Handbook of Practical Neurophysiotherapy

HANDBOOK OF
PRACTICAL NEUROPHYSIOTHERAPY
HANDBOOK OF
PRACTICAL NEUROPHYSIOTHERAPY
Pushpal K Mitra
B Sc Physiotherapy, MD (Alt. Med.) MIAP
Senior Faculty, NIOH, Kolkata, India
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Handbook of Practical Neurophysiotherapy
© 2009, Pushpal K Mitra
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted
in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior
written permission of the author and the publisher.
This book has been published in good faith that the material provided by author is original. Every effort is
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any inadvertent error(s). In case of any dispute, all legal matters are to be settled under Delhi jurisdiction
only.
First Edition: 2009

ISBN: 978-81-8448-693-3
Typeset at JPBMP typesetting unit
Printed at
To
My dear students and patients
from whom I have learnt all
that I know and wish to share
the same through my writings
PREFACE
Our nervous system is the most complex of all living organisms on the
planet earth, consisting of maze of very delicate tissues, which are
responsible for regulation and coordination of virtually each and every
function in our body. It is this nervous system, consisting of a highly
evolved brain, a sophisticated spinal cord and a vast network of peripheral
nerves, that is more complicated than the processor of a super computer,
which has given us the edge to evolve as the most successful species
among all others in the creation. It is our nervous system, particularly
our brain, which has given us the consciousness of our identity, our
thought, and ultimately our soul. However, in spite of all the advances
that we have made over the past century in the field of science and
technology, it is only in recent years that we are beginning to understand
how all the components of the nervous system fit together and work as
a cohesive unit.
Being extremely delicate and highly specialized, nervous tissue can
be easily damaged, often irreversibly, due to different causes, ranging
from trauma to infection to degeneration. In clinical practice, neurological
disorders pose the greatest challenge to a physiotherapist. This is not
only due to the complexity of the nervous system, but also due to the
diversity of clinical presentation, response and outcome of treatment. As
such two similar cases may turn out to be totally different. As a result,
long-term morbidity and physical disability is frequently associated with
neural disorders. To treat such disorders a team approach is essential,
where along side physicians and nurses, a physiotherapist, especially
skilled in the art of Neuro-rehab can render yeoman service.
Neuro-physiotherapy is a niche specialty area, concerned with
acquiring of specialized skill sets to evaluate, quantify, plan and execute
appropriate interventions, to minimize the extent and severity of the
dysfunction arising from a neurological disorder.
Since neurological patients with moderate to severe dysfunction forms
the staple case load for any physiotherapy set up, the author, in his third
offering to the students and practitioners of this noble art, has opted to
pen down his humble views on the physiotherapy principle and
techniques of managing neurogenic dysfunctions.
viii Handbook of Practical Neurophysiotherapy
Along with time tested methods adopted in dealing with neurological

disorders, many concepts in management that have been proposed in
this volume are relatively new and may be, at times, unfamiliar to the
reader. As in the case of the preceding two volumes in the handbook
series, I have made every attempt to make this volume as free of factual
errors as possible. However, I shall be eternally grateful for any feedback
from the readers regarding the quality and the veracity of the information
presented in this volume.
If you like this volume as much as you did my previous publications
in the series of handbooks, that alone shall be my ample reward.
Pushpal K Mitra
ACKNOWLEDGEMENTS
I wish to thank my dear friend Dr Sanjay Sahu, MD, for contributing the
excellent radiographic material along with their interpretations, which in
my view has added new dimensions to this volume.
I humbly acknowledge the of eager anticipation of my beloved
students, encouragement of my colleagues and the support of Dr Ratnesh
Kumar, Director, NIOH, for providing the motivation to present this
volume, third in the series of handbooks on practical aspects of
physiotherapy.
CONTENTS
1. Rehabilitation Process of the Neurological Disorders ....................... 1

2. A Primer to the Anatomy of the Nervous System ................................. 6
3. Essentials of Neurological Assessment ...............................................27
4. Fundamentals of Neuroimaging and Electrodiagnosis ....................49
5. Physiotherapy in Neurological Dysfunctions ....................................72
6. Disorders of the Brain: CVA, TBI and Brain Tumors ...................... 105
7. Parkinsonism ....................................................................................... 153
8. Disorders of the Spinal Cord ............................................................. 184
9. Disorders of the Peripheral Nerves ................................................... 242
10. Disorders of Balance, Coordination and Equilibrium .................... 288
11. Cerebral Palsy ...................................................................................... 317
Annexures .............................................................................................. 339

Index ...................................................................................................... 363
Rehabilitation Process of
1 the Neurological Disorders
INTRODUCTION
The human nervous system is a complex maze of very delicate tissues.
In spite of all the advances that we have made over the past century in
science and technology, using latest techniques of imaging, and advanced
laboratory tests, it is only for past few years that we are beginning to
understand how all the components of the nervous system fit together
and work as a cohesive unit.
Nervous tissues can be easily damaged, often irreversibly, due to
different causes. The ranges of disorders that affect the nervous system
are very wide. In clinical practice, neurological disorders pose the greatest
challenge. This is not only due to the complexity of the nervous system,
but also due to the fact that the diversity of presentation, patient response
and outcome of treatment in two similar cases may turn out to be totally
different. As a result, long-term morbidity and physical disability is
frequently associated with neural disorders.
Points to Ponder
• Accurate assessment of a neurological disorder is the foundation for
successful rehabilitation.
• Assessment helps the clinician to draw up a problem list, which can
then be addressed in a logical sequence.
• Though neurogenic dysfunctions can be divided into broad categories
like UMN and LMN syndromes, each neurological patient is unique,
as are the problems faced by him or her.
• Such a patient needs the expertise of professionals from different
specialties to solve these problems, so that he/she can get back to
near normal life. It is like fitting the pieces of a jigsaw puzzle together,
until the whole picture emerges.
• Satisfactory outcome of any neurological dysfunction can only be
achieved by a multidisciplinary, holistic approach; by addressing the
physical impairments, behavioral problems, associated medical issues,
anxiety, depression and socio-economic concerns of the patient.
2 Handbook of Practical Neurophysiotherapy
• Psychological support and physical rehabilitation go hand-in-hand,

because unresolved psychological issues, like post-traumatic stress
disorder (PTSD) may contribute to or exacerbate any physical
disability.
• Discharge to home or transfer to the local hospital from a referral
hospital should be anticipated well in advance and must only be
undertaken when the patient’s rehabilitation needs can be adequately
provided for at their local or community level.
• Joint therapy sessions between the patient’s current therapists, with
whom the patient and the family can become much attached and the
therapists who will be involved in the long-term rehabilitation
following discharge or transfer will facilitate the ease of transition of
care.
• Most survivors of neurological disorders may regain basic function
of affected parts and may achieve acceptable functional ambulation,
depending upon the severity of the lesion, although this may take up
to two years of close nursing and therapy and even then the patient
may never be completely normal. This factor has to be made clear to
the patient and the family, so that false hopes are not nurtured.
NEURO REHAB TEAM

The rehabilitation of a patient with neurological dysfunction needs the
involvement of a team of professionals. Such a team is commonly led by
the Neuro physician/surgeon, assisted by the Nursing staff,
Physiotherapist, Occupational therapist, Orthotist, Speech therapist,
Clinical psychologist, and Social and Vocational counselors.
Physiotherapy—Role and Scope

• The physiotherapist should be involved in the primary care of the
patient from the time of admission. This helps familiarize the therapist
to the problems of the patient right from the beginning.
• In the acute stage, chest physiotherapy may help to prevent atelectasis
and pooling of secretions in the lungs of a patient, who has lost
consciousness or may be unable to breath deeply enough or cough
effectively due to the weakness of respiratory muscles.
• Passive physiotherapy is important in the mobilizing of the
unconscious/paralyzed patient, preventing contractures (with early
and appropriate splinting), and slow down muscle wasting (through
massage and electrical stimulation).
• As the patient gains some power and control over his movements,
Orthosis may be used primarily to prevent deformities and
secondarily to help the patient regain functional independence.
• At some stage during rehabilitation, the rate of recovery will slow
down and it is often at this stage that the patient will be discharged
home.
Rehabilitation Process of the Neurological Disorders 3
• Before discharge from a health care institution, a program of exercises

or activities to be carried on at home should be taught to the caregiver
by the physiotherapist.
• Fatigue may become more evident as more and more activities are
taken on. The patient and their families should be forewarned of this
phenomenon.
• Patients should not attempt to resume their former activities or sports
without clearance from the therapist. It is important to re-integrate
the patient slowly into “normal” activities.
• Exercising too quickly leads to fatigue. This fatigue may become
chronic and subsequently difficult to overcome.
• Swimming as in hydrotherapy, walking and cycling are all helpful
recreational activities that have positive effects on the long-term
functional recovery of the patient.
• Follow-up should be regular and at least once in every six months
until either complete recovery or a clear plateau in recovery is reached.
Rehab Nurses—Role and Scope

• The rehab nurse is like the conductor of an opera.
• She coordinates various aspects of patient care in hands on manner,
identifying day-to-day problems and monitoring progress.
• She liaises between various team members of the rehab team and
looks after critical executive function as far as administration of drugs,
implementation of positioning, splinting at the right time and manner,
nutrition, as well as, maintenance of hygiene and comfort of the
patient.
• She also acts as the spokesperson for the patient to highlight their
problems and needs to the team.
Occupational Therapist—Role and Scope

• If the physiotherapist is the blacksmith of the human body, the
occupational therapist is the goldsmith.
• Where the Physio is primarily concerned with getting the movement
back to the patient, the occupational therapist ensures that such
movements are precise, coordinated and overall useful for activities
of daily living and vocational engagement.
• This is achieved by the occupational therapist through supervized
implementation of activities to sharpen various motor and sensory
faculties of the patient.
• Fine motor coordination, sensory integration, and adaptations of the
environment are the tools of the trade for the occupational therapist,
which helps in the final and total integration of the disabled into
mainstream of life.
Clinical Psychologist—Role and Scope

• It is important to tell the patient at an early stage that, while
improvement is certain and many people recover completely, 10-
20% is left with residual symptoms, which may be severe in 10%.
Relapses occur in only 10% of patients, usually within two years.
• Physiotherapists need to reinforce the advice of the psychologist,
that major improvement is likely and complete recovery is possible
to reduce the risks of prolonged illness behavior.
• The “acute stress reaction” to any neurological disorder is likely to
be more intense than all other disorders and last longer in some
patients than others. This depends on many factors: severity of the
illness, personality of the patient, the way in which people are given
information about their illness, and practical and emotional support
from professionals and relatives.
• A clinical psychologist should be involved from an early stage, as
soon as sedation has been reduced or withdrawn.
• Most people with neurological disorders, whether or not they make
a good physical recovery, will usually make a good psychological
recovery. A significant number experience severe emotional
disturbance, including anxiety, depression and post-traumatic stress
disorder.
• Embarrassment, self-consciousness, mood swings are not uncommon
and the patients need reassurance during this time.
• Patients should have access to an informed Therapist, GP and a
neurology consultant for follow-up. Ongoing management may
include counseling, anti-depressants, relaxation techniques and graded
exercise.
• The various support groups may provide invaluable support and
counseling because of the “I’ve been through it myself” phenomenon.
• Fatigue may be severe and may persist for years, even after what
appears to have been a full physical recovery and this may contribute
to the development of clinical depression and post-traumatic stress
disorder.
Social and Vocational Counselors—Role and Scope

• Feeling of helplessness and hopelessness overwhelms a breadwinner
when he/she is rendered invalid by any neurological disorder.
• Financial and social implications of such disability are enormous,
often leading to the breakdown of the social and family support
system.
• Counseling the patient to maximize confidence, optimize residual
functional ability and exploring options that can be used to generate
income, even in spite of the disability, is a major task that has to be
shared by the neuro-rehab team.
• Exhaustive planning and training is necessary to take up a new

profession or to even join back in the old one, when one has to cope
with a disability. The Physiotherapist must coordinate with
occupational therapists, social workers; vocational counselors and
placement agencies to put the patient back to work.
• Adverse attitude of some employers may be a hindrance to successful
re-integration of a disabled person in the workforce. A neuro-rehab
team member may be called upon to act as the spokes person for the
disabled, as he/she will be armed with the functional potential of
the client, the evidence of the physical abilities and legislations in
force that assure fair dealing of the disabled in the job market.
Orthotist—Role and Scope

• Wheel chairs or walking aids may be needed on a temporary or
permanent basis.
• Home/school adaptations may be necessary and may include
wheelchair ramps, walking frames on wheels, disabled toilets,
cushioned chairs, etc.
• The capabilities of the carers and extended family should also be
taken into consideration.
• The appropriate aids need to be arranged prior to discharge home.
• Disabled welfare services of state or central government responsible
for disabled education, employment and rehabilitation may provide
financial assistance, aids and appliances. These issues may take
considerable time to organize and plan and should be made weeks
before the expected discharge.
A Primer to the Anatomy
2 of the Nervous System
INTRODUCTION
Successful implementation of any treatment strategy depends on a sound
knowledge of the anatomy and physiology of the concerned system. It is
deemed that most of the readers will have prior working knowledge of
the human nervous system. This chapter is specifically designed to refresh
that knowledge.
The nervous system of any animal, including human, perform the
following primary actions:
• Coordinates the activity of the muscles
• Monitors different systemic organs
• Receives, interprets, initiates appropriate response based on inputs
received from different sense organs.
Nervous system is made of neurons, which, organized into various
discreet functional units such as Central Nervous System, Peripheral
Nervous System and Autonomic Nerveous System, play crucial roles in
coordination of all life processes.
STRUCTURE OF THE BASIC NEURON

The brain is made of approximately 100 billion nerve cells, called neurons.
Neurons have the amazing ability to gather and transmit electrochemical
signals—they are something like the circuit in computer.
Neurons consist of three basic parts (Fig. 2.1):
Cell body: This main part has all of the essential components of the
cell, such as the nucleus (contains DNA), endoplasmic reticulum and
ribosomes (for building proteins) and mitochondria (for making energy).
If the cell body dies, the neuron dies.
Axon: This long, cable-like projection of the cell carries the
electrochemical message (nerve impulse or action potential) along the
length of the cell.
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Fig. 2.1: Basic neuron design, showing a cell body or neuron, its axon with myelin
sheath and the dendrites at the end of the axon. Note the inset showing breaks in
the myelin sheath, the Node of Ranvier.
Depending upon the type of neuron, axons can be covered with a

thin layer of myelin, like an insulated electrical wire. Myelin is made of
fat and it helps to speed transmission of a nerve impulse down a long
axon. Myelinated neurons are typically found in the peripheral nerves
(sensory and motor neurons), while nonmyelinated neurons are found in
the brain and spinal cord.
Dendrites or nerve endings: These small, twig-like projections of the
cell make connections to other nerve cells and allow the neuron to talk
with one another or perceive changes in the environment. Dendrites can
be located on one or both ends of the nerve cell.
Neurons come in many sizes. For example, a single sensory neuron from
your fingertip has an axon that extends the length of your arm, while
neurons within the brain may extend only a few millimeters. Neurons
have different shapes depending on what they do. Motor neurons that
control muscle contractions have a cell body on one end, a long axon in
the middle and dendrites on the other end; sensory neurons have
dendrites on both ends, connected by a long axon with a cell body in the
middle (Fig. 2.2).
Neurons also vary with respect to their functions:
• Sensory neurons carry signals from the outer parts of your body
(periphery) into the central nervous system.
• Motor neurons carry signals from the central nervous system to the
outer parts (muscles, skin, glands) of your body.
Fig. 2.2: Examples of some types of neurons: From left to right (a) Bipolar
interneuron, (b) Unipolar sensory neuron motoneuron (c) Multipolar motor neuron
and (d) Cortical pyramidal cell
• Receptors sense the environment (chemicals, light, sound, touch)

and encode this information into electrochemical messages that are
transmitted by sensory neurons.
• Interneurons connect various neurons within the brain and spinal
cord.
Monosynaptic Reflex Arc

The simplest type of neural pathway is a monosynaptic (single connection)
reflex arc or pathway (Fig. 2.3), like the knee-jerk reflex (Fig. 2.4).
Fig. 2.3: Monosynaptic reflex arc

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Fig. 2.4: The knee jerk reflex: When one taps the right spot on patellar tendon with
a reflex hammer, receptors send a signal into the spinal cord through a sensory
neuron. The sensory neuron passes the message to a motor neuron that controls
quadriceps muscle. Nerve impulses travel down the motor neuron and stimulate
the quadriceps muscle to contract. The sudden knee extension that happens does
not involve the brain
PARTS OF THE NERVOUS SYSTEM

There are three essential parts of the nervous system. These include the
brain, the spinal cord, and the peripheral nerves (Fig. 2.5). Each
organized in discrete but interdependent functional units, forming the
nervous system (Fig. 2.6). The brain has three main parts: the cerebrum,
the cerebellum and the brainstem.
Each part of the brain has specific function.
• The cerebrum looks after high-order thinking, planning and learning
• The cerebellum manages learned automatic bodily functions,
including walking, jumping, and running
• The brainstem processes simple body functions, such as breathing
and digestion.
Brain works like the main server in a telephone network.
The spinal cord is the area where reflexes are made. Split-second decisions
do not go back to the brain and then back to the organ or body part. This
would take too long and the nerve impulse would arrive too late to
prevent the stimulus from becoming reality. For instance, if a ball was
thrown at an individual’s head, the reflex to move out of the way would
come from the spine, not the brain, thus lowering the reaction time. The
spine is also the “highway” which passes inputs from the sensory
receptors to the brain and the commands from the brain to the motor
nerves. It works like the main cable in a telephone network.
Fig. 2.5: The layout of the nervous system
Fig. 2.6: Functional organization of the nervous system

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The peripheral nerves are the telephone lines of the body. They
carry messages in the form of electrical impulses to and from different
parts of the body. There are four kinds of nerves: motor, sensory,
autonomic and interneurons. Messages carried in all nerve types travel
in only one direction.
CENTRAL NERVOUS SYSTEM (CNS)

The central nervous system (CNS) represents the largest and the most
sensitive part of the nervous system and includes the brain and the
spinal cord. Together with the peripheral nervous system, it has a
fundamental role in the control of all body systems. The CNS is contained
within the dorsal cavity, with the brain within the cranial vault, and the
spinal cord in the spinal canal.
The CNS is widely believed as a system devoted to information
processing, where an appropriate response is computed based on a
sensory input. Yet, many threads of research suggest that motor activity
may exist well before the maturation of the sensory systems and that the
senses can only influence response to a certain degree, without dictating
it. This has brought the concept of the CNS as an autonomous entity.
Embryology of the CNS—Sequential Development

• In the developing fetus, the CNS originates from the neural plate, a
specialized region of the ectoderm, and the outermost of the three
embryonic layers.
• During embryonic development, the neural plate folds and forms
the neural tube.
• The internal cavity of the neural tube gives rise to the ventricular
system. The regions of the neural tube differentiate progressively
into transverse systems.
• First, the whole neural tube differentiate into its two major
subdivisions: Brain (rostral/cephalic) and Spinal cord (caudal).
• Subsequently, the cephalic part of the neural tube differentiates into
brainstem and prosencephalon.
• Later, the brainstem subdivides into rhombencephalon and
mesoncephalon, and the prosencephalon into diencephalon and
telencephalon.
• The rhombencephalon gives rise to the pons, the cerebellum and the
medulla oblongata and its cavity becomes the fourth ventricle.
• The mesencephalon gives rise to the tectum, pretectum, cerebral
peduncle and its cavity develops into the mesencephalic duct or
cerebral aqueduct.
• The diencephalon gives rise to the subthalamus, hypothalamus,
thalamus and epithalamus and its cavity to the third ventricle.
• Finally, the telencephalon gives rise to the corpus striatum (caudate
nucleus and putamen), the hippocampus and the neocortex and its
cavity becomes the lateral (first and second) ventricles.
Being extremely sensitive, the entire CNS is protected by the

meninges, a tough fibrous sheath called the duramater, the brain is
protected by the skull vault and the spinal cord by the bony roof of the
vertebrae.
ANATOMY OF THE HUMAN BRAIN

The human brain is the most complex organ in the body. It controls the
CNS and by the way of spinal cord and the PNS, it regulates virtually all
human activity. Involuntary, or “lower,” actions, such as heart beat,
respiration and digestion are unconsciously governed by the brain,
specifically through the autonomia nervous system. Complex, or “higher,”
mental activity, such as memory, thought, and reasoning is consciously
controlled.
The human brain is vast and complex. It contains some one hundred
billion neurons, which are capable of transmitting electrical and chemical
communication from the control center of the brain with tens of thousands
of other nerve cells. Nerve cells in turn rely on some quadrillion (1015)
synaptic connections for their communications.
Anatomically, the brain can be divided into three parts: the forebrain,
midbrain and hindbrain.
• The forebrain includes several lobes of the cerebral cortex that control
higher functions.
• The mid- and hindbrain includes insular and limbic lobes, cerebellum
and the brainstem, which are more involved with unconscious and
autonomic functions.
The cerebral cortex is bulbous in shape, composed of convoluted
grey matter internally supported by deep white matter. The two
hemispheres of the brain are separated by a prominent central fissure
and connect to each other at the corpus callosum. A well-developed
cerebellum is found at the back of the brain. Brainstem structures are
almost completely enveloped by the cerebellum and telencephalon, with
the medulla projecting through the foramen magnum to merge with the
spinal cord (Fig. 2.7).
The weight of adult human brain is typically between 1 and 1.5 kg
(3 lb) and has an average volume of 1.6 liters. The mature human brain
consumes some 20-25% of the energy prduced by the body, while the
developing brain of an infant consumes around 60%.
Blood Supply to Brain

The blood reaches the brain through the vertebral artery and the internal
carotid artery (Fig. 2.8). Both arteries communicating with each other
through the Circle of Willis (Fig. 2.9). Blood drains from the brain through
a network of sinuses that drain into the right and left internal jugular
veins.
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Fig. 2.7: The human brain has two paired hemispheres, each with six distinct lobes,
the frontal, the parietal, the temporal, the occipital, the insular and the limbic. The
brainstem extends below the cerebellum and connects the brain to the spinal cord
Fig. 2.8: The blood supply to brain through the vertebral

artery and the internal carotid artery
Fig. 2.9: The Circle of Willis is an arterial anastomosis supplying blood to the
brain. It is formed by the anterior cerebral arteries, the posterior cerebral arteries,
the anterior artery communicans, the posterior artery communicans and the internal
carotid artery
Protecting the Brain

The primary protection to the brain is provided by the bony skull vault
which encloses this delicate organ. The second layer of protection is
provided by the dura mater, a tough fibrous lining, anchored on the
inner surface of the skull vault. Further, the brain is suspended in
cerebrospinal fluid (CSF), which also fills the space between the skull
vault and the brain, as well as, empty spaces called ventricles inside the
brain. The dense fluid protects the brain and spinal cord from shock.
Movement of fluid within the brain is limited by the blood-brain barrier
and the blood-CSF barrier.
The brain is easily damaged by compression, so the fluid surrounding
the central nervous system must be maintained at a constant volume.
Humans are estimated to produce about 500 ml or more of cerebrospinal
fluid each day, with an estimated 150 ml of CSF at any given time is
located in the ventricles of the brain. The remainder fills the subarachnoid
space, which cushions and separates the delicate tissues of the brain and
spinal cord from the hard surrounding bones of skull vault and vertebrae.
Elevated levels of CSF are associated with inflamation of the brain or the
spinal cord, e.g. traumatic brain injury, spinal cord injury, cerebral
hemorrhage, hydrocephalus etc. Increased fluid pressure for long duration
can result in permanent neural damage to the brain and may lead to
permanent disability or death.
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Why the Volume of CSF should be Limited?
Rigid bony skull prevents the human brain from getting even bigger. At
birth, the human skull is rather soft, and it deforms somewhat during its
passage through the birth canal, then recovers its shape. This allows it to
expand to make room for the growing brain, which continues to grow,
at the same rate as that of an unborn fetus, for an additional year or two.
After the skull sutures have hardened, there is no way that it can
accommodate a larger volume within the skull vault without squeezing
the delicate nerve tissues of the brain. Such squeezing by excess fluid,
creating raised intracranial pressure, whether by blood clot or excess CSF
may have deadly consequences like herniation or irreversible damage to
the brain matter.
Function of the Human Brain
The human brain is the source of the conscious, cognitive mind. The
mind is the set of cognitive processes related to perception, interpretation,
imagination, memory, and crucially language of which a person may or
may not be aware.
The human brain appears to have no localized center of conscious
control (Fig. 2.10). The brain seems to derive consciousness from
interaction among numerous systems within the brain. Midbrain functions
include routing, selecting, mapping, and cataloging information, including
information perceived from the environment and information that is
remembered and processed throughout the cerebral cortex. Endocrine
functions housed in the midbrain play a leading role in modulating arousal
of the cortex and of autonomic systems.
Nerves arising from the brainstem complex, where autonomic
functions are modulated, join nerves routing messages to and from the
cerebrum in a bundle that passes through the spinal cord to related parts
of a body. Twelve pairs of cranial nerves, including some that innervate
parts of the head, follow pathways from the medulla oblongata outside
the spinal cord.
Grey matter, the thin layer of cells covering the cerebrum, was
believed by most scholars to be the primary center of cognitive and
conscious processing. White matter, the mass of glial cells that support
the cerebral grey matter, was assumed to primarily provide nourishment,
physical support, and connective pathways for the more functional cells
on the cerebral surface. But recent research suggests that glial cells serve
a computational role beyond merely transmitting processed signals
between more functional parts of the brain, which in part contributes to
the human consciousness.
Fig. 2.10: The frontal lobe of the brain is concerned with personality, emotions,
problem solving and reasoning powers. The parietal lobe concerns the motor and
sensory abilities of the individual. The temporal lobe controls language, speech
and hearing, whereas the occiputal lobe controls the vision. The cerebellum is
responsible for balance and co-ordination of movements and the brain stem
regulates basic body functions like respiration, heart beat etc. Different areas of
the human brain represent various functions, though the human consciousness is
sum total of all these functions, hence can’t be localized
CRANIAL NERVES
Cranial nerves are nerves that emerge directly from the brain. Although
thirteen cranial nerves in humans fit this description, twelve are
conventionally recognized. The nerves from the third onward arise from
the brainstem. Except for the tenth and the eleventh nerve, they primarily
serve the motor and sensory systems of the head and neck region.
The twelve pairs of cranial nerves are traditionally abbreviated by
the corresponding Roman numerals. They are numbered according to
where their nuclei lie in the brainstem, e.g. Cranial Nerve III (the
Oculomotor nerve) leaves the brainstem at a higher position than Cranial
nerve XII, whose origin is located more caudally (lower) than the other
cranial nerves. Please refer to Annexure 5 for details of cranial nerves,
their function and testing methods.
SPINAL CORD
The spinal cord is a thin, tubular structure that is an extension of the
CNS from the brain and is enclosed in and protected by the bony vertebral
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coloumn. The main function of the spinal cord is transmission of neural

inputs between the periphery and the brain.
Structure of the Spinal Cord

The spinal cord extends from the medulla oblongata in the brainstem up
to the conus medullaris near the lumbar level at L1-2, terminating in a
fibrous extension known as the filum terminale. The spinal cord is about
45 cm long in men and 43 cm long in women, ovoid-shaped, and is
enlarged in the cervical and lumbar regions. The peripheral regions of
the cord contain neuronal white matter tracts containing sensory and
motor neurons. The central region is four-leaf clover shaped that
surrounds the central canal (an anatomic extension of the fourth ventricle)
and contains nerve cell bodies, motor nerve roots exiting in the ventral
aspects and sensory nerve roots entering in the dorsal aspects. The ventral
and dorsal roots later join to form paired spinal nerves, one on each side
of the spinal cord (Fig. 2.11).
The three meninges that cover the spinal cord — the outer dura
mater, the arachnoid membrane, and the innermost pia mater—are
continuous with that in the brainstem and cerebral hemispheres, with
CSF found in the subarachnoid space. The cord within the pia mater is
stabilized within the dura mater by the connecting denticulate ligaments
which extend from the pia mater laterally between the dorsal and ventral
roots.
Fig. 2.11: Structure of spinal cord and its cross-sectional diagram showing motor
and sensory nerves arising from the ventral and the dorsal horns
Spinal Cord Segments

There are 31 spinal cord nerve segments in a human spinal cord (Fig. 2.12):
• 8 cervical segments
• 12 thoracic segments
• 5 lumbar segments
• 5 sacral segments
• 1 coccygeal segment
Because the vertebral column grows longer than the spinal cord, spinal
cord segments become higher than the corresponding vertebra, especially
in the lower spinal cord segments in adults. In a fetus, the vertebral
levels originally correspond with the spinal cord segments. In the adult,
the cord ends around the L1/L2 vertebral level at the conus medullaris,
with all of the spinal cord segments located superiorly to this. For example,
the segments for the lumbar and sacral regions are found between the
vertebral levels of T9 and L2. The S4 spinal nerve roots arise from the
cord around the upper lumbar/lower thoracic vertebral region, and
Fig.2.12: Spinal cord segments

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descend downward in the vertebral canal. After they pass the end of the
spinal cord, they are considered to be part of the cauda equina.
There are two regions where the spinal cord enlarges:
• Cervical enlargement—corresponds roughly to the brachial plexus
nerves, which innervate the upper extremities. It includes spinal cord
segments from about C4 to T1. The vertebral levels of the enlargement
are roughly the same (C4 to T1).
• Lumbosacral enlargement—corresponds to the lumbosacral plexus
nerves, which innervate the Lower extremities. It comprises of the
spinal cord segments from L2 to S3, and is found about the vertebral
levels of T9 to T12.
Embryology
In the human fetus, the spinal cord develops from the nural tube and
extends all the way down to the sacral vertebrae. As a person matures,
the rest of the body grows faster than the spinal cord, so that by adulthood,
the spinal cord reaches only to the level of the first or second lumbar
vertebrae. There is no spinal cord below this level, only the individual
spinal nerves that form the cauda equina.
Injury
Spinal cord injuries can be caused by falling on the neck or back, or
having the spinal cord moved or disrupted in another way. The vertebral
bones or intervertebral disks can shatter, causing the spinal cord to be
punctured by a sharp fragment of bone. Usually victims of spinal cord
injuries will suffer loss of feeling in certain parts of their body. In milder
cases a victim might only suffer loss of hand or foot function. More
severe injury may result in paraplegia, tetraplegia, or full body paralysis
below the site of injury to the spinal cord. The two areas of the spinal
cord most commonly injured are the cervical spine (C1-C7) and the lumbar
spine (L1-L5).
PERIPHERAL NERVOUS SYSTEM

The peripheral nervous system or PNS, is a part of the nervous system,
and consists of the nerves and neurons that extend outside the CNS. The
peripheral nervous system, made up of nerves arising from the spinal
cord, is divided into the somatic and autonomus nervous systems. Unlike
the CNS, however, the PNS is not protected by bone or the blood-brain
barrier, leaving it exposed to toxins and mechanical injuries.
Spinal nerves originate from the spinal cord. They control the
functions of the rest of the body. In humans, there are 31 pairs of spinal
nerves: 8 cervical, 12 thoracic, 5 lumber, 5 sacral and 1 coccygeal. By
convention, a spinal nerve root is named after the vertebra immediately
above it. Thus the fourth thoracic nerve root originates just below the
fourth thoracic vertebra. This convention breaks down in the cervical
spine. The first spinal nerve root originates above the first cervical
vertebra and is called C1. This continues down to the last cervical spinal
nerve root, C8. There are only 7 cervical vertebrae and 8 cervical spinal
nerves.
Myotome and Dermatomes

Spinal nerves have motor fibers and sensory fibers. The motor fibers
innervate certain muscles, while the sensory fibers innervate certain areas
of the skin. A skin area innervated by the sensory fibers of a single nerve
root is known as a dermatome. A group of muscles primarily innervated
by the motor fibers of a single nerve root is known as a myotome.
Each muscle in the body is supplied by a particular level or segment
of the spinal cord and by its corresponding spinal nerve. The muscle and
its nerve make up a myotome (Fig. 2.13).
Dermatomes
Dermatome is a Greek word which literally means “skin cutting”. A
dermatome is an area of the skin supplied by nerve fibers originating
from a single dorsal nerve root. The dermatomes are named according
to the spinal nerve which supplies them. In diagrams or maps, the
boundaries of dermatomes are usually sharply defined. However, in real
life there is considerable overlap between adjacent dermatomes.
Dermatome and myotome correspond closely to each other, hence
knowing the dermatome will guide the clinician to appropriate myotome
in most cases. Please refer to Annexure 7 for dermatome map of the
human body.
Fig. 2.13: Myotome
Spinal Nerve Plexus

A plexus resembles an electrical junction box, which distributes wires to
different parts of a house. Much like the electrical junction box in a
house, a nerve plexus is a network of interwoven nerves. In a plexus,
nerve fibers from different spinal nerves are sorted and recombined so
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that all fibers going to a specific body part are put together in one nerve.
Damage to nerves in the major plexuses causes problems in the arms or
legs that these nerves supply. The major plexuses are the brachial plexus,
which is located in the neck and distributes nerves throughout the arms,
and the lumbo-sacral plexus, which is located in the lower back and
distributes nerves to the pelvis and legs (Fig. 2.14). Please refer to
Annexure 6 for details selected spinal nerves and their function.
Fig. 2.14: Four nerve plexuses arise from the spinal cord
• The cervical plexus provides nerve connections to the head, neck,

shoulder and diaphragm.
• The brachial plexus provides connections to the chest, shoulders,
upper arms, forearms, and hands.
• The lumbar plexus provides connections to the back, abdomen, groin,
thighs, knees, and calves.
• The sacral plexus provides connections to the pelvis, buttocks, genitals,
thighs, calves, and feet. Because the lumbar and sacral plexuses are
interconnected, they are sometimes referred to as the lumbo-sacral
plexus. The spinal nerves in the chest do not join a plexus; they are
called the intercostals, which are located between the ribs.
Cervical Plexus
The nerves formed by the cervical plexus supply the back of the head,
the neck and the shoulders (Fig. 2.15). The C1 posterior primary ramus
does not usually supply the skin. The C2 posterior primary ramus forms
the greater occipital nerve which supplies the posterior scalp. The upper
four anterior primary rami form the cervical plexus. The cervical plexus
supplies the skin over the anterior and lateral neck to just below the
clavicle. The plexus also supplies the muscles of the neck including the
scalene, the sternocleidomastoid muscles, and the diaphragm.
The lesser occipital, greater auricular, transverse cervical and
supraclavicular are cutaneous nerves formed by the cervical plexus. They
lie in the posterior triangle and emerge around the posterior border of
the sternocleidomastoid to supply the skin. The supraclavicular nerve
forms medial, intermediate and lateral branches in the posterior triangle
to run over the clavicle to innervate the skin.
The deep branches of the cervical plexus innervate muscles. The
fibers from C1 innervate the deep muscles of the neck. Fibers from C2, 3, 4
Fig. 2.15: Nerves formed by the cervical plexus

1. Spinal accessory nerve
2. Supraclavicular nerve
3. Transverse cervical nerve
4. Great auricular nerve
5. Lesser occipital nerve
6. Greater occipital nerve
7. Facial nerve
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supply sternocleidomastoid, Trapezius and Levator scapulae muscles.

The spinal accessory nerve also supplies sternocleidomastoid and
trapezius. The Phrenic nerve is formed by fibers from C3, 4, 5. The right
and left Phrenic nerves pierce the diaphragm to supply it. The phrenic
nerve also supplies the mediastinal pleura with sensory fibers.
Brachial Plexus
The brachial plexus is an arrangement of nerves (a plexus) arising from
C5 to T1 nerve roots, through the neck, the axilla and into the arm. All
nerves of the arm stem from the brachial plexus. Please refer to Annexure
8 for nerves of the brachial plexus and muscles supplied by them.
Therefore, lesions of the plexus can lead to severe functional impairment
of the upper extremities.
The brachial plexus starts from the five anterior rami of the spinal
nerves, after they have given off their segmental supply to the muscles
of the neck. These are the five roots. These roots merge to form three
trunks;
• “Upper” C5-C6
• “Middle” C7
• “Lower” C8-T1.
Each trunk then splits to form an anterior and a posterior division.
These six divisions will regroup to become three cords. The cords are
named by their position in respect to the axillary artery (Fig. 2.16).
• The posterior cord is formed from the three posterior divisions of the
trunks.
• The lateral cord is made of the anterior divisions from the upper and
middle trunks.
• The medial cord is simply a continuation of the lower trunk.
Injuries to the Brachial Plexus

The brachial plexus is susceptible to injuries that are produced by
abduction/traction of the upper limb from the body wall or a direct blow
to the lateral surface of the scapula. Two injuries types are recognized in
brachial plexus injuries: Traumatic and Obstetric. Traumatic injuries often
are the result of high velocity RTA’s (Road Traffic Accidents). The most
common form of injury are the motorcycle drivers falling, with either the
head/neck pushed to the side (upper plexus lesions) or with their arm
abducted (stretched upwards) which produces a lower plexus injury.
The cardinal signs of brachial plexus avulsion are:
• Weakness in the arm
• Diminished reflexes
• Corresponding sensory deficits
Fig. 2.16: Brachial plexus
Mechanism of Injury
Since the meningeal coverings of the nerve roots are thinner than those
in the peripheral nerve, the nerve roots are stretched or torn from their
origin by traction trauma. The epineurium of the peripheral nerve is
contiguous with the dura mater, providing extra support to the peripheral
nerves. In cases where the nerve roots have been torn, recovery is unlikely
without new experimental surgical techniques.
The diagnosis may be confirmed by an electromyography and nerve
conduction examination after 3-5 days of injury. The evidence of
denervation will be evident. If there is no nerve conduction 72 hours
after the injury, then root avulsion is most likely.
Lumbo-sacral Plexus
Lumbo-sacral plexus is derived from L4-5 and S1-2-3-4 roots, each giving
rise to anterior and posterior branches. Anterior branches supply flexor
and posterior branches supply extensor and abductor muscles of lower
limbs (Fig. 2.17).
• Superior gluteal nerve having root value of L4 and 5 supplies G
Medius, G Minimus and Tensor fascia latte.
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Fig. 2.17: Lumbo-sacral plexus
• Inferior gluteal nerve having root value of L5, S1 and S2 supplies G.

Maximus.
• Small nerves arising from L4, 5, S1, 2 and 3 supply lateral rotators of
the hip excluding obturator externus, which is innervated by
Obturator nerve.
• Sciatic nerve is the largest nerve arising from lumbo-sacral plexus,
which supplies the hamstrings and all muscles of the ankle and foot.
• Pudendal nerve, supplying the perineum and external genital organs
arises from the ventral rami of S2-S4
Injury of Lumbo-sacral Plexus

Lumbo-sacral plexus is commonly injured with pelvic ring trauma,
involving the nerve roots arising from L4 and 5 portions of the lumbo-
sacral trunk.
AUTONOMIC NERVOUS SYSTEM (ANS)

ANS is a part of the PNS that maintains the constant level of gasses, ions
and nutrients in tissues, so essential for survival. This essential act is
done mostly by the ANS without conscious effort or volition. It does so
mostly by controlling cardiovascular, digestive, endocrine and respiratory
functions, but also salivation, perspiration, vasodilatation, vasoconstriction,

adjusting the diameter of the pupils depending upon the ambient light,
micturition of urine, and erection. Most of the activities of the ANS are
involuntary. However, breathing, for example, can be in part consciously
controlled. Indeed, although breathing is a purely homeostatic function
in aquatic vertebrates, in land vertebrates it accomplishes much more
than oxygenating the blood: it is essential to sniff a prey or a flower, to
blow a candle, to talk or sing. This example, among others, illustrates
that the so-called “autonomic nervous system” is not truly autonomous.
It is anatomically and functionally linked to the rest of the nervous system
and a strict delineation is impossible.
The ANS is nevertheless a classical term, still widely used throughout
the scientific and medical community. Its most useful definition could
be: The sensory and motor neurons that innervate the viscera. These
neurons form reflex arcs that pass through the lower brainstem. This
explains that when the central nervous system (CNS) is damaged above
brainstem level, a vegetative life is still possible, because cardiovascular,
digestive and respiratory functions are still working.
Function
Sympathetic and parasympathetic divisions of the spinal nerves typically
function in opposition to each other. But this opposition is better termed
complementary in nature rather than antagonistic. For an analogy, the
sympathetic division works as the accelerator and the parasympathetic
division as the brake. The sympathetic division typically functions in
actions requiring quick responses. The parasympathetic division functions
with actions that do not require immediate reaction. Consider sympathetic
as “fight or flight” and parasympathetic as “rest and digest”.
Generally, these two systems should be seen as permanently
modulating vital functions, in usually antagonistic fashion, to achieve
homeostasis or balance in the physiology of the organism. Some typical
actions of the sympathetic and parasympathetic systems are listed in
Annexure 9.
Essentials of Neurological
3 Assessment
Accurate clinical assessment is the key component in the care of a

neurological patient. It can help the therapist to:
• Detect the presence of a neurological disease or injury
• Shortlist the nature of problems created by the disease or injury
• Monitor progression of the disorder
• Determine the type of care the patient needs, and the expected
outcome of therapeutic interventions.
The initial assessment of a patient with neurogenic dysfunction should
be a comprehensive clinical examination, covering following critical areas
concerning the function of the nervous system:
• Level of consciousness and orientation
• Function of cranial nerves
• Presence or lack of movement
• Presence or lack of sensation
• Cerebellar function, indicated by the presence or lack of balance
• Presence or lack of coordination
• Muscle tone, power, deep tendon and superficial reflexes.
This initial examination will establish baseline data with which to
compare subsequent assessment findings. Once a thorough neurological
examination has been done at the time of admission or at the beginning
of physiotherapy intervention, subsequent assessments should be
problem-oriented, focusing only on the parts of the nervous system
affected by the patient’s condition. The patient’s diagnosis and the acuity
of the clinical condition will determine how extensive the problem-
oriented assessments will be and how frequently it will need to be
repeated. On an average, the review assessments may be done every
three weeks.
ASSESSMENT OF NEUROLOGICAL DISORDERS

The crisis of the neurological system can be the most challenging to
monitor and evaluate. This is because of the inability of medical science
to control neurological symptoms as easily as we do in case of the
cardiopulmonary or gastrointestinal crisis. The neurological system is

still quite out of our control. Sometimes, the only option is to allow a
neurologically compromised person to die, while monitoring, charting
the progression, reporting to the physician, and holding the hands of
those involved. The therapist and the nurse are essential participants in
these processes. Whether it’s a brief check of neurological status or a
comprehensive neurological evaluation, in a crisis your assessment may
uncover critical nervous system dysfunction before it is too late.
Three key aspects of the neurological assessment are:
• The interview
• The physical examination
• The specific diagnostic tests.
History Taking: The Art of Interviewing the Patient/Care-giver

History taking is not about hearing, but about really listening to the
patient. One of the most essential skills for a clinician is the ability to
listen to the account of the sufferer, stated as far as possible in his or her
own words, with undivided attention, trying to hear what is being said
and even what may remain unsaid. Only then a clear picture of the
sequence of events leading to the present problems affecting the patient
may be ellicitated, based on which the clinician may develop a working
hypothesis about the disorder in question. In many cases, the neurological
patient is disoriented or unable to talk. It may be necessary to obtain the
interview from the patient’s family or close friend.
Key Questions
Ask the patient/relative if there is any:
• A history of past neurological disorders
• Record in detail the description of the development of the current
signs and symptoms
• Ascertain the time of onset, the duration of signs and symptoms
• The precipitating factors and the sequence of signs and symptoms
• Question if there were any recent illnesses, such as a head cold or
sore throat
• Document the patient’s medications, both prescribed and over the
counter, including vitamins and herbal remedies
• Conclude the interview with a review of symptoms.
Any or all the preceding information collected during the interview
may give clues to the cause of the neurological damage.
• For example, if the patient has a history of chronic atrial fibrillation
and does not adhere to his anticoagulant drug regime, this may
explain why he developed CVA.
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Assessment 29
While interviewing the patient, be careful not to suggest symptoms,

with close ended questions such as:
“Do you have a stabbing headache?”
Instead use open-ended sentences, such as:
“Can you describe the type of pain you are feeling in your head?”
Note down the details, as far as possible, in own words of the patient.
The precipitating factors, mode of onset and the course of the current
illness are particularly important. Document the progression of the signs
and symptoms. While interviewing a relative, be sure that the person
who is giving the information is oriented and knowledgeable of the
patient’s problems and current illnesses.
In particular, inquire if the patient has a history of diabetes mellitus,
pernicious anemia, cancer, chronic infections, thyroid disease,
hypertension or any addiction, since these factors may affect the nervous
system.
Medication, prescribed by a doctor or obtained by the patient over
the counter, may be significant in producing neurological symptoms. A
person with history of chronic neurological disease may be taking
antiseizure medications such as Phenobarbital, Carbamazepine (Tegretol),
or Phenitoin (Dilantin), which may give rise to some neurological
symptoms such as diplopia, ataxia, drowsiness or mental slowing. These
side effects may be misinterpreted by the patient and cause non-
compliance with the regime of medication. Document the medication,
dosage, schedule and when the patient last took the medication.
Points to Ponder
• Note the onset, progression and the nature of the presenting
symptoms to get an insight into the condition you are dealing with.
• Check the past history to identify other pre-existing conditions,
surgeries and health related issues.
• Take note of the social history to specify current living conditions,
family/social support, level of education, employment and lifestyle
of the patient.
GENERAL EXAMINATION OF NEUROLOGICAL DISORDERS

OBSERVATIONS
Level of Consciousness (LOC)
The single most important aspect of neurological assessment is the
assessment level of consciousness and cognition. Worsening of either
indicates deteriorating neurological status.
Points to Ponder
The following terms are commonly used to describe various stages of
decreased LOC, so it is useful to be familiar with them:
• Full consciousness: The patient is alert, attentive, and follows
commands. If asleep, he responds promptly to external stimulation
and, once awake, remains attentive.1
• Drowsiness: The patient is drowsy but awakens—although not fully—
to stimulation, he will answer questions and follow commands, but
will do so slowly and inattentively.1
• Semi conscious: The patient is difficult to arouse and needs constant
stimulation in order to follow a simple command. He may respond
verbally with one or two words, but will drift back to sleep between
stimulation.
• Stupor: The patient arouses to vigorous and continuous stimulation;
typically, a painful stimulus is required. He may moan briefly but
does not follow commands. His only response may be an attempt to
withdraw from or remove the painful stimulus.
• Coma: The patient does not respond to continuous or painful
stimulation. He does not move—except, possibly, reflexively—and
does not make any verbal sounds.
Since these and other terms used to categorize LOC are frequently
used imprecisely, you’d be wise to avoid using them in your
documentation, instead, describe how the patient responds to a given
stimulus. For example, write: “the patient moans briefly on painful
stimulus, but does not open eyes or follow commands.” Bear in mind
that recognizing and describing a change in LOC is more important than
appropriately naming it.
When assessing LOC, there are several tools you can choose from.
Typically, though, it is the Glasgow Coma Scale (GCS) that is dedicated
and internationally accepted neurological assessment tool. It’s especially
useful for evaluating patients during the acute stages of head injury.
Glasgow Coma Scale (See Annexure 1)

The Glasgow Coma Scale allows us a standard reference for monitoring
or assessing a patient with confirmed or suspected brain damage. A GCS
score is based on three patient responses to stimuli:
• Eye opening
• Motor response
• Verbal response.
To each of these responses, a score is assigned and the GCS is interpreted
as follows.
Scoring of GCS
• The patient receives a score for best response in each of these areas,
and the three scores are added together.
Assessment 31
• The total score will range from 3 to 15; the higher the number, the
better the level of consciousness.
• A score of 8 or lower usually indicates coma.
• A score of 15 is the highest, and 3, the lowest.
• An awakened person, who has orientation to person, time and place,
and can also follows simple commands, such as squeeze my hand,
has a Glasgow score of 15.
• A patient, oriented to self, but not to time and place, yet follows all
simple commands, has a score of 14.
• An aphasic person may score a 2 on verbal response, but then total
a twelve, as he will follow simple commands and open eyes
spontaneously.
Any change in the level of consciousness is an important indicator of a
person’s neurological status. Impaired cerebral blood flow results in an
altered LOC. Frequent assessments are necessary on the person at risk,
because the sooner the neurological compromise is recognized, the better
the prognosis.
Orientation
If the patient is alert or awake enough to answer questions, you’ll also
need to assess orientation. Determine if he is oriented to person, place,
and time by asking questions like: What is your name? Where are you right
now? Why are you here? What year is it? Who is the president of India?
A comprehensive evaluation of orientation will include tests of higher
intellectual function, as well. To test abstract reasoning, for example, you
might ask the patient to interpret a well-known proverb.
Abnormal posturing
Abnormal flexion or extension of the head, neck, trunk and limbs are
ominous signs of central nervous system malfunction.
Abnormal flexion or Decorticate posture is an abnormal body posture
indicated by adducted and flexed arms, with the wrists and fingers flexed
on the chest, the legs internally rotated and stiffly extended, with plantar
flexion of the feet (Fig. 3.1).
Fig 3.1: Decorticate posture

Decorticate posture indicates damage to the corticospinal tract, the

pathway between the brain and spinal cord. Although a serious sign, it
is usually more favorable than decerebrate posture. Decorticate posture
may progress to decerebrate posture, or the two may alternate. The
posturing may occur on one or both sides of the body.
Common Causes of Decorticate Posturing

• Brain abscess
• Primary brain tumor
• Secondary brain tumor
• Increased intracranial pressure from any cause
• Stroke
• Head injury.
Abnormal Extension or Decerebrate posturing is an abnormal body
posture indicated by rigid extension of the arms and legs, downward
pointing of the toes, and backward arching of the head. A severe injury
to the brain at the level of the brainstem is the usual cause (Fig. 3.2).
Common Causes of Decerebrate Posturing

• Cerebral infarction (stroke)
• Intracranial hemorrhage
•· Primary brain tumor
• Secondary brain tumor
• Encephalopathy
• Head injury
• Increased intracranial pressure from any cause
• Brainstem tumor
• Hepatic encephalopathy.
Points to Ponder
• Opisthotonus, a severe muscle spasm of the neck and back may
accompany decerebrate posture in severe cases.
• Usually, decerebrate posture indicates organic damage to the
structures of the nervous system, particularly the upper brainstem.
• Decerebrate posture may occur in many patterns. It can occur on one
side, on both sides, or in just the arms.
Fig. 3.2: Decerebrate posturing

Assessment 33
• It may alternate with decorticate posture, i.e. abnormal posturing

due to corticospinal tract injury.
• A person can have decorticate posture on one side and decerebrate
posture on the other.
• The key difference between the two terms, is that in decorticate the
upper limbs are flexed inward towards the center of the body, i.e.
toward the core of the body.
• Generally speaking, with both decorticate and decerebrate posturing,
the patient is either non-responsive or responds to pain stimulus by
adopting abnormal posture.
Abnormal Pupillary Reactions

Pupils are another important component of the neurological examination.
Assessing them is especially important in a patient with impaired LOC.
Like a change in LOC, a change in pupil size, shape, or reactivity can
indicate increasing intracranial pressure (ICP) from a mass or fluid.
Always check pupils as part of the cranial nerve assessment.
Points to Ponder
• The therapist will need to frequently assess the pupils of the patient
at risk neurologically.
• If the patient is unable to open the eyes to request, gently lift the
upper lids.
• Compare the two pupils for size, shape and equality.
• Utilize a chart in order to evaluate pupil size more precisely.
• The pupil size ranges from 1 to 6 millimeters.
• Unequal pupils are not always abnormal. Additionally, eye surgery
may have altered the shape and size of the pupil.
Method of Testing the Pupillary Reaction

• Obtain a penlight and darken the room to assess the pupils’ direct
light response.
• Hold one eyelid open and shine the light directly into the eye. The
pupil will constrict immediately.
• When the light is removed, the pupil will dilate immediately.
• Now ask the patient to hold both eyes open, shine the light into one
eye and watch for consensual response. Normally, the eye not
exposed to light will also constrict.
• To assess accommodation, hold a finger six inches from the patient’s
nose. Ask the patient to focus on the finger, then to focus on an
object farther away, such as a wall clock. The pupils should dilate as
they focus on objects farther away, and constrict when the object is
closer.
• The assessment of pupils is not always easy. It may be difficult to see

the pupils clearly on people with dark eyes. If you are unsure, ask
for a second opinion, particularly if you notice other neurological
alterations. The extra effort you make may save your patient’s life.
ASSESSMENT OF VITAL SIGNS

Though it is a common convention that vital signs are checked and
monitored by physicians and nurses, the therapist attending an unstable
patient in ICU, with a neurological disorder, must be aware of and be
able to interpret changes in vital signs to alert the physician in time to
prevent a crisis.
Points to Ponder
• Slower heart rate, widening of pulse and irregular respiration, known
as Cushing’s triad, may be present in CVA or TBI, along with a
change in body temperature. These are indications of active
inflammatory changes taking place in the CNS and should be watched
very carefully during therapy.
• Detailed documentation and prompt reporting of any change in LOC,
Pupilary reaction, BP, Pulse rate, SaO2 and ECG trace is necessary to
alert others of the patient’s current status, so any subtle changes will
be obvious.
• At times, it may be tempting to allow a neuro-patient to sleep through
a neuro-check, but “the sleep” may be end up being permanent if
neuro-checks aren’t frequently performed.
What do Vital Signs Reveal About Neuro Status?

• Because the brainstem and vagus nerve (CN X) play an important
role in vasomotor tone, conditions affecting these areas can cause
vital signs to change. A change in vital signs, however, is not a
reliable indicator of neurological deterioration, as they tend to change
too late to prevent irreversible brain damage.
• Raised intracranial pressure produces a specific set of changes known
as Cushing’s triad. Present in herniation syndromes, Cushing’s triad
consist of: increasing systolic blood pressure with a widening pulse
pressure, bradycardia, and bradypnea.6
• Cushing’s triad is a late sign of increased ICP. Once this pattern of
vital signs occurs, brainstem herniation is already in progress and it
may be too late to reverse it. To detect increasing ICP before it reaches
this point, be alert for earlier signs, for example a subtle change in
LOC or pupils.
• Accurate and consistent documentation helps ensure that subtle
changes in neuro status are caught early on. Whether the unit you’re
working in uses computerized charting, flow sheets, or hand-written
Assessment 35
notes, it’s essential that you compare your findings to those of previous
exams. Through comparison, you’ll be able to spot changes and trends
and, when necessary, intervene quickly and appropriately.
• Verbal communication is important, too. In many ICU, a bedside
neuro exam is done as a part of the change-of-shift report, so that the
off-going and oncoming nurses and therapists can assess the patient
together. The off-going staff can then verify that the patient’s status
is unchanged, perhaps saving the patient an unnecessary CT scan.
RADIO IMAGING
• The Computed Axial Tomography commonly called the CAT scan
is used to visualize the blood vessels and to identify disruptions of
the blood-brain barrier. It is a noninvasive procedure, although an
intravenous injection of radiopaque contrast material may be given
to enhance visualization of the vessels. The X-rays are done at
progressive levels along the brain, resulting in a series of “slices” of
the brain in black and white pictures. The computer detects differences
in tissue densities and radiation absorption too subtle to be picked
up by conventional radiography. A variety of disorders may be
diagnosed utilizing the CAT scan, including hemorrhages, cysts,
infarction, tumors, brain atrophy and cerebral edema. Remove all
objects, such as hair pins or a wig, from the patient’s head before the
scan. The patient should be fasting for at least six hours prior to the
CAT to prevent nausea and vomiting that may be provoked by the
injection of the contrast. Upon administration, the contrast may cause
a warm, flushed feeling and a metallic taste in the mouth. The scan
with contrast takes about an hour, and without contrast, takes about
twenty minutes. If the patient receives contrast, encourage the patient
to drink extra fluids after the scan.
• Magnetic Resonance Imaging (MRI) is used to visualize structures
in the base of the brain and the posterior fossa. While placed within
a large magnetic field, bursts of radiofrequency magnetism are applied
at an angle to the larger magnetic field. This process causes hydrogen
protons to escape from alignment and then to realign. The signals
are used to generate an MRI picture, which will readily detect brain
edema or infarcted tissue. Gadolinium is a magnetic enhancing agent,
which may be given intravenously to allow for better interpretation.
All metal objects must be removed from the patient prior to magnetic
scanning. A person with a metal hip prosthesis, pacemaker or other
implanted metal object may not undergo the MRI procedure or be in
the exam room. When a healthcare provider is required to enter the
MRI room with an unstable patient during the magnetic scan, the
provider must remove all jewelry, metal objects and ID badge. The
MRI takes about one hour to complete. For both the MRI and the CT,
the patient must lie very still in a small confined space. Because
some people have fear of small, confined spaces (claustrophobia),

the physician may order an anti-anxiety medication, such as valium,
to relax the patient and promote compliance.
PHYSICAL EVALUATION
Assessing for Signs of Motor Dysfunction (See Annexure 2)
A neuro assessment almost always includes an evaluation of motor
function. Since you’ll be assessing the ability to move on command, it is
important that the patient must be awake, willing to cooperate, and able
to understand what you are asking to be done.
Changes in Muscle Tone

Clinically, the muscle tone is defined as resistance offered by a resting
muscle to rapid passive movement, while the patient is attempting to
maintain a relaxed state of muscle activity. It is assessed clinically using
rapid passive movements about a joint to determine the degree of muscular
resistance to the passive movement. Muscle tone is perceived by an
examiner but not directly perceived by the patient. Assessment should
include palpation of muscles to estimate the resting (baseline) state of
muscle activity.
Points to Ponder
• Abnormalities of muscle tone are an integral component of many
chronic neurological disorders.
• These disorders may result from diseases or injury to the developing
or mature motor pathways in the cortex, basal ganglia, thalamus,
cerebellum, brainstem, central white matter, or spinal cord.
• When such a disorder is seen in children before 2 years of age, the
term cerebral palsy (CP) is often used; when it occurs in adults, a
variety of descriptive labels have been applied, depending on the
cause.
Neurogenic motor disorders are commonly classified into hypertonia or
hypotonia on the basis of the abnormality of muscle tone.
Hypertonia (See Annexure 2A, C and D)

Hypertonia is defined as abnormally increased resistance to passive movement
of a joint. It may be caused by spasticity, dystonia, rigidity, or a
combination of these features. Physiotherapists should, as far as possible,
use the terms spastic hypertonia, dystonic hypertonia or rigid hypertonia
to distinguish the primary clinical feature of the underlying disorder.
Mechanisms that lead to increased tone may also contribute to poor
voluntary motor performance or involuntary muscle contractions, but
assessment of muscle tone is independent of strength, dexterity,
coordination, or involuntary movements.
Assessment 37
Spasticity
Spasticity is a velocity-dependent resistance offered to passive stretch by any
hypertonic muscle. This resistance must be different for high versus low
speeds of passive movement and for flexion versus extension about the
joint. A “spastic catch” is often felt during passive movement and that
may represent the threshold for onset of the stretch reflex in the affected
muscle.
Points to Ponder
• Spasticity can vary depending on patient’s state of alertness, activity,
or posture.
• Spasticity can be increased by anxiety, emotional state, pain, surface
contact, base of support or other non-noxious sensory inputs.
• Spasticity may worsen with low base of support or antigravity posture.
• The presence of spasticity suggests the presence of hypertonia, thus
the terms spasticity and spastic hypertonia are used interchangeably.
• Electrophysiological studies of spastic muscles show changes in the
threshold of the tonic stretch reflex, so that resistance increases in
magnitude or occurs sooner as speed of passive movement increases.
Dystonia
Clinically dystonia can be defined as a movement disorder in which
involuntary sustained or intermittent muscle contractions cause twisting and
repetitive movements, abnormal postures, or both.
Points to ponder
• Dystonia may cause hypertonia, but hypertonia is not always present in
dystonia
• Dystonia is commonly triggered or exacerbated by attempted
voluntary movement and may fluctuate in severity in an individual
at different times, depending upon body position, specific tasks,
emotional state, or level of consciousness.
• However, if dystonia is present at rest and causes an involuntary
posture, then it may be a cause of hypertonia, giving rise to the term
dystonic hypertonia.
• To diagnose dystonic hypertonia, there must be observable dystonic
postures that do not relax during the examination of tone. The body
part being examined must be supported against gravity to ensure
that postural muscle activity is not contributing to the apparent
increase in tone.
In Dystonic hypertonia we can find all of the following:
1. Resistance to passive joint movement is present at very low speeds of
movement and is not depend on speed or angle of movement.
2. Simultaneous co-contraction of agonists and antagonists may occur,

and this is reflected in an immediate resistance to a rapid reversal of
the direction of passive movement about a joint.
3. The limb tends to return toward a fixed involuntary posture, and
when symptoms are severe, the limb tends to move toward extremes
of joint angles.
4. Hypertonia is triggered or worsened by voluntary movement or
posture of the affected and other body parts and may be strongly
dependent on a particular movement or posture attempted or the
activity of distant muscle groups.
5. The pattern as well as the magnitude of involuntary muscle activity
varies with arousal, emotional and behavioral state, tactile contact, or
attempted task.
Dystonia may be sub-classified as:
• Action induced
• Posture induced.
Points to Ponder
• In adults, the actions that lead to dystonia may be restricted to certain
attempted tasks, although task specificity is less common in children.
• When dystonia is present at rest or with posture, certain attempted
postures may be impossible to attain.
• Dystonia may be triggered or worsened by self-consciousness,
distraction, startle, overuse, fatigue, touch, or pain.
• Dystonia is sensitive to antigravity posture and it must therefore be
tested in sitting, standing, supine, and with major joints in both flexion
and extension.
• Dystonia is not necessarily a primary disorder of muscle tone, but it
may appear because of the inability to relax the muscles fully.
• Dystonia may be focal when it affects a single body part, segmental
when it affects one or more contiguous body parts, multifocal when
it affects two or more noncontiguous body parts, generalized when it
affects one leg and the trunk plus any other body part or both legs
plus any other body part, and hemidystonia when it affects only one
half of the body.
• The anatomic localization of lesions that lead to dystonia has not yet
been identified with certainty. It is likely that lesions in the basal
ganglia cause them.
Rigidity
Rigidity is a common muscle tone disorder in which the resistance to passive
movement is independent of posture and speed of movement. In adults it is
frequently seen in Parkinsonism. The presence of rigidity suggests the
Assessment 39
presence of hypertonia; thus, the terms rigidity and rigid hypertonia may be
used interchangeably.
Clinically rigidity may defined as a hypertonia in which all of the
following are present:
1. Unlike in spasticity, the resistance to passive movement in rigidity
does not depend on speed, and angle. Further the limb does not tend
to return toward a particular fixed posture or extreme joint angle as
in dystonia, i.e. Absence of synergy.
2. Simultaneous co-contraction of agonists and antagonists may occur,
and this is reflected in an immediate resistance to a reversal of the
direction of movement about a joint, i.e. Lead Pipe.
3. Voluntary activity in distant muscle groups does not lead to
involuntary movements about the rigid joints, although rigidity may
fluctuate, i.e. Cogwheel.
4. At rest the rigid muscles may exhibit fluctuating tone, i.e. Tremor.
5. Rigidity may be associated with bradykinesia, tremor, flexed posture,
and gait instability, known as Parkinsonism. Other forms of
hypertonia.
Resistance to passive movement may be due to disorders of spinal cord,
peripheral nerve, muscle, or connective tissue. Such disorders include
startle syndromes, stiff person syndrome, MND, myotonia, neuro
myotonia, myokymia, and childhood movement disorders such as
athetosis, chorea, ataxia, as well as the hyper kinetic features of dystonia,
myoclonus, tremor, and tic disorders.
Assessment of Muscle Power

Most commonly accepted format of assessment of muscle power is the
MRC scale. Power of a muscle is graded from 0-5 depending upon its
ability to generate torque, from complete inactivity to maximum
power (See Annexure 2B).
TESTING REFLEXES
Reflex assessment encompasses deep tendon, superficial, and brainstem
reflexes.
• Deep tendon reflexes include the triceps jerk, biceps jerk, brachio-
radialis jerk, patellar tendon jerk, and achilles tendon jerk
(Annexure 3).
Although all deep tendon reflexes aren’t routinely assessed, they
should be tested in any patient with suspected CNS disorders, neuropathy,
and peripheral nerve or spinal cord injury.
• The plantar reflex is the only superficial reflex that’s commonly
assessed and should be tested even in comatose patients and in those
with suspected injury to the lumbar 4-5 or sacral 1-2 areas of the
spinal cord as well as in neuropathy and peripheral nerve injuries.
Points to Ponder
1. Stimulate the sole of the foot with the handle of a reflex hammer or
the tip of a key.
2. Begin at the heel and move up the foot, in a continuous motion,
along the outer aspect of the sole and then across the ball of the toes
to the base of the big toe.
3. The normal response is plantar flexion (curling under) of the toes.
Extension of the big toe, known as the Babinski’s sign is abnormal,
except in children younger than the age of 2 years.
• Brainstem reflexes must be assessed in drowsy or comatose patients
to determine if the brainstem is intact. Brainstem reflexes are mainly
protective.
Points to Ponder
1. You’ll need to check for the protective reflexes, i.e. coughing, gagging,
and the corneal response, as part of the cranial nerve assessment.
2. To test the oculo-cephalic, or doll’s eye reflex, turn the patient’s
head briskly from side to side; the eyes should move to the left while
the head is turned to the right, and vice versa. If this reflex is absent,
there will be no eye movement.
3. To test the oculo-vestibular reflex, also known as the ice caloric or
cold caloric reflex, a physician will instill at least 20 ml of ice water
into the patient’s ear. In patients with an intact brainstem, the eyes
will move laterally toward the affected ear. In patients with severe
brainstem injury, the gaze will remain at midline.
EVALUATING SENSATION (ANNEXURE 4)

The sensory exam evaluates the patient’s ability, or inability to perceive
and identify specific sensations with her eyes closed. It is done only if
there’s a specific need, as in spinal cord injury or peripheral nerve lesions.
The patient must be alert enough to be able to cooperate with the
examination and to tell whether she feels the sensation and whether both
sides of her body feel it equally. Testing must begin with the feet and
move up the body to the face, comparing one side with the other.
Points to Ponder
• To assess sensation to light touch use your fingertips or cotton.
• To test superficial pain sensation, use a clean, unused, blunted safety
pin. Be sure not to break the skin, and discard the pin appropriately
after you’ve finished using it on a patient. Also, test sensation using
a blunt object, like point of a key. The patient should be able to
distinguish sharp from dull.
Assessment 41
• To test temperature sensation, you can use test tube of hot and cold
water.
• To test vibratory sensation, use a tuning fork.
• To test proprioception, or position sense, move the patient’s toes and
fingers up or down. Grasp the digit by its sides and ask the patient
tell you which way it’s pointing.
EVALUATING CEREBELLAR FUNCTION

Move on to the cerebellar assessment, if indicated. It may not be necessary
in a specific problem-focused examination for nerve or spinal injury, and
it can’t be done if the patient can’t or won’t follow commands.
Points to Ponder
• If the patient is in bed, you may not be expected to assess the balance
and gait. In that case, limiting the testing to coordination only is
acceptable. Hold up your finger and have the patient quickly and
repeatedly move her finger back and forth from your finger to her
nose. Then have her alternately touch her nose with her right and
left index fingers. Finally, have her repeat these tasks with her eyes
closed. The movements should be precise and smooth.
• To assess the lower extremities, have the patient bend her leg and
slide that heel along the opposite shin, from the knee to the ankle.
This movement, too, should be accurate, smooth, and without tremor.
• If the patient is able to stand and not restricted to bed, you can assess
balance using the Romberg test. Have the patient stand with her feet
together, arms at the sides, and eyes open; she should be able to
stand upright with no swaying. If she can do that, have her close her
eyes and stand the same way. If she falls or breaks her stance after
closing the eyes, the Romberg test is positive, indicating Proprioceptive
or Vestibular dysfunction.
ASSESSING THE CRANIAL NERVES (ANNEXURE 5)

There are 12 pairs of cranial nerves—some sensory, some motor, and
some both. The table in Annexure 5 lists the functions of each nerve and
explains how to test them.
Points to Ponder
A summary of focused Neurological Exam for Physiotherapist
The following passage attempts to provide the reader with a brief
but comprehensive review of the neurological examination. An
understanding of neuroanatomy is necessary to appreciate the fine points
of the neurological examination. In any case, neuroanatomy has to be
reviewed several times before a complete understanding is obtained
(Table 3.1).
A physiotherapist should conduct any neurological assessment to

answer the following questions:
1. Is there a lesion?
2. Where is the lesion?
3. What caused the lesion?
4. What are the key losses of function?
5. What are the necessary therapeutic interventions?
Table3.1: Key functional areas to be tested

Exam Localization
Mental status Cortex
Cranial nerves Brainstem
Motor and reflexes Upper motor and lower motor neurons
Sensory Sub cortical (thalamus), spinal cord
Coordination Cerebellum
The mental status is indicated by four basic parameters (Table 3.2).

• Level of consciousness: GCS score is often used to establish a baseline
LOC. Orientation to person, place and time should also be determined.
• Concentration and attention: Patients should be asked to perform serial
seven subtractions that is count backwards from 100 decreasing by
seven each time.
• Language by fluency of the patient’s speech, testing for comprehension
of simple commands such as repetition of words, naming of objects,
writing a sentence and reading a phrase.
• Memory should be tested regarding immediate, recent and remote
events.
Table 3.2: Interpretation of what each area of brain does in terms of mental status
Frontal cortex Intellectual function, production of speech (i.e. non-
fluent ‘expressive’ aphasia’s), motor control
Parietal cortex Analysis of sensory information, also serves a role in
intellectual function (e.g. visual-spatial neglect)
Temporal cortex Comprehension of speech (i.e. fluent ‘receptive’
aphasia)
Occipital cortex Vision
• The cranial nerve examination is an excellent way to localize a

brainstem lesion. Most cranial nerves originate in the brainstem,
because their nucleus resides there. A lesion in the cortex will cause
a contralateral deficit of the cranial nerve while an infranuclear
lesion will cause an ipsilateral deficit.
Assessment 43
• The cortex controls motor function. It begins in the upper motor

neurons. (Betz cells of the precentral gyrus). The axons project via
the posterior limb of the internal capsule, travel through the brainstem
(the pyramidal tract), cross in the lower medulla, then descend in the
spinal cord (corticospinal tract within the lateral column) to the lower
motor neurons in the spinal cord.
• The lower motor neuron originates from the anterior column of the
spinal cord and ends in the motor end plate. The distinction between
an upper motor and lower motor neuron is important because a
lesion in either of the pathways gives markedly different clinical
presentation.
• The standard motor examination should include five areas, strength,
tone, posture, involuntary movements and reflexes. A rating scale
for motor examination is important for two reasons. Identifying
motor deficits allows for localization (i.e., which side of the brain is
involved). With the rating of the motor deficits one can follow
progression or improvement that has important
prognostic implications.
• Muscular bulk and tone will help in differentiating between upper
and lower motor neuron deficits.
• Abnormal postures–Decorticate and Decerebrate. Decorticate
posturing is extension of the lower extremities and flexion of the
upper extremities whereas decerebrate rigidity is extension and
internal rotation of all extremities. Both are upper motor neuron
problems.
• Decorticate posturing suggests a supratentorial pathology whereas
decerebrate posturing indicates an infratentorial pathology. Because
the lesion goes deeper in the brainstem, decerebrate posturing has a
worse prognosis.
• Involuntary movements indicate involvement of the extra-pyramidal
system, which includes complicated neuronal tracts between the basal
ganglia and cerebellum.
• Deep tendon reflexes are important to note because they give
information about the upper motor neuron verses lower motor neuron
lesions and lateralization. Symmetric abnormality verses asymmetric,
indicating systemic verses isolated neurological pathology.
• Superficial reflex such as the Babinski sign, i.e. toe fanning and
extension of big toe upon stimulation of the lateral aspect of the sole
of the foot from heel to big toe is important to note. The presence of
a Babinski sign indicates an upper motor lesion.
• Sensory examination is often difficult because it is a very subjective
examination. With an uncooperative patient the sensory exam may
be impossible to perform accurately. But when it can be done, the
sensory exam will reveal information about where lesions are located.
• Sensations are transmitted from the peripheral nerves to the spinal

cord. Once in the spinal cord, the nerve transmissions ascend through
several tracts or columns.
• Pain and temperature are located in the lateral column and decussates
(cross to the other side) at the level of entry.
• Proprioception and vibration travels through the posterior columns
and decussate at the level of the brainstem.
Superficial touch travels through both the lateral and posterior
columns, proving that the body has redundant systems for important
functions.
• Dermatomes are the peripheral distribution of the specific spinal
cord roots.
• Coordination and gait is an integration of multiple tracts including
the pyramidal, extra pyramidal, posterior columns and cerebellar
tracts and together, coordination and gait can be thought of as the
“final exam of the nervous system”. Many patients deemed “non-
focal and intact” might reveal significant dysfunction in Coordination
and gait.
• Ataxia is the classic neurological abnormality indicating cerebellar
dysfunction, which can be in the upper extremities, the lower
extremities or in the trunk. Ataxia is manifested by a lack of smooth
and coordinated movements.
POINTS TO PONDER
How to Localize a Lesion?
Knowing where the lesion is not just an intellectual exercise to be
completed by the therapist to prove that they know their neuroanatomy.
Localization of a lesion has important implications in terms of
diagnostic and therapeutic interventions.
The four major areas of lesion in the nervous system are as follows:
A. Cortex
B. Sub cortex: Thalamus, basal ganglia and internal capsule
C. Brainstem
D. Spinal cord.
Features of Cortical Lesions

There are five major findings associated with lesions in the cortex.
1. Dysphasia: Any disorder of language, which includes expressive,
receptive, global aphasia, naming and reading.
Geographic area: Frontal or temporal cortex.
2. Cortical Sensory loss: Which includes an inability to identify objects
in your hand (stereognosis), loss of two point discrimination and the
inability to discern writing on one’s palm (graphesthesia).
Geographic area: Post central gyrus.
Assessment 45
3. Weakness of face and extremity muscles with possible paresthesia:

• If the arm is more involved, the lesion is in the middle cerebral
artery territory. If the leg is more involved, then it is in anterior
cerebral artery territory.
4. Conjugate Gaze Palsy: There are three gaze centers, two reside in
the cortex and one in the brainstem. The major one is the frontal
cortex gaze center.
The eyes will deviate toward the cortical lesion, because the right
frontal gaze center is responsible for looking to the left and vice
versa. The eyes will look towards the lesion.
So when the right frontal cortex gaze (Fig. 3.3) center is knocked
out, the conjugate gaze will be toward the right and vice versa. And
if the eyes deviate together at all, the most likely lesion is in the
frontal cortex.
Fig. 3.3: Frontal cortex
5. Seizures: Seizures associated with hemiplegia or TBI are most likely

due to a cortical lesion. Seizures generally originate in the cortex.
Features of Sub-cortical Lesions

This comprises lesions of internal capsule, basal ganglia and thalamus
1. Visual field defects: When a patient has difficulty with detecting
simultaneous movements in certain visual fields, the lesion is likely
to be in the cortex or the sub cortical area. For example, presence of
the left homonymous hemianopsia (Fig. 3.4) indicates a sub cortical
lesion in the visual pathway.
Fig. 3.4: Homonymous hemianopsia

2. Dystonia: Unusual, uncoordinated movements such as

choreoathetosis (involuntary jerky movements), hemiballismus (slow,
bizarre movements of half the body), or simply a loss of harmony of
refined movements is indicative of basal ganglia lesions. Remember
that the basal ganglia help modulate movement, and refine the motor activity
of the pyramidal system.
3. Face and extremity weakness: When the face, arm and leg are equally
involved then the lesion must reside in the internal capsule.
4. Dense Sensory Loss: Loss of pain and touch in face and extremities
signifies a lesion in the thalamic area. The thalamus is a sensory
relay switch as well as a primary receptive center, so in a thalamic
lesion there will be abnormality of the sensation in the face and extremities.
Features of Brainstem Lesions

Brainstem consists of midbrain, pons and medulla, and cerebellum.
Lesions in the brainstem result in crossed abnormalities.
1. Crossed hemiplegia: The cranial nerves will be affected on one side,
while the extremity motor deficits are on the other side. The brainstem
lesion will affect the infranuclear cranial nerves ipsilaterally, and the
motor tract contralaterally, because the motor tract decussates (crosses)
just above the spinal cord.
2. Cerebellar findings: Ipsilateral ataxia, dysmetria (misjudge distance
between finger to nose).
3. Nystagmus: The medial longitudinal fasciculus helps to coordinate
eye movement and resides in the brainstem axis. It connects the two
nuclei of CNIII and CNVI, which allow conjugate gaze to occur. A
problem in the brainstem could result nystagmus. The nystagmus
could be horizontal, vertical or rotary.
4. Lower cranial nerve findings: Cranial nerves VIII-XII project from
the lower brainstem. Thus lesions in this area will cause hearing loss
and vertigo (CN VIII), dysarthria (difficulty with articulation),
dysphagia (CN IX-X) (difficulty with swallowing), and tongue
deviation (XII).
Features of Spinal Cord Lesions

Lesions in the spinal cord cause predictable deficits. Assuming there is
normal cortical, sub cortical and brainstem functions, the possible findings
are listed below.
1. Motor deficits can be in one extremity (monoplegia), both lower
extremities (paraplegia), one side of the body (hemiplegia) and in
four extremities (quadriplegia).
In the case of monoplegia or hemiplegia, the lesion will be
ipsilateral.
Assessment 47
2. Sensory loss may be bilateral or ipsilateral or contralateral because

pain and temperature fibers cross immediately after entering the cord.
A sensory level along with a no man’s land may be present in most
cases.
Clinical Implication of Dominance

• The controlling hemisphere in most human beings is the left side of
the brain.
• The dominant hemisphere really controls most things in the body.
• Physiotherapists should know whether a patient is right-handed or
left-handed.
• Right-handed people are left hemisphere dominant.
• Most left handed people are also left hemisphere dominant except
for about 10% which will be right hemisphere dominant.
• The reason dominance is so important is that a stroke in a dominant
hemisphere for the same sized lesion can be more disabling.
• The speech centers are located in the cortex of the dominant
hemisphere. Aphasia does not occur when the non-dominant
hemisphere is involved.
When the Non-dominant Hemisphere is Involved, the Following

Symptoms May Result
a. Inattention and denial: These patients neglect the left side of the
body despite having significant deficits. These patients will not see
you if you stand on their left. They may not shave the left side of
their face. They remain unconcerned about their deficits; because
they do not believe they have any damaged side.
b. Constructional apraxia: Patients are unable to do a motor task without
having any motor deficit. They just won’t be able to do it. They may
not be able to open the door even though they have the motor
capability to do so.
c. Spatial Disorientation: Patients are able to get lost in their own
home.
d. Confusional State: This occurs infrequently in severe lesions.
Final Word of Caution

• No matter how brief or extensive your neuro assessments are,
comparing your findings to those of previous exams is essential.
• When assessing motor response in an unconscious patient, use sternal
pressure judiciously. Deep sternal pressure can cause bruising.
• In many ICUs, a bedside neuro exam is done as a part of the change-
of-shift report so that both sets of nurses and therapists can assess
the patient together. This facilitates any change of status to be detected
at the earliest.
BIBLIOGRAPHY
1. Bader MK, Littlejohns LR. AANN core curriculum for neuroscience nursing
(4th ed). Philadelphia: Saunders 2004.
2. Hickey JV. The clinical practice of neurological and neurosurgical nursing
(6th ed). Philadelphia: Lippincott 2003.
3. Kerr ME. Intracranial problems. In SM Lewis, MM Heitkemper, SR Dirksen
(Eds), Medical surgical nursing (5th ed). St Louis: Mosby 2000.
4. Mashall RS, Mayers SA. On call neurology (2nd ed). New York: WB Saunders
2001.
5. Messner R, Wolfe S. RN’s pocket assessment guide. Montvale, NJ: Medical
Economics 1997.
6. Vos H. The neurological assessment. In E Barker (Ed), Neuroscience nursing:
Spectrum of care (2nd ed) St Louis: Mosby 2002.
Fundamentals of Neuroim-
4 aging and Electrodiagnosis
As recently as in the 1970s, the diagnosis of most disorders, particularly

those affecting the nervous system, depended mainly on clinical
examination. Some of these disorders, such as brain tumors, often required
exploratory surgery, aspiration or biopsy for visible or histological or
biochemical evidence of disorders. The risks of infection, anesthesia, and
imperfect healing weigh against exploratory surgery, but the diagnostic
benefits make the risk worth taking. In the last few decades, however, a
variety of medical imaging and electrodiagnosis techniques, among other
advanced procedures have made most exploratory surgery and other
invasive procedures redundant and has greatly accelerated progress in
neuro-medicine. Although the basic principles of some of these techniques
have been known for quite some time, they did not become clinically
useful until computer technology had advanced for enough to process
data into clear images of the body.
As a primary caregiver a physiotherapist must be conversant with the
fundamentals of these investigative procedures and be capable of understanding
their interpretations for facilitating process of rehab goal setting and planning
therapeutic interventions.
COMPUTED TOMOGRAPHY (CT)

Formerly called a CAT scan, computed tomography (CT) is a more
sophisticated use of X-rays to produce finely detailed images. The patient
is moved through a machine that emits low-intensity X-rays on one side
and receives them with a detector on the other side. By imaging body
slices as thin as a few millimeters, CT scans show less overlap of organs
than conventional X-rays and thus produce sharper images. CT scans are
useful for identifying tumors, aneurysms, cerebral hemorrhages, kidney
stones, and other disorders. In a brain CT, a beam of X-rays is shot
straight through the brain. As it comes out the other side, the beam is
blunted slightly because it has hit dense living bone on the way through.
Blunting or “attenuation” of the X-ray comes from the density of the
tissue encountered along the way. Very dense tissue like bone blocks lots
of X-rays, grey matter blocks some and fluid even less. X-ray detectors
positioned around the circumference of the scanner collect attenuation
readings from multiple angles. A computerized algorithm then
reconstructs an image of each slice (Fig. 4.1 and Photo gallery).
MAGNETIC RESONANCE IMAGING (MRI)

With magnetic resonance imaging (MRI), a cylindrical device surrounds
the body with a magnetic field three thousand to sixty thousand times as
strong as Earth’s. Hydrogen atoms align themselves with this field. The
patient is then irradiated with radio waves. Hydrogen ions absorb this
energy and align in a new direction. When the radio waves are turned
off, they realign to the magnetic field and emit energy at rates that vary
with the type of tissue. This emitted energy is received by a detector and
analyzed by a computer into an image of the body’s interior. MRI can see
through cranial and vertebral bone to visualize brain and spinal cord
tissue in finer detail than CT (Fig. 4.2 and Photo gallery).
How an MRI Image is Formed

• When protons in the body tissue are placed in a magnetic field, they
oscillate.
• The frequency at which they oscillate depends on the strength of the
magnetic field.
• Protons are capable of absorbing energy if exposed to electromagnetic
field at the matching frequency of oscillation.
• After they absorb energy, the nuclei release this energy so that they
return to their initial state of equilibrium.
• This re-radiation of energy by the nuclei as they return to their initial
state is what is observed as the MRI signal.
• The return of the nuclei to their equilibrium state does not take place
instantaneously, but rather takes place over two stages within a period
of time.
• The return of the nuclei to their initial state is governed by two
physical processes:
– The relaxation back to equilibrium of the component of the nuclear
magnetization which is parallel to the magnetic field.
– The relaxation back to equilibrium of the component of the nuclear
magnetization which is perpendicular to the magnetic field.
• The time that it takes for these two relaxation processes to take place
is roughly equal to:
– Time T1 for the first process
– Time T2 for the second process.
• The strength of the MRI signal depends primarily on three parameters.
– Density of protons in a tissue: The greater the density of protons,
the larger the signal will be.
Fundamentals of Neuroimaging and Electrodiagnosis 51
– T1
– T2
• The contrast between brain tissues is dependent upon how these 3
parameters differ between tissues.
• For most “soft” tissues in the body, the proton density is very
homogeneous and therefore does not contribute in a major way to
signal differences seen in an image.
• However, T1 and T2 can be dramatically different for different soft
tissues, and these parameters are responsible for the major contrast
between soft tissues.
• T1 and T2 are strongly influenced by the viscosity or rigidity of a
tissue. Generally speaking, the greater the viscosity and rigidity, the
smaller the value for T1 and T2.
• It is possible to manipulate the MR signal by changing the way in
which the nuclei are initially subjected to electromagnetic energy.
• This manipulation can change the dependence of the acquired signals
on the three parameters: proton density, T1 and T2. Hence, one has
a number of different MR imaging techniques (“weightings”) to
choose from, which accentuate some visual characteristics of the tissue
and not others (Table 4.1).
Table 4.1: Key to interpretation of X-ray / CT / MRI: A simplified tabulation of

tissue image characteristics
Normal tissue MR-T1 MR-T2 X-ray / CT
Dense bone Dark Dark Bright
Air Dark Dark Dark
Fat Bright Bright Dark
Water Dark Bright Dark
Brain tissue “Anatomic” Interim. Interim.
Abnormal tissue
Infarction Dark Bright Dark
Hemorrhage Bright Bright Bright
Tumor Dark Bright Dark
Glial plaques in MS Dark Bright Dark
Image characteristics Tissue abnormality

Dark on T1 weighted images Edema, tumor, infarctions, inflammation,
infections, hemorrhage, calcification
Bright on T1 weighted images Fat, sub-acute hemorrhage, stasis of blood,
laminar necrosis following infarctions
Dark on T2 weighted images Calcification, fibrous tissue, pus
Bright on T2 weighted images Fat, sub-acute sub-dural hemorrhage, edema,
tumor, Infarctions, inflammation, infections,
hemorrhage, calcification
Bright means high signal intensity, high density/high attenuation of

X-rays. Dark means low signal intensity, density and attenuation. Interim
means intermediate Anatomic- Gray matter appears gray, white matter
white.
To detect bleeding in brain- for MR use gadolinium; for CT, iodinated
contrast material.
POSITRON EMISSION TOMOGRAPHY (PET) (FIG. 4.3)

Positron emission tomography (PET) is used to visualize the metabolic
state of a tissue. The patient receives an injection of radioactively labeled
glucose, which emits charged particles called positrons. When a positron
and electron meet, they annihilate each other and give off gamma rays
that are picked up by a detector and analyzed by computer. The result
is a color coded image that shows which tissues were using the most
glucose that is, where most metabolically active is taking place at the
time. In cardiology, a PET scan can show the location and extent of dead
heart tissue. In neuroscience, it can show which parts of the brain are
active from moment to moment as a person engages in various sensory,
motor, or intellectual tasks.
SPECT/PET Scans (Single Photon/Positron Emission Computed

Tomography) (Fig. 4.4)
When radio-labeled compounds are injected in tracer amounts, their
photon emissions can be detected much like X-rays in CT. The images
made, represent the accumulation of the labeled compound. The
compound may reflect, for example, blood flow, oxygen or glucose
metabolism, or dopamine transporter concentration. These images are
shown with a color scale as depicted in plate at the right.
Functional MRI (F MRI)

A new variation of MRI, functional MRI (f MRI) detects the anaerobic
activity of active neurons of the brain. It can pinpoint brain activity to
within 1 or 2 millimeters, and is even more precise and useful than PET
scans for studies of brain function. It also has the advantage of requiring
no injections or radioactive isotopes, and it is much quicker than a PET
scan. The PET and f MRI techniques not only have been valuable for
clinical diagnosis but have added enormously to our knowledge of brain
function, pinpointing abnormalities correlated with depression,
schizophrenia, and attention deficit disorder. They have also provided
images of the mind at work, so to speak, identifying areas involved in
consciousness, memory, thought, musical perception, reading, motor
control, and speech.
The changing face of imaging technology- photo gallery (Figs 4.1
to 4.6)
Fig. 4.1: CT scan – A computerized tomography is a special X-ray used as second

line of investigation. X-ray beams that passes to the different slices of the brain
(like a knife through a loaf of bread) is picked up by a detector and fed into a
computer which reads the information. Brain fluid shows up black and the brain
appears in different shades of gray on CT scan. This test is used to check for
stroke, tumor, infection or bleeding
Fig. 4.2: MRI scan – A MRI measures Fig. 4.3: PET – Positron emission
radio-waves which are detected by the tomography scans to see the chemical
machine and feeds the information to the activity in the brain. This test uses
computer to construct the brain images. radioactive glucose to measure brain
This test is used to check for brain activity. Low brain activity is colored blue,
tumor, infection or cyst medium activity is yellow, and high
activity is pink
Fig. 4.4: SPECT/PET scans (Single photon/positron emission tomography)
Fig. 4.5: Arteriogram – This procedure is used to study the blood vessels of the
brain. The imagologist injects dye into a major artery to outlines the arteries of the
brain. Then it is possible to see if these blood vessels have a bulging weakness of
the wall (aneurysm) or blockage or a break, all of which may causes a stroke
Fig. 4.6: X-ray skull – A plain X-ray is used primarily to take a picture of bony
skull vault to detect if one has broken or fractured the skull
Photo Gallery of Typical CT Scan Images (Figs 4.7 to 4.18)
Fig. 4.7: The CT scan image of a normal brain
Fig. 4.8: CT scan showing cerebral infarction of the left hemisphere
Fig. 4.9: CT scan of the brain showing left cerebral hemorrhage

Photo Gallery of Typical MRI Scans Images
Fig. 4.10: Normal MRI of the brain showing landmarks in the brain viewed in
coronal section
Fig. 4.11: MRI of a massive cerebral Fig. 4.12: Acute cerebral hemorrhage
hemorrhage of the left hemisphere of the can be seen in MRI below in the left
brain, which had been fatal hemisphere of the brain
Fig. 4.13: MRI showing acute cerebral

infarction the right pre-central gyrus.
Abnormally bright signal is seen here
because of the presence of excess water
which has a prolonged relaxation time.
As tissue has become infarcted and
edematous, the sulcus is no longer
identifiable. Compare the infarcted side
with the normal right side
Fig. 4.14: MRI of a metastasis of adeno- Fig. 4.15: Metastasis of bronchogenic

carcinoma, note clear encapsulation with carcinoma- note the diffuse margins
well defined margins of the SOL
Figs 4.16A and B: Comparison of MRI and CT scans

of hypertensive encephalopathy
Figs 4.17A and B: Comparison between PET and enhanced MRI of the same
condition as shown above
Fig. 4.18: MRI showing stenosis of cervical spine. The cervical cord is markedly
compressed. The patient also had degenerative disease of C3-4 and C4-5
RADIOGRAPHY
Radiography, use of X-rays, is the oldest imaging technique (Fig. 4.6). In
the term “X-ray” can refer either to the type of radiation used or to the
photographic image produced (the radiogram). X-rays were discovered
in 1885, and Marie Curie (1867–1934) trained military doctors in the use
of X-ray machines in World War I. X-rays are relatively simple and
inexpensive to make, and they are commonly used in dentistry,
mammography, chest examinations, and diagnosis of fractures. They are
best used for dense structures such as bone, but hollow organs can be
visualized by filling them with a radiopaque substance such as barium,
given by swallow or enema to X-ray the stomach or colon. Angiography

is the X-ray visualization of blood vessels after injection with a radio-
paque dye.
Photo Gallery of Some Typical X-rays (Figs 4.19 to 4.21)
Fig. 4.19: A normal cervical spine X-ray
Fig. 4.21: Compressive myelopathy

detected by X-ray of cervical spine lateral
view in extreme flexion showing
Fig. 4.20: A prolapsed disc anterolysthesis at C4 and C5 with C5 and
between C6 and 7 C6
ELECTRO-DIAGNOSTIC STUDIES: EEG, EMG AND NCV’S

A. Electroencephalogram (EEG)
Introduction
The electroencephalogram (EEG) is a recording of the electrical activity
of the brain from the scalp (Fig. 4.22). The first recordings were made by
Hans Berger in 1929 although similar studies had been carried out in
animals as early as 1870.
The waveforms recorded are thought to reflect the activity of the
surface of the brain, the cortex. This activity is influenced by the electrical
activity from the brain structures underneath the cortex.
The nerve cells in the brain produce signals that are called action
potentials. These action potentials move from one cell to another across
a gap called the synapse. Special chemicals called neuro-transmitters
help the signals to move across the gap. There are two types of neuro-
transmitters; one will help the action potential to move to the next cell,
the other will stop it moving to another nerve cell.
Fig. 4.22: Tracing of an electroencephalogram
The brain normally works hard to keep an equal amount of each of

these neurotransmitters in the brain.
EEG activity is quite small, measured in micro volts (µV) with the
main frequencies of interest up to approximately 30 Hertz (Hz).
EEG Electrodes
Small metal discs called electrodes are placed on the scalp in special
positions. These positions are identified by the operator who measures
the head using the International 10/20 System (Fig. 4.23). This relies on
taking measurements between certain fixed points on the head. The
electrodes are then placed at points that are 10% and 20% of these
distances.
Each electrode site is labeled with a letter and a number. The letter
refers to the area of brain underlying the electrode, e.g. F – Frontal lobe
and T – Temporal lobe. Even numbers denote the right side of the head
and odd numbers the left side of the head.
Fig. 4.23: 10/20 System of electrode placement

There is a great variety of electrodes that can be used. The majorities
are small discs of stainless steel, tin, gold or silver covered with a silver
chloride coating. These normally have a lead attached. Alternative
methods consist of a cap in which the electrodes are already embedded.
Montages
EEG machines use a differential amplifier to produce each channel or
trace of activity. Each amplifier has two inputs (Fig. 4.24). An electrode
is connected to each of the inputs.
Differential amplifiers measure the voltage difference between the
two signals at each of its inputs. The resulting signal is amplified and
then displayed as a channel of EEG activity.
EEG Applications
One of the major roles of EEG is as an aid to diagnose epilepsy. Abnormal
patterns such as spikes, sharp waves and/or spike and wave complexes
can be seen. The type of activity and the area of the brain that it is
recorded from will assist the physician in prescribing the correct
medication for that type of epilepsy.
Fig. 4.24: EEG machine

Patients with epilepsy that can not be controlled by medication will

often need surgery in order to remove the damaged tissue. The EEG
plays an important role in localizing this tissue. Special electrodes can be
inserted through the cortex or alternatively a grid of electrodes placed
directly on the surface of the cortex. These recordings, often called Long
Term Monitoring for Epilepsy (LTME), can be carried out for periods
ranging from 24 hours to 1 week. The EEG recorded will indicate which
areas of the brain should be surgically removed.
EEG studies can also be used in patients who are deeply unconscious,
to distinguish between brain death and possible reversible conditions.
Electrocerebral inactivity (ECI) or electro-cerebral silence (ECS) is
defined as no EEG activity over 2 µV in amplitude when recording from
electrodes on the scalp, that are 10 cm or more apart.
Using the 10/20 International System of electrode placement, the
average distance between electrodes in an adult is 6 to 6.5 cm. Activity
recorded using these distances and at a normal display sensitivity may
suggest ECS. However if the same activity was recorded using longer
inter-electrode distances, some activity might be seen. Therefore some
double distance electrode linkages are recommended, e.g. FP1-C3, F3-P3,
C3-O1 etc.
Display sensitivities of a minimum of 2 µV/mm are required.
However digital EEG systems have the added advantage of having
sensitivity values of 1.5 and 1 µV/mm. This 50-100% increase in sensitivity
will allow a more confident assessment of the presence or absence of a
2 µV signal.
The EEG is also used to investigate other conditions that may affect
brain function such as strokes, brain injuries, liver and kidney disease
and dementia.
EEG Activity
EEG activity can be broken down into 4 distinct frequency bands:
Beta activity > 13 Hz (Fig. 4.25).
Beta activity is a normal activity present when the eyes are open or
closed. It tends to be seen in the channels recorded from the center or
front of the head. Some drugs will increase the amount of beta activity
in the EEG.
Alpha activity 8 Hz-13 Hz (Fig. 4.26).
Fig. 4.25: Beta activity
Fig. 4.26: Alpha activity

Alpha activity is also a normal activity when present in waking adults.

It is mainly seen in the channels recorded from the back of the head. It
is fairly symmetrical and has amplitude of 40-100 µV. It is only seen
when the eyes are closed and should disappear or reduce in amplitude
when the eyes are open.
Theta activity 4 Hz-7 Hz (Fig. 4.27).
Fig. 4.27: Theta activity
Theta activity can be classed as both a normal and abnormal activity

depending on the age and state of the patient. In adults it is normal if the
patient is drowsy. However it can also indicate brain dysfunction if it is
seen in a patient who is alert and awake. In younger patients, theta
activity may be the main activity seen in channels recorded from the
back and central areas of the head.
Delta activity < 4 Hz (Fig. 4.28).
Fig. 4.28: Delta activity
Delta activity is only normal in an adult patient if they are in a

moderate to deep sleep. If it is seen at any other time it would indicate
brain dysfunction. Abnormal activity may be seen in all or some channels
depending on the underlying brain problem.
There are a number of other waveforms which tend to be a little
more specific to certain conditions. For example spike and wave activity
indicates a seizure disorder and may be seen in the EEG even if the
patient is not having an epileptic seizure.
Other epileptic conditions may be diagnosed if spikes or sharp waves
(Fig. 4.29) are seen.
Tri-phasic waves are sometimes seen if the patient has severe liver
or kidney disease that is affecting brain function.
These are just brief descriptions of some of the simpler waveforms
that may be seen in any one EEG recording. Combinations of any of the
above patterns are possible which can make interpretation of the record
difficult. Abnormal activity is not always specific to any condition and
may suggest a few different diagnoses.
Fig. 4.29: Spike and wave activity
EEG Recording
The EEG recording can last from anything between 15 minutes to 1 hour
or longer depending on the patient. Typically the patient will be lying
down or sitting relaxed in a chair. Most of the recording is taken with the
eyes closed, although the patient will be frequently asked to open the
eyes for short periods.
Most patients will be asked to carry out a period of deep breathing
for approximately 3 minutes. This may produce some abnormal activity
which would not be seen while the patient is relaxed. The physiological
effect of deep breathing is to increase the amount of carbon dioxide
(CO2) being removed from the bloodstream. This fall in CO2 produces a
fall in blood pressure and at the same time blood vessels in the brain
become constricted. This reduces blood flow and the delivery of oxygen
and glucose to the brain. This in turn may produce some abnormal brain
activity not seen in the resting record.
Photo stimulation is also carried out. A strobe lamp is placed 30 cm
from the patient’s eyes. Brief flashes of light (2-5 seconds in duration) at
a number of different flash frequencies are delivered to the patient with
both eyes open and eyes closed. A continuous flash with increasing and
decreasing flash frequencies is sometimes used.
Some patients who are sensitive to flashing lights may show abnormal
activity in the EEG.
Throughout the test, the operator is constantly annotating the record
with any patient movements, or tasks that they are carrying out.
Other signals may also be recorded in conjunction with the EEG
such as heart rate (ECG), respiration, eye movements (EOG), and muscle
activity (EMG).
EEG Analysis
The EEG reports consist of a number of different sections. The operator
may prepare a report describing the type of activity seen in the record
together with changes produced by deep breathing and photo stimulation.
They will also comment on the patient’s state during the recording. The
physician will then interpret these changes with regard to the medical
problem being investigated.
With an increase in the number of long recordings being carried out,
many clinical and law enforcement specialties may make use of detection
algorithms such as spike and seizure detection..
Other methods of analyzing EEG data include Power Spectrum

Analysis. A Fast Fourier Transform (FFT) is performed on sections of
EEG data to determine the power content of the four main frequency
bands. The resulting waveforms can be displayed as a brain map which
will show the scalp distribution of the power within each frequency
band.
The amplitude of the different waveforms at a single point can also
be displayed in a similar format.
This type of display provides a more objective analysis of the EEG
activity compared to a subjective visual analysis by a physician.
Video Monitoring
Simultaneous video monitoring of the patient during the EEG recording
is becoming more popular. It allows the physician to closely correlate
EEG waveforms with the patient’s activity and may help produce a more
accurate diagnosis.
Domestic video recorders and cameras can be connected to an EEG
machine using a time code generator. This records an accurate time signal
onto the videotape. When the videotape and EEG are reviewed together
the two signals are accurately synchronized together.
Video monitoring is always used for Long-term Monitoring recordings
as the patient is unattended. The patient may also have an event button
connected to the EEG machine so that times when the patient thought
they were having an epileptic attack can be easily identified.
Sleep Studies
The EEG is frequently used in the investigation of sleep disorders
especially sleep apnea. EEG activity together with other physiological
signals such as heart rate, airflow, respiration, oxygen saturation and
limb movement are measured simultaneously. These recordings are
usually carried out overnight although some sleep studies can be carried
out in the department during the day under strictly controlled conditions.
The EEG record can be broken down into epochs which are normally
of 30 seconds duration. Using the EEG activity, each epoch is classified
into one of 5 sleep stages. This is displayed visually as a Sleep Histogram.
Respiration and airflow are used to look for periods of apnea which
occur when the patient stops breathing. These are then correlated with
the sleep stage in which they occurred and the level of the oxygen
saturation fell to during the apnea.
Electromyogram (EMG) and Nerve Conduction Velocity (NCV)

Studies
Electromyography (EMG) and Nerve Conduction Velocity (NCV) studies
are done to evaluate for injury or disease of muscle, nerve roots, and
peripheral nerves. These studies are normally done together and are
usually performed as a workup for complaints of pain, weakness,
numbness, or tingling.
Unlike radiographic or imaging tests that evaluate structure, electro-
diagnostic studies assess physiology or biochemical function.
Think of a malfunctioning telephone. A photograph of the phone
would miss the problem entirely, but with a volt-ohm meter a technician
could determine if there was a bad connection in the cable or in the
phone itself or the phone line, or at the telephone pole.
Nerve Conduction Studies
• During the nerve conduction study, mild electrical impulses are sent
along the course of a nerve in the arm or the leg. The electrical
impulse will make the muscles in the arm and leg contract. The
patient feels an electric shock every time the nerve is stimulated by
the NCV stimulator.
• Electrode patches are placed along the known course of the nerve, as
shown in the above illustration (Fig. 4.30).
• When the nerve is stimulated, it must transmit the signal along its
course.
• An electrode placed further down the arm or leg captures the signal
as it passes by. A healthy nerve will transmit the signal faster and
stronger than a sick nerve.
Fig. 4.30: Electrode placement for NCV study

• Nerve conduction velocity studies (NCV) look at the efferent and

afferent function of peripheral nerves. They measure the conduction
velocity of an electrical impulse along the axon (or trunk) of a
peripheral nerve. It tells us to what degree a nerve is physically
“pinched” or damaged.
• The nerve is tested at various points to determine if there is a “block”
along the direction of travel.
In order to understand nerve conduction studies we need to
understand how nerves respond to injury. Nerves are compound
structures consisting of many individual wires in an insulating covering
called “myelin”.
When there is compression on a nerve, a “conduction block” will
occur as shown in the Figure 4.31. This often temporarily blocks the
nerve impulse from traveling along the axon of the nerve. This happens
when you cross your legs and your foot falls asleep. When the pressure
is removed, the nerve usually returns to normal function. This “reversible
conduction block” is short-term and most often results in no permanent
neurological deficit. It will usually yield a normal NCV test.
If pressure remains on the nerve for a long enough period of time,
the nerve will lose some of its myelin sheath. This will cause the nerve
to conduct impulses more slowly, causing an increased conduction time
or decreased velocity. This will usually yield a slowed speed of conduction
along a nerve or what’s called an “increased latency” in an NCV test.
This may or may not result in permanent neurological deficit depending
upon the degree and extent of injury.
If pressure remains on a nerve for long enough, the nerve will die.
This will result in a decrease in amplitude of the overall “nerve signal”
as well as a decrease in velocity along the nerve axon. This usually results
in some degree of permanent neurological deficit and/or atrophy of the
innervated muscle.
Fig. 4.31: Progressive degeneration of nerves

Electromyography
• The needle EMG study involves the insertion of very thin pin
electrodes into the skin.
• The electrode is moved around slightly after its insertion.
• There are two kinds of electrodes used for EMG studies: Concentric
and Monopolar. Monopolar electrodes are designed for minimal pain
and discomfort.
• Muscles normally receive constant electrical signals from healthy
nerves, and in return “broadcast” their own healthy electrical signals.
• Once inserted into a muscle, the EMG electrodes record the resting
electrical potentials generated by the muscle.
• If the muscle is diseased or injured, or if it does not receive adequate
signals from its nerve supply, then the muscle signals that are
broadcast back through the EMG electrode will show the abnormal
insertional and resting potential activity.
• EMG confirms what is seen on the NCV and will often help
determine the difference between a nerve root and peripheral nerve
problem.
• It the nerve to a muscle is damaged, the muscle will start to atrophy
or degenerate. As it atrophies, its outer sheath (the sarcolemma)
becomes more sensitive, often causing the muscle to fire
spontaneously.
• In the beginning, this occurs in just a few muscle fibers so it can’t
been seen with the naked eye but is seen on the EMG. After sufficient
degeneration, one can often visually see the muscle firing; this is
called a fasiculation.
• Degeneration causes the muscle to become weaker and when it
contracts, will have an incomplete or diminished ability to contract,
also seen with the EMG.
• As the muscle gains its nerve supply back, it does so with larger
motor units, increasing the muscles action potential amplitude which
is also measurable.
• EMG helps us to see if a nerve and muscle are damaged, and whether
it is improving or getting worse.
• Nerves can heal. As long as the epineural sheath (the outer covering
of the nerve) remains intact, the nerve may regenerate some of its
myelin sheath, sprout new axons to innervate the muscle and return
to normal function. Since nerves usually grow at a rate of
approximately one inch per month, electrodiagnostic studies can
answer the following:
1. Location of the lesion- muscle or nerve?
2. Status of the lesion- improving or not
3. Nature of the lesion
4. How long it is likeley to take to recover?
EVOKED POTENTIALS
Electronic averaging has permitted the recording of low amplitude
potentials evoked by different types of sensory stimulus. These responses
are commonly used in the diagnosis of Multiple Sclerosis (MS), a relapsing
and remitting condition which is characterized by patchy inflammation
affecting the myelin sheath of the central nervous system. The object is
to demonstrate abnormalities in regions of the nervous system not known
from clinical manifestations to be involved -silent lesions. For example,
the finding of abnormal VEPs or BAEPs in a patient with paraparesis
would demonstrate abnormalities in at least 2 sites of the central nervous
system characteristic of MS.
Visual Evoked Potentials (VEPs)

The visual evoked potential is a gross electrical signal recorded from the
occipital cortex in response a systematic change in some visual event
such as a flashing light or an alternating chequered pattern. The recording
electrode is placed over the occipital cortex and the amplitude and latency
of the waveform generated can be measured (Fig. 4.32).
Figs 4.32A to C: Normal VEP in adults with 20/20 vision

This method currently provides the most sensitive means of detecting

subclinical lesions of the optic nerve and may enable a diagnosis of MS
to be made at an earlier time. Abnormality in the VEP is also encountered
with compressive lesions of the anterior visual pathways. In the pediatric
age group, the flash.
VEP may be used as a screening test for the visual pathway.
Brainstem Auditory Evoked Potentials (BAEP)

If one could record directly from several different levels of the subcortical
auditory pathway, one would see during the first 10 milliseconds
following an appropriate acoustic stimulus, a series of potentials
corresponding to the sequential activation of peripheral, pontomedullary,
pontine and midbrain portions of the pathway. When these acoustic nerve
and brainstem potentials are volume conducted to surface recording
electrodes at the vertex and earlobe, they form a composite series of
waves known as brainstem auditory evoked potentials. Since the
amplitude of these responses are very small (about 1/100 of spontaneous
EEG activity), special computer averaging technique is required.
The neurologic applications of BAEPs have been proven useful in
the diagnosis of MS. It may be used as a screening test for early detection
of acoustic neuromas and in the assessment of comatose patients. Like
the VEPs, it may also be a useful screening test for hearing in the pediatric
age group such as neonatal screening and those who do not cooperate
sufficiently with behavioral testing.
Somatosensory Evoked Potentials (SSEP) (Fig. 4.33)

SEPs can be recorded from electrodes placed over the somatosensory
cortex of the cerebral hemisphere contralateral to the applied stimulus.
Automatic averaging techniques are used to facilitate recording of these
small potentials. In the upper limb, the stimulus is usually applied to the
median or ulnar nerve whereas in the lower limb the tibial nerve is most
frequently used. Stimulation of the median nerve at the wrist elicits a
response at the brachial plexus at about 9 msecs (N9), the cuneate nucleus
12 msec (N12) and somatosensory cortex at 20 msec (N20).
Clinical uses of SSEP

The SSEP findings may help in the detection and localization of lesions
of the central somatosensory pathways but are not pathognomonic of
specific diseases. In Multiple Sclerosis (MS) the presence of SSEP
abnormalities may reveal subclinical lesions involving the central
somatosensory pathways thus aiding in early diagnosis. In patients with
definite MS, the incidence of SSEP abnormality is about 80% whereas in
the category of possible MS, the yield is only about 30%. The interpretation
of electrophysiologic results must therefore always be taken in a clinical
context.
Fig. 4.33: Normal SEPs elicited by stimulation of the median nerve and recording
at Erb’s point (EP), the 7th and 2nd cervical spine (CV7 and CV2) and
somatosensory cortex (C4)
ACKNOWLEDGEMENT
1. Radio-images and their interpretations were kindly contributed by Dr Sanjay
Sahu MD (Radiodiagnosis), Silliguri.
Physiotherapy in Neuro-
5 logical Dysfunctions
INTRODUCTION
Physiotherapists are clinicians who focus on symptomatic management
of a disorder. In case of neurological conditions, symptoms often relate
to dysfunctions. The first part of this chapter describes the nature of
neurogenic dysfunctions, why they develop, how to identify typical
symptoms and the principles of management of these symptoms, as well
as, the resultant dysfunction.
The second part of this chapter presents a pictorial guide to different
techniques of physiotherapy used at different stages of the evolution of
neurological dysfunction from acute to chronic to residual stages in a
logical sequence. The reader is advised to pick and choose different
exercises as deemed appropriate for the condition depending on their
own clinical correlation.
SECTION 1
PRINCIPLES OF PHYSIOTHERAPY MANAGEMENT

Neuro-physiotherapy is a specialized branch of physiotherapy used for
minimizing the morbidity, preventing disability and enhancing functional
ability in those who have sustained a neurological impairment due to an
injury to the brain, spinal cord or peripheral nerves, or are suffering from
neurological disease process such as CVA, Parkinson’s disease, Motor
Neuron Disease, Poliomyelitis, Peripheral neuropathies, etc.
What are Major Dysfunctions Associated with Neurological Disorders?

Any neurological disorder gives rise to a set of abnormalities in function,
which manifests as dysfunction. The physiotherapist has to tackle mainly
three kinds of abnormalities dealing with neurological disorders.
Physiotherapy of the Nervous
in Neurological System
Dysfunctions 73
These are:
• Motor abnormalities like increased or decreased tone, abnormal reflex
reactions and weakness of muscle, all of which independently or in
combination lead to movement dysfunction.
• Sensory abnormalities like increased or decreased sensory acuity, tingling,
numbness, loss of kinesthetic sensation, loss of proprioceptive sensation and
pain. All of these sensory abnormalities, individually or in combination
lead to self-inflicted trauma, perceptual dysfunctions and to a great
extent contribute to movement dysfunction. Sudomotor (abnormality
of sweating) and vasomotor deficits (abnormality of skin vascularity)
affect the integrity of the skin.
• Behavioral abnormalities like anxiety, depression, emotional lability,
neglect, loss of body image etc. lead to cognitive, perceptual and social
dysfunctions.
All of the above-mentioned abnormalities may coexist in most of the
neurological disorders, one type of dysfunction contributing to the other,
usually as a vicious cycle. Hence the approach of the physiotherapist has
to be holistic, where not a single presenting symptom should be ignored.
What can a Physiotherapist do to Help Treat Neurological Impairments?

A physiotherapist with interest in the treatment of neurological conditions
uses special set of skills for evaluation and treatment to help patients
with neurological dysfunction to:
• Re-learn purposeful movements of the extremities and trunk in bed
or out of bed.
• Facilitate recovery of postural control and balance in lying, sitting
and standing.
• Avoid secondary complications of prolonged bed rest or hypo
mobility.
• Help in inhibition of abnormal manifestation of primitive reflexes
and movement synergies.
• Help regain movement and co-ordination of the body parts.
• Stimulate hand movement and gain fine motor function.
• Teach functional mobility skills, including walking, needed for
performing activities of daily living independently or with minimum
of assistance.
• Assess the need for and prescribe aids, appliances and mobility
devices.
There is a common misconception that any neurological disorder
invariably leads to muscle paralysis and loss of sensation. In reality,
when a patient has sustained damage to the nervous tissues, it isn’t
always necessary that the muscles power or sensation is lost.
It’s often seen that muscles are not getting the right messages from
the brain to function effectively and the sensory feedback mechanism
either overreacts or reacts wrongly to a given stimulus.
For example, imagine that when ever you want to move your wrist,
your whole arm moves simultaneously, and no matter what you do you
can’t get your brain to give the right message to the muscles of the wrist
to perform the desired movement, keeping the rest of the arm relaxed.
The job of the physiotherapist is to help the patient with such
neurological problems, to relearn which muscles to use, when and how,
so that he can do only the movement that he wants, when ever he wants
it.
The path to recovery following any neurological damage is often a
long and difficult one, so the physiotherapist has to have the skill,
knowledge, patience and understanding to achieve satisfactory
rehabilitation of the patient.
A detailed assessment is necessary to highlight the problem areas
before starting treatment. Treatment goals should be structured primarily
to work towards solving immediate problems, to achieve goals that are
desired by the patient.
The long-term goals should focus on regaining as much independence
as possible in the activities of daily living, to be able to enjoy life once
again. This should be the foundation of the physiotherapy approach.
How does a Physiotherapist Treat Neurological Impairments?

Physiotherapists, like the homeopaths, treat the symptom of a disorder,
rather than the disorder itself. Hence, while treating a Neuro-disorder,
the diagnostic nomenclature has little significance in directing the
therapeutic approach. From the point of view of a physiotherapist any
neuro-disorder may be classified symptomatically, as either one of the
following:
• Upper motor neuron syndrome
• Lower motor neuron syndrome.
Each of the above syndromes has a set of typical symptoms,
impairments, and resultant dysfunction characteristic of the disorder.
The successful outcome of any therapeutic intervention can be assured
only when the nature of the disorder is correctly identified and appropriate
measures are taken to solve the problems.
Typical features of principal neurogenic syndromes are as follows:
Upper Motor Neuron Syndromes

The upper motor neuron (UMN) syndrome is a collective term for motor
symptoms seen in patients who have sustained lesions to the motor cortex
or the descending corticospinal system. Lesions producing UMN
dysfunction may occur in patients with congenital disorders like cerebral
palsy, neurodegenerative diseases such as multiple sclerosis or
Parkinsonism, vascular brain damage due to stroke, injuries to the brain
and spinal cord or hypoxic damage to the brain or the spinal cord.
Dysfunctions 75
UMN have a number of positive and negative signs (Table 5.1) which
impair motor skills required for normal mobility, activities of daily living,
and independence, thereby adversely affecting a person’s quality of life.
Table 5.1: Typical positive and negative motor signs in the UMN syndrome
Negative Signs Positive Signs
• Weakness • Exaggerated tonic • Associated reactions
• Loss of dexterity and phasic stretch (synkinesias)
• Loss of selective reflexes • Spastic dystonia
control of limb • Flexor and extensor • Increased muscle
movement spasms stiffness that may lead
• Co-contraction to contracture
Lower Motor Neuron Syndromes

The lower motor neuron (LMN) syndrome is a collective term for motor
symptoms seen in patients who have sustained lesions to the four
anatomical stations listed below. (Fig. 5.1 and Table 5.2)
1. The anterior (ventral) horn cell, as in polio, MND, etc.
2. The peripheral nerve, arising from ventral and dorsal nerve roots, as
in radiculopathy or neuropathy.
3. The neuromuscular junction as in myasthenia gravis.
4. The skeletal muscles as in myopathies.
Fig. 5.1: The four anatomic stations underlying lower motor neuron weakness
Table 5.2: Comparison of signs and symptoms in the UMN and LMN syndrome
Lower motor neuron weakness (LMN) Upper motor neuron weakness
(UMN)
Flaccidity Spasticity
Decreased tone Increased tone
Decreased muscle stretch reflexes Increased muscle stretch reflexes
Profound muscle atrophy Minimal muscle atrophy
Fasciculation present Fasciculation absent
May have sensory disturbances May have associated sensory
disturbances
CURRENT CONCEPTS IN NEUROPHYSIOTHERAPY

While treating neurogenic dysfunctions, the fundamental issue for the
physiotherapist to overcome is the limitation of function in day-to-day
life. The most frequently asked questions by the patient/care/giver
focuses on “When will I/he be able to do this or that?”
The common problem in all such patients may be
• Motor weakness
• Abnormal tone
• Abnormal sensation
• Abnormal control of movements.
Physiotherapy approach that is able to address these issues effectively
will be most appropriate in dealing with the dysfunctions associated
with neurological problems and provide relief to the patient.
Before we can identify how to solve these issues, we should be able
to say why these problems arise and how does physiotherapy actually
work in resolving the problems. Different groups of workers in the field
of neuro-rehabilitation have, over the years, developed different treatment
protocols for management of motor and sensory deficits arising out of
neurological disorders.
The fundamental concept behind these protocols is that the nervous
system, the brain in particular, can regenerate and reorient itself, even
after a devastating injury, through the little understood phenomena of
Neuro-plasticity, which is the ability of dormant nerve cells to activate
and/or orient themselves to undertake new functions, when the original
cells have been destroyed.
What should be Done? A Problem Solving Approach to

Neurophysiotherapy
The simplest way to plan physiotherapy treatment for any neurological
disorder would be to first isolate what is the actual dysfunction? Such
dysfunctions may be weakness of muscle, poor coordination of movements
and/or sensory abnormality.
The second question to be answered will be what are the key
components of the dysfunction?
A physiotherapist is primarily concerned with disorders of normal
movement, which may be caused by various components like:
Muscle weakness caused by
• Abnormal muscle tone, power, stretch reflex
Lack of coordination due to
• Liberation of primitive reflexes
• Aberration of sensory feedback
• Lack of perception and cognitive ability etc.
Dysfunctions 77
Once the key component causing the dysfunction and the contributing
factors has been identified, the therapist will know which defective
component in the functioning of the patient is causing maximum
problem and device means to minimize this particular dysfunction.
Goal Setting
The most essential goal for the physiotherapist, when treating a patient
with any Neuro-disorder, is to try to normalize defective movements,
teach appropriate responses to sensory stimuli and train appropriate
cognitive and behavioral responses. This is the key to regaining normal
functional ability. To achieve this goal the therapist must be able to identify
the most troublesome components of dysfunction and deal with them in
logical sequence.
What is Normal Movement?

It is the most energy efficient and economical way of moving the body
segments under voluntary control, to perform any desired task. To achieve
any normal movement, stability of the body and mobility of the body
segments to complete the desired task is essential.
What are the Factors that Determine the Stability of the Body at Rest
and Efficiency in Motion?
Background muscle tone is the most important element necessary to hold
the body segments together in an acceptable arrangement in relation to
one another with minimum expenditure of energy, otherwise known as
posture. Muscle tone is inversely proportional to the base of support
(BOS) of the body and directly proportional to the height of the center
of gravity (CG) of the body from the ground. The sensory feedback
received constantly from the peripheral receptors regarding BOS and CG
in any given posture are processed in the brain, which then determines
how much tone should be appropriate in which segment of the body to
perform any given task. Hence, apart from regulation of muscle tone,
ability of the sensory mechanisms to pick up and analyze feedback from
various receptors is also essential for stability of the body and economy
of motion.
How does Adverse Tone Affect the Stability and Mobility of the Body
in Neuro-disorders?
In neuro-disorders, the skeletal muscle tone may either be too high
(hypertonia) or too low (hypotonia). If the tone is too high, it may interfere
with proper alignment of body segments, by pulling each or any segment
away in the wrong direction due to over activity. This becomes even
more pronounced whenever any active movement is attempted. In UMN
lesions like the stroke, hypertonia of skeletal muscles may give rise to
unnecessary mass movement or synergy, whereas in parkinsonism it

may lead to rigidity of muscles, creating a poverty of movement. In
either case both the static and dynamic posture becomes defective, leading
to poor stability as well as mobility. In LMN lesions, hypotonia of key
skeletal muscles fail to support the weight of the body segments against
gravity. This may cause buckling or sagging of body segments against
one another, resulting in an unstable posture.
How does Impaired Sensory Feedback Mechanism Affect the Stabil-

ity and Mobility of the Body in Neuro-disorders?
Impaired feedback may mean either poor pick up of peripheral stimulus
from sensory receptors, as in LMN disorders or faulty interpretation in
the brain, of the sensory stimuli picked up by intact peripheral receptors,
as seen in UMN syndromes. In either case the brain as the master organ
responds to inadequate or improper sensory feedback. Hence the quality
and quantity of response is bound to be defective.
GENERAL PRINCIPLES OF MANAGEMENT OF HYPERTONIA-

SPASTICITY AND RIGIDITY OF MUSCLES
Hypertonia is a condition marked by an abnormal increase in muscle
tension and a reduced ability of a muscle to stretch. It is caused by injury
to motor pathways in the central nervous system, which carry information
from the central nervous system to the muscles and helps control posture,
muscle tone, and reflexes. Hypertonia can be so severe that joint
movement is not possible. Untreated hypertonia can lead to loss of
function and deformity. Hypertonia may manifest as spasticity, dystonia
or rigidity. Spastic hypertonia involves uncontrollable muscle spasms,
stiffening or straightening out of muscles, shock-like contractions of all
or part of a group of muscles, and abnormal muscle tone. It is seen in
disorders such as cerebral palsy, stroke, and spinal cord injury. Dystonic
hypertonia refers to muscle resistance to passive stretching and a tendency
of a limb to return to a fixed involuntary and abnormal) posture following
movement. Rigidity is an involuntary stiffening or straightening out of
muscles, accompanied by abnormally increased muscle tone and the
reduced ability of a muscle to stretch. This type of hypertonia is most
common in parkinsonism.
The initial management of hypertonia should focus on reducing
external triggering factors before specific treatment is considered. The
clinical management depends on a variety of different approaches,
necessitating the involvement of a comprehensive rehabilitation team. In
general terms, there are four potential aims of treatment of spasticity:
a. To improve function
b. To reduce the risk of unnecessary complication
c. To alleviate pain
Dysfunctions 79
d. To make nursing easier for the maintenance of hygiene, dressing and

transferring.
Physiotherapists usually address most hypertonia as spasticity. The
following passage discusses in detail the different approaches to reducing
hypertonia, whether spastic, dystonic or rigid in presentation.
Physiotherapy Treatment Techniques of Hypertonia

A physiotherapist has a vital role to play in the assessment and
management of spasticity through positioning, seating, splinting and
casting, and the use of orthotic devices.
• Controlling factors which exacerbate spasticity

Spasticity has a variety of triggers. Common causes for the exacerbation
of spasticity are urinary retention or infection, severe constipation, skin
irritation such as pressure sores or increased sensory stimuli from external
causes such as ill-fitting orthotic appliances and catheter leg bags.
Occasionally, exacerbation of spasticity may be due to an underlying
abdominal emergency or lower limb fracture, particularly in those who
are unable to appreciate pain and not able to localize their problem.
Often taking care of these triggers can reduce spasticity to a manageable
level.
• Positioning and seating

Correct positioning, particularly for the immobile patient, is an
important aspect of management of spasticity. Incorrect positioning in
bed, particularly in the early stages after stroke or brain injury, is a major
cause of unnecessary spasticity. The supine position easily exacerbate
extensor spasm by facilitation of the tonic labyrinthine supine reflex.
Similarly, a number of patients exhibit an asymmetric tonic neck reflex
after brain injury which, in the supine position, will encourage a
windswept posture characterized by asymmetric position of the pelvis,
with one hip assuming a flexed position in abduction and external rotation
whilst the other assumes an adducted and internally rotated posture.
This may lead to secondary orthopedic problems, particularly subluxation
of the hip on the adducted side.
Proper seating is vital. The fundamental principle of seating is that
the body should be contained in a balanced, symmetrical and stable
posture which is both comfortable and maximizes function. There are
many different types of seating system. All should have the ultimate aim
of stabilization of the pelvis without lateral tilt or rotation, but with a
slight anterior tilt so the spine adopts a normal lumbar lordosis, thoracic
kyphosis and cervical lordosis. The hip should be maintained at an angle
of slightly more than 90°; which is often facilitated by a seat cushion with
a slight backward slope. Knees and ankles should be at 90°.
In people with severe spasticity, this posture may not be possible or

may require a variety of seating adjustments such as foot straps, knee
blocks, adductor pommels, lumbar supports, lateral trunk supports and
a variety of head and neck support systems. An adaptable and adjustable
system is useful, particularly in people with complicated disabilities and
in those with variable conditions such as multiple sclerosis.
• Passive movements and reeducation of postures
It is sometimes a matter of trial and error to find an appropriate
posture that reduces spasticity. Functional postures like half lying, side
lying, sitting and standing can all be helpful in different circumstances,
with the primary aims of reducing spasticity and stretching the spastic
muscles, as well as facilitating the use of antagonistic muscle groups. In
order to prevent contractures, each joint should be put through a full
range of movement for at least 2 hr in every 24 hrs.
• Splinting and casting
The application of splints and casts can prevent the formation of
contractures in the spastic limb and serial casting can improve the range
of movement in a joint that is already contracted; a new cast being applied
every few days as the range improves. It is not known whether this is
purely a mechanical effect or whether splinting actually reduces spasticity.
Unfortunately, there is no clear agreement on the most appropriate design
nor the length of time a splint should be applied to give the desired
effect.
• Modalities
Cold inhibits spastic muscles, but the effect is short-lived, lasting for
about half an hour.
Heat is also used for relaxation of a spastic muscle. Unfortunately, the
anti-spastic effect of heat is relatively short-lived.
Electrical stimulation has been used in some centers. Alfieri found that
10 min of surged faradic stimulation to the finger extensors produced a
decrease in spasticity and improved ROM for up to 3 hrs.
Seib et al recently found that surged faradic stimulation of the tibialis
anterior muscle has an anti-spastic effect that lasts for up to 24 hrs.
Potissk and colleagues have confirmed similar findings with the use
of a transcutaneous electrical nerve stimulation, but the effects only persisted
for up to 45 min.
Unfortunately, the role of electrical stimulation and other related
techniques, such as electromyographic biofeedback and electrical
vibration, is still not clear. None of these appear to have much long-term
benefit but can have useful short-term effects, particularly when used as
an adjunctive treatment in combination with other measures, such as the
fitting of orthoses, weight transfer and remedial positioning.
Dysfunctions 81
There are a number of different dynamic physiotherapy techniques,

which claim an antispastic effect. There is, however, little evidence that
any particular technique is better than the other for the management of
spasticity.
• Oral Medication
Oral anti-spastic medication can be helpful. Oral medication is
adequate in for milder cases. However, in severe and focal spasticity, the
side effects, like drowsiness and weakness commonly seen in large doses,
restrict the usefulness of these drugs. Sudden withdrawl of these drugs
may cause convulsions.
A. First choice anti-spastic drug is baclofen, a GABA B receptor agonist
that cause pre-synaptic inhibition on the release of excitatory
neurotransmitters reducing muscle spasm. The standard daily dosage
of Baclofen is 80 mg, administered in divided doses. It may cause
drowsiness and weakness and occasionally induce hallucinations.
B. An alternative agent is dantrolene sodium, which works by
suppression of release of calcium ions from the sarcoplasmic reticulum
of muscle, with consequent inhibition of excitation, and contraction
of muscles It is an effective drug if introduced in slow incremental
doses up to a maximum of 400 mg daily in divided doses. In addition
to drowsiness, weakness and fatigue, it may cause impairment of
liver function, which necessitates monitoring liver function tests.
C. Diazepam is the earliest anti-spastic agent. It causes severe drowsiness
and fatigue. A new agent, tizanidine, take effect by preferential
inhibition of poly-synaptic spinal excitatory pathways. It works as
efficiently as baclofen with fewer side effects.
• Nerve blocks
a. Phenol/Alcohol Peripheral Nerve Block

Percutaneous phenol for selective peripheral nerve block was first used
by Khalili et al to manage focal spasticity. A surface electrode is used to
locate the motor point of a peripheral nerve, where phenol/alcohol is
injected. Any accessible peripheral nerve can be blocked in this manner.
The obturator is the commonest and most accessible nerve and gives rise
to very satisfactory reduction in adductor spasticity. The posterior tibial
nerve is also a useful injection site for the relief of calf muscle spasticity
and often abolishes troublesome clonus or facilitates the fitting of an
ankle-foot orthosis. Hamstring spasticity can be controlled by blocking
the sciatic nerve or directly the hamstring muscle. It is less easy to block
the femoral nerve to release the quadriceps muscle and the iliopsoas for
the relief of hip flexor spasticity. It is also possible to block the median
and ulnar nerves as well as the musculo-cutaneous nerve for the relief of
flexor spasticity at the elbow. If there is any doubt as to the potential
benefits of the nerve block then a local anesthetic may be used before
definitive block with phenol or alcohol. The effective duration of phenol

and alcohol nerve blocks are variable, ranging from a few days to several
months and are useful to treat focal spasticity either as definitive
procedures or as an adjunct to other techniques. The commonest side
effects of this technique are burning and loss of motor function.
b. Botulinum Toxin Block

Botulinum toxin type A produces dose-related weakness of skeletal
muscle by impairing the release of acetylcholine at the neuromuscular
junction. It is now an established first-line treatment for focal dystonia.
A number of studies have now shown that botulinum toxin is useful for
the management of spasticity. It is particularly helpful for spasticity in
the hip adductors, calf muscles and the upper limb flexors.
The technique is simple; botulinum toxin is diluted in normal saline
and is injected intramuscularly at the motor point. The dose varies
considerably depending on the bulk of the muscle and the number of
muscles to be injected. Botulinum toxin injection is a safe and effective
technique with very few side effects reported in the literature.
Occasionally, weakness of the injected muscle or of neighboring muscles
can be a problem, but no general systemic weakness has been reported.
The disadvantages are the cost of the toxin, the need for repeat injections
every 2-3 months and a risk of developing antibodies.
c. Intrathecal Baclofen Techniques

The use of intrathecal baclofen for the treatment of severe spasticity of
the lower limbs in paraplegia was first described by Penn and Kroin in
1984. Surgical implantation of a sub-cutaneous pump allows
programmable intrathecal delivery of baclofen via a silastic catheter, dose
being adjusted according to clinical effect.
• Surgical and orthopedic procedures
Surgical procedures for the management of spasticity is needed
primarily for release of fixed contractures.
Anterior and posterior rhizotomy have been performed traditionally
for the treatment of severe spasticity. An advanced technique pioneered
by Sindou and Jean Monod works through a microsurgical lesion in the
dorsal root entry zone (‘DREZ-otomy’). The procedure can be used for
both upper and lower limbs giving good results with minimal morbidity.
Occasionally, surgical repositioning of joints and limbs can alter the
BOS, facilitate proper seating and reduce spasticity. Common orthopaedic
intervention is Achilles tendon lengthening for a fixed equinus deformity,
often with associated correction of a varus deformity. Hindfoot varus is
normally caused by spasticity of the tibialis posterior whilst mid-foot
varus is normally caused by tibialis anterior spasticity. Often equino-
varus deformity needs the combination of Achilles tendon lengthening,
Dysfunctions 83
tibialis posterior lengthening and split anterior tibialis transfer procedures,

sometimes in combination with lengthening of the toe flexors. Similar
lengthening procedures, tenotomy and transposition can be undertaken
on the hamstring muscles. Obturator neurectomy or adductor tenotomy
can be carried out in more resistant cases of adductor spasm Hip flexion
deformities are easily corrected by iliopsoas release.
Surgery in the upper limb is not generally as successful as in the
lower limbs but various tenotomy or tendon-lengthening procedures are
possible, including lengthening of the biceps and brachio-radialis,
lengthening of the flexor carpi ulnaris and flexor carpi radialis tendons
for wrist flexor spasticity.
Points to Ponder
• Physiotherapy is vital for correct positioning, seating, use of orthoses,

splints and casts and for other anti-spastic measures such as use of
heat and cold and electrical stimulation.
• The use of oral medication and peripheral nerve blocks and botulinum
toxin are treatments which are proving very useful and are under-
used and undervalued.
• In more severe cases intrathecal medication can be helpful.
• Surgical procedures such as rhizotomy and orthopedic corrections
may sometimes be necessary, but usually only for the most severe
cases or for those who have been poorly managed in the earlier
stages.
Goals and Outcomes
• The treatment of spasticity, like all rehabilitation processes, must

start with the establishment of specific achievable goals and a carefully
planned strategy to achieve those goals.
• The final question is: Is it necessary to treat the spasticity at all?
Spasticity can be useful for the individual. For example, spasticity in
a lower limbs may serve as a brace to support the individual’s weight
for transferring or walking.
GENERAL PRINCIPLES OF MANAGEMENT OF HYPOTONIA- FLAC-

CIDITY AND WASTING OF MUSCLES
Hypotonia means “low tone,” and may refer to a physiological state in
which a muscle has decreased tone, or tension, often seen in normal
newborns and infants. Hypotonia is more of a description than a diagnosis.
Abnormal (Pathological) hypotonia is the clinical manifestation of a
disrupted reflex arc, commonly associated with Lower Motor Neuron
disorders affecting the Peripheral Nervous System.
Causes and Symptoms

The causes of pathological hypotonia are varied and numerous. Some
involve trauma to, or diseases of, the brain or spinal cord (CNS), while
others affect the peripheral nerves, neuromuscular junction, or the muscles
themselves. Common disorders giving rise to hypotonia of muscles are
lower spinal cord injuries, poliomyelitis, anterior horn cell diseases (MND),
Peripheral neuropathies and Nerve injuries.
CNS trauma and infection are perhaps the most common cause of
hypotonia in infants and in children. Insult to the brain may occur before
birth, around the time of birth, or after birth. Certain maternal/fetal
infections, maternal diseases, birth asphyxia, or maternal use of harmful
substances such as alcohol or certain drugs may cause prenatal CNS
damage. Infants who are born healthy may sustain post-natal brain injury
if they suffer from breathing difficulties, develop meningitis, or suffer
some other type of brain trauma.
Hypotonia may develop in an adult as a result of trauma or disease
affecting the cerebellum. A number of different genetic disorders are
associated with hypotonia, and may affect the nerves and by extension
the muscles supplied by them or the muscles only. Most genetic conditions
are generalized affecting multiple muscle groups and are progressive,
like myopathies.
In addition to low muscle tone, patients with hypotonia may also
exhibit excessive flexibility of the joints decreased deep tendon reflexes,
muscle weakness and weak gross motor skills such as sitting up, and
walking. They may also have difficulties with coordination.
Diagnosis
Diagnosis of the cause of hypotonia may involve a number of different
procedures, and tests. These include:
• A physical examination determines the presence and degree of
hypotonia by passive movements stretching the affected muscles.
• An electromyography (EMG) study measures extent of muscle fiber
activation during voluntary contraction.
• A nerve conduction velocity (NCV) study measures a nerve’s ability
to transmit electrical impulses to and from the muscle
• A muscle biopsy to analyze the affected muscle.
• Biochemical tests (CPK) of muscle tissue and blood.
• Genetic tests (Gene mapping) to look for possible hereditary genetic
causes affecting the brain, nerves, and/or muscles.
• MRI of the brain and spinal cord to locate possible changes like
demyelination, neuronal degeneration etc.
Determining which tests to use depends on the history and physical
findings. Depending on the cause and progression of hypotonia, treatment
and evaluation may be needed throughout life.
Dysfunctions 85
Treatment
Unlike the wide array of potential causes of hypotonia, treatment options
for low muscle tone are somewhat limited. In most cases, treatment may
be primarily supportive, such as mechanical assistance with basic life
functions like breathing and feeding, physical therapy to prevent muscle
wasting and maintain joint mobility, aids and appliances like calipers,
braces, wheelchairs etc to maintain mobility. Treatments to improve
neurological status might involve medication or corrective surgery to
help relieve contractures. Physical and occupational therapy helps to
maintain or improve muscle tone, strength, and coordination.
Recovery and Rehabilitation

In all cases, frequent or periodic monitoring of muscle tone and
performance (muscle charting), along with neurological status, should be
done to determine if the hypotonia is worsening, static, or improving.
Effective recovery and rehabilitation can only be achieved if an accurate
status of the condition is known. Since muscle weakness often
accompanies hypotonia, efforts to improve muscle strength through
resisted exercises or functional electrical stimulation may also improve
low muscle tone. Occupational and physical therapy can assist individuals
in developing alternative methods for accomplishing some everyday tasks
(Trick movements) they may find difficult. Speech therapy is beneficial
at any age if the muscles of the face and throat are hypotonic.
GENERAL PRINCIPLES OF MANAGEMENT OF INCOORDINATION

AND ATAXIA
Ataxia describes a lack of ability to move the muscles in a coordinated
fashion. People with ataxia have irregular or awkward movements.
Though most commonly used to describe the way a person walks, this
condition can affect any of the muscles in the body. Incoordination can
be due to many different types of problems, ranging from drinking alcohol
to having a stroke. Ataxia and incoordination may cause problems with
everyday activities, such as tying a shoelace or driving a car.
There are many possible causes for ataxia and incoordination.
Examples include:
• Damage to the brain from head injury, stroke, brain tumors or multiple
sclerosis
• Infection such as meningitis, syphilis etc.
• Effects of alcohol, barbiturates, seizure medications or “sniffing glue”
• Poisoning
• Vitamin deficiencies, such as lack of vitamin B2/B6/B12
• Hormone abnormalities, such as hypothyroidism
• Inherited conditions, such as Friedreich’s ataxia or ataxia-telangiectasia
• Sensory and motor nerve lesions, which often affect walking and
may occur with diabetes, lead poisoning, or certain cancer
chemotherapy medications
• Movement disorders such as Parkinson’s disease or Huntington’s
chorea
• Balance problems due to irritation or infections of the middle ear,
such as Meniere’s disease.
Depending on the cause of ataxia, there may or may not be long-
term effects. For example, ataxia from alcohol usually goes away when
the person is no longer intoxicated. If ataxia is related to a brain tumor
or cancer, death may occur. Multiple sclerosis can result in permanent
disability and severe weakness.
Treatment is directed at the underlying cause. For example, drugs
can help reduce ataxia if Parkinson’s disease is the cause. Antibiotics
may be needed for an infection. Surgery may remove a brain tumor. If
a stroke is the cause, the only treatment may be physical therapy to
improve function as much as possible.
Treatment may be short-term or lifelong. Those with Huntington
chorea, for example, may need treatment and care for the rest of their
lives.
Monitoring depends on the underlying cause. Those with diabetes or
AIDS often need close monitoring with frequent visits to the physician
hospitals and have blood tests.
Though the common aim of all therapeutic protocols are to reduce
morbidity and hasten recovery of function, these protocols have been
developed and tested under widely divergent conditions, on different
groups of patients. As such they are often contradictory to each other. A
standardized protocol of management is yet to be developed.
Principles of physical therapy for treatment of ataxia and
incoordination:
• Rehabilitation of patients with ataxia has traditionally included
Frenkel’s exercises, rhythmic stabilization, and the use of walking
aids and weights.
• Proprioceptive neuromuscular facilitation (PNF), including resistive
exercises helps improve strength, coordination, endurance, balance,
and gait, but no research studies of the efficacy of PNF for patients
with cerebellar disorders have been reported.
• In general, rehabilitation interventions for patients with chronic
cerebellar dysfunction have, in the past, been restricted to conservative
management (e.g. maintaining range of motion) and compensation
strategies (e.g. recommending that patients increase their base of
support or use assistive devices to improve stability.
• More recently, balance rehabilitation that increasingly challenges body
stability has been tried, using neuromuscular retraining methods.
Treatment is based on the premise that the patients needed to
Dysfunctions 87
reacquire proper motor control and associated balance through

adaptation to increasingly demanding conditions. Therefore, upper-
extremity use during balance and gait activities is minimized to
facilitate independent balance control. Improvement in functional
ambulation is often judged by the type of assistive device used,
amount of upper-extremity weight bearing on the device, level of
assistance required to walk, and maximum distance covered.
GENERAL PRINCIPLES OF MANAGEMENT OF SENSORY ABNOR-

MALITIES—NUMBNESS, PAIN, PARESTHESIA, ANALGESIA
Numbness usually arises from damage or disease of nerves. Numbness
is often associated with or preceded by abnormal pain-like sensations
often described as pins-and-needles, prickling or burning sensations. Any
numbness or abnormal sensation symptoms need prompt professional
medical advice.
The following medical conditions are some of the possible causes of
numbness.
• Nerve entrapments
• Nerve compression syndromes
• Repetitive motion disorders
• Carpal tunnel syndrome
• Circulatory disorders
• Diabetes
• Multiple sclerosis
• Stroke, transient ischemic attack.
Panic attack - some patients report numbness or tingling in panic
attacks (but only with many other symptoms including panic). Numbness
can affect various body parts and its cause depends on the location of the
numbness.
The cause of numbness may be more easily identified if other
symptoms exist.
Pain is an important sensory symptom. Milder abnormal nerve
sensations such as pins-and-needles, tingling, burning, prickling are all
known as “paresthesias” and can lead to numbness. The various senses
can have problems; giving rise to vision symptoms, hearing impairment,
taste symptoms, and temperature sensitivity. Any sensory symptoms need
medical investigation
Paresthesia
Paresthesias are abnormal sensations, such as numbness or tingling, which
may occur secondary to lesions anywhere in the nervous system. They
may be accompanied by hypoesthesia (decreased sensation), most
commonly noticed in response to painful or tactile stimuli. The etiology
of paresthesia is usually suggested by the distribution of the finding and
the associated symptoms.
Causes of Paresthesia
• Nerve compression or entrapment neuropathy caused by:
– Lumbosacral disc herniation with nerve root compression
– Posterior tibial nerve compression (tarsal tunnel syndrome)
– Peroneal nerve compression (foot drop)
– Cervical spine spondylosis/disc herniation with nerve root
compression
– Median nerve compression (carpal tunnel syndrome, often seen
in hypothyroidism or pregnancy)
– Ulnar nerve compression
– Long thoracic nerve compression (winged scapula)
• Infections (e.g., HIV/AIDS, herpes zoster, Lyme disease)
• Diabetic neuropathy (bilateral symptoms)
• Alcoholic neuropathy causing thiamine deficiency (vitamin B1) and/
or direct toxic effect of alcohol
• Vitamin B12 deficiency
• Uremia
• Vasculitis or collagen vascular disease
• Tumor– Carcinomatous infiltration or direct compression
• Toxins –Industrial exposures (e.g., lead, mercury, pesticides)
• Medications (e.g., pyridoxine, isoniazid, antiretrovirals)
• Guillain-Barré syndrome (usually bilateral)
• Hereditary motor or sensory neuropathies
• Amyotrophic lateral sclerosis
• Trigeminal neuralgia.
Diagnosis
A complete history and physical examination is necessary to determine
the etiology especially–Time of onset, anatomic distribution (focal, unilateral,
bilateral), history of trauma, diabetes, alcohol abuse, cancer, or collagen vascular
disease, associated weakness, cramping, pain, or loss of position or temperature
sense and comprehensive neurological exam with a focus on cervical or
lumbosacral nerve patterns.
Initial lab tests may include fasting blood sugar, electrolytes, calcium,
magnesium, TSH, glucose, BUN/creatinine, hemoglobin A1C, ESR, vitamin
B12, thiamine level, and chest X-ray.
Electromyography may be used to differentiate neuropathic versus
myopathic causes of associated muscle atrophy, nerve conduction studies,
nerve biopsy (usually the sural nerve) is reserved for proof of histological
causes, e.g. amyloidosis.
Dysfunctions 89
Treatment
• In compression or entrapment neuropathy
– Avoid aggravating activities and repetitive trauma
– Immobilization/splinting of affected limb
– Physical therapy and proper ergonomics/biomechanics
– NSAIDs and/or acetaminophen
– Epidural steroids in severe cases
– Surgical release of entrapped nerve/herniated disc if conservative
measures fail and symptoms persist
– Surgical removal of compressive tumors
• Treat and control underlying systemic diseases (e.g., diabetes,
alcoholism, HIV, renal disease, vasculitis)
• Treat underlying infections with antibiotics
• Supplement vitamin deficiencies
• Discontinue offending medications or toxic exposures
• Painful peripheral neuropathies (diabetic, alcoholic) may be relieved
by amitriptyline or desipramine, phenytoin or carbamezapine, or
topical capsaicin cream.
• Counter irritation caused by physical modalities like ice, dry heat,
TENS, iontophoresis, didynamic current are sometimes useful.
Analgesia
Analgesia, the absence of sensitivity to pain, is an important sign of
central nervous system disease, commonly indicating a specific type and
location of spinal cord lesion. It always occurs with loss of temperature
sensation (thermo anesthesia) because these sensory nerve impulses travel
together in the spinal cord. It can also occur with other sensory deficits
— such as paresthesia, loss of proprioception and vibratory sense, and
tactile anesthesia — in various disorders involving the peripheral nerves,
spinal cord, and brain. However, when accompanied only by thermo
anesthesia, analgesia points to an incomplete lesion of the spinal cord.
Analgesia can be classified as partial or total below the level of the
lesion and as unilateral or bilateral, depending on the cause and level of
the lesion. Its onset may be slow and progressive with a tumor or abrupt
with trauma. Transient in many cases, analgesia may resolve
spontaneously.
Emergency Interventions
Always suspect spinal cord injury if the patient complains of unilateral
or bilateral analgesia over a large body area, accompanied by paralysis.
Immobilize his spine in proper alignment, using a cervical collar and a
long backboard, if possible. If a collar or backboard isn’t available, position
the patient in a supine position on a flat surface and place sandbags
around his head, neck, and torso. Use correct technique and extreme
caution when moving him to prevent exacerbating spinal injury.

Continuously monitor respiratory rate and rhythm, and observe him for
accessory muscle use because a complete lesion above the T6 level may
cause diaphragmatic and intercostal muscle paralysis. Have an artificial
airway and a handheld resuscitation bag on hand, and be prepared to
initiate emergency resuscitation measures in case of respiratory failure.
History and Physical Examination

First, take the patient’s vital signs and assess his level of consciousness.
Then test pupillary, corneal, cough, and gag reflexes to rule out brainstem
and cranial nerve involvement. If the patient is conscious, evaluate his
speech, gag reflex, and ability to swallow.
If possible, observe the patient’s gait and posture and assess his
balance and coordination. Evaluate muscle tone and strength in all
extremities. Test for sensory deficits over all dermatomes (individual
skin segments innervated by a specific spinal nerve) by applying light
tactile stimulation with a tongue depressor or cotton swab. Perform a
more thorough check of pain sensitivity, if necessary, using a pin. Also,
test temperature sensation over all dermatomes, using two test tubes—
one filled with hot water, the other with cold water. Test vibration sense
(using a tuning fork), in each arm and leg, proprioception, and superficial
and deep tendon reflexes. Check for increased muscle tone by passive
movements of elbows and knees.
Focus your history taking on the onset of analgesia (sudden or
gradual) and on any recent trauma—a fall, sports injury, or automobile
accident. Obtain a complete medical history, noting especially any
incidence of cancer in the patient or his family.
Causes
• Anterior cord syndrome: With anterior cord syndrome, analgesia
and thermo anesthesia occur bilaterally below the level of the lesion,
along with flaccid paralysis and hypoactive deep tendon reflexes.
• Central cord syndrome: Typically, analgesia and thermo-anesthesia
occur bilaterally in several dermatomes, in many cases extending in
a cape like fashion over the arms, back, and shoulders. Early weakness
in the hands progresses to weakness and muscle spasms in the arms
and shoulder girdle. Hyperactive deep tendon reflexes and spastic
weakness of the legs may develop. However, if the lesion affects the
lumbar spine, hypoactive deep tendon reflexes and flaccid weakness
may persist in the legs.
• Brown-séquered syndrome (spinal cord hemi section): Contra lateral
analgesia and thermo anesthesia occur below the level of the lesion.
In addition, loss of proprioception, spastic paralysis, and hyperactive
deep tendon reflexes develop ipsilaterally. The patient may also
experience urine retention with overflow incontinence.
Dysfunctions 91
• Brainstem syndrome: With brainstem involvement, additional

findings include facial analgesia and thermo anesthesia, vertigo,
nystagmus, atrophy of the tongue, and dysarthria. The patient may
also have dysphagia, urine retention, anhidrosis, decreased intestinal
motility, and hyperkeratosis.
• Drugs: Analgesia may occur with use of a topical or local anesthetic.
Special Considerations in Analgesia
• Focus on preventing further injury to the patient because analgesia

can mask injury or developing complications. Guard against scalding
by testing the patient’s bathwater temperature before he bathes; advise
him to test it at home using a thermometer or a body part with intact
sensation.
• Prevent formation of pressure ulcers through meticulous skin care,
massage, use of lamb’s wool pads, and frequent repositioning,
especially when significant motor deficits hamper the patient’s
movement.
• Because a child may have difficulty describing analgesia, observe
him carefully during the assessment for nonverbal clues to pain,
such as facial expressions, crying, and retraction from stimuli.
Remember that pain thresholds are high in infants, so your assessment
findings may not be reliable. Also, remember to test bathwater
carefully for a child who’s too young to test it himself.
PHYSIOTHERAPY CONCEPTS OF MANAGEMENT

Present day approach of physiotherapy in tackling neurogenic dysfunction
has taken shape over the last century through trials and errors of various
clinicians, working with different patient groups, at different clinical
settings. Each of these clinicians has proposed their own techniques for
management of the neurogenic dysfunction studied by them. However,
due to lack of any standardized scientific validation and contradictory
nature, these proposed techniques have not developed into clinical
protocols and should be treated only as concepts of management. The
following passage details several concepts of management used
worldwide by physiotherapists. It is desired that the reader explore
applicability of each concept to the clinical problems they are facing, pick
out the most appropriate components and, by trail and error, try to
develop their own protocol for managing neurogenic dysfunctions.
THE REMEDIATION/FACILITATION CONCEPT

In this concept emphasis is placed on neuromuscular facilitation, sensory
stimulation and remedial exercises to minimize morbidity and enhance
recovery of lost function. Emphasis is placed on the development
patterns/activities to promote recovery of function through neuro-

muscular facilitation. The following techniques of remediation/facilitation
are adopted worldwide:
Proprioceptive Neuro-muscular Facilitation Approach (PNF)

This technique was initially introduced by Herman Kabat and later
developed by Knott and Voss. It proposes using the proprioceptors like
the muscle spindle (stretch receptors) to facilitate contraction in the target
muscle (Table 5.3). The PNF concept focuses on total patterns of movement
during voluntary activities to promote motor learning in synergistic
(having similar action) muscle groups. Normal movements are usually
spiral and diagonal in nature. PNF exercises are therefore usually given
in such patterns (Table 5.4). Proprio-ceptive elements ellicitated by
maximal resistance or stretch to a target muscle is integrated into such
movement patterns to result in spreading (irradiation) of activation from
stronger muscle of a group to the weaker muscles used in a specific
movement pattern. This serves as a preparatory step to achieve movement
and posture control in a total pattern, before advanced motor skills can
be learned.
Points to Ponder
1. Stretch is first applied on a muscle to stimulate the receptors (muscle
spindles) within the muscle. This facilitates stronger contraction of
the muscle/muscle group.
2. Once the target muscle/muscle group has been sufficiently aroused,
movement is attempted passively by the therapist in a functional
pattern, which is usually diagonal or spiral in nature. This is essential,
since all normal functional movements occur in a diagonal plane and
spiral axis of the body.
3. The grip of the therapist is the key to success of such training, e.g.
grip used by the therapist may provide stretch/resistance/traction
to the proprioceptors, as may be required.
4. The patient is asked to follow the movements with his eyes and at
a later stage to participate to the best of his ability. This creates
activation of hitherto inactive muscles. As the pattern is repeated
time and again, weak muscles gain power.
5. Impulses may overflow from the stronger, active muscles to weaker
muscles in the group that are required to act simultane-ously to
produce the pattern of movement.
6. Functional movement training must start from mastering the rotatory
component in the distal part, gradually progressing to the proximal
part of the extremity. Repeated practice, under the manual guidance
of the therapist helps in mastering the movements one by one.
Dysfunctions 93
7. Traction to the joints may be used when attempting movements in

an antigravity plane and joint compression may be incorporated when
performing the same movements in a gravity-assisted plane.
8. Clear and audible verbal commands from the therapist are essential.
In rehabilitation of the neurogenic dysfunctions, PNF is primarily
used for strengthening and elongation of shortened muscles.
Table 5.3: Specific techniques applied for PNF

What? How? Why?
Approximation Compression force Simulates afferent feed-
applied to joint surfaces back. Facilitates extensor
activity. Stabilizes posture
Agonist reversal Slow isotonic concentric Strengthens weak hypo-
contraction followed by tonic postural muscles.
eccentric action of the Improves postural control
same muscle group during weight transfers
through a desired ROM
Alternating isometrics Alternating isometric Improves stability in static
setting of muscle groups and dynamic posture.
on one side a joint Increases antigravity
followed by those on the control in weakness or
opposite side, in anterior- ataxia
posterior, medial-lateral
and diagonal patterns
Contract-relax Isotonic movement in Reduces limitation of
rotation range of large ROM due to muscle
joint is performed followed tightness and spasticity
by isometric hold of tight
antagonists against
slowly increasing
resistance and then
relaxing suddenly. It must
be followed up with
movement in active ROM
gained in the agonist
pattern.
Hold-relax-active Isometric contraction of Improves ability to initiate
motion agonists in mid-range to muscle contraction in
inner-range followed by hypotonia, weakness and
relaxation and then by muscle imbalance
passive movement into
the ROM gained. This is
immediately followed up
with resisted active
movement of the agonist
through full range
Contd...
Contd...
Hold-relax Isometric contraction of Relaxation technique
tight antagonist against performed at the point of
slowly increasing limitation of ROM caused
resistance followed by by muscle tightness,
sudden relaxation and spasm or pain
passive movement into the
newly gained ROM in
agonist pattern
Maximal resistance Resistance is applied to Improves muscle strength
stronger muscles to cause and imbalance
overflow of stimulus to
weaker muscle in the
same or opposing groups
Repeated contractions Repeated isotonic Improves incoordination,
contractions induced by a weakness, endurance and
series of quick stretches muscle imbalance
and enhanced by
resistance throughout the
ROM in one direction till
the point of weakness
Resisted progression Tracking resistance is Improves weakness,
applied to facilitate endurance, timing and
progression in weight control of movements
transfers, kneel walking
and gait training
Rhythmic initiation Passive to assistive to light Reduces spasticity, rigidity,
tracking resistance in one and inability to initiate
or both direction of limb movements (apraxia)
ROM
Rhythmic rotation Passive to assistive to light Reduces spasticity, rigidity,
tracking resistance in one and inability to initiate
or both direction of trunk or movements (apraxia)
limb rotation
Rhythmic stabilization Simultaneous isometric Improves instability in
contraction of agonist and weight bearing, antigravity
antagonist control, weakness and
ataxia
Slow reversal Slow isotonic contraction Improves inability to
of the in agonist and then change direction,
antagonist pattern incoordination, imbalance
and weakness
Timing of emphasis Maximum resistance to Improves instability in
elicit a sequence of weight bearing, antigravity
contraction from strong to control, weakness and
weaker components of a ataxia
muscle group
Contd...
Dysfunctions 95
Contd...
Traction Distraction force applied Simulates afferent feedback.

to joint surfaces Facilitates flexor activity.
Reduces stiffness
Table 5.4: Diagonal patterns of movements used in PNF

Upper limbs D1F D1E D2F D2E
(supine position Flexion- Extension Flexion- Extension
movement occ- Adduction- Abduction Abduction Adduction
urs at shoulder Ext. Rotation Int. Rotation Ext. Rotation Int. Rotation
joint elbow, may
remain straight
or flex and
extend)
Lower limbs D1F D1E D2F D2E
(supine position Flexion- Extension Flexion- Extension
movt. occur at Adduction- Abduction Abduction- Adduction
hip joint knee Ext. Rotation Int. Rotation Int. Rotation Ext. Rotation
may remain
straight or flex
and extend)
Trunk Upper trunk Upper trunk Lower trunk Head and neck
(supine or Flexion and Extension and Flexion and flexion with
sitting; head and rotation in the rotation in the rotation, knee rotation to right
trunk moves direction of UL direction of UL flexed or or left
together) moving in D1E moving in D1F extended
pattern pattern
Neuro-developmental Technique (NDT/Bobath Approach)

Dr Karl Bobath and Ms Berta Bobath primarily developed this concept
for management of CP children in 1940. Normal movement sequences,
patterns and balance reactions are focus of this concept. Therefore accurate
analysis of the patient’s movement pattern is essential. The therapist
should be able to answer, “Why does he move the way that he does”?
Answers are usually abnormal tone, liberated primitive reflexes (tonic
reflexes) and mass movement patterns, producing faulty posture and
interfere with the process of motor relearning.
Once the key component causing the faulty movement pattern has been
identified, motor relearning can be promoted by inhibition of abnormal
tone and reflexes by adopting reflex inhibiting postures will allow normal
movements and the motor relearning to take place.
Points to Ponder
1. Physiotherapists, for treatment of patients with abnormal tone and
movements like CP, developed this approach.
2. Neuro facilitation concept used in this approach believes that if the
patients’ body is handled/positioned in a particular way it helps in
reducing the abnormal reflexes, hypertonia and thereby gains control

of movement.
3. Most important contribution of NDT concept was that it tried to
explain the role of motor control in normal and abnormal movements.
4. NDT concept depended on the theory of release of primitive reflexes
to explain neurological movement dysfunction.
5. Postural reflexes that are present normally in an infant are integrated
as the infant grows to an adult.
6. In the event of an injury to the immature brain (as in CP) or to a
mature brain (as in CVA/TBI), these primitive reflexes may be
released, resulting in abnormal movements and postures.
7. Bobath et al. proposed that such abnormal reflexes are best inhibited
by positioning the limbs and body in a reflex inhibiting posture
(Passive correction).
8. Once the body has gained ability to sustain such reflex inhibiting
postures without assistance, movements may be attempted in similar
reflex inhibiting patterns to gain some degree of functional
independence.
9. Feedback, mostly sensory, is believed to provide stimulus for
adaptation. Adverse feedback generated by faulty posture or
movements tends to reinforce faulty patterns. Hence inhibition of
wrong feedback plays an important role in developing treatment
strategy under NDT.
• Movement therapy in Hemiplegia or TBI using Brunnstrom’s approach
Sensory-motor recovery of hemiplegia following CVA (stroke) occurs in
a specific sequential pattern. The rate of recovery varies between limbs,
i.e. lower limbs recover faster than upper limbs. Even within the same
limb, the recovery is usually faster in proximal muscle groups than distal,
i.e. in upper limb, shoulder recover function faster than the hand. Such
recovery may reach a plateau within a period of six to eighteen months
of the stroke.
Brunnstrom’s concept of assessment can identify the stage of recovery
in a stoke patient and provide an accurate prognosis of the recovery. It
also provides a clear understanding of faulty movements in hemiplegia
so that appropriate remedial measures can be adopted.
Brunstrom’s technique of treatment is used to develop tone in flaccid
stage of UMN syndromes arising from pure pyramidal lesions like stroke
or traumatic brain injury.
Points to ponder
1. This technique utilizes reflex responses, which are trained to be under
voluntary control.
2. Head and neck control is trained stimulating tonic neck reflexes
(ATNR, STNR), tonic lumbar and tonic labyrinthine reflexes.
Dysfunctions 97
3. Trunk control is developed through righting reactions and balance

training in various postures.
4. Associated reactions are used to develop further functional ability,
e.g. hyperextension of thumb producing release of finger flexors.
• Sensory stimulation techniques (Rood’s approach)
CVA Patients, having difficulty in initiating and sustaining movement,
benefit from extra feedback in the form of proprioceptive, tactile or
vestibular stimulus in the early stages of motor relearning. Response to
such stimulus depends on the extent of CNS damage, level of arousal,
type and amount of stimulus. Multiple stimuli (spatial summation) or
repetition of the same stimuli (temporal summation) may be necessary in
patients with low LOC. Patients having the ability to initiate, sustain and
self-correct voluntary movements should not be treated with this
approach.
Techniques
• Proprioceptive stimulation—One may use quick stretch or tapping
to facilitate muscle contraction, slow stretch to release spasm,
resistance to movement to increase feedback, joint approximation to
increases tone and Traction to reduce spasm through activation of
afferents, vibration- 100-200 Hz activates muscle spindles, relaxes
muscle spasm and inhibits antagonists.
• Exteroceptive stimulation: One may use Quick stoking/icing for
facilitation, firm pressure for inhibition, slow stroking and neutral/
moist warmth for relaxation, prolonged icing for reducing muscle
tone/spasm.
• Vestibular stimulation: Such as slow rocking to reduce tone, Fast
rolling/spinning for increasing tone, coordination and retinal image
stability and Head down position to activate generalized extensor
tone.
MOTOR CONTROL AND MOTOR LEARNING CONCEPT

This concept aims at gaining functional independence through learning
task specific movement control using motor control strategies and motor
relearning strategies.
• Motor control strategies
Motor control strategies consist of five components:
1. Motor program is a set of pre-set sequence of muscle activation
producing a coordinated voluntary movement. Such program is
usually learned and can be carried out irrespective of peripheral
feedback.
2. Motor plan is an overall strategy for movement requiring coordination
of several motor programs.
3. Feedback mechanism are incoming (afferent) information sent to

the control centers in the brain from the peripheral receptors, updating
the control centers regarding accuracy of the movement while it is
taking place and the adaptations necessary to meet the demands of
the environment.
4. Feed forward mechanism readies the musculo-skeletal system in
anticipation of a movement or changes an ongoing movement pattern
in response to sensory feedback.
5. Motor skill acquisition is goal directed, problem-solving behavior
organized through development of motor programs and their
integration to form a motor plan, which can be adapted to changes
in environmental demands.
SECTION 2
PICTORIAL GUIDE TO PHYSIOTHERAPY TECHNIQUES IN

MANAGEMENT OF NEUROLOGICAL DYSFUNCTIONS
Mat exercises: The mat exercises are done on a floor mat or on a padded
wooden plinth. The area of an exercise mat should be minimum 6’ × 6’.
Mat exercises are used for progressive mobilization of a bed-ridden
patient. Purposes of mat exercises are to activate, re-educate and
strengthen postural muscles of the trunk and those of the extremities and
to teach the patient to move and change position on his own. Started as
soon as the patient is stable, these exercises contribute in prevention of
pressure sores, postural instability, deformities of the spine and limbs, etc.
Mat exercises start with rolling as seen in the Figure 5.2. The patient
is supine with the therapist sitting on his knees beside him. The patient
tries to roll over to either side using the leverage of both his upper limbs
and trunk. The therapist guides the movement of rolling, keeping a sharp
eye on the symmetry of patient’s posture. Repeat 5 times on either side
Fig. 5.2: Rolling

Dysfunctions 99
and as the patient gets better control he may try to roll on to his chest
and then on to his back like a log.
Pelvic rolling as shown in the Figure 5.3 follows rolling. The starting
position is supine. The patient flexes both hip and knee to 90 degrees and
then keeping the both feet and the upper extremities on the plinth, rotates
his spine to touch his flexed lower limbs to the plinth on the ipsilateral
side. The therapist kneels to one side of the patient, stabilizing the contra
lateral shoulder on the mat. This exercise mobilizes and strengthens the
lower trunk muscles. Repeat 5-10 times on either side.
Abdominal muscle strengthening exercises, as shown in the Figure 5.4
is a preparatory exercise for sitting up. The patient starts from supine,
holding on to the arm of the therapist with both hands. He takes a deep
breath, lets it out and then tries to pull him self up to sitting keeping his
elbow in extension, using the strength of his abdominal muscles. Repeat
5 times to start with, overdoing may cause abdominal muscle cramps.
Bridging as demonstrated in the Figure 5.5 is exercise of choice for
early strengthening of spinal and hip extensor muscles. The starting
position is supine. The patient rests both his palm on the plinth and
raises his buttocks off the plinth arching his back. Therapist kneels by the
side guiding the movement. Repeat 10-20 times in one sitting.
Fig. 5.3: Pelvic rolling
Fig. 5.4: Abdominal exercises

Fig. 5.5: Bridging
If the patient is allowed to lie on his stomach, further progression

of spinal extension can be done by the exercise as shown in the Figure 5.6.
He tries to lift his chest off the bed using the combined power of upper
limbs and back muscles. Therapist kneels by his side, guiding the
movement and keeping the spine straight. Repeat 10-20 times.
Fig. 5.6: Spinal extension
Fig. 5.7: Prone kneeling

Dysfunctions 101
Prone kneeling is the logical progression from prone spinal extension

(Fig. 5.7). In this position, like our ancestors, the great apes, the patient
begins to learn to transfer weight through all his extremities (Figs 5.8A
and B). This is an essential exercise to train for prerequisites for walking.
Remember, a chimpanzee can walk slowly for short periods on two feet
but if it has to move fast it does so on four feet because the larger base
of support in four-point weight bearing provides greater stability and
safety. Hence this exercise is most useful for patients who have not walked
for long and may also have weak lower limbs (Figs 5.9A and B). Ideal for
spastic para and in hemiplegia the flexed hip and knee inhibits extensor
spasticity, while the loading of upper limbs help build power and inhibit
flexor synergy.
Figs 5.8A and B: From prone kneeling position the patient may alternately extend
one lower limb or an upper limb, maintaining balance on a three-point weight bearing
as shown above. This progression from prone kneeling helps train better balance
and postural control, as well as, increases the power of extensors of the extremities
and spine. Repeat 5-10 times in a sitting. The therapist must be close to the patient,
kneeling by his side, ready to support if the patient tends to be misbalanced. It is a
difficult maneuver to master, particularly for a patient who till recently has been bed
ridden. Be careful!
Figs 5.9A and B: Kneel standing (left) and half kneeling (right is the first step in the
quest for gaining standing balance. In either case the therapist must adopt identical
position in front of the patient. In the beginning the patient may hold on to the
shoulder of the therapist, more for reassurance than for support. The therapist
guides the pelvis of the patient to maintain midline symmetry and proper pelvic tilt
and obliquity
Sitting balance training and weight transfer through upper limb (Fig. 5.10)
is seen in the picture at the left. Patient sits in high sitting at the edge of
the plinth, with both feet planted on the ground. The therapist kneels
behind the patient, ensuring symmetry, keeping the elbow of the weight
bearing upper limb straight and if required mobilizing the central key
point of the patient (located at the solar plexus) about the weight bearing
line of the body, to gain better control of the trunk. As the patient gains
balance and confidence in this position, he tries to manipulate his own
key points. Practice for 10-20 cycles in a sitting.
After achieving unsupported sitting balance the patient may be
progressed on to vector exercises, as demontrated in the picture at the
left. In high sitting position, the patient clasps both hands in the front
and then touches the hand of the therapist held at different angles of the
clock in the front of the patient (Fig. 5.11). Initially the therapist places
his hand within easy reach of the patient. As the patient gains trunk
Fig. 5.10: Sitting balance training and weight transfer through upper limb
Fig. 5.11: Vector exercises to gain trunk control and eye hand coordination
Dysfunctions 103
balance and eye-hand coordination the therapist progresses the exercise

by moving his hand little away so that the patient has to lean further,
within his base of support, at different alngles of the clock, to touch it.
Repeat for 10-20 cycles in clockwise and anticlokwise direction.
• In the first photo (Figs 5.12A to C) at the left the patient rests his
buttocks at the edge of the plinth in 3/4th standing, while transferring
almost full weight of his body through the lower limbs. Since his
lower limbs are weak and may buckle, therapist, sitting in front,
crosses his knee in front of the patient’s to prevent sudden buckling.
The patient holds on to the shoulder of the therapist for additional
security.
• In the second picture you see the patient moving away from the
edge of the plinth to full weight bearing, the therapist guiding the
pelvis into proper alignment, while keeping his knee against the
knee of the patient as an insurance against buckling.
• The third picture shows a patient learning to stand for prolonged
periods in an Oswestry standing frame. This kind of standing frame
is simple to make, low cost, wooden structure that allows even a
wheel chair borne patient to stand for physiological benefits. The
patient is standing in front of a full-length posture mirror to correct
his posture through visual feedback.
Paraplegia patients may stand for prolonged periods with help of two
straps, one under buttocks and the other in front of the knee to hold the
patient upright. The tray in front allows the support of upper limbs in
patients with poor trunk control.
Figs 5.12A to C: The series of three pictures above demonstrate the steps to
achieving standing balance
Once the patient has gained—

• Sufficient strength in his lower extremities
• Good trunk balance
• Confidence.
He may be started on gait training. The choice of mobility aids will vary
depending on the three factors mentioned above. In the pictures above
the patient is being trained to walk with a pair of elbow crutches, using
a four-point gait (Figs 5.13A and B).
Figs 5.13A and B: Gait training
Four-point gait is ideal for neurological conditions since it offers

greatest base and points of support during locomotion, which is useful
for safety in presence of motor weakness and incardination.
Disorders of the Brain:
6 CVA, TBI and Brain Tumors
INTRODUCTION
The Brain is a delicate organ. A focal lesion in any one of the hemisphere
of the brain, primarily caused by either Cerebrovascular Accidents (CVA)
or Trauma or Tumor or Infection, may result in motor, sensory and
cognitive impairments in the contralateral side of the body, presenting
clinically as hemiplegia, i.e. half sided paralysis of the body.
A generalized damage to the brain, either due to cerebral anoxia
occuring at birth, or edema and/or diffuse axonal disruption as secondary
complications of trauma or CVA, may result in widespread damage to
the brain cells of both hemispheres, which may cause motor and sensory
involvement of both extremities and trunk, as well as loss of perception,
cognition and other higher functions like emotion, memory, speech, vision,
presenting clinically as encephalopathy, i.e generalized brain dysfunction
involving the entire body.
What ever the cause and nature of the dysfuntion of the brain, the
basic principles of assessment, goals and interventions as far as
physiotherapy is concernerd are similar in nature.
The following chapter is thus divided into three separate sections,
covering Stroke (CVA), Traumatic Brain Injury (TBI), and Brain tumors
based on the presenting symptoms of each disorder.
The principle of physiotherapy management in these disorders of
the brain is decided, based on the nature of symptoms and can be used
interchangeably, irrespective of the cause. As far as treatment techiniques
are concerned, like positioning, facilitation, etc. whatever is appropriate
for treating himeplegia caused by CVA may be equally useful to treat
dysfunctions caused by a TBI or tumor and vice versa.
SECTION 1
CEREBROVASCULAR ACCIDENTS (CVA) OR STROKE

INTRODUCTION
Alternative names: Brain stroke, Brain attack
Definition: A cerebral stroke or CVA consists of a series of cataclysmic
events occurring throughout the body due to temporary or permanent
cut off of the blood supply to any part of the brain. Commonest
manifestation of such disruption of cerebral blood supply is paralysis of
half side of the body, called hemiplegia.
Categories
1. Ischemic Stroke resulting from:
• Cerebral thrombosis, caused by formation of blood clot within
the cerebral artery network
• Cerebral embolism, caused by bits of matter like broken blood
clots, fat globules, tissue particles, air bubbles or clumps of
bacteria, travelling through the blood stream, that block a narrow
part of cerebral blood vessles and cut off blood supply to brain
tissue.
2. Hemorrhagic Stroke resulting from Cerebral hemorrhage caused by
rupture of an artery in the extradural, subdural, subarachnoid or
intracerebral space of the brain.
About 20% of strokes are hemorrhagic where as the remaining 80%
are ischemic in nature. Which ever way a CVA occurs, the end result is
usually irreversible damage to the brain tissue on the affected
hemispehere, which manifests as motor, sensory and perceptual loss on
the opposite side of the body (Fig. 6.1).
Fig. 6.1: Hemorrhagic stroke (left) compared to ischemic stroke (right)

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Pathophysiology of Stroke
The damages caused to the brain by CVA are three fold:
• Cerebral anoxia or lack of oxygen supply to the brain tissue due to
disruption of blood supply, if extended more than 4-6 minutes, causes
irreversible brain damage.
• Cerebral infarction or rotting of brain tissue due to lack of blood
supply.
• Cerebral edema or accumulation of fluid in the interestitial spaces of
the brain tissue, causing raised intracranial pressure, thus further
damage to the brain.
Risk Factors for Stroke

• Atherosclerosis and high blood pressure are the primary reasons
for stroke. The risk of stroke is further increased by age, family
history of stroke, smoking, diabetes, high blood cholesterol, and
heart disease.
• Certain medications increase the chances of clot formation, and
therefore chances for a stroke. Birth control pills can cause blood
clots, especially in woman who smoke and who are older than 35.
• Men have more strokes than women. But, women have a risk of
stroke during pregnancy and the weeks immediately after pregnancy.
• Cocaine and alcohol abuse, head injury, and bleeding disorders
increase the risk of bleeding into the brain.
ISCHEMIC CVA
Alternative Names
Cerebral ischemia, Cerebral thrombosis, TIA, Stroke in evolution
Definition: If blood flow is stopped for longer than a few seconds to the
brain, it cannot get enough blood and oxygen. Due to ischemia, i.e. lack
of blood supply, brain cells die, causing permanent neurological damage.
This is the most common type of stroke or CVA. Usually this type of
stroke results from clogged arteries, a condition called atherosclerosis.
Fatty deposits and blood platelets collect on the wall of the arteries,
forming a sticky substance called plaque. Over time, the plaque builds
up. Often, the plaque causes the blood to flow abnormally, which can
cause the blood to clot.
There are two types of clots that can block blood supply to the brain:
• A clot or plaque that grows within the blood vessels in the brain,
progressively narrowing its lumen, causes Cerebral Thrombosis
• A clot that breaks loose from elsewhere in the body and moves
through the bloodstream to the brain, cutting off blood supply at the
narrowest part, causes a cerebral embolism.
Points to Ponder
Other important causes of cerebral embolisms are:
• Fractures of long bones releasing droplets of fat in the blood stream
• Internal bleeding releasing blood clots, following surgery or
pregnancy
• Tissue debris arising from rheumatic heart disease and the use of a
mechanical heart valve
• Formation of gas bubbles in the blood stream due to sudden
decompression, as seen in deep sea divers, commonly called bends.
A clot can form at any of these sites, break off, and travel to the brain
through the blood stream as an embolus.
Blood supply to the brain may also be interrupted temporarily for a
few seconds or less due to atrial fibrillation, cervical spondylosis
compressing vertebro-basillary artery, atherosclerosis of cerebral arteries
or idiopathic arterial spasm. This temporary cessation of blood supply
creates momentary CVA and are called Transient Ischemic Attack (TIA).
HEMORRHAGIC CVA
Alternative Names
Brain bleeding; Brain hemorrhage; Cerebral hemorrhage, Cerebral
aneurysm.
Definition: The second major cause of stroke is bleeding in the brain.
Hemorrhagic stroke involves bleeding within the brain, damaging nearby
brain tissue. This can occur when small blood vessels in the brain become
weak and burst, often due to uncontrolled blood pressure. Some people
have congenital defects in the blood vessels of the brain (Cerebral
Aneurysms) that make such sudden ruptures more likely. The flow of
blood after the blood vessel ruptures damages brain cells.
Patho-Physiology of Hemorrhagic Stroke

Hemorrhagic stroke occurs when a blood vessel bursts inside the brain,
breaking the blood-brain barrier. The brain is very sensitive to bleeding
and damage can occur very rapidly, either because of the presence of the
blood itself, or because the extra fluid increases pressure on the brain
tissue and harms it by pressing it against the skull.
Bleeding irritates the brain tissue, causing swelling. The surrounding
tissues of the brain resist the expansion of the bleeding, which finally clot
forming a hematoma. Both the swelling and the hematoma will compress
and displace normal brain tissue.
Points to Ponder
• Most often, hemorrhagic stroke is associated with high blood
pressure, which stresses the artery walls until they break.
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• Another cause of hemorrhagic stroke is an aneurysm. This is a weak

spot in an artery wall, which balloons out because of the pressure of
the blood circulating inside the affected artery. Eventually, it can
burst and cause serious harm. The larger the aneurysm is, the more
likely it is to burst. It is unclear why people develop aneurysms, but
genes may play a role, since aneurysms run in families.
• Hemorrhagic stroke can also be caused by the accumulation of a
protein called amyloid within the artery walls, particularly in the
elderly. This makes the arteries more prone to bleeding.
• Some people with brain hemorrhage may have abnormal connections
between arteries and veins, called an arterial-venous malformation
(AVM). Under normal circumstances, circulating blood travels
through the arteries into the capillaries, where it provides nutrients
and oxygen to the tissues. Once the blood has deposited the nutrients
and oxygen, it is carried back to the heart from the capillaries via the
veins. In an AVM, however, an artery may connect directly to a vein,
instead of going through the capillaries. Since blood pressure in the
arteries is much greater than in the veins, in case of sudden increase
in blood pressure the veins may rupture, causing bleeding into the
brain.
• Another important cause that can cause bleeding in the brain is
secondary metastasis of cancer cells to the brain from distant organs,
such as the breast, skin, and thyroid.
• Ischemic stroke can also sometimes lead to secondary brain
hemorrhage because the affected brain tissue softens and this can
lead to breaking down of capillaries in the area.
• In addition, brain hemorrhage can also occur when people have
problems in forming blood clots. Clots, which are the body’s way of
stopping any bleeding, are formed by proteins called coagulation
factors and by sticky blood cells called platelets. Whenever the
coagulation factors are missing or platelets are not available in
sufficient quantity, people may develop a tendency to bleed
excessively.
• Some medications are often used to prevent ischemic stroke, work
by blocking the production of clotting factors (such as warfarin) or
interfering with the function of platelets (such as aspirin) may
occasionally, as an adverse side effect, cause bleeding in the brain.
Illicit drugs, such as cocaine, can also cause hemorrhagic stroke.
GENERAL SIGNS AND SYMPTOMS OF STROKE

The symptoms of stroke depend on which part of the brain is damaged.
Development of one or more of the following signs and symptoms
indicates a CVA:
• Weakness or paralysis of muscles of one side extremities, trunk, and
face
• Tingling, numbness or decreased sensation on the affected side of

the body
• Loss or changes in visual acuity
• Slurred speech, inability to speak or understand speech
• Problem in swallowing or drooling from the corner of the mouth
• Loss of memory
• Head reeling, loss of balance and coordination
• Personality and mood changes, usually depressed or apathetic
• Drowsiness, confusion and unconsciousness
• Involuntary eye movements and drooping of the eye lids (Ptosis).
If one or more of these symptoms is present for less than 24 hours,
it is called to be a transient ischemic attack (TIA) or a stroke in evolution.
A TIA is a temporary loss of brain function and a warning signal for
possiblity of a major stroke in near future. If these changes last for more
than 24 hours a full blown CVA is suspected.
Specific Signs and Symptoms of Hemorrhagic Stroke

Hemorrhagic stroke symptoms are typically of sudden onset and may
quickly become worse. Apart from hemiplegia, sensory deficits and other
common problems seen in all types of CVA, following possible problems
may be seen:
• Sudden and severe headache
• Impaired level of consciousness
• Dizziness, vertigo, nausea and vomiting
• Impaired breathing and cough reflexes
• Difficulty in swallowing and frequent choking
• Decreased or partial loss of vision
• Speech difficulties
• Inability to recognize or identify familiar things
• Loss of coordination in movements.
DIAGNOSIS OF STROKE
For diagnosing a stroke, knowing how the symptoms developed in a
proper sequence is important. The symptoms may be severe at the
beginning of the stroke, or they may progress gradually for the first few
days, i.e. stroke in evolution. Once there is no further deterioration, the
stroke is considered complete.
During the clinical examination the clinician should look for specific
neurologic, motor, and sensory deficits. These often correspond closely
to the location of the lesion in the brain. An examination may show
changes in vision or visual fields, abnormal reflexes, abnormal eye
movements, muscle weakness, decreased sensation, and other changes.
A “bruit” (an abnormal sound heard with the stethoscope) may be heard
over the carotid arteries of the neck. There may be signs of atrial
fibrillation.
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Routine tests are performed to determine the type, location, and cause
of the stroke and to rule out other disorders that may be responsible for
the symptoms.
These Tests Include—
• CT or MRI scan of the brain: Commonly used to determine whether

the stroke was caused by hemorrhage or ischemia or any other lesions
and to define the location and extent of the stroke.
• ECG: Used to determine the status of heart function and to diagnose
underlying heart disorders.
• EEG: Used to determine the status of brain function, especially in
embolic stroke.
• Carotid Doppler Study: Used to determine if the cause may be carotid
artery stenosis, i.e. narrowing of the carotid artery supplying blood
to the brain.
• Cardiac Monitor: Worn while in the hospital to determine if cardiac
arrhythmias may be responsible for the stroke.
• Cerebral Angiography: May be done to identify the blood vessel
responsible for the stroke or to look for aneurysm, particularly if
surgical repair is being considered.
• Hematological analysis may be done to exclude immune conditions
or any abnormality in clotting of the blood.
Specific Tests for Detecting Hemorrhagic Stroke

A neurological exam in an acute CVA is almost always abnormal. The
patient may look drowsy and confused or be unconscious. The patient
may have neck rigidity, abnormal postures, reflexes, muscle tone and
muscle power. However, these findings are seen in most CVA and are
not specific to brain hemorrhage only.
In Hemorrhagic CVA
• An eye examination may show abnormal eye movements, and

hemorrhagic changes may be seen upon retinal examination
(examination of the inner surface of the eye ball with an instrument
called ophthalmoscope).
• The most important test to rule out the presence of a brain hemorrhage
is a CAT scan which should be obtained without delay. A MRI scan
can be obtained later to better understand what caused the bleeding.
• An angiography, consisting of series of X-ray or CT scan slices of the
cerebral arteries using radiopaque dye/contrast medium may be
required to identify aneurysms or AVM.
Other Tests Needed in Hemorrhagic Stroke Include

• BT/CT (Bleeding time/Clotting time)
• Prothrombin/Partial Thromboplastin time (PT/PTT)
• Biochemical study of CSF to detect presence of blood.
MEDICAL MANAGEMENT OF STROKE

A stroke is a medical emergency. Getting treatment immediately can
save lives and reduce disability. Treatment varies, depending on the
severity and cause of the stroke. For virtually all strokes, hospitalization
is required, possibly in intensive care and sometimes on life support. The
goal of the primary caregiver should be to get the person to the emergency room
of a hospital immediately, determine if he or she is having a stroke from bleeding
or a stroke from a blood clot, and start therapy, all within 3 hours of when the
stroke began.
ACUTE CARE STROKE (SEE ALSO ANNEXURE 11)

Thrombolytic medicines break up blood clots and restore blood flow to
the damaged area of the brain. People who receive this medicine are less
likely to have long-term impairment. However, there are strict criteria
for who can receive thrombolytics. For a successful outcome, the patient
must be evaluated accurately and treated by a specialized stroke team
within 3 hours of when the symptoms started. In most cases blood thinners
such as heparin is used to treat ischemic stroke. Aspirin and other anti-
platelet agents may be used as well. If the stroke is hemorrhagic, anticoagulant
treatment can make the damage worse, hence care is needed to diagnose the
cause before giving treatment.
Anti-hypertensive medication may be needed to control high blood
pressure in all types of CVA.
Nutrients and fluids may be given through an intravenous tube (IV)
or a feeding tube in the stomach (Ryle’s tube), especially if the patient
has swallowing difficulties Difficulty in swallowing may lead to choking,
which in its turn may result in aspiration pneumonia. Swallowing
difficulties may be temporary or permanent depending upon the area
and the extent of the brain lesion.
ICU Management
Initial treatment is ideally administered in an intensive care unit, where
complications can immediately be detected. Medical personnel pay careful
attention to breathing because sometimes persons with brain hemorrhage
may develop very irregular breathing patterns or even stop breathing
entirely.
Initial treatment includes intubations in unconscious patients, moist
oxygen inhalation, starting life support with ventilator if needed, starting
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IV fluids for administering nutrients and medication to repair the cause

and minimize the effect of ischemia/hemorrhage, preventing chest
complications, and maintainance of general/oral hygiene.
A person having acute CVA may be unable to protect the airway by
coughing or sneezing because of impaired consciousness. Saliva or other
secretions may go down the airway, which is potentially serious and
may cause lung problems such as aspiration pneumonia. To treat or
prevent these breathing problems, an endotracheal tube may need to be
placed through the mouth into the trachea.
Hemorrhage in the brain may cause brain edema, and this may
require hyper osmotic agents like mannitol, glycerol, and hypertonic
saline solutions to get rid of the excess fluid.
The blood pressure may be too high or too low in patients with
acute CVA. These problems need to be addressed immediately.
Bed rest may be advised to avoid increasing the intracranial pressure.
Stool softeners or laxatives may prevent straining during bowel
movements because straining also causes increased intracranial pressure.
Pain killers may relieve headache but should be used with caution
because they may reduce consciousness. This may produce false
impression that the patient is getting worse.
Anticonvulsive medications such as phenytoin may be needed to
prevent or treat seizures.
Intravenous nutrients and fluids may need to be supplemented
through a nasogastric tube (Ryle’s tube) passed through the mouth into
the stomach, especially in presence of swallowing difficulties.
Positioning, passive range-of-motion exercises and chest
physiotherapy are essential components of acute care, to prevent
complications such as pressure sores, contractures/tightnesss/deformities
of musculoskeletal system and maintaining hygiene of the airway.
SURGICAL INTERVENTIONS IN BRAIN HEMORRHAGES

For hemorrhagic stroke, emergency surgery is often required to remove
pooled blood from the subdural and subarachnoid space of the brain and
to repair damaged blood vessels. For intra-cerebral hemorrhage (ICH)
surgery is not recommended.
The type of surgery depends upon the specific cause of brain bleeding.
For example, a hemorrhage due to an aneurysm requires special type of
repair of the cerebral arteries by a highly skilled neurosurgeon, whereas
for subdural/sub arachnoid bleeding, removal of the hematoma may
occasionally be needed, through a “Burr Hole” drilled through the skull.
Researchers are currently investigating whether a “clot buster drug
injection” inside the hematoma can facilitate the removal of brain
hematoma through needles or catheters, needing less invasive surgery.
One common complication of brain hemorrhage, resulting in raised

intracranial pressure, is hydrocephalus. It is the accumulation of fluid in
cavities within the brain, called the ventricles. The excess fluid is drained
with diuretics, hyper osmosis or ventriculostomy.
For AVM, different treatments are available, including surgical
removal of the AVM network, radio surgery using ionizing radiation to
reduce the size of the AVM and intra-arterial embolization, a procedure
in which a special type of glue is injected into the AVM to close the
connection between arteries and veins.
Prognosis of Stroke
Stroke is the third leading cause of death in India. About one-fourth of
people who have a stroke die as a result of the stroke or its complications,
about one-half have long-term disabilities, and about one-fourth recover
most or all function.
The long-term outcome from a stroke depends on the extent of
damage to the brain, the presence of any associated medical problems,
and the likelihood of recurring strokes.
Hemorrhagic stroke is less common but more frequently fatal than
ischemic stroke.
COMMON COMPLICATIONS FOLLOWING STROKE

• Loss of mobility due to joint contractures or due to abnormal tone of
skeletal muscles
• Loss of sensation of a part of the body
• Loss of cognitive functions
• Impaired communication or social interaction
• Reduced ability to function or care for self
• Decreased life span
• Side effects of medications
• Aspiration
• Malnutrition
• Pressure sores
• Urinary and respiratory tract infections
• Bladder and bowel incontinence.
Prevention of Stroke
Most cases of hemorrhagic stroke are associated with specific risk factors,
such as high blood pressure, smoking, or cocaine use. Controlling blood
pressure and avoiding smoking and cocaine can reduce the chances of
brain bleeding. Surgery to correct blood vessel abnormalities like
aneurysms or AVMs is sometimes advisable to prevent bleeding.
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If a person has had a TIA or ischemic stroke in the past, or have

heart arrhythmias, mechanical heart valve, diabetes or high blood
pressure, he/she may have to take antihypertensive, aspirin or other
blood thinners.
Points to Ponder
Persons at risk of CVA should
• Get screened for high blood pressure at least twice a month, especially
if he/she have a family history of high blood pressure
• Have blood cholesterol checked
• Treat high blood pressure, diabetes, high cholesterol, and heart disease
if present
• Follow a low-fat diet
• Quit smoking
• Exercise regularly
• Lose weight if overweight
• Avoid excessive alcohol use (no more than 1 to 2 drinks per day).
PRINCIPLES OF NURSING CARE IN ACUTE CVA

Stroke can be a debilitating condition. However, with appropriate
treatment and willpower, many patients can regain part of their function.
Nursing care of a CVA, particularly in the acute stage is crucial for long
term well-being of these patients.
1. Improve patient’s quality of life: Pay attention to both physical and
psychological aspects.
2. Enhance the patient’s self-care ability: Teach appropriate skills in
restoring normal daily activities and minimize dependence. This can
slow down the aging process and reduce carers’ burden.
3. Maintain limb and body function to avoid bed sore, chest infection,
aspiration and frozen shoulder.
A CVA can cause various degrees of brain damage that may lead to
different levels of physical, cognitive and speech impairment. Such
disability affects the daily living and self-care ability of stroke patients.
Applying the appropriate care is of utmost importance in helping the
stroke patient to cope with these disabilities and to improve their quality
of life, particularly in the early stages.
Simple Tips for the Caregiver

Encouragement of Self-care
Encourage patients to take responsibility of their personal hygiene such
as combing and changing clothes according to their functional ability.
Provide them with a well-ventilated, warm and clean living environment.
Understanding the Psychology of Stroke Patients

A warm, caring approach is important in helping stroke patients to cope
with the tremendous changes and challenges ahead. However the care
giver should seek professional help if patients develop symptoms or
signs of depression.
Nutritional Care
A balanced diet using the principles of the food-guide pyramid should
be offered to the patient in order to ensure adequate nutrition and to
maintain ideal body weight. Easily digestible food is preferred. Offer
choice of food to the patient.
Bowel and Bladder Care

Identify the causes of incontinence so as to provide specific management.
For those using indwelling urinary catheters (Foleys catheter), the catheter
should be changed whenever necessary, clamped properly, and removed
as early as possible, since they are a prime cause for urinary infections.
Check for any sign and symptom of urinary tract infection and seek
medical advice when necessary.
Limb Exercises
Performing passive mobilization exercises and maintaining a good posture
helps to maintain the range of joint movements and prevent deep vein
thrombosis/contractures. Techniques such as proper positioning and
range-of-motion exercises employed by therapists allow early return of
usable muscle tone, prevent CTD and bed sores.
Communication
A patient with speech or comprehension difficulties may experience
significant communication problems. Patience and appropriate
encouragement helps the patient to communicate more effectively. The
use of simple words, body language, real objects, picture cards and word
cards may help the patient in overcoming his communi-cation problems.
Prevention of Secondary Complications of Acute CVA

Pressure-sore
Being bed-ridden together with reduced activity increase the risk of
localized skin damage due to prolonged pressure.
For Prevention:
• Relieve localized pressure over the skin by turning every 2 hours
• Protect the skin by keeping it dry, clean and soft
• Perform regular exercises and improve nutritional status.
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Chest infection
Being bed-ridden and lacking in physical activities, stroke patients often
develop reduced inflation of the lungs (Hypostasis), have reduced ability
in clearing secretions from their lungs and have weakened body resistance.
Hence, they are prone to chest infections.
For Prevention:
• Increase body resistance by performing exercise and eating a balanced
diet
• Change body positions frequently, make the patient sit upright when
eating, increase fluid intake and perform deep breathing exercises.
Choking
Patients may have difficulties in swallowing after a stroke. Prepare food
according to dietician’s advice and closely observe the patients when
they eat. Feeding must always be done in sitting/propped up position.
Prevention:
• Encourage patients to take in small amounts at a time and prepare
food in small pieces for easy swallowing.
• Avoid sticky, dry or hard food.
PHYSIOTHERAPY IN ACUTE CARE OF CVA

Essential Observation in Acute Stage of CVA
• Look for signs of raised intracranial pressure, i.e. Headache, altered
level of consciousness, vomiting, neck rigidity, constricted pupil in
one eye, agitation, etc. If any of the above signs are present the
therapist must proceed with extreme caution, keeping your eyes on
the bedside monitors for any sudden change in pulse rate, respiratory
rate, ECG trace, etc. Alert the medical staff immediately of any changes
that you may notice. Avoid straining the patient and unnecessary
changes of head position during therapy.
• Look for abnormal posturing, often due to decerebrate/decorticate
presentation. This usually indicates ongoing abnormal neurogenic
activity and needs to be handled with care. Any sudden stretch or
movement may trigger abnormal posturing.
• Look for abnormal position of trunk and extremities, often due to
hypotonic muscles, which in the long run may lead to contractures.
• Look for reddening of skin over bony pressure points, often leading
to pressure sores. Start changing of side every two hours, ask for a
water mattress and instruct the nurses to keep the skin clean and
dry.
• Look for swelling of extremities, often due to lack of muscle
contraction leading to venous stasis or inflammation of veins at IV
sites leading to thrombophlebitis. Start with elevation of the part

and apply pressure hose to extremities to minimize the risk of DVT.
For inflammation of veins and the surrounding soft tissues, apply
Magsulph fomentation or IR radiations.
• Look for early signs of chest complication, usually manifested by
increased respiratory and heart rate, fever, wheezing and crackling
in the chest. Start a daily regime of chest percussion, vibration and
end expiratory squeeze from day one.
Caring Goal
The primary aim of physiotherapy for stroke patients in the acute stage
is to prevent secondary complications of immobility. Physiotherapy can
improve level of function and improve self-care ability in the convalescent
stage, through appropriate positioning, passive exercises and education
to the caregiver about proper handling in the acute stage of the disorder.
General Caring Tips

To Maintain and Improve the Mobility of Affected Limbs
• Passive movements are to be performed daily, for at least five
repetitions on each extremity. Stretching of vulnerable areas like the
calf facilitates venous return.
• As the patient stabilizes they should be encouraged to use their
affected limbs, if needed with the help of sound limbs, especially for
bed mobility.
Patients should do exercise exactly according to physiothera-pist’s
instruction, because faulty patterns of movement, once developed in
the early stage don’t go away easily.
To Increase the Awareness of Affected Side of the Body

• Try to approach the patient on the affected side during feeding,
conversation or transfer. This way the patient could be assisted more
effectively. Besides, it could improve the awareness for the affected
limbs so as to stimulate the patient’s usage of the affected limbs and
side of the body.
• Place objects of daily need next to the affected side.
To Prevent Injury
• Avoid placing objects, which are too hot, too cold or sharp near the
affected side.
Adopting Proper Posture

The patient must adopt proper posture as the following so as to prevent
increase of spasticity.
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• Position the patient on bed in such a way that he has to interact with
his immediate environment through his affected side of the body.
This will prevent neglect or ignorance of the affected side (Fig 6.2).
• Use a firm mattress of approximately 5 cm thick to provide adequate
support to the spine and the affected limbs maintained in neutral
abduction and slight flexion.
• Use a firm pillow with a suitable thickness so as to give good support
to the neck. The head should be in horizontal alignment with the
trunk and the neck should not be bent or dropped backward.
• When lying on affected side, support the trunk and affected limbs in
relaxed position with 3-4 pillows, with the affected side shoulder
abducted, elbow and fingers straightened and the knee slightly bent.
• When lying on sound side, support the trunk and sound limbs in
relaxed position with 3-4 pillows, with the affected side scapula
protracted, shoulder flexed, elbow and fingers, hip and knee in
extension.
• Turn the patient into different positions every two hours if the patient
cannot move on his/her own.
• As soon as the vital signs of the patient have stabilized and the
stroke is deemed to be complete, the therapist must encourage on
bed and out of bed mobility.
• This may be started with sitting propped up on the bed with the aid
of a backrest.
• Attention should be paid to keep the shoulders level and prevent
slumping forward, using a number of pillows.
• The duration of sitting must be progressed slowly to increase vascular
tone and exercise tolerance, particularly in hemorrhagic strokes,
keeping a sharp look out for any abnormal sweating, breathlessness,
dizziness, alteration of consciousness, etc.
• If and when the patient is able to tolerate sitting propped up on bed
for ½ hour at a stretch, he must be encouraged to sit up on a chair
at the bedside (Fig 6.3).
Fig. 6.2: Positioning in supine lying position

Fig. 6.3: Positioning in sitting position
• Choose a suitable chair with backrest, arm rest and firm seat to
provide good support
• Support the affected upper limb with a pillow or armrest, with the
elbow and fingers straightened.
• The depth of the seat should be appropriate so that the patient can
sit straight with his/her back supported by the backrest.
• The height of the chair should be appropriate so that the patient’s
feet can be placed on the floor comfortably, with the hip and knee
flexed at 90°.
Care of Swelling of Extremities

• If required, patient should wear elastic stockings on the affected limbs
and therapist should apply passive movements and effleurage
massage from the distal to the proximal end of the extremity.
• Support the affected limbs in an elevated position with several pillows
above the level of the heart when resting.
Maintain Good Personal Hygiene

• Observe good personal hygiene standards.
• Keep the web spaces and joint lines of fingers and toes clean and dry
in order to prevent body odor and skin diseases.
Adopting Proper Lifting and Transferring Technique

• Patients should adopt proper transferring technique to prevent
worsening of spasticity of affected limbs. For example:
– Don’t pull on the rail of the bed to sit up from lying
– Don’t only bear weight on the unaffected leg in transferring or
standing, share the body weight equally on both legs.
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• Therapist should assist Caregivers and patients by teaching proper

lifting and transferring technique.
– Hold the patient firmly without pulling the affected upper limb
to avoid causing injury to the shoulder.
– Caregivers should maintain a proper posture by keeping close to
the patients, the back straight and knees bent during the transfer
process so as to prevent back injury
PHYSIOTHERAPY IN LONG-TERM CARE OF CVA (SEE ALSO AN-

NEXURE 9)
Points to Ponder
• Recovery time and the need for long-term treatment are highly
variable in each case of stroke. Physical therapy benefits most patients.
Activity should be encouraged within the person’s physical
limitations.
• A safe environment for exercise and training must be considered.
Some people with stroke appear to have no awareness of their
surroundings on the affected side. Others show a marked indifference
or lack of judgment, which increases the risk of injury to the part and
hence need for safety precautions.
• In patients having difficulty in communicating due to language
deficits, alternative forms of communication such as pictures, verbal
cues, demonstration may be needed.
• Speech therapy, occupational therapy, or other interventions may
increase the ability to function.
• Catheterization of the bladder or bowel control programs may be
required to control incontinence.
• In home based care, apart from a visiting physiotherapist, it is essential
to have a safe environment, trained nurses for regular nursing care,
and attending physician to meet physiologic needs.
• Reality orientation, with repeated reinforcement of environmental
and other cues, may help reduce disorientation.
• Family counseling may help in coping with the changes required for
home care.
GOALS AND MANAGEMENT OF POST-STROKE SEQUEL

Residual effects of CVA depend on the area of the brain, which has been
deprived of blood supply. This in turn depends on which of the major
artery or its branches that has been affected. As such, vascular syndromes
commonly seen in CVA are as follows:
• Anterior cerebral artery stroke presents with opposite side hemi
paresis with sensory loss, lower limbs more affected than upper limbs.
• Middle cerebral artery stroke presents with opposite side hemi
paresis with sensory loss, upper limbs more affected than lower limbs.
• Posterior cerebral artery stroke presents with opposite side sensory

loss, thalamic pain with sensory disturbances and transient loss of
motor power on the opposite side of the body.
• Vertebro-basiliar artery stroke presents with progressive vertigo,
ataxia, hemi or quadriplegia, occasionally with bulbar palsy and coma.
It is essential that the clinician identify the vascular syndrome
accurately before planning the treatment and rehab strategy to ensure
best possible outcome.
STAGING OF RECOVERY IN CVA (AS PER BRUNNSTROM)

A patient of CVA passes through several stages during progressive
recovery of function. These stages provide an insight into the actual
status, potential for recovery and may provide an approximate time frame
for getting back near normal function. Brunnstrom staging is the first
cornerstone in assessment of CVA for the planning of rehab.
Stage 1: Initial flaccidity marked with complete hypotonia of all muscles
on the affected side of the body. This usually indicates the stage of cerebral
shock.
Stage 2: Emerging hypertonia, hyperreflexia and mass pattern of
movements (synergies), indicating subsiding of the cerebral shock and
commencement of cerebral function.
Stage 3: Beginning of voluntary movements, only in mass pattern, with
very strong background spasticity.
Stage 4: Regaining of voluntary control in some joints, with concurrent
reduction in spasticity and subsiding of mass pattern of movements.
Stage 5: Increasing voluntary control out of mass pattern, with deficits in
coordination.
Stage 6: Voluntary control and coordination near normal.
PHYSICAL ASSESSMENT OF POST-STROKE SEQUEL

Assessment of Speech and Communication
• Check for Aphasia, typically present in left hemiplegia, due to lesions
of Parieto-occipital cortex of the dominant hemisphere.
• Check for perceptual deficits, typically present in right hemiplegia,
due to lesions of Parietal lobe of the non-dominant hemisphere.
Assessment of Changes in Behavior

• Slow, cautious, hesitant and insecure are noted in patient with right
hemiplegia due to lesions in left hemisphere.
• Impulsive, quick, indifferent behavior with poor judgment of safety,
frequently overestimating their ability and underestimating their
problem is seen in patients with left hemiplegia due to lesions in
right hemisphere.
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Assessment of Sensory Deficits

• Assess superficial, Proprioceptive and combined sensation of both
affected and unaffected extremities, trunk and face. Significant
aberration in sensory interpretation may be noted, due to which the
patient may wrongly interpret a type of stimulus, e.g. simple touch
may be felt as pricking or vibration as warmth etc. Such faulty sensory
ability can some times be a hindrance to rehab.
• Assess hearing and Vision, because deafness, tinnitus, Diplopia or
double vision and homonymus hemianopia or half visions are
frequently seen in CVA. During rehab these additional impairments
have to be kept in mind.
• Specifically check cranial nerve functions in suspected brainstem
and Vertebro-basiliar artery lesions.
Assessment of Deficits in Motor Control

• Abnormal muscle tone (Hypo- or Hyper-tonia), along with Hypo-
or Hyper-reflexia, with liberation of primitive reflexes may be present.
• Losses of selective movements are the commonest motor control
loss seen in CVA. Presence of basic limb synergies or mass pattern
of movements pose the biggest challenge to the therapist, which may
manifest as follows:
a. Upper extremity flexion synergy with retraction/elevation of
scapula, adduction and external rotation of shoulder, elbow
flexion, forearm supination and flexion of wrist and fingers.
b. Upper extremity extension synergy with protraction of scapula,
adduction and internal rotation of shoulder, elbow extension,
forearm pronation and flexion of wrist and fingers.
c. Lower extremity flexion synergy with retraction of pelvis, flexion,
adduction and external rotation of hip, knee flexion, ankle
dorsiflexion and inversion of foot.
d. Lower extremity extension synergy with extension, adduction
and internal rotation of hip, knee extension, ankle plantar flexion
and inversion of foot.
Points to Ponder
• Whenever the patient tries to perform any voluntary movement in
an extremity, any the above mentioned synergies or mass movement
patterns may appear.
• Common combination of mass pattern is flexion in the upper and
extension in the lower extremities.
• As such the patient will be unable to perform selective movements
freely, say flexion of elbow, without retraction of scapula, adduction
of shoulder, etc. taking place at the same time. This causes severe
wastage of energy and prevents purposeful movement impossible.
• Presence of muscle weakness, in-coordination and lack of motor

planning (Apraxia) may further complicate voluntary control in many
patients of CVA.
Assess for Deficits in Balance Reactions and Postural Control

• Poor and adverse tone of postural muscles results in defective posture
and poor balance in most patients. Basal ganglion lesion usually
present with poor postural control and balance reactions. Marked
hypotonic lower limbs causing unsteady gait or ataxia characterize
Cerebellar lesions. Vertebro-basiliar artery lesions present with
positional vertigo.
Assessment of Functional Mobility Skills (FMA)

• Bed mobility is the first thing that the therapist should check in a
patient of CVA. Begin with the attitude of the body in supine lying.
a. Observation: Check for abnormal posturing, symmetry of the body
segments, attitude of the extremities and ability to move individual
extremities. Due to maximum base of support, background muscle
tone is lowest in supine lying. Even in presence of severe spasticity,
and limb synergies, any CVA patient, in supine lying, should be able
to perform some selective movement of extremities in supine position.
b. Testing: Ask the patient to roll alternately to either side from supine
lying, shift from side to side and up-down on the bed, taking note of
the way he initiates this movement. Patients with hemiplegia tend to
have greater difficulty lying on the affected side. The affected upper
limb tends to get in the way and the patient does not know how to
position the affected upper limb in a position of comfort. The
extremities of the sound side are frequently used to compensate, to
push or prop the affected side of the body in the desired position.
Turning to the sound side is much easier.
• Sitting up on bed, initially with support and later without support,
in long sitting and high sitting position should be checked. Sitting
entails smaller base of support than lying, hence greater background
tone and interference from synergies. Note for any deviation in
posture while sitting and the extent of assistance needed achieve
sitting, the support needed to maintain the position and the confidence
level of the patient while in sitting.
• Standing up from sitting involves getting the body segments in
alignment over the smallest base of support. The background tone
and the synergies should be most pronounced and therefore a
deterrent. To compensate the patients may adopt a wide base or lean
on the sound side, taking maximum load on the sound limb. In
either case, standing becomes inefficient and not conducive to the
next logical step, walking.
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• Assessment of gait
Hemiplegic patients present with typical gait deviation. Typical
deficits resulting in such gait deviations are due to:
a. Hip joint- Retracted and flexed hip with compensatory backward
leaning of trunk, with trendelenburg limp due to weak abductors
and scissoring due to spastic adductors create a poor starting
position of hip in the stance phase and in-sufficient pelvic rotation
during swing, further complicates the matter. Weak hip flexors
may produce insufficient ground clearance during swing; hence
the typical circumduction gait.
b. Knee joint: The knee may remain flexed during the stance phase
due to weak quadriceps, resulting in compensatory locking of
the knee in extension. With extensor synergy dominant in lower
limbs, spastic quadriceps may pull the knee into recurvatum
(Hyperextension).
c. Ankle joint: The ankle is put in planter flexion due to spastic
calf muscles, leading to tightening of the Tendo-Achilles, resulting
in foot drop. The heel does not touch the ground and the patient
develops an equious gait (tiptoe like a horse). Further, due to
predominant inversion pattern, weight of the body is transferred
to the lateral border of the foot. This results in instability at the
ankle, which are likely to be sprained repeatedly.
d. Unequal load transfer: Due to inefficient weight bearing and the
presence of synergy, the affected lower limb doesn’t advance
smoothly from heel strike, through stance phase up to toe off.
The duration of load transfer to the affected lower limb is
momentary. Hence the cadence is reduced, step length becomes
unequal and the timing becomes uneven.
Uses of FME
The purpose of functional mobility evaluation in a post stroke sequel is
to detect at what stage the patient is stuck in his path to recovery. Given
time, all hemiplegics will relearn basic functional movements on their
own. However the qualities of such movements are poor and there is
always a risk of fall. Accurate assessment by a therapist pinpoints the
short fall in the functional mobility skills, which can be then overcome
by painstaking motor relearning program.
SPECIALIZED STROKE ASSESSMENT TOOLS

Stroke assessment tools are specific regime of evaluation, focusing on a
key parameter of hemiplegia. They have laid down protocols and are
often named after their authors. All have their merits and demerits and
have their fan following among therapists. The main aims of all such
tools are to provide a measure of progress in a case of stroke. A brief
outline of few popular stroke assessment tools are presented below:
• Brunnstrom hemiplegia classification and progress record is based

on six sequential recovery stages discussed earlier in this chapter. It
mainly plots the emergence, dominance and variation of movement
synergies on a time scale.
• Bobath evaluation of motor patterns focuses on qualitative
assessment of movement and postural patterns, based on three
recovery stages, i.e. stage of flaccidity, stage of spasticity and stage
of relative recovery. This protocol emphasizes descriptive recording
of movements out of synergy and the influence of spasticity on
movements.
• Fugl-meyer assessment of physical performance ( FMA) expands
on the recovery stage concept of Brunnstrom, providing objective
criteria for scoring synergy and out of synergy movements.
• Carr and Shephard motor assessment scale measures functional
capabilities using 8 categories of movements, providing objective
criteria for scoring performance.
SUMMARY OF LONG-TERM PROBLEMS OF STROKE PATIENTS

Impairments, such as hemiplegia, spasticity, and aphasia, are the primary
neurological disorders caused by stroke.
Points to Ponder
• Activity limitations or “disabilities” are manifested by reduced ability
to perform daily functions, such as dressing, bathing, or walking.
• The magnitude of disability is generally related to but not completely
dependent on the severity of stroke.
• Other factors that influence disability include intrinsic motivation
and mood, adaptability and coping skill, cognition and learning ability,
severity and type of pre-existing and acquired medical co-morbidity,
medical stability, physical endurance levels, effects of treatments in
acute stage, and the amount and type of rehabilitation training
received by the patient.
• Therapeutic interventions to improve sensory-motor performance after
stroke vary considerably. Rehabilitation can be effective in improving
both intrinsic motor control and functional status.
• Although 14% of stroke survivors achieve a full recovery in physical
function, between 25-50% of cases require at least some assistance
with activities of daily living, and almost half of the number of cases
experience severe long-term effects such as partial half body paralysis
or hemi paresis.
• Common tasks need considerably greater energy in hemiplegia.
Energy expenditure in hemiplegia patients varies with the degree of
disuse weakness, spasticity, loss of coordination etc. This in turn
leads to decreased activity and greater exercise intolerance, leading
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to secondary complications such as reduced cardio respiratory fitness,

muscle atrophy, osteoporosis, and impaired circulation to the lower
extremities in stroke survivors.
• In addition, a diminished self-efficacy, greater dependence on others
for activities of daily living, and reduced ability for normal social
interactions can have a negative psychological impact.
• Stroke usually does not occur in isolation. Patients with stroke have
a high prevalence of associated medical problems. These conditions
may be “pre-existing conditions” or occur for the first time after stroke
as “post stroke complications”. In particular, cardiac disease has been
reported to occur in up to 75% of stroke survivors.
• Since physical activity places greater energy demands on the
cardiovascular system of hemiplegia patients than on that of able-
bodied subjects, stroke survivors with pre-existing cardiac disease
may be at an increased risk for cardiac complications.
GOALS OF REHAB IN CVA

Traditionally, the physical rehabilitation of individuals with stroke
typically ended within six months after stroke because it was believed
that most, if not all, recovery of motor function occurred during this
interval. Nevertheless, recent research studies have shown that aggressive
rehabilitation beyond this time period increases aerobic capacity and
sensory motor function.
• The first rehabilitation goal for the stroke patient is to regain pre-
stroke levels of activity as soon as possible.
– For inpatients, exposure to simple orthostatic or gravitational
stress, i.e. mat activity; intermittent sitting or standing during
hospital stay has been shown to reduce deterioration in exercise
tolerance.
– After discharge from hospital, the exercise therapy may range
from mat activity to standing with support, static march and
remedial gait training.
• The second rehabilitation goal for the stroke survivor is to prevent
recurrent stroke and cardiovascular events by reduction of risk factors.
An aerobic exercise program can enhance glucose regulation, decreases
body weight and fat, reduce blood pressure, C-reactive protein, and
regulate levels of total blood cholesterol, serum triglycerides, and
low-density lipoprotein cholesterol.
• The third rehabilitation goal should be to improve fitness,
notwithstanding residual functional limitations. Evidence is
accumulating that stroke risk can be reduced with regular physical
activity in individuals of all ages and both sexes.
• Traditional stroke rehabilitation programs emphasize functional
training as a means to help the individual gain and maintain as much
independence as possible.
Training in the performance of mobility and personal care tasks,

together with attempts to improve muscle strength and coordination,
continue to form the central areas of focus of most rehabilitation programs.
ROUTE MAP TO STROKE REHAB

• Maintain ROM and prevent CTD with the help of relaxed passive
movements through full range of the affected side extremities should
be performed routinely, at least for five repetitions daily. As soon as
possible, ask the patient to participate in the movement, the therapist
providing only minimum required assistance to complete the ROM.
Composite movements like hip-knee flexion with ankle dorsiflexion
are most useful in regaining the sense of movement and ultimately
function in the affected extremities. Ask the patient to follow the
movement with his eyes. This will reinforce the body image and
sense of movement.
• Teach and maintain optimal remedial positioning by using pillows
and towel rolls to maintain the affected side in a posture that inhibits
reflex patterns commonly seen after CVA. Remedial positioning can
be given in lying, sitting and standing. The thing to remember is to
maintain a posture that is exactly the opposite of what the synergy
is trying to do. If the upper limb is being held in adduction- internal
rotation of at the shoulder, flexion at elbow, wrist and fingers with
pronated forearm, you should try maintaining the shoulder in
abduction and external rotation, elbow, wrist and fingers in extension.
Progressively reduce the base of support from lying to sitting to
standing while training optimal remedial positioning.
Precaution: Avoid traction to sensitive joints like the shoulder while
handling and positioning as it may lead to painful shoulder.
• Promote awareness, active movements and function of the
hemiplegic side through remediation-facilitation approach. Start with
normalization of tone in the affected side. In case of hypotonic
muscles, brisk massage or surged faradic stimulation over the affected
muscle surface may be applied as a preparation for exercises. In
hypertonia, selective cooling of the spastic muscles, load bearing in
reflex inhibiting postures, surged faradic stimulation of opposite
groups of muscles are useful. Try to apply all these measures while
maintaining optimal remedial position.
• Teach selective movements in out of synergy pattern only when the
tone has been optimized. Start teaching such movements using simple
patterns, with the body in maximum base of support, e.g. in lying.
Common PNF diagonal patterns in spiral axis (D1 and D2) may be
used. Gradually progress to more complicated patterns and by
adopting smaller base of support like sitting. Emphasis should be on
functional patterns of movement.
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• Improve posture, symmetry and balance using verbal and visual

feedback through mirrors. Attention to symmetry and posture should
commence from the acute stage in bed and carry over to sitting and
standing in rehab stage. Unequal weight transfer through points of
weight bearing in sitting and standing is the main cause of postural
asymmetry. Two bathroom scales under each foot may be used to
show the patient the inequality of load bearing. Balance reactions are
best trained on wobble boards.
COMPLICATIONS FOLLOWING STROKES AND THEIR MANAGEMENT

Sensory Disturbances Including Pain
Stroke patients may lose the ability to feel touch, pain, temperature, or
position. Sensory deficits may hinder the ability to recognize objects
through touch. Some times it can be severe enough to cause loss of
recognition of the affected side body or limbs. Some stroke patients
experience pain, numbness or odd sensations of tingling or prickling or
paresthesia in the affected side
Stroke Patients frequently have a variety of chronic pain syndromes
resulting from stroke-induced damage to the nervous system (neuropathic
pain) or from biomechanical imbalance between hyper tonic and normal
muscles.
• Hemiplegic’s shoulder pain

Patients who have a seriously weakened or paralyzed UL, frequently
with subluxation of the shoulder joint, commonly experience moderate
to severe pain that radiates outward from the shoulder, extending all the
way to wrist and hand. Autonomic dysfunction may set in creating reflex
sympathetic dystrophy (RSD). The extremity, particularly the hand may
be swollen, tender to touch and discolored. Most often, the pain results
from a joint in the involved limb becoming immobilized due to lack of
movement and the tendons and ligaments around the joint become fixed
in one position. This is commonly called a “frozen” joint; “passive”
movement at the joint in a paralyzed limb is essential to prevent painful
“freezing” and to allow easy movement if and when voluntary motor
strength returns. In some cases, excessive traction may be applied on a
flaccid joint while shifting the patient passively, leading to trauma to
joint capsule and the surrounding soft tissue.
• Thalamic pain syndrome

In some stroke patients, pathways for sensation in the brain are
damaged, causing the transmission of false signals that result in the
sensation of pain in a limb or side of the body that has the sensory
deficit. The most common of these pain syndromes is called “thalamic
pain syndrome,” which can be difficult to treat even with medications.
Bladder and Bowel Incontinence

The loss of urinary continence is fairly common immediately after a
stroke and often results from a combination of sensory and motor deficits.
Stroke survivors may lose the ability to sense the need to urinate or the
ability to control muscles of the bladder. Some may lack enough mobility
to reach a toilet in time. Loss of bowel control or constipation may also
occur. Permanent incontinence after a stroke is uncommon. But even a
temporary loss of bowel or bladder control can be emotionally difficult
for stroke survivors.
Problems Using or Understanding Language (Aphasia)

At least one-fourth of all stroke survivors experience language
impairments, involving the ability to speak, write, and understand spoken
and written language. A stroke-induced injury to any of the brain’s
language-control centers can severely impair verbal communication.
Damage to a language center located on the dominant side of the brain,
known as Broca’s area, causes expressive aphasia. People with this type of
aphasia have difficulty conveying their thoughts through words or
writing. They lose the ability to speak the words they are thinking and
to put words together in coherent, grammatically correct sentences. In
contrast, damage to a language center located in a rear portion of the
brain, called Wernicke’s area, results in receptive aphasia. People with this
condition have difficulty in understanding spoken or written language
and often have incoherent speech. Although they can form grammatically
correct sentences, their utterances are often devoid of meaning. The most
severe form of aphasia, global aphasia, is caused by extensive damage to
several areas involved in language function. People with global aphasia
lose nearly all their linguistic abilities; they can neither understand
language nor use it to convey thought. A less severe form of aphasia,
called anomic or amnesic aphasia, occurs when there is only a minimal
amount of brain damage; its effects are often quite subtle. People with
anomic aphasia may simply selectively forget interrelated groups of
words, such as the names of people or particular kinds of objects.
Problems with Thinking and Memory

Stroke can cause damage to parts of the brain responsible for memory,
learning, and awareness. Stroke survivors may have dramatically
shortened attention spans or may experience deficits in short-term
memory. Individuals also may lose their ability to make plans,
comprehend meaning, learn new tasks, or engage in other complex mental
activities. Two fairly common deficits resulting from stroke are anosognosia,
an inability to acknowledge the reality of the physical impairments
resulting from stroke, and neglect, the loss of the ability to respond to
objects or sensory stimuli located on one side of the body, usually the
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stroke-impaired side. Stroke survivors who develop apraxia lose their

ability to plan the steps involved in a complex task and to carry the steps
out in the proper sequence. Stroke survivors with apraxia may also have
problems following a set of instructions. Apraxia appears to be caused
by a disruption of the subtle connections that exist between thought and
action.
Emotional Disturbances
Many people who survive a stroke feel fear, anxiety, frustration, anger,
sadness, and a sense of grief for their physical and mental losses. These
feelings are a natural response to the psychological trauma of stroke. The
physical effects of brain damage cause some emotional disturbances and
personality changes. Clinical depression, which is a sense of hopelessness
that disrupts an individual’s ability to function, appears to be the
emotional disorder most commonly experienced by stroke survivors. Signs
of clinical depression include sleep disturbances, a radical change in eating
patterns that may lead to sudden weight loss or gain, lethargy, social
withdrawal, irritability, fatigue, self-loathing, and suicidal thoughts. Post-
stroke depression can be treated with antidepressant medications and
psychological counseling.
SECTION 2
TRAUMATIC BRAIN INJURY (TBI)
INTRODUCTION
A traumatic brain injury arising from a sudden blow to the head is a
major public health problem. Currently it’s a leading cause of disability
among young adults. Many face lasting impairments that affect their
independence and daily lives.
Fall from a fast motorcycle while riding without helmet; a crash into
the windshield of a fast car while driving without seat belts; the scenarios
are endless the end result is the same; a traumatic brain injury.
Characterized by a blow to the head, this type of injury suddenly
damages the brain and its function. Survivors can experience a range of
lasting impairments, including problems with speech, emotion, sensation,
movement, or thinking. And due to inadequate treatments, many face
the prospect of experiencing significant disabilities for the rest of their
lives.
CAUSES OF HEAD INJURIES—TRAUMATIC BRAIN INJURIES

Brain and head injuries can occur almost anywhere. Traumatic brain
injury, as the name suggests, is caused by a trauma. Traumatic brain injury
(TBI) most often occur in road accidents, many types of falls, ejection
from a vehicle at high speeds, roof crush or roof collapse in a rollover,
objects falling and striking the person on the head, impacts of a child’s
head onto a floor or in vehicles interior during collision, motorcycle
accidents even with a helmet, from violent explosions and many other
situations both industrial and residential.
Injuries involving some type of blow or striking of one’s head are
among the most common in our society and about 10-15% are left
permanently disabled. Head injuries can range from relatively minor
damage to the scalp and face such as lacerations, abrasions and bruising
to more serious consequences involving damage to the brain, brain stem
injuries, frontal lobe brain injury, anoxic brain injury and other closed
head injury complications. While traumatic brain injury occurs much less
frequently, it is important to know how it is identified and what to do
for the person.
• Loss of consciousness, even for a very brief period, is one of the
clearest indications that a blow to the head may have affected the
brain.
• A confusional state involving uncertainty about time, date, and
location and/or a period of memory loss for the events surrounding
the head injury are also indicators of trauma to the brain.
• Any of these symptoms following a blow to the head should be
taken seriously.
Traumatic brain injury is a serious and debilitating injury. Persons
with a severe brain injury often have problems with mental and physical
functioning, and may require on-going supervision and assistance, as a
result of post concussion syndrome. Even a person who has suffered a
head or brain injury, with little or no documented loss of consciousness,
may have permanent deficits which make it impossible for them to return
to their previous lifestyle and sphere of activities.
TYPES OF HEAD INJURIES

Head injuries are basically of two types; open and closed head injury.
• In the relatively rare and usually devastating open head injury, the
skull vault is fractured, creating a communicating passage between
the sealed cranial cavity and the external atmosphere. There may be
leakage of CSF from the cranial cavity and entry of air into the skull
vault. Broken pieces of skull bones may lacerate the delicate brain
tissue.
• Closed head injuries are said to occur when the skull vault remains
intact, though the brain tissue are damaged to inertial forces acting
on the brain when the skull is struck by a powerful blow. This type
of head injuries are far more common than open head injuries and
since they do not have dramatic initial presentation, are likely to be
ignored with possible deadly outcome for the patient.
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MECHANISM OF BRAIN DAMAGE IN CLOSED HEAD INJURIES

In closed head injuries, brain tissue damage arises from three
characteristics of this brain-skull anatomy:
• The rigidity and internal contours of the skull
• The incompressibility of brain tissue
• The susceptibility of the brain to shearing forces.
The first two characteristics give rise to contusions or hematomas
(i.e., bleeding) on the surface of the brain, one of the most common
outcomes of brain injuries. There are usually two contusion sites in a
brain injury. One occurs at the site of the blow to the brain and is called
the coup injury. The other arises on the opposite side where the brain
bounces off the skull when it has been pushed away by the original
blow. The contusion here is termed the counter coup injury (Fig. 6.4).
Some bleeding may also arise at the suture points when the dura
mater is torn away from the inside of the skull.
The third characteristic, susceptibility to shearing forces, plays a role
primarily in injuries which involve rapid and forceful (whiplash)
movements of the head, such as in car accidents. In these situations
rotational forces in whiplash-type injuries are particularly important.
These forces, associated with the rapid acceleration and deceleration of
the head, are smallest at the point of rotation of the brain near the lower
end of the brainstem and successively increase at increasing distances
from this point. The resulting shearing forces cause different levels in the
Fig. 6.4: Coup and counter coup injury with shearing injury of the brain
brain to move relative to one another. This movement produces stretching

and tearing of axons (diffuse axonal injury) and the insulating myelin
sheath (Fig. 6.5). These injuries are the major cause of loss of consciousness
in a head injury. Small blood vessels are also damaged causing bleeding
deep within the brain.
Collectively these injuries can result in Cerebral Edema (swelling of
the brain). Cerebral edema leads to raised intra cranial pressure (ICP).
Since the rigid skull vault can’t expand, if the pressure within the skull
is not relieved through surgery, cooling or medication, the brain will
gradually be pushed down through the opening at the base of the skull,
the foramen magnum (Herniation). Nuclei in the brain-stem controling
breathing and cardiac function will eventually be compressed resulting
in death.
Although much damage is caused by the initial impact or primary
injury, additional factors can cause further damage to the brain. This is
known as secondary injury. Most of the care that a person receives in the
hospital after a brain injury is meant to minimize the effects of secondary
injury since the primary injury (the impact) has already happened.
Fig. 6.5: Mechanism of axonal damage due to shearing forces acting on the
axons in the brain
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Raised ICP affects the drainage from the brain and cause fluid to build
up causing hydrocephalus. ICP can get so high that it cuts off blood flow
to the brain, causing further damage. A number of things can be done to
minimize brain swelling including: intravenous medicines,
hyperventilation on a ventilator or even surgery to open the skull and
relieve some of the pressure.
Another main cause of secondary injury is bleeding in or around the
brain. During the acute hospitalization, doctors are closely watching for
developing blood clots (hematomas) that can cause damage to the brain
tissue directly and cause build up of ICP.
Finally, problems like low blood pressure or low oxygen levels in
blood due to depressed breathing can cause further damage to the already-
injured brain. Infections, abnormalities in blood’s chemistry and prolonged
seizures can also affect brain function.
In summary, damage to the brain is caused by many factors, in
addition to the original trauma. The brain injury represents all these
different factors together.
EFFECTS OF INJURY TO THE BRAIN

Effects of a brain injury will depend on the location of the injury and the
amount of damage to particular brain parts. This is because different
parts of the brain control different functions. This means that no two
people will have identical symptoms from a brain injury. Every brain
injury is different. Thus, one person may have problems with memory
and concentration while another may have weakness or paralysis of
muscles. Almost any mix of symptoms or impairments can occur.
Examples of traumatic brain injury symptoms include:
• Physical impairments: Muscle weakness or paralysis, loss of
coordination, problems with vision or smell, slurred speech, difficulty
swallowing, spasticity (severely increased muscle tone) and pain.
• Cognitive impairments (trouble with thinking): Poor memory, lack
of concentration, slowed thinking, inability to plan and problems
with perception.
• Emotional and behavioral issues: Lack of awareness of problems,
depression, irritability, poor judgment, low motivation, poor emotional
control and agitation.
ACUTE CARE OF A TBI PATIENT

Acute medical care of TBI usually begins when paramedics or emergency
medical technicians arrive on the scene of an accident or when a TBI
patient arrives at the emergency department of a hospital. Because little
can be done to reverse the initial brain damage caused by trauma, medical
personnel try to stabilize the patient and focus on preventing further
injury. Primary concerns in the acute care include:
• Insuring adequate oxygen supply to the brain and the rest of the
body
• Maintaining adequate blood flow to the brain and other vital organs
• Controlling blood pressure, heart rhythm and rate.
At the site of the accident and during transit, paramedics may have
to intubate or open the patient’s airway through a tracheotomy to make
sure of air entry. They may also need to perform CPR or use defibrillator
to keep the failing heart pumping blood, and they may need to stabilize
other injuries like fracture and to control bleeding.
Because many head-injury patients may also have spinal cord injuries,
paramedics have to take great care while moving and transporting the
patient to the hospital emergency. Ideally, the patient is placed on a
back-board and in a neck restraint collar. These devices immobilize the
patient and prevent further injury to the head and spinal cord.
As soon as the patient arrives at the ER, the attending medical
personnel have to stabilize the head injured patient. Once the patient’s
breathing and heart function has been stabilized the ER medical team
assess the patient’s condition by measuring vital signs and reflexes and
by performing an initial neurological examination. They check the patient’s
vitals, such as temperature, blood pressure, pulse, breathing rate, and
pupil size in response to light. They assess the patient’s level of
consciousness and neurological functioning using the Glasgow Coma Scale
(Table 6.1), a standardized, 15-point test that uses three measures - eye
opening, best verbal response, and best motor response- to determine the
severity of the patient’s brain injury.
Table 6.1: Glasgow Coma Scale

The eye opening part of the Glasgow Coma Scale has four scores:
• 4 indicate that the patient can open his eyes spontaneously.
• 3 indicate the patient can open his eyes on verbal command.
• 2 indicate that the patient opens his eyes only in response to painful stimuli.
• 1 indicates the patient does not open his eyes in response to any stimulus.
The best verbal response part of the test has five scores:
• 5 indicate the patient is oriented and can speak coherently.
• 4 indicate patient is disoriented but can speak coherently.
• 3 indicate the patient uses inappropriate words or incoherent language.
• 2 indicate the patient makes incomprehensible sounds.
• 1 indicates that the patient gives no verbal response at all.
The best motor response test has six scores:
• 6 means the patient can move his arms and legs in response to verbal
commands.
• A score between 5 and 2 is given if the patient shows movement in response
to a variety of stimuli, including pain.
• 1 indicates that the patient shows no movement in response to stimuli.
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The results of the three tests are added up to determine primarily the
patient’s level of consciousness (LOC), as well as, the overall neurological
condition. A total score of 3 to 8 indicates a severe head injury, 9 to 12
indicates a moderate head injury, and 13 to 15 indicate a mild head
injury.
Radio-imaging tests help in determining the diagnosis and prognosis
of a TBI patient. Patients with mild to moderate injuries may have skull
and neck X-rays done to check for bone fractures or spinal instability.
The patient should remain immobilized in a neck and back restraint until
it is certain that there is no risk of spinal cord injury.
For moderate to severe cases, the imaging test of choice is a computed
tomography (CT) scans. The CT scan creates a series of cross sectional X-
ray images of the head and brain and can show bone fractures as well
as the presence of hemorrhage, hematomas, contusions, brain tissue
swelling, and tumors.
Magnetic resonance imaging (MRI) may be used after the initial assessment
and treatment of the TBI patient. MRI uses magnetic fields to detect
subtle changes in brain tissue content and can show more detail than X-
rays or CT. Unfortunately, MRI is not ideal for routine emergency imaging
of TBI patients because it is expensive, time-consuming and is not available
in all hospitals.
Other imaging and diagnostic techniques that may be used to confirm a
particular diagnosis include cerebral angiography, electroencephalo-
graphy (EEG), transcranial Doppler ultrasound, and single photon
emission computed tomography (SPECT).
Approximately half of severely head-injured patients will need surgery
to remove hematomas or repair contusions. Patients may also need surgery
to treat injuries to the skull, scalp and other parts of the body. These
patients usually go to the intensive care unit after surgery.
If there are signs of raised ICP following a closed head injury, such as
worsening LOC, headache, projectile vomiting, blurring of vision, slurring
of speech, etc. medical personnel monitor Intra Cranial Pressure (ICP)
using a probe or catheter. The probe is inserted through the skull to the
sub-arachnoid space and is connected to a monitor that registers the
patient’s ICP. If a patient has dangerously high ICP, he or she may have
to undergo a ventriculostomy, a procedure that drains cerebrospinal fluid
(CSF) from the brain to bring the pressure down. Drugs that can be used
to decrease ICP include diuretics like mannitol or sedatives like
barbiturates, although the safety and effectiveness of the latter are
unknown.
How Does a TBI Affect Consciousness?

A TBI can cause problems with arousal, consciousness, awareness,
alertness, and responsiveness. Generally, there are six abnormal states of
consciousness that can result from a TBI: stupor, coma, vegetative state,
persistent vegetative state, locked-in syndrome, and brain death.
1. Stupor is a state in which the patient is unresponsive but can be
aroused briefly by a strong stimulus, such as sharp pain.
2. Coma is a state in which the patient is totally unconscious,
unresponsive, unaware, and unarousable. Patients in coma do not
respond to external stimuli, such as pain or light, and do not have
sleep-wake cycles. Coma results from widespread and diffuse trauma
to the brain, including the cerebral hemispheres of the upper brain
and the lower brain or brainstem. Coma generally is of short duration,
lasting a few days to a few weeks. After this time, some patients
gradually come out of the coma, some progress to a vegetative state,
and others die.
3. Vegetative state, in which patients are unconscious and unaware of
their surroundings, but they continue to have a sleep-wake cycle and
can have periods of alertness. Unlike coma, where the patient’s eyes
are closed, patients in a vegetative state often open their eyes and
may move, groan, or show reflex responses. A vegetative state can
result from diffuse injury to the cerebral hemispheres of the brain
without damage to the lower brain and brainstem. Anoxia, or lack of
oxygen to the brain, which is a common complication of cardiac
arrest, can also bring about a vegetative state.
4. Persistent vegetative state (PVS); patients who do not recover from
a vegetative state within 30 days are said to be in a PVS. The chances
of recovery depend on the extent of injury to the brain and the
patient’s age, with younger patients having a better chance of recovery
than older patients. Generally adults have a 50 percent chance and
children a 60 percent chance of recovering consciousness from a PVS
within the first 6 months. After a year, the chances that a PVS patient
will regain consciousness are very low and most patients who do
recover consciousness experience significant disability. The longer a
patient is in a PVS, the more severe the resulting disabilities will be.
Rehabilitation can contribute to recovery, but many patients never
progress to the point of being able to take care of themselves.
5. Locked-in syndrome is a condition, in which a patient is aware and
awake, but cannot move or communicate due to complete paralysis
of the body. Most locked-in syndrome patients can communicate
through movements and blinking of their eyes, which are not affected
by the paralysis. Some patients may have the ability to move certain
facial muscles as well. The majority of locked-in syndrome patients
do not regain motor control, but several devices are available to help
patients communicate.
6. Brain death is the lack of measurable brain function due to diffuse
damage to the cerebral hemispheres and the brainstem, with loss of
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any integrated activity among distinct areas of the brain. Brain death
is irreversible. Removal of life support devices like ventilator will
result in immediate cardiac arrest and cessation of breathing.
What are the Complications of Acute TBI?

Complications of Acute TBI include seizures, hydrocephalus or post-
traumatic ventricular enlargement, CSF leaks, infections, cerebro-vascular
injuries, cranial nerve injuries, pain, bed sores, multiple organ system
failure in unconscious patients, and associated trauma to other parts of
the body.
1. Seizures: About 25 percent of patients with brain contusions or
hematomas and about 50 percent of patients with penetrating head
injuries develop seizures that occur within the first 24 hours of the
injury. Generally, medical professionals use anticonvulsant
medications to treat seizures in TBI patients only if the seizures persist.
2. Hydrocephalus or post-traumatic ventricular enlargement occurs
when CSF accumulates in the brain resulting in dilation of the cerebral
ventricles and an increase in ICP. This condition can develop during
the acute stage of TBI or may not appear until later. Generally it
occurs within the first year of the injury and is characterized by
worsening neurological outcome, impaired consciousness, behavioral
changes, ataxia, incontinence, or signs of elevated ICP. The condition
may also develop secondary to meningitis, subarachnoid hemorrhage,
intracranial hematoma, or other types of CVA. Treatment includes
shunting and draining of CSF as well as any other appropriate
treatment for the root cause of the condition.
3. CSF leaks occur due to bony fragments from a fractured skull tearing
the meninges. A tear between the dura and the arachnoid membranes,
called a CSF fistula, can cause CSF to leak out of the sub-arachnoid
space into the sub-dural space; called a sub-dural hygroma. CSF can
also leak out from the nose and the ear. The tears in the meninges
that cause CSF leakage can also allow air and bacteria to enter into
the skull vault, causing infections such as meningitis. Pneumocephalus
occurs when air enters the intracranial cavity and becomes trapped
in the sub-arachnoid space.
4. Infection within the intracranial cavity is a dangerous complication
of TBI. They may occur outside of the dura, below the dura, below
the arachnoid causing meningitis or within the space of the brain
itself causing abscess formation. Most of these life threatening
complications develop within a few weeks of the initial trauma.
Standard treatment involves antibiotics and sometimes surgery to
remove the infected tissue. Meningitis may be especially dangerous,
with the potential to spread to the rest of the brain and nervous
system.
5. Cerebro-vascular lesions- Any damage to the head or brain usually

results in some damage to the vascular system of the brain. The
body’s immune system can repair damage to small blood vessels,
but damage to larger vessels can result in serious complications.
Damage to any one of the major arteries leading to the brain can
cause a stroke, either a hemorrhagic stroke or an ischemic stroke,
with symptoms of headache, vomiting, seizures, hemiplegia and
impaired consciousness, all developing within several days of a head
injury. Thrombosis-ischemic strokes are treated with anticoagulants,
while surgery is the preferred treatment for hemorrhagic stroke. Other
types of vascular injuries include vasospasm and the formation of
aneurysms.
6. Cranial nerve injuries can occur due to fractures at the base of the
Skull. This can cause compressive cranial neuropathies. The seventh
cranial nerve, called the facial nerve, is the most commonly injured
cranial nerve in TBI and damage to it can result in paralysis of facial
muscles.
7. Headache is the most common form of pain experienced by TBI
patients, but other forms of pain can also be problematic.
8. Pressure sores, urinary tract infection, pneumonia or other life-
threatening infections, and progressive multiple organ failure are
serious complications for patients who are unconscious, in a coma,
or in a vegetative state following TBI.
9. Associated trauma- Most TBI patients have injuries to other parts of
the body in addition to the head and brain. These injuries require
immediate and specialized care and if neglected can complicate
treatment and recovery from the TBI. Some common associated
traumas are whip lash injury to cervical spine, blunt trauma to the
chest wall, fractures of extremities, nerve injuries, deep vein
thrombosis etc.
What Disabilities Can Result from a TBI?

The extent, type and severity of disabilities resulting from a TBI depend
upon the severity of the injury, the location of the injury, and the age and
general health of the patient. Some common disabilities of TBI are:
1. Problems with cognition (thinking, memory, and reasoning)
2. Disorder of sensory processing (sight, hearing, touch, taste, and smell)
3. Difficulty in communication (expression and understanding)
4. Abnormal behavior or mental health (depression, anxiety, personality
changes, aggression, acting out, and social inappropriateness).
• Post-concussion syndrome (PCS)): Approximately 40% of TBI patients,
even with mild injuries, develop a host of troubling symptoms
collectively called post-concussion syndrome (PCS), which include
headache, dizziness, vertigo, defective memory, poor attention span,
insomnia, restlessness, irritability, apathy, depression, and anxiety.
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These symptoms may last for a few weeks after the head injury. This
syndrome is more prevalent in patients with history of depression or
anxiety before the injury. Treatment for PCS may include pain killers,
psychotropic drugs, counseling, psychotherapy and occupational
therapy to develop coping skills.
• Cognitive impairment: Most patients with severe TBI, if they recover
consciousness, suffer from cognitive disabilities, the most common
being memory loss, characterized by some loss of specific memories
and the partial inability to form or store new ones, become easily
confused or distracted and have poor concentration and attention.
They also have problems with higher level executive functions, such
as planning, organizing, abstract reasoning, problem solving, and
making judgments, which may make it difficult to resume pre-injury
work-related activities. Recovery from cognitive deficits is greatest
within the first 6 months after the injury and more gradual after that.
• Visual impairment: Many TBI patients have problems with vision.
Patients may not be able to register what they are seeing or may be
slow to recognize objects. Also, TBI patients often have difficulty
with hand-eye coordination. Because of this, TBI patients may be
prone to bumping into or dropping objects, or may seem generally
unsteady. TBI patients may have difficulty driving a car, working
complex machinery, or playing sports.
• Sensory impairment: Other sensory deficits may include problems
with hearing, smell, taste, or touch. Some TBI patients develop
tinnitus, a ringing in the ears. A person with damage to the part of
the brain that processes taste or smell may develop a persistent bitter
taste in the mouth or perceive a persistent noxious smell. Damage to
the part of the brain that controls the sense of touch may cause a TBI
patient to develop persistent skin tingling, itching, or pain.
• Language and communication problems are common disabilities in
TBI patients. Some patients may experience aphasia, defined as
difficulty with understanding and producing spoken and written
language; others may have difficulty with the more subtle aspects of
communication, such as body language and emotional, non-verbal
signals.
1. In non-fluent aphasia, also called Broca’s aphasia or motor aphasia,
TBI patients have trouble recalling words and speaking in complete
sentences. They may speak in broken phrases and pause frequently.
Most patients are aware of these deficits and may become extremely
frustrated.
2. Patients with fluent aphasia, also called Wernicke’s aphasia or
sensory aphasia, display little meaning in their speech, even though
they speak in complete sentences and use correct grammar. Instead,
they speak in flowing gibberish, drawing out their sentences with
non-essential and invented words. Many patients with fluent aphasia
are unaware that they make little sense and become angry with others
for not understanding them.
3. Patients with global aphasia have extensive damage to the portions
of the brain responsible for language and often suffer severe
communication disabilities.
4. TBI patients may have problems with spoken language if the part of
the brain that controls speech muscles is damaged. In this disorder,
called dysarthria, the patient can think of the appropriate language,
but cannot easily speak the words because they are unable to use the
muscles needed to form the words and produce the sounds. Speech
is often slow, slurred, and garbled.
5. Some may have problems with intonation or inflection, called
prosodic dysfunction. An important aspect of speech, inflection
conveys emotional meaning and is necessary for certain aspects of
language, such as irony.
Communication disabilities such as language and speech problems
are common among TBI patients. Above, a speech therapist uses a mirror
in her work, performing exercises to help a patient relearn speaking
skills.
These language deficits can lead to miscommunication, confusion,
and frustration for the patient as well as those interacting with him or
her.
• Most TBI patients have emotional or behavioral problems that fit
under the broad category of psychiatric health. Family members of
TBI patients often find that personality changes and behavioral
problems are the most difficult disabilities to handle. Psychiatric
problems that may surface include depression, apathy, anxiety,
irritability, anger, paranoia, confusion, frustration, agitation, insomnia
or other sleep problems, and mood swings. Problem behaviors may
include aggression and violence, impulsivity, disinhibition, acting
out, noncompliance, social inappropriateness, emotional outbursts,
childish behavior, impaired self-control, impaired self-awareness,
inability to take responsibility or accept criticism, egocentrism,
inappropriate sexual activity, and alcohol or drug abuse/addiction.
Some patients’ personality problems may be so severe that they are
diagnosed with borderline personality disorder, a psychiatric
condition characterized by many of the problems mentioned above.
Sometimes TBI patients suffer from developmental stagnation,
meaning that they fail to mature emotionally, socially, or
psychologically after the trauma. This is a serious problem for children
and young adults who suffer from a TBI. Attitudes and behaviors
that are appropriate for a child or teenager become inappropriate in
adulthood. Many TBI patients who show psychiatric or behavioral
problems can be helped with medication and psychotherapy.
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What are the Long-term Problems Associated with a TBI?

Long-term problems after a TBI include Parkinson’s disease and other
motor problems, Alzheimer’s disease, dementia pugilistica, and post-
traumatic dementia.
Alzheimer’s disease (AD) – AD is a progressive, neurodegenerative
disease characterized by dementia, memory loss, and deteriorating
cognitive abilities. Recent research suggests an association between head
injury in early adulthood and the development of AD later in life; the
more severe the head injury, the greater the risk of developing AD. Some
evidence indicates that a head injury may interact with other factors to
trigger the disease and may hasten the onset of the disease in individuals
already at risk. For example, people who have a particular form of the
protein apolipoprotein E (apo E4) and suffer a head injury fall into this
increased risk category. (ApoE4 is a naturally occurring protein that helps
transport cholesterol through the bloodstream).
Parkinson’s disease and other motor problems: Movement disorders as a
result of TBI are rare but can occur. Parkinson’s disease may develop
years after TBI as a result of damage to the basal ganglia. Symptoms of
Parkinson’s disease include tremor or trembling, rigidity or stiffness, slow
movement (bradykinesia), inability to move (akinesia), shuffling walk,
and stooped posture. Despite many scientific advances in recent years,
Parkinson’s disease remains a chronic and progressive disorder, meaning
that it is incurable and will progress in severity until the end of life.
Other movement disorders that may develop after TBI include tremor,
ataxia (uncoordinated muscle movements), and myoclonus (shock-like
contractions of muscles).
Dementia pugilistica: Also called chronic traumatic encephalopathy,
dementia pugilistica primarily affects career boxers. The most common
symptoms of the condition are dementia and Parkinsonism caused by
repetitive blows to the head over a long period of time. Symptoms begin
anywhere between 6 and 40 years after the start of a boxing career, with
an average onset of about 16 years.
Post-traumatic dementia: The symptoms of post-traumatic dementia
are very similar to those of dementia pugilistica, except that post-traumatic
dementia is also characterized by long-term memory problems and is
caused by a single, severe TBI that results in a coma.
Dementia pugilistica is a condition caused by repetitive blows to the
head over a long period of time. Symptoms of the disorder, which
primarily affects career boxers, include dementia and Parkinsonism.
What Kinds of Rehabilitation Should a TBI Patient Receive?

Rehabilitation is an important part of the recovery process for a TBI
patient. During the acute stage, moderately to severely injured patients
may receive treatment and care in an intensive care unit of a hospital.
Once stable, the patient may be transferred to a subacute unit of the

medical center or to an independent rehabilitation hospital. At this point,
patients follow many diverse paths toward recovery because there are a
wide variety of options for rehabilitation.
TBI patients must receive an individualized rehabilitation program
based upon the patient’s strengths and capacities and that rehabilitation
services should be modified over time to adapt to the patient’s changing
needs. Moderately to severely injured patients receive rehabilitation
treatment that draws on the skills of many specialists. This involves
individually tailored treatment programs in the areas of physical therapy,
occupational therapy, speech/language therapy, physiatry (physical
medicine), psychology/psychiatry, and social support. Medical personnel
who provide this care include rehabilitation specialists, such as
rehabilitation nurses, psychologists, speech/language pathologists,
physical and occupational therapists, social workers, and a team
coordinator or administrator.
The overall goal of rehabilitation after a TBI is to improve the patient’s
ability to function at home and in society. Therapists help the patient
adapt to disabilities or change the patient’s living space, called
environmental modification, to make everyday activities easier.
Some patients may need medication for psychiatric and physical
problems resulting from the TBI. Great care must be taken in prescribing
medications because TBI patients are more susceptible to side effects and
may react adversely to some pharmacological agents. It is important for
the family to provide social support for the patient by being involved in
the rehabilitation program. Family members may also benefit from
psychotherapy.
It is important for TBI patients and their families to select the most
appropriate setting for rehabilitation. There are several options, including
home-based rehabilitation, hospital outpatient rehabilitation, inpatient
rehabilitation centers, comprehensive day programs at rehabilitation
centers, special school based programs for children, and others. The TBI
patient, the family, and the rehabilitation team members should work
together to find the best place for the patient to recover.
How Can TBI be Prevented?

Unlike most neurological disorders, head injuries can be prevented by
following the simple tips listed below:
• Wear a seatbelt every time you drive or ride in a car.
• Buckle your child into a child safety seat, booster seat, or seatbelt
(depending on the child’s age) every time the child rides in a car.
• Wear a helmet and make sure your children wear helmets when
riding a bike or motorcycle; Playing a contact sport; Using in-line
skates or riding a skateboard; Batting and close fielding in cricket or
Riding a horse.
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• Keep firearms and bullets stored in a locked cabinet when not in use.
• Avoid falls by- Using a step-stool with a grab bar to reach objects on
high shelves; Installing handrails on stairways; Installing window
guards to keep young children from falling out of windows; Using
safety gates at the top and bottom of stairs when young children are
around. Make sure the surface on a child’s play area is made of
shock-absorbing material (e.g., sand).
SECTION 3
BRAIN TUMORS
GENERAL CONSIDERATIONS
What is a Brain Tumor?

A tumor is an abnormal growth of tissue. Brain tumors are the most
common solid tumors seen in the human body. Brain tumors, either
malignant or benign, are tumors that originate in the cells of the brain.
A benign tumor does not contain cancer cells and usually, once
removed, does not recur. Most benign brain tumors have clear borders,
meaning they do not invade surrounding tissue. These tumors can,
however, cause symptoms similar to cancerous tumors because of their
size and location in the brain.
Malignant brain tumors contain cancer cells. Malignant brain tumors
are usually fast growing and invade surrounding tissue. Malignant brain
tumors very rarely spread to other areas of the body, but may recur after
treatment. Sometimes, brain tumors that are not cancer are called
malignant because of their size and location, and the damage they can
do to vital functions of the brain.
Brain tumors can occur at any age. Brain tumors that occur in infants
and children are very different from adult brain tumors, both in terms of
the type of cells and the responsiveness to treatment.
What Causes Brain Tumors?

The majority of brain tumors have abnormalities of genes involved in
cell cycle control, causing uncontrolled cell growth. These abnormalities
are caused by alterations directly in the genes, or by chromosome
rearrangements which change the function of a gene.
Patients with certain genetic conditions (i.e., neurofibromatosis, von
Hippel-Lindau disease, Li-Fraumeni syndrome, and retinoblastoma) also
have an increased risk to develop tumors of the central nervous system.
There have also been some reports of members of the same family
developing brain tumors that do not have any of these genetic syndromes.
Research has been investigating parents of children with brain tumors

and their past exposure to certain chemicals. Some chemicals may change
the structure of a gene that protects the body from diseases and cancer.
Workers in oil refining, rubber manufacturing, and chemists have a higher
incidence of certain types of tumors. Which, if any, chemical toxin is
related to this increase in tumors is unknown.
Patients who have received radiation therapy to the head as part of
prior treatment for other malignancies are also at an increased risk for
new brain tumors.
What are the Symptoms of a Brain Tumor?

The following are the most common symptoms of a brain tumor. However,
each patient may experience symptoms differently. Symptoms vary
depending on size and location of tumor. Many symptoms are related to
an increase in pressure in or around the brain. There is no spare space
in the skull for anything except the delicate tissues of the brain and its
fluid. Any tumor, extra tissue, or fluid can cause pressure on the brain
and result in the following symptoms:
• Increased intracranial pressure (ICP) - caused by extra tissue or
fluid in the brain. Pressure may increase because one or more of the
ventricles that drain cerebrospinal fluid (CSF, the fluid that surrounds
the brain and spinal cord) has been blocked, causing the fluid to be
trapped in the brain. Increased ICP can cause the following:
• Headache
• Vomiting (usually in the morning)
• Nausea
• Personality changes
• Irritability
• Drowsiness
• Depression
• Decreased cardiac and respiratory function and eventually coma
if not treated.
Symptoms vary depending upon which part of the brain the tumor is
found. Symptoms of brain tumors in the cerebrum (front of brain) may
include:
• Seizures
• Visual changes
• Slurred speech
• Paralysis or weakness on half of the body or face
• Increased intracranial pressure (ICP)
• Drowsiness and/or confusion
• Personality changes.
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Symptoms of brain tumors in the brainstem (middle of brain) may include:

• Seizures
• Endocrine problems (diabetes and/or hormone regulation)
• Visual changes or double vision
• Headache
• Paralysis of nerves/muscles of the face, or half of the body
• Respiratory changes
• Increased intracranial pressure (ICP).
Symptoms of brain tumors in the cerebellum (back of brain) may include:
• Increased intracranial pressure (ICP)
• Vomiting (usually occurs in the morning without nausea)
• Headache
• Uncoordinated muscle movements
• Problems walking (ataxia).
The symptoms of a brain tumor may resemble other conditions or medical
problems.
How is a Brain Tumor Diagnosed?

In addition to a complete medical history, assessment procedures for a
brain tumor may include:
• Neurological exam - test reflexes, muscle strength, eye and mouth
movement, coordination, and alertness.
• Computed tomography scan (CT or CAT scan.): A diagnostic imaging
procedure that uses a combination of X-rays and computer technology
to produce cross-sectional images (often called slices), both
horizontally and vertically, of the body. A CT scan shows detailed
images of any part of the body, including the bones, muscles, fat,
and organs. CT scans are more detailed than general X-rays.
• Magnetic resonance imaging (MRI): A diagnostic procedure that
uses a combination of large magnets, radiofrequencies, and a
computer to produce detailed images of organs and structures within
the body. A MRI of the brain usually shows more details of the brain
than a CT scan, and is the diagnostic test of choice in brain tumors.
• Bone scan: Pictures or X-rays taken of the bone after a dye has been
injected that is absorbed by bone tissue. These are used to detect
tumors and bone abnormalities.
• Myelogram: An X-ray of the spine, similar to an angiogram.
• Lumbar puncture/spinal tap: A special needle is placed into the lower
back, into the spinal canal. This is the area around the spinal cord.
A small amount of cerebral spinal fluid (CSF) can be removed and
sent for testing. CSF is the fluid which bathes the brain and spinal
cord. There may be situations in which a lumbar puncture would be
contraindicated in brain tumors.
Diagnosis of a brain tumor depends mostly on the types of cells

in which the tumor begins and the tumor location.
What are the different types of brain tumors?
The different types of brain tumors include the following (Fig. 6.6)
Gliomas
The most common type of brain tumor is a glioma. Gliomas begin from
glial cells, which are the supportive tissue of the brain. There are several
types of gliomas, categorized by where they are found, and the type of
cells that originated the tumor. The following are the different types of
gliomas:
Astrocytomas
Astrocytomas are glial cell tumors that are derived from connective tissue
cells called astrocytes. These cells can be found anywhere in the brain or
spinal cord. Astrocytomas are the most common type of childhood brain
tumor. Astrocytomas are generally subdivided into high-grade or low-
grade tumors. High-grade astrocytomas are the most malignant of all
brain tumors. Astrocytomas are further classified for presenting signs,
symptoms, treatment, and prognosis, based on the location of the tumor.
The most common location of these tumors is in the cerebellum, where
they are called cerebellar astrocytomas. These persons usually have
symptoms of increased intracranial pressure, headache, and vomiting.
There can also be problems with walking and coordination, as well as
double vision.
Fig. 6.6: Types and common location of brain tumors

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Brainstem Gliomas
Brainstem gliomas are tumors found in the brainstem. Most brainstem
tumors cannot be surgically removed because of the remote location and
delicate and complex function this area controls. Brainstem gliomas occur
almost exclusively in children; the group most often affected is the school-
age child. The child usually does not have increased intracranial pressure,
but may have problems with double vision, movement of the face or one
side of the body, or difficulty with walking and coordination.
Ependymomas
Ependymomas are also glial cell tumors. They usually develop in the
lining of the ventricles or in the spinal cord. The most common place
they are found in children is near the cerebellum. The tumor often blocks
the flow of the CSF (cerebral spinal fluid, which bathes the brain and
spinal cord), causing increased intracranial pressure. This type of tumor
mostly occurs in children younger than 10 years of age. Ependymomas
can be slow growing, compared to other brain tumors, but may recur
after treatment is completed. Recurrence of ependymomas results in a
more invasive tumor with more resistance to treatment.
Optic Nerve Gliomas

Optic nerve gliomas are found in or around the nerves that send messages
from the eyes to the brain. They are frequently found in persons who
have neurofibromatosis, a condition a child is born with that makes him/
her more likely to develop tumors in the brain. Persons usually experience
loss of vision, as well as hormone problems, since these tumors are usually
located at the base of the brain where hormonal control is located. These
are typically difficult to treat due to the surrounding sensitive brain
structures.
Primitive Neuroectodermal Tumors (PNET)

PNET can occur anywhere in the brain, although the most common place
is in the back of the brain near the cerebellum. When they occur here,
they are called medulloblastomas. The symptoms depend on their location
in the brain, but typically the patient experiences increased intracranial
pressure. These tumors are fast growing and often malignant, with
occasional spreading throughout the brain or spinal cord.
Medulloblastomas
Medulloblastomas are one type of PNET that are found near the midline
of the cerebellum. This tumor is rapidly growing and often blocks drainage
of the CSF (cerebral spinal fluid, which bathes the brain and spinal cord),
causing symptoms associated with increased ICP. Medulloblastoma cells
can spread (metastasize) to other areas of the central nervous system,

especially around the spinal cord. A combination of surgery, radiation,
and chemotherapy is usually needed to control these tumors.
Craniopharyngioma
Craniopharyngioma are benign tumors that occur at the base of the brain
near the nerves from the eyes to the brain, and the hormone centers.
Most persons with this type of brain tumor develop symptoms before the
age of 20. Symptoms include headache, as well as problems with vision.
Hormonal imbalances are common, including poor growth and short
stature. Symptoms of increased intracranial pressure may also be seen.
Although these tumors are benign, they are hard to remove due to the
sensitive brain structures that surround them.
Pineal Region Tumors

Many different tumors can arise near the pineal gland, a gland which
helps control sleep and wake cycles. Gliomas are common in this region,
as are pineal blastomas (PNET). In addition, germ cell tumors, another
form of malignant tumor, can be found in this area. Tumors in this
region are more common in children than adults, and make up 3 to 8
percent of pediatric brain tumors. Benign pineal gland cysts are also seen
in this location, which makes the diagnosis difficult between what is
malignant and what is benign. Biopsy or removal of the tumor is
frequently necessary to tell the different types of tumors apart. Persons
with tumors in this region frequently experience headaches or symptoms
of increased intracranial pressure. Treatment depends on the tumor type
and size.
Treatment for Brain Tumors

Specific treatment for brain tumors will be determined by
• Age, overall health, and medical history
• Type, location, and size of the tumor
• Extent of the disease
• Tolerance for specific medications, procedures, or therapies
• Expectations for the course of the disease
• Patient’s opinion or preference
Treatment may include (alone or in combination):
Surgery
Surgery is usually the first step in the treatment of brain tumors. The
goal is to remove as much of the tumor as possible while maintaining
neurological function. Surgery for a biopsy is also done to examine the
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types of cells the tumor is made of, for a diagnosis. This is frequently
done if the tumor is in an area with sensitive structures around it that
may be injured during removal.
• Chemotherapy
• Radiation therapy
• Steroids (to treat and prevent swelling especially in the brain )
• Anti-seizure medication (to treat and prevent seizures associated
with intracranial pressure)
• Ventriculo-peritoneal shunt (Also called a VP shunt).
A VP shunt may be placed in the head to drain excess fluid from inside
the brain. A VP shunt helps control the pressure inside the brain (Fig. 6.7).
• Lumbar puncture/spinal tap is done to test pressure in the central
nervous system, to look for suspicious cells, and give medication if
needed. There may be situations in which a lumbar puncture would
be contraindicated in brain tumors
• Rehabilitation: Supportive care for side effects of brain tumor or
treatment includes to regain lost motor skills and muscle strength;
speech, physical, and occupational therapists may be involved in the
healthcare team
• Antibiotics: To treat and prevent infections
• Continuous follow-up care: To manage disease, detect recurrence of
the tumor and to manage late effects of treatment.
Fig. 6.7: Placement of a ventriculo-peritoneal shunt

Long-term Outlook for a Patient with a Brain Tumor

As with any cancer, prognosis and long-term survival can vary greatly
from individual to individual. Prompt medical attention and aggressive
therapy are important for the best prognosis. Continuous follow-up care
is essential for a person diagnosed with a brain tumor. Side effects of
radiation and chemotherapy, as well as second malignancies, can occur
in survivors of brain tumors.
Rehabilitation for lost motor skill and muscle strength may be required
for an extended amount of time. Speech therapists and physical and
occupational therapists may be involved in some form of rehabilitation
in the lines of TBI or stroke management.
7 Parkinsonism
INTRODUCTION
Parkinsonism is the term used to describe the group of symptoms, seen
typically in Parkinson's disease, but are largely common in majority of
degenerative disorders affecting the brain.
The characteristic symptoms Parkinsonism consists of:
• Tremor
• Rigidity
• Bradykinesia
• Postural instability
• Loss of short-term memory
• Limited attention span.
Parkinsonism is a general term and not all patients with symptoms
of Parkinsonism may have Parkinson disease. Early in the disease process
it may be difficult to know whether a patient has typical Parkinson disease
or any other form of brain degeneration that share the same symptoms.
Later, due to appearance of additional symptoms and the subsequent
course of the disease, the correct diagnosis may be reached.
From the point of view of the physiotherapists, treatment is largely
based on symptoms of a disorder. Hence we shall consider the term
Parkinsonism as our point of reference while dealing with similar
degenerative disorders affecting the brain.
Outcome of physiotherapy may vary to some extent depending upon
the underlying diseases process. Since the physiotherapist will be seeing
the patient on day to day basis, he is best equipped to notice even slight
changes in symptoms, common in these patients. It is the responsibility
of the therapist to communicate such changes in symptoms to the
neurologist/physician at the earliest. To get best results with
physiotherapy it is essential to modify treatment techniques depending
on presenting symptoms and appropriate titration of drugs by the
neurologist.
PARKINSON'S DISEASE (PRIMARY PARKINSONISM)

Dr James Parkinson, a British physician, first described the symptom
complex of the shaking palsy in 1817; hence the name Parkinson disease
(PD). Presently it is referred to as primary Parkinsonism. It is a disease
of the elderly, characterized by four major clinical features:
• Shaking of the limb at rest (Resting tremor)
• Slowness of movement (Bradykinesia)
• Stiffness, increased resistance to passive movement of the limbs or
trunk (Rigidity)
• Poor balance in standing and walking (Postural instability).
When at least two of these symptoms are present, and especially if they are
more evident on one side of the body than the other, a diagnosis of PD is made,
unless there are any atypical features that suggest an alternative diagnosis.
Patients may first realize something is wrong when they experience
stiffness in extremities or back, for which they may seek the advice of a
therapist. Complaints of a frozen shoulder or dragging foot or chronic
low back pain are common initial symptoms of PD.
Since the symptoms come on gradually, older patients may attribute
these to "aging". The movements are progressively slowed and activities
take longer to perform. They may develop a tremor in one limb and/or
have balance problems. The tremor is mistaken as "shakiness,"
bradykinesia is regarded as normal "slowing down," and stiffness is
attributed to "arthritis". The stooped posture, common to PD, may be
attributed simply to "aging and osteoporosis".
Changes occur in facial expression, so that there is a certain facial
fixity, blank expression showing little emotion or a staring appearance
due to reduced frequency of eye blinking.
Initially, symptoms are a variable combination of tremor,
bradykinesia, rigidity and postural instability. Symptoms typically begin
on one side of the body and spread over time to the other side. Patients
may experience initial symptoms for a year or more before seeking medical
advice.
Age of Onset
Parkinson disease affects 1 in 100 people over the age of 60. In 5-10% of
patients with PD, the disease can affect younger people in the age group
of 40 years or younger.
Pathophysiology
After Alzheimer's disease, Parkinson disease is the most common
degenerative disease of the brain, but unlike Alzheimer's the symptoms
of PD can be reversed or controlled significantly with medication, making
it the only degenerative disorder of the brain that is partly treatable.
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• It is a chronic, progressive disease that results nerve cells degeneration

in a part of the midbrain, called the substantia nigra.
• These nerve cells produce dopamine, an important chemical messenger
that transmits signals from the substantia nigra to another part of the
brain called the corpus striatum.
• These signals allow for smooth coordinated voluntary movement.
• When the dopamine-secreting cells in the substantia nigra die, the other
movement control centers in the brain become unregulated.
• These disturbances in the control centers of the brain cause the
symptoms of PD. When 80% of the dopamine-producing cells in the
substantia nigra are depleted, symptoms of PD develop.
Clinical Features
Initial symptoms of PD are mild, usually on one side of the body, and may be
ignored by the patient, as they do not require medical treatment.
Resting tremor is a major characteristic of PD, and the most common
presenting symptom, but some patients may never develop it. Tremor
may be the least disabling symptom, but is often the most embarrassing to
the patient. Patients may keep their affected hand in their pocket, behind
their back, or hold something to control the tremor, which may be more
psychologically distressing than any physical limitation that it imposes.
Over time, initial symptoms become worse. A mild tremor gradually
becomes more troublesome and noticeable. Difficulties may develop with
cutting food or handling utensils with the affected limb.
Bradykinesia (slowness in movement) becomes a significant problem
and the most disabling symptom. Slowness may interfere with daily
ADL. Mobility is impaired and difficulty develops in getting into or out
of a chair or a car, or turning over in bed. Walking is slower and there
is a stooped posture, with the head and shoulders hanging forward.
The voice becomes soft and monotonous.
A disturbance of balance may lead to repeated falls and result in
fractures.
Handwriting becomes small ("micrographic") and illegible.
Automatic movements, such as arm swing when walking, are reduced.
Symptoms may originally be restricted to one limb, but eventually
progress to the other side of the body.
As the symptoms progress, the patients should inform their
physicians, so that optimal treatment can be established. The rate of
progression and resulting level of disability vary in different patients.
When the disorder is such that normal activities of daily living (ADL) are
impaired, at least to some extent, symptomatic treatment is begun.
The goal of treatment is not to abolish symptoms, but to help the patient
control their symptoms and function independently. The patient must be
explained that the illness will not go away, but controlling its symptoms
will reduce extent of disability. However, if the patients are made aware
of the progressive nature of the illness, they usually become anxious and
depressed. Hence counseling becomes an essential aspect of the treatment.
PARKINSONISM SYNDROMES (SECONDARY PARKINSONISM)

Recognizing Secondary Parkinsonism
A number of patients with Parkinsonism do not have Parkinson's disease.
One study of patients with features of Parkinsonism found that
• 65% had classical PD
• 18% had drug-induced Parkinsonism
• 7% had vascular Parkinsonism or Multiple infarct dementia arising
from multiple minute infarctions of the brain due to blocking-up of
the small blood vessels in the brain
• 10% had atypical Parkinsonism.
Atypical Parkinsonism should be suspected particularly if the patient:
• Don't respond to dopaminergic (Parkinson) drugs
• Has early loss of balance
• Has marked intellectual changes (dementia)
• Has rapid onset and progression of symptoms
• Has conspicuous postural hypo-tension
• Has little or no tremor.
Secondary Parkinsonism may be caused by following disorders:
Drug-induced Parkinsonism
Antipsychotic drugs, metaclopramide, reserpine, tetrabenazine and some
calcium-channel blockers may cause Parkinsonism, as adverse side effect.
Such Parkinsonism usually resolves within weeks or months after
discontinuing the offending medication.
Progressive Supranuclear Palsy (PSP)

PSP is characterized by
• Early onset of imbalance and frequent falls
• Rigidity of the trunk
• Abnormality of eye-movements.
Symptoms of PSP usually begin after the age of 50 and progress
more rapidly than with Parkinson disease. The most characteristic eye
movement abnormality is loss of up gaze and down gaze. Patients may
have frequent falls while walking downstairs, because they cannot look
down. Dementia develops later in the disease. There is no specific
treatment for PSP. Dopaminergic treatment should be tried but often
provides little benefit. Supportive treatments such as speech therapy,
physical therapy, and antidepressants may help.
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Cortico-basal Degeneration (CBD)

CBD is the least common cause of the atypical Parkinsonism. It often
affects the body asymmetrically and progresses more rapidly than
Parkinson disease. The initial symptoms of CBD usually develop after
age 60 and include asymmetric bradykinesia, rigidity, limb dystonia
(abnormal postures), postural instability, and disturbances of language
(speech expression or comprehension). There is often marked and
disabling apraxia, i.e. difficulty to use the affected limb even though
there is no weakness or sensory loss. There is no specific treatment for
CBD. Supportive treatment such as botulinum toxin for dystonia,
antidepressants, speech therapy and physiotherapy may help. Levodopa
and dopamine agonists seldom offer any benefit.
Multiple System Atrophy (MSA)

MSA is a neurodegenerative disease of unknown cause. Initially it may
be difficult to distinguish from Parkinson disease, but it is far less common
and progresses more rapidly. The mean age of onset is in the mid-50s,
occurring equally in both sexes. Clinically, it presents with bradykinesia,
poor balance, abnormal autonomic function, rigidity, difficulty with
coordination, or a combination of these features. Abnormalities of
autonomic function include impotence, low blood pressure upon standing,
excessive or reduced sweating, and constipation.
There are three subtypes of this disorder, each affecting different
systems of the CNS.
1. Striatonigral degeneration (SND) – is characterized by Parkinsonism,
but without much tremor and with poor response to Sinemet.
2. Shy-Drager syndrome – Parkinsonism and autonomic abnormalities
are conspicuous.
3. Olivo-ponto-cerebellar atrophy (OPCA) – patients have lack of
coordination and clumsiness, which affect balance and gait.
As MSA progresses, other symptoms and signs develop that reflect
involvement of a different system. The Parkinsonian presentation typically
has an asymmetrical tremor, bradykinesia, rigidity and postural instability.
Men often develop impotence; both men and women often experience
urinary urgency and incontinence.
Although 30% of patients with MSA have short-term benefit from
Levodopa and dopamine agonists, the symptoms of Parkinsonism in
most patients respond poorly to such medications. Dyskinesia and
dystonia emerge in half of treated patients.
Vascular Parkinsonism (Multiple infarct dementias)

Multiple small strokes (TIA) can cause Parkinsonism. Patients with such
disorder are more likely to present with gait difficulty, rather than tremor
and have worse symptoms in the lower limbs as compared to the upper
limbs. Some will also report sudden onset of symptoms, others give a
history of step-wise deterioration, i.e. symptoms get worse, and then
reach plateau for a period, before worsening again. Treatment is the
same as for Parkinson disease, but the results are often disappointing.
Supportive treatments such as speech therapy, physical therapy, and
anti-depressants may help.
PRINCIPLES OF MANAGEMENT OF PARKINSONISM

Till date no treatment has been shown to effectively stop the progression
of Parkinsonism. Goal of treatment is to control most troublesome
symptoms, either in Parkinson disease or Secondary Parkinsonism.
Primary treatment measures include medications like dopamine
replacement therapy, and surgical intervention like brain lesioning or
deep brain stimulation (DBS). Supplementary measures include physical
therapy occupational therapy, speech therapy and lifestyle modifications
like diet, rest and activity.
Medications for Parkinson’s Disease/Parkinsonism

Patients with PD or Parkinsonism may have a wide range of symptoms,
in varying degree of severity. Hence the choice of medication and dosage
varies considerably between individuals. Moreover, over time, as the
disease progress, the dose of medications may need to be increased or
new medications added.
Some commonly prescribed medications are:
1. Levodopa: The introduction of Levodopa (or L-dopa) more than 30
years ago revolutionized treatment of Parkinson disease. L-dopa is
modified by brain enzymes to produce dopamine which reduces the
symptoms of slowness, stiffness and tremor and to date remains the
most effective treatment for Parkinson disease. Since blood enzymes
would break down most of the L-dopa before it reaches the brain, it
is always combined with an enzyme inhibitor called carbidopa. After
being absorbed in the gastrointestinal tract, L-dopa is transported to
the brain, where it is converted into dopamine. It is subsequently
released by brain cells and activates dopamine receptors allowing for
normal function of the movement control centers of the brain.
Levodopa is available as a standard (or immediate) release
formulation or a long-acting or "controlled-release" formulation.
Controlled release may provide a longer duration of action by increasing
the time it takes for the gastrointestinal tract to absorb Levodopa.
Over the years, a number of substitutes for levodopa have been
developed. Unlike levodopa, these medications do not have to be modified
by brain enzymes in order to activate dopamine receptors. As a class,
these medications are called dopamine agonists and may be used in
place of levodopa or in combination with it.
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A number of other medications can be used alone or in combination

with levodopa or a dopamine agonist to improve movement for people
with PD. These medications do not stimulate dopamine receptors but
alter the movement control center by other means. The most commonly
used medications are amantadine, anticholinergic medications, and
selegiline.
2. Amantadine: It was initially developed as an antiviral medication.
By coincidence it was found to help the symptoms of Parkinson
disease. It may be used alone or in combination with levodopa or
dopamine agonists. Amantadine reduces symptoms of fatigue, tremor
and bradykinesia in some people with early Parkinson disease. For
people with more advanced PD, amantadine may reduce motor
fluctuations, in particular, Dyskinesia.
3. Anticholinergic medications are the oldest class of medications
available for Parkinson disease. Anticholinergic medications may
reduce tremor or rigidity. They can be taken alone or in combination
with levodopa. These drugs are rarely used in elderly patients or
those with cognitive problems, because increased confusion can be
one of their side effects.
4. Selegiline: It is an inhibitor of the enzyme MAO-B (monoamine
oxidase B). Since this enzyme breaks down dopamine, inhibiting it
prolongs the action of dopamine in the brain, and may improve the
symptoms of Parkinson disease. It also has a mild antidepressant
effect. Although early studies of selegiline initially led physicians to
believe that it may delay the progression of Parkinson disease,
currently there is no firm evidence that this is so.
Neuroprotective Treatments
Current treatments (PD medications) can significantly reduce symptoms
of the disease. They do not, however, prevent disease progression. There
is great interest in the development of neuroprotective therapies to halt
the disease or delay its onset. Cell loss in the Substantia nigra is the cause
of symptoms of PD. Why that it occurs is still unclear. It is believed that
oxidation results in the production of free radicals that may be harmful
to brain cells and lead to their death. Neuroprotective treatment through
anti-oxidant agents prevents this oxidative degeneration. However this
treatment is effective at an early stage of PD.
1. Coenzyme Q-10: Cells need energy to survive and function. They
contain mitochondria, which are "batteries" that produce energy. In
Parkinson disease, there seems to be a disturbance in the function of
these batteries. Coenzyme Q-10 affects the energy-generating
mechanisms in cells. A recent study suggested that treatment with
1200 mg/day of coenzyme Q-10 resulted in less disability over the
fixed period of the study than lower doses of the same compound or
a placebo.
2. Dopamine agonists: have been shown experimentally to protect

dopamine-producing cells. They may have antioxidant effects,
inhibiting free radical formation and scavenging free radicals. They
may also slow programmed cell death in Parkinson disease.
Experimental Treatments
"Restorative" therapies are a category of procedures that includes
transplantation of fetal cells or stem cells, injection of growth factors, or
gene therapy. The goal of these procedures is to correct the basic chemical
defect of Parkinson disease by increasing the production of dopamine in
the brain. Presently, the restorative therapies are only experimental and
are not available as treatment.
Surgical Treatments in Parkinsonism

For most people with Parkinson disease, levodopa and other medications
are effective for maintaining a good quality of life. As the disorder
progresses, however, some patients develop variability in their response
to treatment, called "motor fluctuations." During an "on" period, a person
can move with relative ease, often with reduced tremor and stiffness.
"Off" periods describe those times when a person is having more difficulty
with movement. A person with Parkinson disease may experience an
"off" period just prior to taking the next dose of levodopa, and this is
called "drug wearing off." Another form of motor fluctuation is
uncontrolled writhing movement (choreiform movement) of the body or
a limb, which is called "dyskinesia." For most people with Parkinson
disease, wearing off and dyskinesias can be managed with changes in
drugs. However, when medication adjustments do not improve mobility
or when medications cause significant side effects, surgical treatment
may be considered.
Surgery for Parkinson’s Disease

The different types of surgery for Parkinson disease are summarized
below:
• Lesioning or ablation procedures: The first surgical procedures
developed were the "ablative or brain lesioning" procedures, e.g.
Pallidotomy. In lesioning, a surgeon uses a heat probe to destroy a
small region of brain tissue that is abnormally active in Parkinson
disease. No instruments or wires are left in the brain after the
procedure, which produces a permanent effect on the brain. In general,
it is not safe to perform lesioning on both sides of the brain. Thalamic
surgery is generally reserved for patients with essential tremor and
is not recommended any longer for patients with Parkinson disease.
• Deep brain stimulation procedures (DBS): In addition to lesioning
surgery, many surgical teams now offer an alternative treatment called
deep brain stimulation (DBS). It involves placing a thin metal electrode
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into one of several possible brain targets and attaching it to a

computerized pulse generator, which is implanted under the skin in
the chest, like a heart pacemaker. All parts of the stimulator system
are internal; there are no wires coming out through the skin. To
improve control of symptoms, a physician or nurse using a
programming computer held next to the skin over the pulse generator
can adjust the stimulator during a routine office visit. Unlike lesioning,
DBS does not destroy brain tissue. Instead, it reversibly alters the
abnormal function of the brain tissue in the region of the stimulating
electrode. Although deep brain stimulation is a major new advance,
it is a more complicated therapy that may demand considerable time
and patience before its effects are optimized.
Targets for Deep Brain Stimulation

There are now three possible target sites in the brain that may be selected
for placement of stimulating electrodes: the globus pallidus (GPi), the
sub thalamic nucleus (STN), and the thalamus, specifically called "Vim"
(ventro-intermediate nucleus). These structures are small clusters of nerve
cells that play critical roles in the control of movement.
Common DBS Procedures

• Thalamic stimulation- Reduces tremor but not the other signs of PD;
approved by US Food and Drug Administration (FDA) in 1997.
• Globus pallidus stimulation- Reduces tremor, rigidity, bradykinesia,
and gait disorder; approved by FDA in 2002.
• Sub thalamic nucleus stimulation- Reduces tremor, rigidity,
bradykinesia, and gait disorder; approved by FDA in 2002.
How does DBS Work?

The theoretical basis for DBS of the GPi or STN in PD was worked out
in the late 1980s and early 1990s. In PD, loss of dopamine-producing
cells leads to excessive and abnormally patterned activity in both the GPi
and the STN. "Pacing" of these nuclei with a constant, steady-frequency
electrical pulse corrects this excessive and abnormal activity. DBS does
not act directly on dopamine-producing cells and does not affect brain
dopamine levels. Instead, it compensates for one of the major secondary
effects of dopamine loss, the excessive and abnormally patterned electrical
discharge in the GPi or the STN. The mechanism by which the constant-
frequency stimulation pulse affects nearby brain cells has not been
determined.
Technique of DBS and Brain Lesioning

The procedures are performed with the patient awake, using only local
anesthetic and occasional sedation. The basic surgical method is called
stereotaxis; a method useful for approaching deep brain targets though

a small skull opening. For stereotactic surgery, a rigid frame is attached
to the patient's head just before surgery, after the skin is anesthetized
with local anesthetic. A brain MRI is obtained with the frame in place.
The images of the brain and frame are used to calculate the position of
the desired brain target and guide instruments to that target, through
coordinates fed in a computer, with minimal injury to the brain. Sedative
medication is given and a patch of hair on top of the head is shaved.
After administration of local anesthetic to the scalp to make it completely
numb, an incision is made on top of the head behind the hairline and a
small opening, of 1.5 cm diameter is made on the skull. At this point, all
intravenous sedatives are turned off so that the patient becomes fully
awake.
To maximize the precision of the surgery, some surgical teams employ
a "brain mapping" procedure in which fine microelectrodes are used to
record brain cell activity in the region of the intended target to confirm
that it is correct, or to make very fine adjustments of 1 or 2 mm in the
intended brain target if the initial target is not exactly correct. The brain
mapping produces no sensation but patients must be calm, cooperative,
and silent during the mapping or else the procedure must be stopped.
The brain's electrical signals are played on an audio monitor so that the
surgical team can hear the signals and assess their pattern. Since each
person's brain is different, the time it takes for the mapping varies from
about 30 minutes to up to 2 hours for each side of the brain. The
neurological status of the patient (such as strength, vision, and
improvement of motor function) is monitored frequently during the
operation by the surgeon or neurologist. If a person undergoes permanent
DBS implantation, once the target site has been confirmed by
microelectrode recording, the permanent DBS electrode is inserted. After
the DBS electrode is inserted and tested, intravenous sedation is resumed
to make the patient sleepy. The electrode is anchored to the skull with
a plastic cap, and the scalp is closed with sutures. The patient then receives
a general anesthetic and is completely asleep for the placement of the
pulse generator in the chest and positioning of a connecting wire between
the brain electrode and the pulse generator unit. This part of the procedure
takes about 40 minutes.
In the case of lesion surgery, a computer-controlled probe is used to
create the desired lesion. This may take several minutes and some of the
benefits may be observed immediately. Once the desired lesion has been
made, the probe is removed and the skull and scalp are closed surgically.
Would both Sides of the Brain be Done at Once, or Only One Side in
DBS?
DBS on one side of the brain mainly affects symptoms on the opposite
side of the body. Many patients have symptoms on both sides of the
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body. DBS leads can be placed on one side or both sides on the same
operating day. The decision to place one or two stimulators in one
operating day is made according to a patient's symptoms and general
health. For elderly patients, or patients concerned about a longer operation,
it may be best to stage the procedures a few weeks or months apart.
What are the Benefits of Surgery?

The major benefit of surgery for PD is that it makes movement smooth
without or with very low dose of medication. Symptoms that improve
with levodopa (slowness, stiffness, tremor, gait disorder) may also
improve with DBS. In addition, it may reduce levodopa-induced
dyskinesias. The procedure is most beneficial for PD patients who cycle
between states of immobility ("off" state) and states of better mobility
("on" state). DBS only suppresses symptoms and does not eliminate need
for medication or alter the progression of PD.
Risk Factors of Pallidotomy or DBS Surgery

The most serious potential risk of the surgical procedures is bleeding in
the brain, producing a stroke in 2% of cases. If stroke occurs, it usually
does so during or within a few hours of surgery. The second most serious
risk is infection, which occurs in about 4% of patients. If an infection
occurs, it is usually not life-threatening, but it may require removal of
the entire DBS system. In most cases, a new DBS system can be re-
implanted when the infection is eradicated. Finally, hardware may break
or erode through the skin with normal usage, requiring it to be replaced.
In the first few days after surgery, it is normal to have some temporary
swelling of the brain tissue around the electrode. This may produce no
symptoms, but it can produce mild disorientation, sleepiness, or
personality change that lasts for up to 1-2 weeks.
What makes a Patient a Good Candidate Surgical Treatment for

Parkinson Disease?
The patients who derive the most benefit from surgery should have good
general health, normal intellectual and memory function for their age,
and continue to experience benefit (however short) from levodopa.
Can Patients Control the DBS Device Themselves?

Following surgery, the patient is given the Medtronic Access Review
unit, a hand-held battery-operated unit that can be used to determine
whether the device is on or off, to turn it on or off, and to check battery
life. The device does not allow the patient to alter the intensity of
stimulation. This is done in the physician's office. Normally, in DBS for
Parkinson disease, the device is left “on” all the time. The next generation
of DBS devices may allow some patient control over the intensity of
stimulation
PRINCIPLES OF PHYSICAL CARE AND NURSING IN PARKINSONISM

Exercise Plan for the Parkinson Patient
Just as running water does not freeze, so moving muscles do not freeze.
The maintenance of normal muscle tone and function is an important
aspect of the treatment of Parkinsonism. In part, medication administered
for the illness achieves this goal. However, to realize the full benefit of
the medication daily exercise and activity are essential. The following
passage outlines exercises capable of maintaining muscle power and tone
and preventing deformities of the limbs and spine. Their daily
performance has proved most beneficial to patients with this illness.
Exercises help strengthen postural and limb muscles and keep them
flexible. Start exercises once a day, at first in lying position on a mat, and
then build up to several times a day, progressing on to sitting and standing
positions. Patients of Parkinsonism must exercise slowly, and take frequent
rests.
The Ten-point Maintenance Exercise Program

1. Bring the toes up with every step you take. In Parkinsonism "you
never make a move", without lifting the toes.
2. Spread the legs (10 inches) when walking or turning, to provide a
wide base, a better stance, and to prevent falling. It may not look
"beautiful," but neither does falling.
3. For greater safety in turning, use small steps, with feet widely
separated. Never cross one leg over the other when turning.
Practice walking a few yards and turn. Walk in the opposite
direction and turn. Do so fifteen minutes a day.
4. Practice walking into tight corners of a room, to overcome fear of
close places.
5. To insure good body balance, practice rapid excursions of the
body. Backward, forward and to the right and left, five minutes,
several times a day. Don't look for a wall when you think you are
falling. It may not be there. Your body will always be there to
protect you, if you will practice balance daily.
6. When the legs feel frozen or "glued" to the floor, a lift of the toes
eliminates muscle spasm and the fear of falling. You are free to
walk again.
7. Swing the arms freely when walking. It helps to take body weight
off the legs, lessens fatigue, and loosens the arms and shoulders.
8. If getting out of a chair is difficult, rise with "lightning speed," to
overcome the "pull of gravity." Sitting down should be done slow,
with body bent sharply forward, until one touches the seat.
Practice this at least a dozen times a day.
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9. If the body lists to one side, carry a shopping bag loaded with
books or other weights in the opposite hand to decrease the bend.
10. Any task that is difficult, such as buttoning a shirt. or getting out
of bed, if practiced 20 times a day, becomes easier the 21st time.
Exercises in Lying Position

Starting Position: Supine on the Floor or Bed,
Lie flat on your back; try to press your body to the floor as flat as possible.
Move your head from right to left as far as possible. Make sure your
head, shoulders, back, touch the surface and remain relaxed.
First stage mat exercises: Bridge, Abdominal Lift (Figs 7.1 and 7.2)
These exercises strengthen abdominal, buttocks, and hamstring muscles.
This helps keep the back stable and aligned when walking. The abdominal
lift strengthens the lower abdominal muscles, helping keep the pelvis
and back stable.
1. Lie on the floor with the back and palms flat on the ground. Bend
your knees. Keep your feet flat on the floor
2. Contract your abdominal and buttocks muscles. Slowly lift the
buttocks off the floor until there is a straight line from the knees to
the shoulders. Hold for 5 seconds. Repeat 10 times. Fig. 7.1.
Fig. 7.1: Bridge
Fig. 7.2: Abdominal lift

1. Lie on the floor with both knees bent. Put the feet flat on the floor
and the arms by the sides. Tighten the abdominal muscles.
2. Lift one bent knee and move it toward the upper body. Keep the
abdominal muscles tight and the back flat on the floor. Hold for 10
seconds. Repeat 3 times. Then, repeat on the other side. Fig. 7.2.
Second Stage Mat Exercises: Leg pull, Hamstring Stretch (Figs 7.3 and 7.4)
Pull one knee to the chest. Hold for 20 seconds. Then release. Repeat
2 times. Switch legs. For a double leg pull, pull both legs to the chest at
the same time. Repeat 2 times.
Put a towel behind one knee or calf. Use the towel to pull the leg
toward the chest, keeping the leg straight or slightly bent. Hold for 20
seconds. Then lower the leg. Repeat twice. Switch legs.
Fig. 7.3: Single/double leg pull
Fig. 7.4: Hamstring stretch

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Third stage mat exercises: Lower back rotation, Hip rotator stretch,
Knee lift (Figs 7.5 to 7.7).
Drop both knees to one side and turn the head, looking in the opposite
direction. Keep shoulders flat on the floor. Hold for 20 seconds. Slowly
switch sides. Repeat 2 times.
Rest your right ankle on your left knee. Place a towel behind your
left thigh and use it to pull the knee toward your chest. Feel the stretch
in your buttocks. Hold for 20 seconds. Release. Repeat 2 times. Switch
legs.
Fig. 7.5: Lower back rotation
Fig. 7.6: Hip rotator stretch
Fig. 7.7: Knee Lift

Lift one bent knee and move it toward your upper body. Keep your
abdominal muscles tight and your back flat on the floor. Hold for 10
seconds. Repeat 3 times. Switch legs.
Fourth stage mat exercises: Back press, Back release, Arm reach, Leg reach
(Figs 7.8 to 7.13)
Starting Position: Prone or Prone Kneeling

Lie on the floor or bed on your abdomen. Do the following exercises one
by one.
Lie prone, feet slightly apart, forehead on the floor. Press up on the
forearms and lift your chest off the floor. Keep the abdomen and hips on
the floor. Hold for 20 seconds. Lower slowly. Repeat 2 times. Return to
starting position (Fig. 7.8).
Fig. 7.8: Elbow press
Do these exercises on your hands and knees. Keep your knees under
your hips and your hands under your shoulders. Keep your spine in a
neutral position (not arched or sagging). Be sure to maintain your neck's
natural curve (Fig. 7.9).
Fig. 7.9: Starting position

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Tighten your abdominal and buttocks muscles to press your back

upward. Let your head drop slightly. Hold for 5 seconds. Return to
starting position. Repeat 5 times (Fig. 7.10).
Fig. 7.10: Back press
Relax your abdominal and buttocks muscles, lift your head, and let
your back sag. Be sure to keep your weight evenly distributed. Don't sit
back on your hips. Hold for 5 seconds. Return to starting position. Repeat
5 times (Fig. 7.11).
Fig. 7.11: Back release
Stretch one arm straight out in front of you. Don't raise your head or
let your supporting shoulder sag. Hold for 5 seconds. Return to starting
position. Repeat 5 times. Switch arms Fig. 7.12.
Fig. 7.12: Arm reach

Extend one leg straight back. Don't arch your back or let your head
or body sag. Hold for 5 seconds. Return to starting position. Repeat 5
times. Switch legs (Fig. 7.13).
Fig. 7.13: Leg reach
Exercises in Sitting Position (Figs 7.14 and 7.15)
Fig. 7.14: Body twist
1. Sit in a chair, facing forward.

2. Place your hands on your shoulders.
3. Turn your head and body to the side as far as possible, as if you were
trying to look behind you.
4. Return to starting position, and then turn to the other side.
5. Repeat 10 times.
Fig. 7.15: Seated march

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1. Sit in a chair, facing forward.

2. Slowly lift one knee as high as you can, then lower your foot to the
floor.
3. Do the same with your other leg. Repeat 10 times with each leg.
Exercises in Standing Position (Fig. 7.16)

1. Stand or sit with your back straight.
2. Hold your arms in front of you. Put your hands and elbows together,
hands pointing toward the ceiling.
3. Move your arms apart as far as possible, pushing your shoulder
blades together.
4. Slowly move your hands back together. Repeat 10 times.
Fig. 7.16: Back stretch
Exercises to Increase Agility

The following exercises help to increase the ease and quickness of
movement. They copy complex everyday moves. The exercises chosen
depend on the type of activities the patient will be doing.
1. Figure of 8 (Fig. 7.17) Follow a large figure 8 at a slow jog or brisk
walk.
2. Keep at it for 2-3 minutes. Then reverse directions.
3. Gradually decrease the size of the figure 8 and increase your speed
and time.
Cross-steps (Fig 7.18)

1. Start with knees bent and feet shoulder-width apart.
2. Cross your right foot in front of your left.
3. With your left foot, step to your left.
4. With your right foot, step behind your left foot.
Fig. 7.17: Figure of 8 exercises helps patient to move around corners and to pivot
Fig. 7.18: Cross steps prepare the patient for complex gait activities
5. With your left foot, step to the left.

6. After doing the cross-step sequence, switch directions.
7. Repeat the entire exercise 10 times.
Side Steps
1. Start with knees bent and feet together.

2. Step to the side with your left foot.
3. Step with your right foot to meet your left foot.
4. Keep your steps short and comfortable.
5. Repeat the sequence in the opposite direction.
6. Continue for 2-3 minutes.
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Short Sprints
1. Sprint forward 10-15 feet. Stop. Feel your muscles absorb the shock.
Sprint backward.
2. Continue for 2-3 minutes.
3. Gradually increase your distance, speed, and total exercise time.
Exercises to Gain Better Balance

Starting position: Stand with hands on hips, feet spread apart
1. Practice marching in place.
2. Practice raising leg straight out to the rear.
3. Practice raising leg out to the side.
4. Practice drawing a circle with the leg.
5. Lean forward and back.
6. Lean to both sides.
7. Lean in a circular motion and reverse the motion.
Gait Training
1. When walking, Remember:
a. Take as large a step as possible.
b. Raise your toes as you step forward, hitting ground with your
heels.
c. Keep legs apart and posture straight.
d. Swing arms and look straight ahead - your feet know where the
floor is located.
2. Collect a dozen magazines; lay them out in a straight line. Space
them so that you can take as long a step as possible. Practice walking
over these magazines without stepping on them.
3. For a better swing to arms, walk holding a rolled magazine in each
hand; keep elbows straight.
4. Practice walking sideways, backwards, and take big steps.
Teaching how to Turn while Walking

1. When practicing turning:
a. Keep feet spread-apart and head high
b. Use small steps; rock front side to side
c. Raise legs from the knees.
2. If you feel glued to the floor:
a. Raise your head, relax back on your heels and raise your toes
b. Rock from side to side, bend knees slightly and straighten up
and lift your toes
c. It sometimes helps if the arms are raised in a sudden short motion.
Teaching how to Get in and Out of a Chair

1. If you become glued a few steps before you reach the chair, try this:
Don't aim for the chair but some object past it. Pass the chair as
closely as possible and as you go by it sit down.
2. To sit down, bend forward as far as possible and sit down slowly.
Get close to the chair. Do not fall into the chair.
3. To get up, move to the edge of the chair, bend forward and push up
vigorously using your arms; try to count 1 2 3 GO! If you have a
favorite armchair, raise the back legs with 4" blocks. This will help
you to get up easily. Don't let people drag you up by your arms, but
help you by pulling you under your arms, or with a slight push on
your back.
Teaching how to Get in and Out of Bed

1. Place blocks under the legs of the head of the bed. This will elevate
the head of the bed, and make it easier for you to sit up and swing
the legs off the bed.
2. A knotted rope tied to the foot of the bed can help you to pull
yourself up.
3. To get to a sitting position, shift the body down and rock yourself by
vigorously, throwing your arms and legs toward the side of the bed.
Teaching how to Use Upper Limbs and Retrain Hand Function

1. Practice buttoning and unbuttoning your clothes; practice cutting
food and writing. Squeeze a ball or work with "Silly Putty." Keep
your fingers busy many times a day. Tear paper; take coins out of the
pocket; play the piano.
2. Always try to dress yourself completely. Use shoehorns, elastic laces,
or extra-long shoelaces to get a better grip. Dress in the most relaxed
and comfortable position, sitting or standing, but make sure you are
in a safe position.
3. To keep elbows straight and shoulders loose, install a pulley in
doorway, place a chair under it or slightly in front. Stretch your arms
and shoulders in all directions. By working the pulley when seated,
you can get a more vigorous pull.
For Correcting Orofacial Problems

1. Practice singing and reading aloud with forceful lip movements. Talk
into a tape recorder, if one is available.
2. Practice making faces in front of a mirror. Recite the alphabet and
count numbers with exaggerated facial motions. Massage your face
with vigor when washing and bathing.
Parkinsonism 175
For easier feeding

• Use non-slip mat to fix utensils. Scoop from a bowl with a raised
curved lip. Weighted cup with enlarged handles reduces tremor.
To avoid choking
• Sit up with the head tilted forwards during meal time. Do not lie
down or tilt the head backwards while eating.
• Cut food into smaller pieces or prepare pureed meals. Food which is
too dry, too hard, chewy or hard to control, or sticky may cause
choking.
• Encourage patients to chew and swallow slowly and do not hurry
them.
To prevent constipation
• Encourage high fiber diet (like vegetables, fruits, oatmeal) and
adequate fluid intake.
Teaching how to Get Dressed

For easier dressing
• Choose clothes which are easier to wear such as clothes with front
opening and large buttons or Velcro. Replace zip with elastic band
for trousers. Shoes fastened by elastic band or Velcro are more
convenient.
To prevent falls while dressing
• Sit down when putting on trousers. Avoid trousers which are too
long or too loose. Shoes should be well-fitted, and preferably with
non-slip soles. Replace shoes when they look worn.
Teaching Transfers
For easier transfer
• Chairs and beds should be of suitable heights such that both feet are
on the ground while the patient is sitting on the bedside. Chairs with
armrests can help with rising from the chair.
To prevent falls while transferring
• Always stand with feet apart for easy balancing.
PARKINSONISM: HOME SAFETY

Teaching Safety in Home Environment
As Parkinson's disease progresses, home safety will be an increasing
concern. This page includes tips that can help make your daily life safer
and easier. Your doctor may also recommend a therapist to advise you
on the best ways to set up your home.
Setting up Living Spaces

Get help from family and friends to make these changes to the home
environment:
• Keep walkways open and free of clutter.
• Move phone and electrical cords out of the way.
• Remove throw-rugs to prevent trips.
• Get a cordless or speaker phone. Program numbers for family and
emergency services.
• Make sure rooms are well lit. Install nightlights along walkways.
• If "freezing" at doorways is a problem, consider placing lines of tape
on the floor between rooms. Stepping over the tape may prompt you
to keep moving.
Teaching Safety in Bathroom and Toilet

Climbing in and out of the bath tub could be dangerous. Shower stalls
are safer. Shower curtain is better than sliding glass door. Alternatively,
a stable shower chair or a bath board can be used. By using a hand-held
shower hose rather than a fixed hose, the patient can wash his/her back
without turning (Fig. 7.19).
Try the following:
1. Place a bench, stool or chair while bathing. Sit on the chair and soap
yourself. Use shower to rinse, or rubber shower extension.
2. Bathroom grab bars that attach securely to the wall must be installed.
Fig. 7.19: Setting up the bathroom

Parkinsonism 177
3. Raised commercially available toilet seats.

4. Toilet armrest for getting on and off the toilet are useful.
• Keep the passageway clear of unnecessary items to allow enough
space for turning and use of walking aid. Loose wires should be
fixed against the wall. Ensure the floor is flat and dry to prevent
falls.
• Ensure adequate lighting. Corridor and bedside lights facilitate
going to the toilet at nighttime.
• Place non-slip mats at toilet and kitchen entrances. Label door
thresholds with sharp-colored strips.
To Prevent Accident
• Install an alarm call system if patient is living alone.
Teaching Communication Skills

To Communicate Effectively
• Reduce background noise. Sit face-to-face with patient. Keep good

eye contact and listen attentively. Ask simple questions.
• Encourage patients to speak slowly and to use simple words or
phrases and body gestures to facilitate communication, e.g. nodding
to represent "yes".
• If patients experience much difficulty with speaking, writing or
drawing pictures on cards can help.
How to Maintain Mental Well-being
• Patients are more prone to depression. Therefore reassurance and

support from family members and therapist are very important.
• Watch for any change in emotion or behavior for early detection of
depression.
• Help the patient take part in the decision making process regarding
his treatment
How to Prevent Complications in Bed-ridden Patients

To Prevent Bedsores
• Keep the skin clean and dry. Observe the skin condition of pressure
areas for any signs of bedsores such as redness and ulcers.
• Change patient's position at least every 2 hours to avoid prolonged
pressure on bony prominences. Avoid placing heavy objects on the
limbs.
• Encourage the patient to perform appropriate exercises.
To Prevent Chest Infection

• Encourage adequate water intake and daily activities, sit up during
meal time, build up the body resistance and perform breathing and
coughing exercises. These can help to reduce the chance of chest
infection since patients may have difficulty in coughing and spitting.
Discharge Instructions for Parkinson's Disease

Here are things the patient can do at home to participate in the treatment
and feel better.
Medications
• Take your medications exactly as directed. Don't skip doses.
• Get a pillbox with sections for each day of the week.
• Try to take your pills about the same time each day.
• Don't run out of medication. Order for more medication when you
still have a 2-week supply left.
• Bring your medication and copies of your prescriptions when you
travel.
• Carry a list of the medications you take.
• Ask your doctor before driving or operating heavy machinery. Some
medications for Parkinson's disease may cause sleepiness.
Activities of Daily Living

• Do one thing at a time.
• Leave yourself plenty of time to get ready for appointments so that
you're not rushed.
• Lay out your clothes nearby.
• Replace buttons with Velcro patches.
• Choose shoes that slip on or that close with Velcro.
• Use kitchen utensils with large handles if you have trouble holding
them.
• If you drink hot liquids, use cups with lids to prevent burns from
spills.
• Install grab bars in the shower or tub to make getting in and out
easier. A shower chair may also be useful.
• Put no-slip decals on the bottom of the tub.
• Remove bathroom rugs, or make sure they have a no-slide rubber
bottom.
• Strengthen your voice by reading aloud. Singing is also a good
exercise.
• Add a voice amplifier to the phone to help you to be heard.
Parkinsonism 179
Avoiding Constipation
• Drink plenty of water. Ask your doctor how much you should drink.
• Eat foods that are high in fiber, such as fruits, vegetables, and whole
grains.
• Use over-the-counter laxatives if needed.
Getting Support
• Remember, Parkinson's is a serious illness. It's normal to feel emotional
while you learn to cope.
• Don't be afraid to ask for help if you feel depressed. Let your family
and doctor know if you feel like harming yourself or others.
• Ask your doctor about support groups in your area.
Follow-Up: Make a follow-up appointment as directed.
COPING WITH PARKINSONISM

Lifestyle Changes
When first diagnosed as suffering from Parkinsonism (primary/
secondary), patients may deny their illness. Going from being a well
individual to someone with a chronic, progressive disease is a major
transition. Patients may question the diagnosis; seek many specialist
opinion, avoid medical appointments or avoid evaluation; refuse to tell
anyone (including family and friends); and refuse dopaminergic treatment,
even if warranted.
Denial can be a barrier to seeking appropriate treatment and support,
alternatively it can also create a positive attitude of "I'm going to fight
this and not let it control me."
The biggest adjustment is the realization that one will never return
to the pre-illness state.. The patient's strongest wish is to return to normal.
It is another adjustment to recognize that the treatment goal is not to
extinguish all signs, but to maintain functionality.
Having a chronic illness raises concerns for the future. Any
progressive chronic illness produces uncertainty. The patient is often
concerned with:
• Will this disease interfere with work?
• Will it interfere with economic well-being?
• Will it interfere with roles as a partner, spouse and parent?
• Will it change privacy, autonomy, independence?
• How quickly will the disease progress?
• Will I become an invalid?
• How will the disease be managed?
• Will adaptation be successful?
Adapting to the illness is difficult for patients. They must adjust to

having a diagnosis, recognize that their life is being changed, maintain
their independence, and at the same time learn to seek help. They need
to recognize that at times they may feel helpless in the face of the disease,
but that they can adapt and live full lives with it.
Common difficulties faced by patients with Parkinsonism can include:
• Anxiety
• Social withdrawal
• Inability to tolerate frustration
• Anger
• Depression.
Adapting to Parkinsonism needs making adjustments in lifestyle
and work, family life and seeking help.
Lifestyle and Work Adjustments

As the symptoms progresses, some changes are required in lifestyle.
Hobbies, once enjoyed, may become more difficult. Patients are often
very creative about substituting activities for things they feel they can no
longer do. Although these changes represent a painful loss to the patient,
adjustments can be made successfully with time.
Lifestyle changes require assessment of what is most important about
the current lifestyle, what can be adjusted, and what has to be completely
changed. Lifestyle changes can be induced by changes in employment,
finances, or disability. Many patients have successful, satisfying work
lives, and often early in the disease make no changes in their normal
work habits or routines.
It is important to ask the patient the following questions:
• Can I continue to function in my job at the same level?
• If not, what part of my job has become more difficult?
• Can adjustments be made so that I can continue to work?
• Is anything at work a safety risk?
• Can or should I change job?
• Should I consider retirement due to disability?
Analyzing the work environment, job duties, performance standards,
and job complexity and type, may provide clues as to what adjustments
can be considered.
• Fatigue may be caused by medications. A mid-day nap during the
lunch-hour can be restorative. Schedule important business meetings
or difficult tasks at a time of the day when one feels best.
• If writing becomes difficult, use a computer or recorder to take notes.
Parkinsonism 181
• If changes in voice volume become problematic in meetings, can

someone else on the team do the presentation.
• Tasks once safely performed may now pose a safety risk. Climbing/
descending a ladder or carrying boxes with both hands may be
hazardous if balance is a problem.
• Individual adjustments to one's job may not be always possible. Talk
to the employer, union representative, manager, or team leader when
considering any changes.
The People with Disabilities Act (PWD) entitles all qualified
individuals the right to a job, regardless of disability. It also requires
reasonable accommodations in the workplace for a disabled worker. This
can include adjustments in work schedule, work assignments, or
modifications in the workplace for equipment or devices. The law
prohibits employers from inquiring about health status, until it directly
impacts on specific areas of performance.
Telling the Employer

Telling the employer about the diagnosis is essential if the nature of the
job poses any hazard. Employers may have noticed some change in
performance, and bringing it up for discussion may give them an
opportunity to understand the situation and make adjustments to patient's
benefit.
Work provides a satisfying arena for individual accomplishment and
satisfaction. For most Parkinson disease patients there is no reason not to
continue working. However, there may come a time when working
becomes increasingly difficult and too demanding, frustrating or
unrewarding.
Family Concerns
Having a chronic illness raises many concerns for the spouse, partner, or
family. They too worry about the unknown future, the risk of disability,
job loss, economic loss and increased dependence. They too can suffer
from anxiety and depression.
Include them in physician visits, so they too have an opportunity to
ask questions or raise concerns that they have. As the patient no longer
is able to do things they once could, the spouse/partner may need to
assume these responsibilities. It is important to discuss these things before
any changes are actually required, giving everyone a chance to assess,
plan, and adjust for the future.
Seeking Help
Help can be obtained in several ways.
• Seeking assistance and permitting others to help the patient at home
or at work.
• Seeking help from specialists for specific PD problems.

• Hiring help, such as housekeeping, shopping, and gardening services.
• Seeking help from support groups.
Patients may be reluctant to seek help. It may mean recognizing that
symptoms are worsening or some new ones have developed. It may
mean spending more time with specialists like physical, occupational, or
speech therapy. This can be frustrating for the family members who are
expecting the patient to act when the patient is unwilling to do so.
Patients value their independence and have their own view of what
makes them appear old or disabled. Often suggestions related to using
a cane, walker, or wheelchair is met with great resistance. Although the
patient is clearly unstable, they avoid using them as they are a visible
sign to the world, and a signal to themselves that they no longer are
completely independent. If it appears that patients are reluctant, keep
the discussion open, be understanding, and allow the patient to articulate
their hesitation.
Support groups offer help from members afflicted with the same
disease. Members can relate to the problems you are experiencing, or
offer helpful tips, as they themselves have experienced the same problems.
Some groups are face-to-face, whereas others may be internet chat rooms.
Patients are often reluctant to attend a support group, as they fear seeing
what they may become.
Tips to Maintaining Optimum Wellness
• Parkinsonism demands adaptation, not despair.

• Learning to pace yourself, prioritize goals, and make timely use of
physical, occupational and speech therapies will enhance your
physical, intellectual, and emotional well-being, and can make all the
difference in how you enjoy life and maintain your independence.
• Establishing an exercise program, learning the most efficient methods
to perform routine activities of daily living, and improving nutritional
status is essential.
• It is important to seek out specialist healthcare providers for who are
both competent and compassionate. Consider choosing a minimum
of two physicians: A neurologist who can advise regarding
adjustments in the anti-Parkinson medications, and a family physician
who is aware of how Parkinsonism affects overall health and can
manage health problems outside the Parkinson arena. Primary care
providers must also include a physiotherapist, competent in neurology
and able to share information with physicians to ensure the best care
possible.
Parkinsonism 183
• It is a good idea to maintain a personal health file at home, including

dates of any major diagnoses, pertinent test reports, immunization
records, dates of any serious illnesses or surgeries, allergies to
medication, and a list of current medications, including non-
prescription drugs and supplements.
• Maintaining a positive attitude is one of the healthiest things one can
do in response to a diagnosis of Parkinsonism. Psychotherapists can
be an important part of adjustment to a diagnosis of Parkinsonism.
Short-term counselling with a capable psychotherapist can be
immensely helpful during this period of depression and anxiety.
Clinical depression can sometimes abate spontaneously, mood
changes persist for more than two weeks, seek advise of a competent
therapist. Antidepressant medication can be safely taken with anti-
Parkinson drugs.
8 Disorders of the Spinal Cord
INTRODUCTION
The spinal cord is the second most important component of the CNS and
connects the brain with all other peripheral organs of the body, through
spinal nerves, helping to control almost every function of the body. When
the spinal cord is damaged it will result in loss of normal movements
due to reduced muscle power, autonomic dysfunctions and/or loss of
sensation in the body at or below the site of the lesion.
Nomenclature
Any damage to the spinal cord, either due to traumatic or non traumatic
causes is broadly called Myelopathy (Myelos- Spinal cord; Pathy- Disorder)
may involve loss of motor, sensory and autonomic function in:
• All four extremities and trunk, involving the urinary and bowel
sphincters, commonly known as quadriplegia or tetraplegia.
• Lower extremities and trunk, mostly involving the urinary and bowel
sphincters, commonly known as paraplegia.
A Myelopathy may be caused by:
• A compressive force, squeezing the delicate nervous tissues of the
spinal cord against the hard bony margin of the spinal canal. This is
called a Compressive myelopathy such compression can be induced
by
1. Nontraumatic causes such as spondylosis, spondylolisthesis,
tumor growing within the spinal canal, collapsed vertebra
2. Inflammatory causes such as edema of the cord.
• A shearing force, causing complete or partial loss of continuity of
the cord, as in a fracture-dislocation of the vertebral column resulting
from accidents, gunshots, sports injuries etc. This is called a spinal
injury.
• A disease/degeneration of the cord, such as Transverse Myelitis,
Acute poliomyelitis, Post polio syndrome, Spina Bifida, Friedreich’s
Ataxia etc. This is called a Noncompressive Myelopathy.
A Primer to the Anatomy of the of
Disorders Nervous System
the Spinal Cord 185
From the point of view of the physical therapist, the signs and symptoms
caused by all three types of spinal cord lesions mentioned above are pretty much
similar and thus may be considered as a group of disorders resulting in the
clinical syndrome of Myelopathy. However for the sake of convenience, henceforth
all types of Myelopathies discussed in this chapter will be referred to as spinal
cord injuries or lesions or damage. (SCI/D/L)
Since the problems faced by the patient of most of these disorders
are same, they follow same format of assessment and has more or less
the same approach to physiotherapy treatment, except in case of traumatic
spinal injuries. In case of spinal trauma the structural derangement of
the vertebral column due to fracture/fracture-dislocation is an added
issue to be considered, over and above the effects of injury to the spinal
cord itself. In the following passages, primarily for the sake of simplicity,
I have attempted to deal with physical therapy approach to the assessment
and management of spinal cord problems as a whole, without getting
bogged down with sign and symptoms of different sub-categories of
spinal cord lesions.
LOCALIZATION OF A SPINAL CORD LESION

The effects of any spinal cord lesion depend on the level and category
of the damage.
Level of a spinal lesion is indicated by the uppermost-uninvolved
spinal segment, which has normal function. The muscles supplied by
nerves originating from this spinal segment must have at least Grade
III+/IV power, intact reflexes and sensation relevant to the spinal segment
in consideration.
• Lesion of the cervical cord occurring between C1-C8 spinal levels
involves all four extremities and trunk, resulting in Quadriplegia or
Tetraplegia, with UMN type presentation of motor, sensory,
autonomic and bladder involvement.
• Lesion of the thoracic cord occurring between T1-T12/L1 involves
the whole of the lower extremities and may involve the trunk partially
or totally, resulting in Paraplegia, with UMN type presentation of
motor, sensory, autonomic and bladder involvement.
• Lesion of the lumbar and sacral segments of the cord occurring below
L1 involves the lower extremities partially or totally, resulting in
Paraplegia, with LMN type presentation of motor, sensory, autonomic
and bladder involvement.
Clinically, spinal cord lesions can be divided into two categories for
classification:
• Complete – Means that there is no function, (no sensation or voluntary
movement) below the level of the injury.
• Incomplete – There is some function below the level of injury. A
person may be able to feel parts of the body that cannot be moved,
they may be able to move one limb more than the other.
RELEVANT ANATOMY OF THE SPINAL CORD

The spinal cord originates from the lower extension of the brainstem.
The spinal cord and meninges covering the cord along its entire length
lie enclosed in the bony vertebral canal. In the 3-month fetus, the spinal
cord and vertebral canal are of the same length but as the child grows,
the vertebral canal grows more rapidly as compared to the spinal cord,
so that in an adult the cord extends from the foramen magnum to the
level of the first or second lumbar vertebra. Thus, the adult spinal cord
occupies only the upper two-thirds of the vertebral canal. The spinal
cord is roughly cylindrical in shape being slightly flattened antero-
posteriorly and possesses cervical and lumbar enlargements from which
originate the nerves supplying the upper limb (C4–T1) and the lower
limb (L1–S3) plexuses respectively.
A total of 31 pairs of spinal nerves emerge from the cord and, since
the adult spinal cord is shorter than the vertebral canal, these nerve roots
descend in the canal, with increasing obliquity and length, to reach their
appropriate inter vertebral lateral foramina, through which they exit the
canal.
The lumbar and coccygeal nerves are the longest and descend beyond
the end of the spinal cord, bunched together to look like a horsetail, the
Cauda Equina (Cauda- Tail; Equina- Horse) (Fig 8.1).
The lower most end of the spinal cord itself tapers to a conical shape
or the conus medullaris and from its end a thin strand of pia mater, the
filum terminale, descends through the Cauda Equina to be attached to
the coccyx.
The cross-section of the spinal cord (Fig. 8.2) shows a central canal
around which is the H-shaped grey matter, the anterior horns of which
contain mainly motor cells. The grey matter of the cord is surrounded by
white matter containing the fibers of the ascending (motor) and
descending (sensory) nerve fibers arranged in discrete bundles of nerve
pathways called the tracts. A median fissure partially divides the white
matter anterior and posterior to the central canal. The central canal
conducts flow of CSF to and from the brain.
Points to Ponder
• The anterior and posterior cerebellar tracts ascend the ipsilateral side
of the cord to the cerebellum.
• The lateral and anterior spino-thalamic tracts convey pain and
temperature sensation. Their fibers ascend the cord in the posterior
horn for a few segments before crossing over to the opposite side to
continue their ascent in the opposite spino-thalamic tracts.
• The posterior columns tracts convey fine touch and proprioception
uncrossed to the medulla and then, after synapsing at brainstem,
extends to the sensory cortex and the cerebellum.
the Spinal Cord 187
Fig. 8.1: General layout of the spinal cord
• The descending tracts are motor in function; the crossed pyramidal

tract conveys the fibers from cells in the opposite motor cortex that
have crossed in the medulla to reach the contra-lateral cord. These
fibers synapse in each segment with motor cells in the anterior horn.
• The direct pyramidal tract descends from the motor cortex without
decussating. Its fibers synapse at each segment with cells in the
anterior horn of the opposite side.
SPINAL MENINGES AND CEREBROSPINAL FLUID (CSF)

The spinal meninges comprise of three membranes surrounding and
supporting the spinal cord; arranged from outside inwards, the dura,
arachnoid and pia mater. The sub-arachnoid space, between the arachnoid
and pia mater contains CSF, a clear, slightly alkaline fluid. The choroid
plexuses of the lateral, third and fourth ventricles of the brain form CSF.
Fig. 8.2: Cross-section of the spinal cord

The dura mater is strong, elastic and fibrous tissue sheath. It is the
outermost covering of the spinal cord and forms the external layer of the
dural sac, the tubular sheath that lies free in the vertebral canal extends
along the dorsal and ventral nerve roots as far as the inter-vertebral lateral
foramina to form dural root sleeves. The space between the bony roof of
the spinal canal and the dural sack is called the epidural space. The
arachnoid mater lines the inside of the dural sac, separated from it by the
sub-dural space. The arachnoid mater is a thin avascular membrane that
covers the spinal cord and the spinal nerve roots inside the dural sleeve.
It is connected to the underlying pia mater by delicate strands of connective
tissue, the arachnoid trabeculae. Between the arachnoid and the pia mater
lies the sub-arachnoid space, which contains the CSF (Fig. 8.3).
Fig. 8.3: The relative arrangement of dura, arachnoid and pia mater
the Spinal Cord 189
The pia mater is the innermost membrane covering the spinal cord
and adheres closely to it. The pia mater envelops the spinal nerve roots
and covers the spinal blood vessels.
BLOOD SUPPLY OF THE SPINAL CORD

Points to Ponder
• Branches of the vertebral, deep cervical, intercostal, and lumbar
arteries contribute to three arteries that run the length of the spinal
cord; the anterior spinal and the two posterior spinal arteries (Fig. 8.4).
• The anterior spinal artery arises at the level of the foramen magnum
by the junction of two branches, one from each vertebral artery.
• Each posterior spinal artery arises from the posterior inferior cerebellar
artery at the same level (Fig. 8.5).
• 21 pairs of segmental Radicular arteries supply the nerve roots and
about half of them contribute to the spinal arteries.
• Of these larger branches, the largest is the great anterior radicular
artery, which supplies the lower thoracic and upper lumbar parts of
the cord.
Since it makes a major contribution to the spinal cord blood supply,
spinal injury or aortic surgery may compromise the blood supply of the
lower part of the spinal cord.
Venous drainage of the cord is usually by three anterior and three
posterior spinal veins, which run longitudinally and receive the radicular
veins.
Fig. 8.4: Shows the vertical distribution

Fig. 8.5: The horizontal distribution of the spinal blood supply.
CLINICAL IMPLICATION
Spinal injuries may damage the radicular arteries, seriously compromising
the function of the spinal cord and cause weakness and paralysis of
muscles. The areas that are most vulnerable are T1–3, T5 and L1. Blockage
of a posterior spinal artery may have little effect owing to the extensive
anastomoses, but occlusion of an anterior spinal artery often produces
ischemia of the anterior central part of the cord causing flaccid paralysis
and loss of pain and temperature sensation. Thrombosis of the great
radicular artery of Adamkiewicz may produce paraplegia because it makes
a major contribution to the blood supply of the lower two-thirds of the
spinal cord.
CLINICAL FEATURES OF SPINAL CORD INJURY/LESIONS

Most common form of spinal cord injury results from Spinal Cord
compression due to traumatic or non-traumatic causes, clinically known
as compressive myelopathy. Cord Compression also involving a nerve
root is called radiculo-myelopathy.
Spinal cord compression may be caused by
• Degenerative diseases of the vertebrae, e.g. osteophyte arising from
spondylosis.
• Compromise of the cord due to fracture/fracture dislocation/
spondylolisthesis of the vertebral bones.
• Intramedullary tumors may compress the cord from inside.
• Extramedullary tumors compress it from the outside. Extramedullary
tumors may be
1. Inside the dura mater (intradural) or
2. Outside the dura mater (extradural).
3. Dumbbell shaped, with intra and extra spinal components.
The spinal cord may also be injured due to non compressive causes
like vitamin deficiencies, infections, autoimmune disorders etc.
the Spinal Cord 191
The primary signs and symptoms of spinal cord lesion consist of

1. Sensory symptoms – Pain, numbness and paresthesia
2. Motor symptoms – Hypo/hyperreflexia, hypo/hypertonia, weakness
and wasting
3. Autonomic disturbances – Loss of vasomotor reflexes- excessive
sweating or dryness or cold skin etc.
The nature and extent of these signs and symptoms of spinal lesions are
related to:
• The level and category of compression/damage caused by the spinal cord
lesion
• The speed with which the compression/damage is accomplished
• The direction from which the cord compression/damage originates.
Based on the above parameters the spinal cord lesions, from whatever
the cause, may present as following clinical syndromes, which may be
used as a road map by the therapist to assess the key areas of loss of
function and plan an appropriate therapy program.
A. Anterior Cord Syndrome

• Caused by damage to the anterior and antero-lateral surface of the
spinal cord, leading to loss of motor function, pain and temperature
sensations and preservation of light touch, proprioception and joint
position senses.
• Anterior and anterolateral compression of the cord usually occurs
due to extramedullary compression due to tumors, osteophyte,
collapsed vertebral body (Wedge Fracture).
• Spinothalamic fibers are most vulnerable to anterolateral
extramedullary compression. The loss of pain and temperature
appears here first, and is most complete in the sacral dermatomes. As
the compression increases, the sensory loss gradually ascends towards
the site of the lesion.
B. Central Cord Syndrome

• Caused by loss of centrally located cervical tracts, characterized by
early loss of motor function (LMN type), pain and temperature sense
in upper extremities, with relative sparing of peripherally located
lumbar and sacral tracts at the early stages.
• Syringomyelia (Gr., syrinx = pipe, myelos = marrow), a cystic
expansion of the central canal or Intra-medullary Tumors that start
within one half of the spinal cord tends to compress the inner parts
of the spinothalamic tract that contain the fibers that had just crossed
over, (i.e. from cells in the opposite dorsal horn at that spinal
segment).
• Therefore in patients with intramedullary tumors, the pain and
temperature loss starts near the level of the tumor (approximately
two levels below).
• As the tumor grows laterally, the pain and temperature deficit

involves Lower regions of the body, that is, the pain and temperature
loss Descends in relationship to the location of the lesion.
• This results in the sparing of the sacral tracts (sacral sparing) before
the sensory loss is complete. Lesions within the center of the spinal
cord damage the pain and temperature fibers as they cross, resulting
in a symmetrical loss of pain and temperature, usually with sparing
of touch and vibration.
• It occurs most commonly in the cervical spinal cord, and therefore
the motor and sensory loss affects the neck and upper extremities in
a cape like fashion. The lower extremities develop UMN signs like
hypertonia and exaggerated reflexes at a later stage when the laterally
expanding lesion affects the peripherally located lumbar tracts.
C. Brown-Séquard Syndrome
Dr Brown-Séquard, one of the founders of clinical neurology and
neurophysiology, noted in the latter half of the 19th century, that “Hemi-
section of the cord or extramedullary tumors that compress the spinal
cord from its lateral or anterior-lateral aspect, causes:
• Impairment of pain and temperature sensation on the opposite side
and at few levels below the lesion, and
• Loss of vibration and position sense, muscle weakness and spasticity
on the same side at the level of the lesion.
D. Dorsal (posterior) Column Syndrome

• Dorsally situated lesions compress the dorsal or posterior column
first, and cause paresthesia (funny sensations), numbness and
impairment of 2-point discrimination, vibration and conscious
proprioception on the side of the tumor.
• Dorsal column lesions may cause a symptom called the “Lhermitte
sign.” The patients experience an electric shock like sensation running
through the back and limbs upon flexion of the neck.
• This is usually associated with lesions in the cervical cord
(compression, multiple sclerosis, sub acute combined degeneration
from B12 deficiency). Flexing the neck stretches the dorsal part of
the cord, thus irritating some of the sick or dying fibers in the fasciculi
gracilis and cuneatus conveying pathological signals.
E. Lateral Corticospinal Tract (LST) Syndrome

Points to Ponder
• Damage of the lateral corticospinal tract in the spinal cord results in
effects on the same side of the lesion.
• The corticospinal tract has most lateral fibers serving the lower limbs.
the Spinal Cord 193
• Slow compression of the corticospinal tract causes an impairment of

motor function called upper motor neuron syndrome or lesion
(UMNL).
• The signs that characterize this syndrome are muscle weakness,
increase in muscle tone and abnormal reflexes, although the chief
complaint may be clumsiness of the hand.
• This tone increase is rate dependent (more resistance is offered, the
faster you try to stretch the muscle) and predominates in the flexors
of the upper limbs and the extensors of the lower limbs.
• Muscle weakness is most marked in the abductors of the fingers and
the extensors of the upper limbs and the flexors of the lower limbs.
• The power of plantar flexion is preserved, whereas dorsiflexion of
the foot is impaired.
• In patients with chronic lateral corticospinal tract damage, spasticity
is the dominant feature, whereas weakness may be mild.
Remember: Antigravity muscles are stronger and become more spastic-
upper limb has spasticity in flexors (biceps), lower limb in extensors
(quads).
• Following UMN lesions deep tendon reflexes are usually increased.
• These “deep tendon” reflexes, i.e. tap on a tendon to initiate the
reflex contraction of the muscle, are really manifestation of muscle
stretch reflexes.
• The stretch activates the afferents that respond to stretch of the nuclear
bag fiber in the muscle spindle.
• Brisk or hyperactive muscle stretch reflexes elicited by tendon tapping
may occur in normal individuals who do not have spasticity
(remember spasticity is increased tone found during passive
movement of a limb, not when tapping a tendon).
• The result of an upper motor neuron lesion affecting the legs is
difficulty in walking. UMNL of the upper extremity results in a stiff,
clumsy and weak hand.
Spinal shock—immediately following a traumatic or ischemic lesion of
the lateral corticospinal tract patients develops “spinal shock.”
• All voluntary and reflex (muscle stretch) movements are lost.
• There is also loss of all sensory modalities and urinary retention (to
be discussed later).
• The sensory deficits do not change, but with time the flaccid weakness
is converted into a spastic upper motor neuron syndrome.
• The first response to stimulation in the course of this transformation
occurs in the plantar response. Normally, on stimulation of the sole
of the foot from heel upwards along the lateral border, the big toe
plantar flexes. This is called the plantar (flexor) response.
• In UMN lesions the plantar response is abnormal because the big toe
goes up (extension). This is called a positive Babinski sign and we
say the plantar response is extensor, versus a normal response about
which we say the plantar response is flexor. The Babinski sign is one
of the cutaneous reflexes (as opposed to the muscle stretch reflex)
and it is pathognomonic (pathognomonikos = skilled in diagnosing)
of an UMN lesion.
F. Disorders of Anterior Horn Cells

Loss of ventral or anterior horn cells or the ventral roots result in a lower
motor neuron (LMN) lesion. You are already familiar with the features
of lower motor neuron lesions. Compression of the cervical or lumbo-
sacral spinal cord may be accompanied by significant lower motor neuron
deficits. This is usually due to direct compression of the ventral horn cell
area or the ventral root.
Autonomic disturbances caused by disorders of anterior horn cells may
involve key physiological functions such as Control of Respiration and
Control of Urinary Bladder. How and why such dysfunctions take place
is detailed below.
Disorder of Control of Respiration

• The tracts sub-serving voluntary (from the cortex) and automatic
(from medullary respiration centers) breathing travel in the ventral
funiculus but are difficult to identify. If this information on both
(bilateral) sides of the spinal cord does not reach the anterior horn
neurons innervating the diaphragm (C3, C4, C5 give rise to the phrenic
nerve) and intercostal muscles (thoracic cord ventral horn cells) the
patient will die if not put on a respirator (Fig. 8.6).
Fig. 8.6: Nervous control of respiration

the Spinal Cord 195
• Severe respiratory compromise involving bilateral lesions usually

results from high cervical cord injuries or anterior horn cell loss from
degenerative diseases like Amyotrophic Lateral Sclerosis. For example,
a bilateral lesion of the ventral funiculus at C1 could interrupt all
descending inputs to cells at C3-C5 that innervate the diaphragm via
the phrenic nerves. Such a lesion also interrupts the descending
input to the cells in the cervical and thoracic cord that innervate the
neck and intercostal muscles which assist in respiration.
Disorder of Control of Micturition

• Normal bladder function depends on the coordinated activity of the
bladder detrusor (smooth) muscles and the sphincter muscles (internal
and external sphincters and muscles of pelvic floor).
• The actual act of voiding is under the control of higher cortical centers
that develops as continence and is achieved in early childhood.
• Incontinence occurs when neuro-anatomic pathways that innervate
the bladder are interrupted or when there are physical problems
with the pelvic floor and sphincter muscles. Incontinence is an
important symptom, particularly if it occurs in association with other
neurological deficits that localize to the spinal cord.
• The important points are that the bladder is controlled by areas of
the brain that send axons down the spinal cord, traveling just medial
to the LCST (Fig. 8.7). These bilateral projections terminate on pre-
ganglionic parasympathetic neurons at S2, S3 and S4. The pre-
ganglionic parasympathetic neurons send their axons out the ventral
roots of S2, S3 and S4 to synapse on post-ganglionic parasympathetic
cells in ganglia near the bladder. These post-ganglionic
parasympathetic cells in turn innervate the detrusor (smooth) muscle
of the bladder for voiding. There are muscle spindles in the detrusor
muscle whose cell bodies lie in dorsal root ganglia at S2, S3 and S4.
• When the bladder fills, these muscle spindles are stretched and
increase their firing. This information enhances neuronal firing of
the pre-ganglionic parasympathetic nerves at S2, S3 and S4 resulting
in contraction of the bladder (voiding). This voiding reflex is normally
controlled by the voluntary descending inputs from cortex.
Lesion 1 – Upper Motor Neuron Type Bladder

Following any acute LCST lesion involving the entire cross-section of the
spinal cord at cervical or thoracic level, initially spinal shock and flaccidity
of the smooth muscles (detrusor) lining the urinary bladder occurs, due
to bilateral damage to the descending pathways involved in bladder
control resulting in urinary retention. (Fig. 8.7). There may be overflow
incontinence when the bladder is filled to maximum capacity.
Fig. 8.7: Mechanism of nervous control of micturition showing the site of damage
(Lesion 1) resulting in UMN type bladder
As the spinal shock wears off and the local reflex arc is established,
spasticity develops in the detrusor (like in the muscles of the arms and
legs) and the bladder contracts at the slightest of stretch. The increased
stretch reflex activates the parasympathetic motor neurons controlling
the detrusor and thus causes sudden reflex contraction of the bladder. This
causes sudden voiding of urine whenever the bladder fills a little. Such
a bladder is called an automatic or spastic bladder.
Lesion 2 – Lower Motor Neuron Type Bladder

When the parasympathetic lower motor neurons are injured or their
axons compressed or disrupted, then the lesion results in LMN type
bladder–
• Weakness, atrophy, and hyporeflexia of the smooth muscles (detrusor)
lining the urinary bladder (Fig. 8.8). The bladder does not contract
and,
• If the afferent sensory nerves are affected, no sensation of a full
bladder will be perceived.
• If sensation is intact, but the efferent motor nerves are affected, then
there is an urge to void but good detrusor contraction is not possible.
Some residual urine will always remain behind in the bladder.
the Spinal Cord 197
Fig. 8.8: Mechanism of nervous control of micturition showing the site of damage
(Lesion 2) resulting in LMN type bladder
Lower motor lesions can occur from a lesion anywhere from

1. The pre-ganglionic parasympathetic neurons at S2, S3 and S4 located
in the conus medullaris
2. The sacral roots in the Cauda Equina
3. The pelvic nerve
4. The pelvic plexus or
5. The second order post-ganglionic parasympathetic neuron that
innervates the detrusor.
Remember: Lesions of the spinal cord higher than the sacral cord result
first in a flaccid bladder in the acute stage followed by a spastic bladder
in the chronic stage. Lesions involving the S1 segments downward result
in only a flaccid bladder.
G. Cauda Equina Syndrome

Lesions below the vertebral level of L1 (beyond the end of the spinal
cord) usually affects the bunch of nerves originating from the lumbar
and sacral roots before it exits the spinal canal, frequently due to traumatic
or compressive causes like prolapse of inter-vertebral discs,
spondylolisthesis, etc.
LMN type presentation of motor power loss and with loss of

superficial sensation in lower extremities, with or without LMN type
autonomous non-reflex bladder may result from a Cauda Equina lesion.
H. Sacral Sparing
Sometimes, even in higher cord lesions, the descending tracts supplying
the sacral segments may be spared, resulting in intact sensation of the
perineum, rectal sphincter tone and active toe flexion.
I. Traumatic Spinal Cord Lesions

Partial or complete transection of the spinal cord may occur due to
traumatic causes like fracture or fracture-dislocation of the vertebral
column, resulting in loss of function below the site of the damage.
Presentation of such damage to the spinal cord is the same as in any
other Myelopathies.
Spinal cord injuries may be caused by fall from a height, vehicular
accidents, diving headfirst in water, gunshot, resulting in sudden and
violent flexion (commonest mode of injury in lumbar spine), flexion-
rotation-lateral flexion (commonest mode of injury in cervical spine),
compression (commonest mode of injury in thoracic spine) and
hyperextension (commonest mode of injury in fracture-dislocation of
spine) of the vertebral column (Fig. 8.9).
PATHO-PHYSIOLOGY OF SPINAL INJURIES

Primary injury to the cord results in loss of blood supply to the cord
followed by secondary sequels such as ischemia, edema, demyelination
the Spinal Cord 199
Fig. 8.9: Mechanism of spinal cord injuries
and necrosis of axons of the spinal cord, which finally stops at scar
formation.
Associated problems in case of traumatic spinal lesions may concern
loss of structural integrity of the vertebral column due to fracture or
fracture dislocation of vertebral bones. Vertebral scoliosis, kyphosis, hyper-
lordosis and instability are the commonest forms of vertebral structural
problems that need to be frequently addressed during the management
of spinal cord injuries.
ASSESSMENT OF SPINAL CORD LESIONS

Points to Ponder
• Observe and record vital signs: Unstable vital signs can be a
contraindication to active intervention by the physiotherapist except
for postural, respiratory, contracture and pressure sore prophylaxis.
• Assess respiratory competence: Particularly in cervical and high
thoracic level of lesion. Respiratory insufficiency and failure is
common in lesions of C1-C3 due to the damage to Phrenic nerve
innervating the diaphragm.
1. Note action of diaphragm by the rise and fall of the abdomen
with each breath cycle.
2. Note for action of intercostal and accessory muscles of respiration
during breathing. Undue effort of these muscles means poor
respiratory reserve.
3. Note the breathing pattern, to detect any abnormality in sharing

the work load of breathing. In normal male persons 3/4th of the
work load of breathing is taken by the diaphragm and 1/4th by
the muscles of the chest. This is denoted by 3D and 1C pattern
of breathing. In a normal female the breathing pattern is 2D and
2C. Any deviation from this pattern means early onset of
respiratory fatigue on exertion.
4. Note the chest expansion, PEFR and the effectivity of cough to
get a general idea of the respiratory efficiency.
• Assess the skin condition: Check sensation and integrity,
particularly below the level of the lesion and over bony prominences.
Teach the patient self-examination using a hand held mirror, to
look for any reddening of the skin. Always check if the sensory
level corresponds to the motor level of involvement. If this doesn’t
happen it may indicate an incomplete lesion and therefore a better
chance of recovery.
• Assess muscle tone, deep tendon reflexes and power: Remember
that the level of spinal cord injury can only be clinically determined
by the presence of minimum 3+/5 power at the muscles innervated
by the lowest unaffected spinal segment. A manual muscle test (MMT)
chart may be prepared as soon as the patient is stable, spinal shock
has settled and in case of vertebral injuries/surgeries, clearance has
been given by the surgeon.
• Assess functional mobility: Assessment of FMA should be done
only when the spinal disorder is no longer progressing and deemed
to be chronic. The FMA is the first step towards rehabilitation and
must include evaluation of ability to move on bed, supine to long
sitting, long sitting to high sitting, bed to wheel chair and wheel
chair to toilet seat transfers, sit to stand and walking. Assessment of
activities of daily living (ADL) is a useful appendage to the FMA and
should include evaluation of abilities to perform self care activities
like toilet, feeding and dressing. The FMA serves as the benchmark
to evaluate further progress as well as to determine the effectivity of
intervention.
• Bladder and bowel assessment: It includes identifying the presence
or absence of incontinence, type of incontinence, secondary
complications of incontinence like urinary tract infections, dribbling,
reflex voiding, constipation, etc.
Based on the motor, sensory and bladder/bowel issues involved and
the FMA, the short-term problems as stated by the patient and the long-
term problems as identified by the rehab team are incorporated in the
management plan (Annexure 12).
the Spinal Cord 201
MANAGEMENT OF SPINAL CORD LESIONS

Persons with spinal cord injuries/disorder (SCI/D) require specialized,
comprehensive inpatient services in the acute stage and institutional/outpatient
rehabilitation programs in the chronic stage to achieve maximum potential.
To treat spinal cord injuries successfully an interdisciplinary team of
neurologist, nurses, occupational therapist and physiotherapist is needed
to offer full assessment and comprehensive rehabilitation programme.
Because the spinal cord serves as the channel for the body’s motor and
sensory message system, most people with this injury lose some or all of
their ability to move and feel.
In the acute stage, the treatment centers on motor paralysis, sensory loss,
autonomic dysfunction and resulting complications. These demand
specialized and intensive treatment program in a hospital having ICU,
neurosurgery, renal, cardio-respiratory, plastic surgery and physiotherapy
support.
In the chronic stage, spinal cord injuries resulting from trauma, vascular
accidents, infections, spinal postoperative complications, vertebral disc
lesions, neuromuscular diseases and other medical conditions, which are
medically stable and able to participate in intense therapy sessions, are
included in the rehab program.
In the residual stage of the spinal disorders, the rehabilitation program
should be patient centered and goal orientated, to enable the patient to
play an active part in making informed decisions in all aspects of their
rehabilitation. The multidisciplinary rehabilitation teams include
physicians, researchers, rehabilitation nurses, physical therapists,
occupational therapists, therapeutic recreation specialists, social workers,
vocational rehabilitation counselors, dieticians, psychologists, biomedical
engineers and orthotists.
Acute Care of Spinal Injuries

In any patient with spinal cord injury the treatment begins with a
comprehensive evaluation of each patient, which the team uses to develop
an individualized treatment plan based upon the patient’s level of injury
and loss of functional ability. The treatment plan is tailored to meet
individual needs most plans include the following:
Medical care: A specialized physician leads spinal cord injury team,
provides medical care for spinal cord inflammation, edema, ischemia
and secondary complications that may occur, prescribes medications, treats
spasticity and contractures and recommends medical treatment and
surgical consultation when necessary. The referring physician is also
invited to be involved with the medical management. A team of
physicians, including neurosurgeons, plastic surgeons, urologists and
orthopedists should be available to assess and treat complications related
to spinal cord injury.
Bed mobility training: Once the spine is stabilized and the patient stable
medically, a mobility-training program begins. The goal is to achieve the
highest level of function within the limits of the injury. Exercise programs
focus on strengthening intact muscles, maintaining or gaining mobility
in bed and building confidence to perform functional activities. These
activities progressively include transfers from bed to the bedpan/toilet
seat, sitting on bed with/without support, physiological standing in a tilt
etc. Aids and appliances needed to maximize stability of the spine and
enhance mobility out of bed are also assessed and prescribed.
Respiratory training: Sufficient respiratory reserve is essential for the
rehabilitation process. For this reason, one should work with spinal cord
patients to strengthen respiratory muscles, improve volume and cough
force, provide pulmonary hygiene and oxygen therapy if needed. The
therapist should also be skilled in providing rehabilitation care to
ventilator-dependent high quadriplegia patients.
Skin care: Because a spinal cord injury usually involves sensory
impairments, skin complications are often a problem. The therapist must
implement an individual skin care program for each spinal cord patient
that includes turning and positioning, bridging, pressure relief raises,
skin checks and teaching patient and family how to prevent pressure
ulcers.
Since our goal is to return the person with spinal cord injury to their
home, work, school and community, each treatment plan includes a
comprehensive plan that prepares the patient for life after acute care,
into rehab and home care. To provide continuity of care, a follow-up
program is prescribed which may include treatment through outpatient
rehabilitation. Spinal cord-injured patients are monitored when ever
possible for ongoing management through outpatient clinic and follow-
up programs.
ADL skills training: Learning how to meet daily needs is an essential
part of rehabilitation for those with spinal cord injuries. Individual and
group treatment programs involve re-learning and managing daily tasks
associated in personal self-care. The occupational therapist prescribes
assistive equipment if needed. Future home and work site assessments
are provided and recommendations for modifications are given to patient,
family and employers.
Education of the individual and family counseling: Counseling and
education sessions help both patient and family understand the
consequences of spinal cord injury and how roles, relationships and
responsibilities are affected. Through adjustment counseling, the team
helps both patient and family deal with these changes and makes plans
for the future. A competent counselor should also offer sexual counseling
and encourage patient and family participation in the activities of a spinal
cord injury groups for paraplegic and quadriplegic reorientation programs.
the Spinal Cord 203
Physical therapy program: In a spinal lesion, at all stages of care revolves

around following principles:
• Helping patients regain physical mobility, strength, balance, and
endurance.
• Physical therapists use treatment methods designed to assist patients
with sitting and standing balance, ambulation, stair climbing, and
wheelchair mobility.
• Physical therapists also provide the patient and family with education
designed to ensure a smooth transition from rehab facility to home
environment.
• In addition, physical therapists assist with acquiring the necessary
equipment for each patient prior to discharge and making sure both
the patient and family are aware of proper equipment usage.
• Physical therapists also provide a written home exercise program.
• After an initial consultation, an individualized treatment program is
designed by the evaluating physical therapist. A team consisting of
a physical therapist and an assistant should care for each patient in
the program. This team cares for the patient through the entire
treatment program, providing the most effective, consistent treatment
possible.
Goals and Interventions of Physiotherapy

The primary task of the therapist, while treating SCI in the acute stage
should be to monitor changes associated with gradual recovery and
prevent secondary complications associated with prolonged bed rest:
Spinal Shock
It is a transient period of diminished reflexes and flaccidity of muscles,
lasting from few hours up to several weeks, usually noticed in the acute
stage of any myelopathy. The main role of the therapist in this stage is
to perform passive movements of extremities in full ROM to maintain
flexibility of joints, suppleness of soft tissue and the length of muscles,
encourage venous return, and to prevent contractures. Proper positioning
with the help of pillows, sand bags and roles of towel help maintain
proper alignment of body segments and prevent deformities.
Onset of Spasticity/Spasm
Tone returns to all the muscles after the remission of the spinal shock. In
an UMN type lesion (cord), the muscles below the level of the lesion
develop exaggerated tone. In incomplete lesions of the cord, this increased
tone may be evident in flexors as well as extensors muscles of the
extremities and the trunk. In complete lesions the tone may selectively be
more in the flexor group of muscles, particularly in lower extremities.
Such hypertonia may be constant (spastic/rigid) or episodic (spasm).

The job of the therapist at this stage, apart from doing PROM exercises,
is to identify the triggering stimulus for increase in tone, such as a blocked
catheter, tight clothing, body position, too high or too low temperature,
urinary infection, pressure injuries to the skin etc. and correct the same
before it can interfere with the rehab process. Selective stretching of
tightened structures to preserve function (Tenodesis grasp) and
prophylactic splinting to prevent deformities are other key components
of care of hypertonic muscles in spinal lesions.
Common Complications of the Acute Stage

1. Autonomic dysreflexia is an emergency situation in which any of
the noxious stimulus listed above may trigger a pathological
autonomic reflex with symptoms of sudden shoot up of blood pressure
(Paroxysmal hypertension), profuse sweating above the level of the
lesion (Diaphoresis), slowing down of heart beat (Bradycardia), severe
headache, flushing of the face, double vision (Diplopia) and/or
convulsions. The therapist must position the patient in a propped up
sitting, check and drain blocked catheter, loosen clothing and call for
the doctor immediately.
2. Heterotopic (Ectopic) bone formation is an abnormal bone growth
in muscles, leading to calcification of soft tissue, commonly associated
with too vigorous PROM exercises. The therapist therefore should be
alert for its early signs such as soft tissue swelling, pain and erythema,
usually seen in the vicinity of a large joint. PROM exercises must be
stopped immediately and application of moist heat and ultrasound
therapy to the tender area may be started.
3. Deep vein thrombosis (DVT) is a formation of blood clot within the
lumen of the veins of mostly seen in the calf, usually caused by
prolonged pressure on deep veins within a flaccid muscle by edge of
the bed or a badly placed towel roll or sand bag. Lack of pumping
action by the paralyzed calf muscles lead to pooling of blood and
altered blood chemistry which further contribute to the formation of
the clot. The therapist should check daily for any tenderness of the
calf muscles and swelling of the feet. In presence of DVT, passive
dorsi-flexion of the ankle will produce pain in the calf. This is called
as the Homan’s sign and is a clinical confirmatory test for DVT. If
DVT is detected, the patient is immediately heparinized to minimize
clot formation. All movements to the affected part are stopped due
to the risk of the tail of the clot breaking off and being carried through
the blood stream as an embolus. Such an embolus may block a narrow
blood vessel and cut off blood supply to a vital sector of brain tissue
or heart muscle resulting in a CVA or a heart attack respectively.
Because DVT are extremely difficult to treat, the emphasis should be
on prevention. Regular PROM exercises for the ankle and foot, active
the Spinal Cord 205
ankle and foot pumping if possible and using pressure garments to

facilitate venous return is the therapeutic line of management for
this complication.
Prevention of Respiratory Complications

Prolonged lack of mobility in the early stages of myelopathy leads to
reduced oxygen demand, resulting in poor respiratory excursion which
in turn leads to shut down of a large number of alveoli in the lungs. This
phenomenon is called pulmonary hypostasis, which is associated with
poor gas exchange, loss of respiratory reserve and poor exercise tolerance.
To prevent such complication the therapist must commence as early as
feasible, deep breathing exercises (10 cycles per sitting twice a day), end
inspiratory holds (for a count of five) followed by a brisk clap between
the scapula (not in cervical/thoracic injuries) to force open the collapsed
alveoli, gentle vibrations of the chest and assisted coughing to clear mucus
from the airway and application of elastic abdominal binders to facilitate
movements of a weak diaphragm.
Maintain Skin Integrity

Prolonged pressure on the skin over bony prominences during
immobilization/bed rest/sitting in wheel chair, along with impaired skin
sensation combine to make the skin of a spinal injured patient extremely
vulnerable to injury, breakdown and formation of indolent ulcers. It will
be wise to remember that skin is the largest organ in the body, with
maximum vascular turn over. It is also the first line of defense for the
body. Any damage to the skin, particularly non-healing, infected pressure
sores have far reaching effects on the well-being of the patient. Since
pressure sores are very difficult to treat the therapist must focus on
prevention. Turning the patient in the bed, every two hours from one
side to the other is the first step in prevention of pressure sores. In case
turning in bed is contraindicated because of immobilization following
fracture of the vertebra or due to unstable vital functions, pressure reliving
measures such as ripple mattress, water bed, circo-electric frame, gel
cushions/water filled surgical gloves/air rings placed under bony
prominences may be opted for. In wheel chair borne patients, it is essential
to select proper seat cushions and teach periodic pushups using the
armrest to relive pressure on ischial tuberosity. The patient must be taught
to perform self-examination of his skin on daily basis to detect first signs
like reddening and blister formation. Using wrinkle free, dry cotton draw
sheets on bed, daily sponging with weak disinfectant solution and
application of zinc oxide cream over bony prominences minimizes the
risk of skin breakdown and formation of pressure sores.
Reorient the patient to the vertical position as early as possible because
prolonged bed rest leads to loss of calcium from the bones causing
osteoporosis, loss of vascular tone causing postural hypotension and loss
of excursion of the lung bases causing pulmonary hypostasis. Best way

to counter such complication is the physiological standing. In the acute
stage, as long as the patient is on bed rest with traumatic spinal lesions
requiring immobilization and traction or following spinal surgeries, this
may be done using a circo-electric bed. The entire bed, moving within a
circular vertical frame, with the patient securely strapped on it, can be
progressively tilted on its long axis from horizontal to vertical, or from
supine to prone or side lying, with the help of an electric motor (Fig. 8.10).
In case no immobilization is needed, the patient on bed rest may be
propped up on the bed using pillows or by lifting the head end of the
bed up to 30° as early as possible. The head end may be elevated daily
by 5-10° till upright position is tolerated for 15-30 minutes. Then the
patient may be transferred to a tilt table (Fig. 8.11).
Fig. 8.10: The circo-electric bed
Fig. 8.11: Electrically operated tilt table

the Spinal Cord 207
Electric Tilt Table tilts from 0-90° and is operated from a hand held
controller. The tilt table consists of an upholstered table-top surface
measuring 28" wide and 78" long. Height is fixed at 33". It has three 4"
restraining straps to hold the patient in position, four 4" locking casters,
and a removable foot board for weight bearing training.
There is an adjustable arm board at the mid thoracic level of the
patients. This board can be used to train hand activities during
physiological standing training on the tilt table.
Improve or maintain the flexibility of soft tissue and strength of all
surviving muscles using PROM exercises/stretching and selective
strengthening of unaffected muscles respectively during the acute phase,
without stretching the diseased/inflamed spinal cord or putting stress
on the vertebral column in case of spinal injury. Hydrotherapy is a
modality that takes care of both of these requirements in complete safety.
As soon as the spinal shock has worn off and the bladder and bowel has
stabilized the patient may be started on Hydrotherapy.
Hydrotherapy
Water is the ideal environment for safe, effective physical rehabilitation
of spinal lesions. Aquatic therapy should be held in a heated aqua-therapy
pool. Perfect for patients not yet ready for traditional physical therapy,
aquatic therapy allows the patient to safely exercise while drastically
reducing stress on joints and muscles (Fig. 8.12).
Aquatic Therapy Programs Usually Include

• Aqua yoga pilates: This program integrates yoga poses and pilates
exercises in a warm-water environment to increase health and muscle
tone, reduce stress and promote relaxation.
• Circuit training: This unique program invites participants to rotate
between stations in the water to work on strength, endurance and
range of motion (Figs 8.12B to D).
Figs 8.12A to D: Common aquatic exercises recommended for strengthening of

lower limbs, improving balance and gait training in the spinal disorders
• Water walking: This independent walking and exercise program is

designed to maintain and improve fitness and wellness in a warm-
water environment (Fig. 8.12A).
the Spinal Cord 209
• Therapeutic aquatic bodywork: This individualized program uses

gentle stretches to increase range of motion throughout the body.
Specific benefits include increased flexibility, increased range of
motion, and increased relaxation. Therapeutic aquatic bodywork also
decreases muscle tension and spasticity (Fig. 8.13).
• Learn to swim again: This program teaches individuals to learn to
swim again after a disabling condition. During individualized
sessions, instructors use various swimming strokes to increase
muscular strength and endurance, range of motion, and balance.
Fig. 8.13: Stretching exercises done in water
Specialized Approaches
• Body-weight support system therapy with the Gait Analysis and
training system is available for walking training, as appropriate in
convalescent stage of the disorders.
• Functional electrical stimulus (FES) training of paralyzed muscles is
available to stimulate physiological function and to increase strength
and endurance in surviving muscles. Experimental modules have
started using FES for substitution of normal muscle action using
electrically stimulated, synchronized muscle contraction through
portable, pre-programmed electrical stimulators worn by the patient.
REHAB LIFE AFTER SPINAL CORD DAMAGE

Adjusting to Life after a Spinal Cord Injury/Damage
Individuals who are newly injured will likely experience grief. This is a
period of mourning that is similar to that following the death of a loved
one. The difference is that the patient is grieving the loss of sense of
touch along with the ability to walk or use hands. He is likely to experience
many different thoughts and feelings after injury. Some may seem extreme
and others mild. There is no step-by-step grieving process, but some
thoughts and feelings are common after injury.
• Denial/Disbelief: The patient may first react to the injury as if nothing

happened. He may refuse to accept that the loss of feeling and
movement is permanent. Instead, he may see the injury as an illness
similar to a cold or flu that will soon pass with time.
• Sadness: Extreme sadness is common after spinal injury because of
great personal loss. However, it is important not to confuse sadness
with depression. Depression is a medical condition that requires
professional treatment. The patient may be diagnosed as depressed
if symptoms such as extreme sadness, inactivity, difficulty in thinking
and concentrating, a significant increase or decrease in appetite and/
or time spent sleeping, and feelings of dejection, hopelessness or
worthlessness are present. He may even have thoughts about suicide
if he has depression.
• Anger: Some people react to their injury with strong feelings of anger.
The patient might lash out verbally or want to become physically
violent towards others. The patient may feel angry toward himself if
his actions resulted in the injury.
• Bargaining: The patient may act as if he accepts the disorder as “the
way things are,” but his acceptance may come with the belief that he
will be rewarded for prayers and hard work in therapy and eventually
recover from the injury at some point in the foreseeable future.
• Acceptance: Grieving usually ends as the patient comes to accept a
realistic view of his current condition and find meaning in his life.
He begins to think and plan about future as an individual with either
a paraplegic or quadriplegic and set goals to pursue in life.
Adjusting to Spinal Cord Injury/Damage

Individuals, who adjust well to unexpected events, generally lead a
healthy, active, and happy life after a disaster like para/quadriplegia.
Individuals who do not adapt well to unexpected events tend to be less
healthy, less active, and unhappier after their injury. Unhealthy behavior
almost always leads to unhealthy results. When someone neglects personal
care, he/she are at greater risk for developing a wide range of health
problems such as respiratory complications, urinary tract infection, and
pressure sores. These problems can limit the ability to participate in rehab
activities. Substance abuse like alcohol or drugs can complicate existing
medical problems or lead to other health problems.
Healthy Adjustment to Spinal Cord Injury/Damage

The key to adjusting to spinal cord injury is personal motivation.
Individuals who are newly injured are often motivated to attend therapy
sessions out of a desire to gain strength and function. They probably
have a strong belief that the paralysis is only temporary, and he will
soon return to his old, “normal” self. This hope is a common reaction
after an injury. Unfortunately, an individual will recover function only
the Spinal Cord 211
based on their level and completeness of injury. In fact, only a few people
actually fully recover from their injury. A healthy approach to this reality
is to move forward with your life after injury with the continued hope
that advances in medicine will one day lead to a cure. People who adjust
well to life after injury are usually motivated to meet personal goals,
such as to get a job, to be the bread earner, to be independent, to be
cherished and to have children in the future. It is up to the patient to find
purpose in his life and the motivation to achieve his goals. There is no
reason that he cannot continue to strive for the same things now that he
has a spinal cord injury/damage.
Healthy Family Adjustment to Spinal Cord Injury/Damage

The family may experience a loss of the way their life was before injury.
For example, they may have to adjust to the role of caregiver. They may
need to work to help with family finances. All of the changes that they
face can lead to added stress and anxiety. Children are naturally curious
and adjust to events by asking questions. They ask questions because
they make few assumptions about how the injury impacts their life.
Therefore, children adjust rather quickly to an injury if their questions
are answered in a clear, honest manner. Adult family members can
minimize stress and anxiety by working to replace false assumptions,
unrealistic ideas, and irrational beliefs. They can start by learning the
facts about spinal cord injury/damage.
Pain after Spinal Cord Injury/Damage

Acute pain is common immediately after a spinal cord injury/damage.
The pain may occur as a result of the inflammation of the spinal cord
itself, or it may occur from secondary damage to other areas of the body.
Chronic pain, often interfering with rehab, can occur due to disorder
of sensory mechanism, in areas totally or partially devoid of sensation.
Such pain is very real and may have a great impact on daily living. A
person in pain has difficulty carrying out daily activities.
Pain Management
Pain management usually includes treatment with medications, modified
activities or a combination of both. Pain management can be a very
difficult process. Many times it is hard to know what is causing the pain
in individuals with Spinal Cord Injury/Damage. It may not always be
possible to completely stop the pain, but an effective pain management
program can lessen the intensity of the pain.
Secondary overuse is often a frequent cause of pain in the chronic stage of
spinal lesions and can be managed by modifying activities that use the
joint or body part that is in pain. This may include limiting or stopping
activities that make the pain worse. For example, it may help to limit
pushing a wheelchair if there is shoulder pain. It may be necessary to

switch from a manual to an electrically powered wheelchair.
It is recommended that the patient may pace himself during certain
activities. Here are some examples on how to effectively pace activities:
1. List all activities that result in pain or fatigue.
2. Note the time that it takes to experience pain or fatigue.
3. Set a time limit for doing the activity that is well below the point
when the patient experiences pain or fatigue.
4. Return to the activity after frequent rest period.
5. Do not get in a rush to complete any activity. One should slowly
increase endurance by increasing the amount of time on activity and
always include adequate rest periods.
If unable to relieve pain through activity modifications like pacing of
activities, it may be necessary to use medication such as opiates or
nonsteroidal anti-inflammatory drugs or physical measures like TENS.
Instructions to Patients in Managing Pain

• Be flexible and cooperative.
• Work collaboratively with health care professionals to find solutions
to managing your pain.
• Follow treatment instructions.
• Take an active role in treatment by asking questions, such as – Are
there alternate drugs that are cheaper/safer?
• Is the prescribed drug or treatment approved?
• Are there side effects from the medications or treatments?
• Are there articles about a procedure or medication that you can read
more about it?
• Are there others who have used a treatment you can talk with about
their experiences?
There are some psychological approaches that help reduce pain. Some
techniques that help include relaxation training, biofeedback and hypnosis.
The Distraction technique may also help reduce chronic pain.
Pressure Sores after Spinal Cord Injury/Damage

Pressure sores are the most common, recurring and devastating
complication of spinal cord injury. They are also referred to as skin sores,
decubitus ulcers, or bedsores. They are more likely to occur after acute
spinal cord injury/damage, due to lack of movement and sensation and
to changes in circulation. In the chronic stage they are frequently caused
by prolonged load bearing on insensitive skin, ill-fitting orthosis, tight
garments, faulty seat cushion and friction during transfers. A pressure
sore begins with redness or break in the skin caused by too much pressure
on the skin for too long a period of time. Sitting or lying in the same
position will begin to cut off the flow of blood to that area, blocking
oxygen and vital nutrients from maintaining healthy tissue. When the
the Spinal Cord 213
tissue becomes starved to too long a period of time it begins to die and
a pressure sore starts to form. Normally the nerves send messages of
pain or feelings of discomfort to the brain to let one know that he needs
to change position, but in SCI damage to spinal pathways keep these
messages from reaching the brain. A pressure sore is serious. It must not
be ignored.
High-risk patients are:
• Chronically ill and bedridden
• Urinary or fecal incontinent
• Overweight or underweight.
Pathophysiology of Pressure Sores

Skin damage from pressure usually begins over bony prominences, i.e.
any place on the body where the bones are close to the skin surface
(Fig. 8.14). Due to the decrease in the rate of circulation that occurs
following spinal cord injury/damage, there is less oxygen available to
the skin, lowering the skin’s resistance to damage. If the skin is deprived
of oxygen due to pressure, the body will try to compensate by sending
more blood to the area. This may result in swelling, which will put even
further pressure on the blood vessels and further block circulation.
How a Pressure Sore Develops

• Stage I – The skin becomes white or lighter in color due to ischemia.
Push-ups and turning schedule so the skin is never deprived of its
blood supply for a long time.
Fig. 8.14: Common sites for developing pressure sores

• Stage II – Skin will redden, it is warm and may be swollen when

pressure is relieved. Stay off red area until all redness is gone. Do not
rub red area or put anything on it. If dark skinned and can’t see
redness, feel for warmth with back of fingers. Redness and warmth
is caused by blood rushing to the area when pressure is relieved. If
redness is not gone 30 minutes after pressure is relieved, it indicates
too much pressure or pressure for too long was applied.
• Stage III – A blister develops over the red area. The skin may have
a bluish color to it. The blister often opens. This stage occurs if pressure
is not completely removed from a red area.
• Stage IV – The center of open sore turns black or brown and/or
there is drainage. Cover with a sterile dressing. Such sore may be
very deep and infected.
Prevention of Pressure Sores

Maintaining a healthy skin is the key to preventing pressure sores. Skin
that is intact, well lubricated with natural oils, and nourished by a good
blood supply will not develop pressure ulcers. Skin stays healthy with a
good diet, good hygiene, regular skin inspection, and regular pressure
relief. By inspecting the skin regularly, one can spot a problem at the
very beginning. In addition to routinely checking skin, a second important
way to prevent pressure sores is to relieve skin pressure by periodically
changing position or being positioned so that pressure is taken off a bony
area. The purpose of relieving pressure is to let the blood supply get to
the skin.
Cushions
Appropriate cushions for chair/wheelchair are essential for skin protection
in spinal injuries with significant loss of sensation. Cushions made of
wooly sheepskin (Fig. 8.15) or air cell mattress provide pressure relief
and weight distribution and thus aid in the prevention of pressure
sores (Fig 8.16). The patient has to be explained that the cushions alone
will not prevent pressure sores. Periodic weight shifts are also essential
to prevent prolonged pressure on the skin, over bony prominences like
ischial tuberosity, while sitting in a wheel chair. A patient with normal
power in upper extremities can shift his weight by pushing up on the
armrest of the wheelchair. In case the patient has no/insufficient power
in UE, weight must be shifted periodically by the caregiver.
Tips to Patients to Prevent Pressure Ulcers

DO
• Make sure your wheelchair foot pedals are adjusted to the right height.
• Use a prescribed cushion on wheelchair seat.
the Spinal Cord 215
Fig. 8.15: Sheep skin
Fig. 8.16: Air mattress
• Sit up straight in wheelchair (slumping or slouching leads quickly to

early skin breakdown over tailbone).
• Check feet carefully when wearing new shoes - shoes should not be
too tight or too large.
• Keep skin clean and dry.
• Use a firm (not hard) mattress, which provides support for your
body.
• Do your wheelchair push-ups or weight shift every 15 minutes.
• Stick to your turning schedule- every two hours.
• Use moisturizing cream if you have dry skin.
• Drink plenty of fluids to keep skin well hydrated.
• Eat a well balanced diet. Foods high in protein, vitamins and minerals
help your skin stay healthy and heal more quickly.
• Check the penis carefully for sores or irritations if you use an external
catheters.
DO NOT
• Use a rubber air ring or any kind of doughnut. They create a lot of
pressure where you don’t want it, and block the flow of blood to skin
inside the ring.
• Wear sanitary belts - they can lead to pressure sores.
• Wear clothing with heavy seams, nylon underwear or tight clothing.
• Put articles in pants pockets or on seat of wheelchair.
• Use alcohol on dry skin.
• Sit in bed with the head raised for long periods - this causes skin to
be squeezed over the lower end of the spine and can lead to sores.
• Smoke – Research shows that spinal cord injury/damage patients
who are heavier smokers have more frequent and more serious
pressure sores, and when they do get sores, the healing process is
slower.
• Abuse drugs or alcohol. Both can damage your skin and can also
lead to other health problems.
THE BLADDER MANAGEMENT

Depending on type of spinal cord injury, bladder may become either
flaccid or spastic.
A flaccid bladder loses detrusor muscle tone (strength) and does not
contract for emptying, can be easily overstretched with too much urine,
which can damage the bladder wall and increase the risk of infection.
Emptying the flaccid bladder can be done with techniques such as Crede,
Valsalva, or intermittent catheterization.
In a spastic (reflex) bladder the detrusor muscles have increased
tone, and may contract automatically, causing accidental voiding.
Dyssynergia occurs when the sphincter muscles do not relax when
the bladder contracts. The urine cannot flow through the urethra. This
can result in the urine backing up into the kidneys. This is called “reflux”
action. The bladder may also not empty completely. Treatments include
medications or surgery to open the sphincter.
Bladder Management Program

A bladder management program helps to effectively prevent infections
and avoid bladder accidents. Level of injury, lifestyle, susceptibility to
infection, and loss of normal urinary system function must be taken into
consideration when deciding which bladder management program works
best for the patient.
Foley or suprapubic catheter: A tube is inserted through the urethra or
abdomen and into the bladder, where a balloon on the end holds it in
place. It remains in the bladder and drains constantly, so the bladder is
never full.
the Spinal Cord 217
Condom catheters: This method uses a cone made of latex rubber or

silicone that covers the penis and attaches to a tube that drains into a
collection bag.
Intermittent catheterization: You drain your bladder several times a day
by inserting a small rubber or plastic tube. The tube does not stay in the
bladder between catheterizations.
Stimulated Voiding
Voiding is encouraged in one of several ways:
• Anal or Rectal Stretch—this method involves increasing pressure
inside the abdomen by bearing down as if going to have a bowel
movement.
• Crede and Tapping—this method involves manually pressing down
on the bladder. The area over the bladder is tapped with the fingertips
or the side of the hand, lightly and repeatedly, to stimulate detrusor
muscle contractions and voiding.
Surgical Alternatives
• Mitrofanoff: A passageway is constructed using the appendix so
that catheterization can be done through the abdomen to the bladder.
• Sphincterotomy: This surgical process weakens the bladder neck and
sphincter muscle to allow urine to flow out more easily. After this
surgery, one urinates involuntarily, and must wear a collection device.
• Bladder augmentation: Surgical enlargement of the bladder.
URINARY TRACT INFECTIONS

What is a urinary tract infection?
Individuals with spinal cord injury/damage are at a high risk for urinary
tract infection (UTI), when bacteria enter bladder or kidneys and cause
you to have symptoms of high grade fever, chills, rigor and cloudy urine.
Causes of UTI
Intermittent Catheterization
Whenever a catheter is passed through the urethra it can pick up
infections. Bacteria can grow and multiply rapidly if residual urine
remains in the bladder for more than 4-6 hours. One can avoid this by
emptying the bladder at least once every 6 hours and by drinking enough
fluids to keep the urine volume between 300 and 500 cc (1-1.5 cups) at
each catheterization. Careful hand washing before and after each
catheterization is essential and will help prevent UTI.
Indwelling (Foley) Catheters
The catheter provides a direct pathway for the bacteria to enter the
bladder. The bacteria that live in the bladder can develop into a UTI if
the catheter becomes blocked, if general resistance to infection decreases,

or if the patient doesn’t drink enough fluids and his urine become
concentrated.
Symptoms of UTI
• Fever, chills, nausea, headache, low back pain
• Increased spasms of legs, abdomen, or bladder
• Urgency to catheterize or pass urine
• Burning of the urethra, penis, or pubic area
• Sediment (gritty particles) or mucus in the urine or cloudy urine
• Bad smelling urine (foul odor)
• Blood in urine (pink or red urine).
When early signs of infection appear, take following steps to help
prevent symptoms of illness:
• Drink more water.
• Stop drinking beverages with sugar, caffeine, and alcohol.
• Catheterize more often.
Preventing Urinary Tract Infections Through Self-care

• Drink plenty of water. The fluid intake should be enough so that the
urine is only slightly yellow in color and clear.
• Changing the catheter every three weeks.
BOWEL MANAGEMENT
The bowel is the last portion of the digestive tract and is sometimes
called the large intestine or colon. The bowel is where waste products are
stored until they are emptied from the body in the form of a bowel
movement as stool. A bowel movement happens when the rectum
becomes full of stool and the anal sphincter opens.
After a spinal cord lesion, damage can occur to the nerves that control
bowel movements. If the spinal cord injury/damage is above the T-12
level, the ability to feel when the rectum is full may be lost. The anal
sphincter muscle remains tight and bowel movements occur as a reflex.
This means that when the rectum is full, the defecation reflex will occur,
emptying the bowel. This is known as a reflex bowel. A reflex bowel can
be managed by having the defecation reflex occur at a socially appropriate
time and place.
A spinal cord injury/damage below the T-12 level may damage the
defecation reflex and relax the anal sphincter muscle. This is known as
a flaccid bowel. Management of this type of bowel problem may require
more frequent attempts to empty the bowel and bearing down or manual
removal of stool. Both types of neurogenic bowel can be managed
successfully to prevent unplanned bowel movements and other bowel
problems such as constipation, diarrhea and impaction.
the Spinal Cord 219
Bowel programs involve training bowels to have a bowel movement

at the time the patient wants. Each person’s bowel program should be
individualized to fit his/her own needs. A bowel program can include
any combination of the following methods for clearing the stool from the
rectum:
1. Manual Removal—Physical removal of the stool from the rectum. This
can be combined with a bearing down technique called a valsalva
maneuver.
2. Digital Stimulation—circular motion with the index finger in the
rectum, which causes the anal sphincter to relax.
3. Suppository—dulcolax suppository which stimulates the nerve endings
in the rectum, causing a contraction of the bowel or glycerin
suppository which draws water into the stool to stimulate evacuation.
4. Mini-enema—softens, lubricates, and draws water into the stool to
stimulate evacuation.
Points to Ponder
• Constipation: Add or increase the dose of a stool softener. Increase
fluid intake, dietary fiber, increase activity level and avoid foods that
can harden stool, such as bananas and cheese.
• Diarrhea: Temporarily discontinue the use of any stool softeners. A
frequent cause of diarrhea is a blockage or impaction of stool.
• Frequent bowel accidents: Ensure rectum is completely empty at the
end of bowel program. Increase the frequency of bowel program in
flaccid. Try using only half of a suppository. Monitor diet for any
foods that may over stimulate bowel, such as spicy foods.
• Mucous accidents: In case of a clear, sticky, sometimes odorous
drainage from the rectum, try switching from a suppository to a
mini-enema, or using only half of a suppository, or try eliminating
suppositories or mini-enemas completely and begin bowel program
with digital stimulation only.
• No results in 3-4 days: Treat constipation as recommended above.
• Rectal bleeding: Keep stool soft. Be very careful to do digital
stimulation gently and with sufficient lubrication.
• Excessive gas: Increase the frequency of bowel programs. Avoid gas-
forming foods, such as beans, corn, onions, peppers, radishes,
cauliflower, sauerkraut, turnips, cucumbers, apples, melons.
• Bowel program takes a long time to complete: Try switching from
a suppository to mini-enemas. Increase intake of dietary fiber and
add or increase the dose of psyllium hydromucilloid. Try switching
program to a different time, and be sure to schedule it after a meal
to help increase intestinal peristalsis.
• Autonomic dysreflexia during bowel program: Use xylocaine jelly

for digital stimulation. Insert some of the jelly into the rectum before
beginning the program. Keep stool as soft as possible. If dysreflexia
persists, consult the doctor for medication to treat or prevent this
condition.
AUTONOMIC DYSREFLEXIA
Autonomic dysreflexia (AD) refers to an over-active autonomic nervous
system, which causes an abrupt onset of excessively high blood pressure.
Persons having injury levels above T-5 are mostly at risk for this problem.
AD can develop suddenly and is potentially life threatening and is
considered a medical emergency. If not treated promptly and correctly,
it may lead to seizures, stroke, and even death.
Anything that is painful, uncomfortable, or physically irritating before
the injury may cause AD after the injury. AD occurs when an irritating
stimulus is introduced to the body below the level of spinal cord injury,
such as an overfull bladder, among others. The stimulus sends nerve
impulses to the spinal cord, where they travel upward until they are
blocked by the lesion at the level of injury. Since the impulses cannot
reach the brain, a reflex is activated that increases activity of the
sympathetic portion of autonomic nervous system. This results in spasms
and a narrowing of the blood vessels, which causes a rise in the blood
pressure.
Stimuli That Cause Autonomic Dysreflexia

Bladder (most common)
• Urinary tract infection
• Urinary retention
• Blocked catheter
• Overfilled collection bag
• Non-compliance with intermittent catheterization program.
Bowel
• Constipation/impaction
• Distention during bowel program (digital stimulation)
• Hemorrhoids or anal fissures
• Infection or irritation (e.g. appendicitis).
Skin-related Disorders
• Any direct irritant like a pressure sore, burn, ingrown toenails, tight
or restrictive clothing or pressure to skin from sitting on wrinkled
clothing below the level of injury.
the Spinal Cord 221
Sexual Activity
• Over stimulation during sexual activity (stimuli to the pelvic region
which would ordinarily be painful if sensation were present)
• Menstrual cramps
• Labor and delivery.
Other
• Acute abdominal conditions (gastric ulcer, colitis, peritonitis)
• Skeletal fractures
• Sitting on one’s scrotum.
Signs and Symptoms

• Pounding headache (caused by the elevation in blood pressure)
• Goose pimples
• Sweating above the level of injury
• Nasal congestion
• Slow pulse
• Blotching of the skin
• Restlessness
• Hypertension (blood pressure greater than 200/100)
• Flushed (reddened) face
• Red blotches on the skin above level of spinal injury
• Sweating above level of spinal injury
• Nausea
• Slow pulse (< 60 beats per minute)
• Cold, calmy skin below level of spinal injury.
Tips for Avoiding Autonomic Dysreflexia

• Apply frequent pressure relief in bed/chair
• Avoid sun burn/scalds
• Maintain a regular bowel program
• Well balanced diet and adequate fluid intake
• Compliance with medications
• If you have an indwelling catheter, keep the tubing free of kinks,
keep the drainage bags empty, check daily for grits (deposits) inside
of the catheter
• If you are on an intermittent catheterization program, catheterize
yourself as often as necessary to prevent overfilling
• Carry an intermittent catheter kit when you are away from home
• Perform routine skin assessments.
Treatment
Treatment must be initiated quickly to prevent complications.
1. Maintain sitting position, but do apply pressure release immediately.
2. You may transfer patient to bed, but always keep the head elevated.
3. Since a full bladder is the most common cause, check the urinary
drainage system.
4. If using a Foley or supra-pubic catheter, check the following:
• Is the drainage bag full?
• Is there a kink in the tubing?
• Is the drainage bag at a higher level than the bladder?
• Is the catheter plugged?
After correcting an obvious problem, and if the catheter is not draining
within 2-3 minutes, it must be changed immediately. If you do not have
a Foley or supra-pubic catheter handy, perform a catheterization with
flexible rubber catheter and empty your bladder. If bladder has not
triggered the episode of AD, the cause may be the bowel. Perform a
digital stimulation and empty the bowel. If the symptoms first appear
when performing a digital stimulation, stop the procedure and resume
after the symptoms subside. If the bladder or bowel is not the cause,
check to see if the patient has a pressure sore, ingrown toenail, or a
fractured bone. Identify and remove the offending stimulus as soon as
possible. Often, this alone is successful in allowing the syndrome to
subside without need for medical intervention. If symptoms persist despite
interventions sugested, notify a physician. It is also good for the person
with the symptoms to be sitting up with frequent blood pressure checks
until the episode has resolved.
Important Reminder
If unable to find the stimulus causing AD, or attempts to relieve the
stimulus fail, the patient needs emergency medical treatment. Since all
physicians are not familiar with AD and its treatment, the patient should
carry a card that describes the condition and the treatment required.
RESPIRATORY COMPLICATIONS AFTER SPINAL CORD INJURY

After spinal cord injury/damage, the airway and lungs are not typically
affected. However, respiratory problems may occur when the signals
sent from the brain can no longer flow through the spinal cord to control
the respiratory muscles. The amount of muscle control that is lost after
a spinal cord injury depends on the level of the injury and the
completeness of the injury. Individuals with injuries below the T12 level
do not usually lose any control of the four respiratory muscle groups
needed for breathing. This means the respiratory system is not usually
affected by injuries in the lumbar or sacral regions of the spinal cord.
the Spinal Cord 223
Complete injuries in the thoracic or cervical regions usually result in

the permanent loss of respiratory muscle function below the level of
injury. The higher the level of injury, the greater the losses to the
respiratory muscle control. However, if that injury is incomplete, it is
impossible to predict whether the individual will regain some or all of
their respiratory function below the level of injury.
• Injuries in the thoracic area (T1-T12) of the spinal cord affect the
control of the intercostal and abdominal muscles.
• With a higher level of injury, such as a T2, individuals will lose most
of their intercostal and abdominal muscle control.
• A lower level of injury, such as a T10, results in losing a small amount
of respiratory muscle control.
• A complete injury between levels C3 and C5 loses all control of the
diaphragm muscles.
• With a complete injury at level C3 and higher the individual loses
control of all four muscle groups that are needed for breathing. A
ventilator is then needed to assist in breathing.
The ventilator does the work of the absent muscles and forces air
into the lungs. Many people with a C4 level of injury, and even some
people with a C3 level of injury, can eventually breathe without the aid
of a ventilator or may only need it for part-time assistance. Those
individuals with complete injuries above C3 use a ventilator for full-time
assistance.
SECONDARY RESPIRATORY COMPLICATIONS

Individuals with a spinal cord injury are at increased risk for developing
following respiratory complications:
• Any loss of respiratory muscle control weakens the pulmonary system,
decreases one’s lung capacity, and increases respiratory congestion.
It does not matter what the level of injury or if the injury is complete
or incomplete. However, the risk for complications is greater for
persons with a complete injury and for persons with tetraplegia.
• For persons with high-level tetraplegia (C5-C1), ventilatory failure is
a common complication after injury. The person typically lacks the
ability to breathe without assistance.
• Another common problem is atelectasis. This is when the lungs
partially collapse because not enough air is getting into the lungs.
• All levels of injury are at risk for pulmonary embolism. Pulmonary
embolism is a blockage in the blood vessels of the lungs. This is the
primary disease of pulmonary circulation and the second leading
cause of death for persons with spinal cord injury/damage within
the first year after their injury.
• Ventilatory failure, atelectasis and pulmonary embolism are all very
serious, life-threatening respiratory complications.
• However, pneumonia is the leading cause of death for all persons

with spinal cord injury. This is true regardless of the level of injury
or duration of injury. Therefore, one should be aware of the symptoms
like shortness of breath, pale skin, high fever, along with a feeling of
heavy chest and an increase in congestion. If you detect symptoms
of pneumonia in the patient, call a doctor immediately for opinion
and advice.
Steps to Prevent Respiratory Complications include

• Medical checkup at least once per year and getting vaccinated against
pneumonia.
• Avoiding buildup of secretion in the lungs by coughing or receiving
cough assist treatments.
• Maintaining proper posture and mobility to prevent buildup of
congestion.
• Wearing an abdominal binder to assist the intercostals and abdominal
muscles.
• Following a healthy diet and managing a healthy weight.
• Drinking plenty of water to keep congestion from becoming thick
and difficult to cough up.
• Not Smoking! The harmful effects of smoking include a decrease of
oxygen in the blood, an increase in congestion in the chest and
windpipe, a reduction in your ability to clear secretions from your
lungs, a destruction of lung tissue, and an increase in the risk for
respiratory infections such as pneumonia and bronchitis.
• Breathing Exercises.
Sleep apnea is a growing respiratory concern for persons with spinal
cord injury. Sleep apnea is a type of breathing disorder. Typically, it is
a stop in breathing during sleep. However, apnea can include other
respiratory difficulties. Increased research in this area suggests that persons
with weakened respiratory muscles may be at high risk for developing sleep
apnea, so persons who are older and persons with tetraplegia may be at a very
high risk.
Symptoms of sleep apnea include irregular breathing or snoring, daytime
sleepiness, problems with memory or concentration, waking up often
during the night, and waking up tired or with a headache.
SEXUALITY AND REPRODUCTIVE HEALTH FOR MEN AND WOMEN

WITH SCI
A spinal cord injury/damage affects a man’s sexuality both physically
and psychologically. After injury, men may face changes in relationships,
sexual activity, and their ability to biologically father children. Men can
also experience emotional changes that can affect sexuality. All of these
the Spinal Cord 225
issues involve both the man with spinal cord injury/damage and his
partner. Therefore, it is very important to understand and confront these
issues as a part of the overall adjustment to life after injury.
Many men with spinal cord injury/damage are capable of having an
erection. However, the erection may not be hard enough or last long
enough for sexual activity. This condition is called Erectile Dysfunction
(ED). There are various treatments and products available for treating
ED but men with spinal cord injury/damage may have special problems
with their use. It is important to see a doctor or urologist for accurate
information on the various treatments and products available. Below are
some of the treatment options currently available:
1. Penile injection therapy involves injecting a single drug or a
combination of drugs into the side of the penis. This produces a hard
erection that can last for one to two hours. These drugs must be used
exactly as prescribed by the physician. If not used correctly, the result
could be a prolonged erection, called priapism. When priapism occurs,
the blood fails to drain from the penis. This can damage the penile
tissue and be extremely painful. Other risks from the injection are
bruising, scarring or infection of the penis. This method is not
recommended for use more than once a week. A penile injection is
a difficult option for a man with limited hand function due to spinal
cord injury. Therefore, he must have assistance in getting the injection.
2. Medicated urethral system erection (MUSE), or transurethral
therapy, is a relatively new treatment option. A medicated pellet is
placed into the urethra where it is absorbed into the surrounding
tissue. This causes the blood vessels to relax and allows blood to fill
the penis. Reported side effects include a risk of infection, a burning
sensation and decreased blood pressure and fainting.
3. The vacuum pump is a mechanical option for producing an erection
that, for most men, is sufficient for intercourse. The penis is placed
in a vacuum cylinder and air is pumped out of the cylinder causing
blood to be drawn into the erectile tissues. The erection is maintained
by placing a constriction ring around the base of the penis. This ring
also prevents urinary leakage that some men with spinal cord injury/
damage experience. It is important to remove the ring after intercourse
to avoid prolonged pressure and the risk of ischemic sores. A battery-
operated vacuum pump is an option for those with limited hand
function.
4. Men with SCI also experience a change in their ability to biologically
father a child. The major factor interfering with a man’s fertility is
primarily due to an inability to ejaculate as a result of damage to the
spinal cord. In fact, 90% of men with SCI are not able to ejaculate
during intercourse; this is called anejaculation. Another problem men
with spinal cord injury/damage may experience is retrograde
ejaculation. This occurs when semen does not leave the urethra but
travels back up the tube and is deposited in the bladder. Men who
are interested in fathering a child should get medical advice and
treatment options from a fertility specialist experienced in issues of
spinal cord injury. The fertility specialist needs to be aware of methods
that can improve sperm quality in men with spinal cord injury/
damage, as well as complications that can occur, such as autonomic
dysreflexia.
5. A romantic and an intimate relationship with a partner can be
developed or maintained after a spinal cord injury. It is important to
keep the lines of communication open as well as an openness to
explore and experiment with different ways to be romantic and
intimate.
Reproductive Health for Women with Spinal Cord Injury/Damage
Women with a spinal cord injury represent about 20% of all individuals
with spinal cord injury/damage and the majority of these women are of
childbearing age. Regardless of a woman’s level of injury or dysfunction,
women with SCI can engage in sexual activity, can have children and
will need to use a contraceptive method if they choose not to have
children. Education is the key for women to understand the facts related
to pregnancy, labor, and delivery.
Women with SCI/D are considered to have “high risk” pregnancies,
and need to take precautions to prevent and treat complications. Pregnant
women with SCI/D are at greater risk for developing:
• Autonomic dysreflexia (AD)
• Changes in bowel function (constipation or diarrhea)
• Bladder spasms resulting from increased weight on the bladder
• Urinary tract infections (a UTI might actually trigger premature labor
if not properly managed)
• Pressure sores resulting from weight gain and/or posture changes
• Respiratory complications
• Muscle spasms
• Swelling of the legs and feet caused by lack of blood flow in the
lower extremities.
Many medications normally used by women with SCI/D can cause
problems during pregnancy and have an adverse effect on fetal growth.
Therefore, it is essential that all medications be evaluated by obstetrician
before pregnancy and continually re-evaluated each trimester.
Although there are risks for complications related to pregnancy in
SCI/D, risks can be reduced and managed through proper prenatal care
and adequate planning.
the Spinal Cord 227
NUTRITION AND WEIGHT CONTROL FOR SCI/D

Basic good nutrition is important for everyone. This does not change
after having a spinal cord injury. After a spinal cord injury it is important
to find a weight that is acceptable and healthy for the patient depending
on metabolic rate, which may be lower after SCI due to lower muscle
mass and a decrease in activity level. The patient needs fewer calories
each day in order to maintain a desirable weight because the ideal body
weight of a person with SCI is lower than an able bodied individual.
Caloric need by an individual with SCI reduces by 5% for those with
paraplegia and 10-15% for those with tetraplegia (quadriplegia) as
compared to the normal person of the same age and sex.
The spinal cord injury puts stress on the body. When the body is
stressed, the metabolic rate is higher. Immediately after an injury, the
body requires more energy and nutrients to repair itself and fight infection
This means that the body burns calories faster. A healthy diet is crucial
at this point. Poor nutrition increases the risk for infections and pressure
sores.
Weight Gain
Weight gain is a common concern of physiotherapists for individuals
with SCI. This may occur because of inability to exercise at a level to
burn the extra calories. In overweight SCI, you will notice a decrease in
mobility, endurance, and balance. This can make transfers difficult. Excess
weight also puts more pressure on the skin. As people gain weight, skin
folds develop which trap moisture, greatly increasing the risk of skin
sores.
Tips to Maintain a Healthy Weight

• Eat foods high in nutrients
• Eat a low fat, high fiber diet
• Cut back on fat, alcohol, sodas, fruit juices, and sweets
• Eat two or three small meals each day
• Avoid “fat-free” foods that are loaded with sugar
• Balance the calories you eat with the calories you burn. Be active and
exercise.
Correct food can benefit individuals with SCI in the reduction of
heart problems, pressure ulcers, kidney and/or bladder stones, urinary
tract infections and irregularities in bowel management. Eating a healthy
variety of foods is the key to good nutrition. Below is a chart that lists the
main nutrients the body needs each day to stay healthy.
Carbohydrates: Serve as the body’s main source of energy, helps to give
the stomach a full feeling. Found in rice, roti, breads, noodles, pasta,
potatoes, fruits, vegetables.
Protein: Builds and repairs body cells, helps prevent skin breakdown
pressure sores; helps fight infection, helps heal wounds. Found in lentils
(dal), bengal gram (chana), paneer (cottage cheese), curd, meat, fish,
poultry, cheese, eggs, dried peas and beans, nuts.
Fats: There are 2 types of fats, unsaturated and saturated:
• Unsaturated fats can actually help reduce cholesterol level in the
blood and are considered “heart healthy”, found in sunflower seeds,
olive oil, sea fish.
• Saturated fats are generally bad for your heart and arteries and should
be avoided, found in butter, lard, coconut oil, palm oil, broiler skin,
red meat.
Vitamin A: Keeps skin and nerves healthy, helps resist infection. Found
in dark green and yellow fruits, carrots, squash, sweet potatoes, apricots,
spinach, egg yolks.
Vitamin B: Helps with digestion, provides energy, keeps eyes, skin, and
nerves healthy. Found in whole grain cereals (Ata), pork, peanuts, red
meats, green leafy vegetables.
Vitamin D: Helps the body use calcium and phosphorus, works with
calcium to form bones. Found in milk, fish liver oils, shrimp, sea fish.
Calcium: Helps build bones and teeth, aids in blood clotting, helps develop
muscle tone. Found in milk, cheese, yogurt (dahi), dried beans (Rajma),
fish with bones, sardines, dark green leafy vegetables.
Iron: Helps build blood cells, carries oxygen to all cells. Found in liver,
lean red meats, dried peas (Matar) and beans (Rajma), green leafy
vegetables, dried fruits, nuts.
Potassium: Regulates muscles and nerves. Found in bananas, apricots,
green coconut water, kiwi, oranges.
Water and Fluids

Water is the most important nutrient. It regulates body temperature,
carries food nutrients through the body, keeps stool soft, carries food
waste out of the body, helps prevent urinary tract infections, helps prevent
kidney and bladder stones, aids with digestion and elimination. It is
recommended that SCI/D patients drink 8-10 glasses of water a day.
Fiber
There are two kinds of fiber, soluble and insoluble. Insoluble fiber (like
wheat bran) speeds up elimination; soluble fiber (oats and fruits) binds
with fats like cholesterol and carries them out of the body. Fibers keep
bowel movements regular, hold food in the stomach longer, slows down
the Spinal Cord 229
calorie absorption, help keep the patient from feeling hungry. Found in
fresh or dried fruits, vegetables, brown rice, dried beans and peas, wheat
germ, popcorn, whole grain breads and cereals.
Remember: Fiber cannot do its job without fluid.
TECHNIQUES OF HANDLING, POSITIONING, MOBILITY AND ADL

TRAINING
This section has several tips in patient handling, positioning, transfer
and mobility training techniques, with details of various apparatus, which
can be used not only for SCI/D as well as for any other disorder like
CVA or traumatic brain lesions or GB syndrome that may render the
patient incapable of moving freely and independently and perform
activities of daily living.
Proper transfer technique must be adopted to move the paralyzed
patient from one surface or from one position to another, since it is an
essential component of patient handling during acute care and rehab of
spinal injuries, as well as other conditions resulting in severe motor
paralysis. Weight shifts done by the patient with or without assistance of
the caregiver to relieve prolonged pressure on the skin and muscle over
bony prominences is also an essential technique for preventing pressure
sores. The technique adopted for transfers and weight shifts vary widely
depending upon the under lying disorder, physical capabilities,
cooperation and motivation of the patient. The following illustrations
attempt to clarify the steps to follow in patient handling during transfers
from stretcher to bed to wheel chair and vice versa or passive repositioning
from supine to sit with maximum safety to the paralyzed patient and the
therapist/nurse (Figs 8.17 to 8.21).
When to Use: Transferring a partial- or non-weight-bearing patient
between 2 horizontal surfaces, such as a bed to a stretcher or trolley in
supine position.
Fig. 8.17: Basic lateral transfer technique

Points to Ponder
• Two caregivers are required to perform this type of transfer.

Additional assistance may be needed for heavier or non-cooperative
residents.
• Height-adjustable trolleys with built-in slide boards are preferred to
minimize physical exertion required by caregiver.
• Always ensure that lifting device is in good working order before
use and is rated for the load weight to be transferred.
• Ensure wheels on equipment are locked.
• Ensure transfer surfaces are same level and at caregiver’s waist level
to avoid extended reaches and back flexion.
Fig. 8.18: Lateral transfer using ceiling-mounted device with horizontal whole
body sling
When to Use: Transferring patients who are totally dependent, non-

weight bearing, have other physical limitations, or are very heavy and
cannot be safely transferred by staff between 2 horizontal surfaces, such
as a bed to a stretcher or gurney in supine position.
Points to Ponder
• Devices are usually ceiling mounted, can be operated by hand-held

control attached to unit or by infrared remote control.
• Always ensure lifting device is in good working order before use
and is rated for the load weight to be lifted.
• On bed using draw sheet – To be used in combination with friction-
reducing devices such as slippery sheets, plastic bags, low friction
mattress covers, or slide boards.
the Spinal Cord 231
Fig. 8.19: Lateral transfer and repositioning patient
When to Use: Transferring or repositioning a patient in bed.
Points to Ponder
• Two caregivers are required to perform this type of transfer.
Additional assistance may be needed for heavier or non-cooperative
patients.
• Use a good hand-hold by rolling up draw sheets or use other friction-
reducing devices with handles such as slippery sheets.
• Narrower slippery sheets with webbing handles positioned on the
long edge of the sheet may be easier to use than wider sheets.
• Look for a combination of devices that will minimize risk of skin
trauma.
• Count down and synchronize the transfer motion between caregivers.
Fig. 8.20: Lifting a patient using a portable hydraulic hoist

When to Use: Lifting patients who are totally dependent, are partial- or
non-weight bearing, are very heavy, or have other physical limitations.
It is perfect for transfers from bed to chair wheel chair, chair or from
floor to bed, lateral transfers or for bathing and toileting in safety and
comfort.
Points to Ponder
• Look for a device with a variety of slings, lift-height range, battery
portability, hand-held control, emergency shut-off, manual override,
and boom pressure sensitive switch.
• Having multiple slings allows one of them to remain in place while
patient is in bed or chair for only a short period, reducing the number
of times the caregiver lifts and positions resident.
• Ensure the hoist is in good working order before use and is rated for
the load weight to be lifted.
• Electric/battery powered hoists are preferred to mechanical/hydraulic
devices to allow a smoother movement for the resident, and less
physical exertion and risk of musculoskeletal injury to the caregiver.
When to Use: For lateral transfer of patients unable to sit up on their
own. Eliminates the need to perform lift transfer in and out of wheelchairs.
Points to Ponder
• Two caregivers are required to perform lateral transfer. Additional
assistance for lateral transfer may be needed for heavier patients.
• Wheelchairs that convert to stretchers may also have a mechanical
transfer aid built in for bed-to-stretcher or stretcher-to-bed type
transfers.
• Motorized height-adjustable devices are preferred to those adjusted
mechanically to minimize physical exertion and risk of
musculoskeletal injury to the caregiver.
Fig. 8.21: Repositioning from lying to sitting position using a wheelchair

convertible to a stretcher
the Spinal Cord 233
• Always ensure device is in good working order before use and is

rated for the load weight to be transferred.
• Ensure wheels on equipment are locked.
• Ensure transfer surfaces are at same level and at a height that allows
caregivers to work at waist level to avoid extended reaches and back
flexion.
Techniques of Progressive Mobilization

As the patient gains stability of the spine and sitting balance, he/she
may be mobilized progressively from the bed to out of bed environment.
This is a preparatory step to wheelchair/gait training. To achieve this
various techniques and aids and appliances are used as detailed below
in Fig. 8.22.
Fig. 8.22: Lateral transfer in sitting
When to Use: Transferring (sliding) patients who have good sitting

balance and are cooperative from one level surface to another, e.g. bed
to wheelchair, wheelchair to car seat or toilet. Patients who require limited
assistance but need additional safety and support can also use it. Movable
seats increase patient comfort and reduce incidence of tissue damage
during transfer.
Points to Ponder
• Ensure clothing is present between the patient’s skin and the transfer
device.
• The seat may be cushioned with a small towel for comfort.
• May be uncomfortable for larger residents.
• Usually used in conjunction with gait belts for safety depending on
resident status.
• Ensure boards have tapered ends, rounded edges, and appropriate
weight capacity.
• Ensure transfer surfaces are at same level.
• Remove lower bedrails from bed and remove arms and foot rests
from wheel chairs as appropriate.
When to Use: Transferring patients who are partially dependent,

cooperative, have some weight-bearing capacity, can sit up unaided and
are able to bend hips, knees, and ankles. It is useful for transfers from
bed to chair, or chair-to-chair, chair or toilet.
Points to Ponder
• Can be used by 1 or 2 caregivers with pivot or transfer disc to assist

transfer as necessary.
• Place sling under patient’s hip.
• Caregiver(s) support patient during the transfer.
• Use for short distance transfer only.
• Sling should not be used to lift patients.
• Position sling so as not to dig into or slip off from the seat of the
patient.
• Ensure sling is in good condition before use and patient is wearing
non-slip clothing.
• Adjust bed height so patient’s feet are flat on floor.
• Use smooth motion by moving feet while pivoting.
After the patient has been taught transfers with or without assistance
the next logical step would be to increase his dimension in terms of
mobility. To this end the therapist has to first come to a decision as to
whether or not the patient is likely to be wheel chair bound for the
remaining life. In case the patient has the potential for ambulation with
orthosis and mobility aids, training should focus on gaining stability in
standing and walking. If the patient doesn’t have such potential, means
have to be found to let the patient achieve physiological standing.
Following are a series of illustrations depicting various aids and appliances
that can be used to reposition a recumbent patient to an upright sitting
or a wheel chair bound to standing position in complete safety
(Figs 8.23 to 8.30).
Fig. 8.23: Lateral transfer in sitting position using transfer slings

the Spinal Cord 235
Fig. 8.24: Transfer from sitting to standing position using powered sit-to-stand or
standing-assist devices
When to Use: Lifting patients who are partially dependent, have some
weight-bearing capacity, are cooperative, can sit up on the edge of the
bed with or without assistance, and are able to bend hips, knees, and
ankles. Useful for transfers from bed to chair/wheel chair or chair to
bed, or for bathing and toileting and for physiological standing to increase
tolerance of upright position, as well as for repositioning where space or
storage is limited.
Points to Ponder
• Usually requires 1 caregiver.
• Look for a device that has a variety of sling sizes, lift-height range,
battery portability, hand-held control, emergency shut-off and manual
override.
Fig. 8.25: Transfer from sitting to standing position using

lift cushions and lift chairs
• Ensure lifting device is in good working order before use and is

rated for the load weight to be lifted.
• Electric/battery powered lifts are preferred to mechanical/hydraulic
devices to allow a smoother movement for the resident, and less
physical exertion and risk of musculoskeletal injury to the caregiver.
When to Use: Transferring patients who are weight bearing and
cooperative but need assistance when standing and ambulating. It can be
used for independent patients who need an extra boost to stand. It can
aid patient independence.
Points to Ponder
• Lift cushions uses a lever that activates a spring action to assist patients
to rise up.
• Lift cushions may not be appropriate for heavier patients.
• Lift chairs are operated via a hand-held control that tilts forward
slowly, raising the patients.
• Patients need to have physical and cognitive capacity to be able to
operate lever or controls.
• Always ensure device is in good working order before use and is
rated for the load weight to be lifted.
Fig. 8.26: Transfer from sitting to standing position and training ambulation using
gait belts/transfer belts with handles
When to Use: Transferring patients who are partially dependent, have

some weight-bearing capacity, and are cooperative. Transfers, such as
bed to chair, chair to chair, or chair to car, when repositioning patients
in chairs, supporting patients during ambulation, and in some cases when
guiding and controlling falls.
Points to Ponder
• May require 1 or 2 caregivers.
• Belts with padded handles are easier to grip and increase security
and control.
the Spinal Cord 237
• Always transfer to patient’s strongest side.

• Use rocking and pulling motion rather than lifting when using a belt.
• Belts may not be suitable for ambulation of heavy or non-weight
bearing patients or patients with recent abdominal or back surgery,
abdominal aneurysm, etc.
• Should not be used for lifting patients.
• Ensure belt is securely fastened and cannot be easily undone by the
patients during transfer (i.e., no Velcro fasteners).
• Ensure a layer of clothing is between patients’ skin and the belt to
avoid abrasion.
• Keep patient as close as possible to caregiver during transfer.
• Lower bedrails; remove arms and footrests from chairs, and other
items that may obstruct the transfer.
Some discs have a stand-assist device attached for independent patients.
When to Use: Transferring patients who are partially dependent, have

some weight-bearing capacity, and are cooperative for transfers such as
from bed to chair, chair to chair, or chair to car. Helps caregivers perform
transfers without twisting.
Points to Ponder
• May require 1 or 2 caregivers.
• The disc is placed on the floor and used to rotate the patients 90
degrees to a bed or chair.
• Lower bed so that patient’s feet are supported on the floor before
standing.
• Patient’s feet should be in the center of the disc, not touching the
outer rim.
• A transfer or gait belt can be used in addition to the disc.
• May not be appropriate for heavier patients. Ensure disc has non-
slip material on either side.
• Ensure wheels on bed/wheel chair are locked and transfer surfaces
are at same level.
• Lower bedrails; remove arms and foot rests from chairs and other
items that may obstruct the transfer.
Fig. 8.27: Transfer from sitting to standing position using pivot discs or boards
When to Use: Patients that have the ability to assist the caregiver during
the activity, i.e. with upper body strength and use of extremities, who
are cooperative and can follow instructions can use the trapeze bar to
shift, raise and reposition themselves on bed.
Fig. 8.28: Self-repositioning using trapeze bar
When to Use: Repositioning patients that have the ability to assist the
caregiver during the activity, with upper body strength and use of
extremities, which are cooperative and can follow instructions. Very useful
during bed making, push up training, sitting on bed pan, periodic pressure
relieving, etc.
Fig. 8.29: Self-repositioning on bed using hand blocks and push up bars
Points to Ponder
• Blocks also enable patients to raise themselves up and reposition
themselves in bed or bed pan.
• Trapeze bars attached to the bed frame serve the same purpose.
the Spinal Cord 239
When to Use: To assist patients who are cooperative and can sit up with
or without assistance, to position on a special bed pan. May reduce need
for extra toileting.
Points to Ponder
Device is positioned under hips and inflates like a pillow to lift hips.
Provide front hand-hold to reduce back flexion.
Fig. 8.30: Self-repositioning on bed pan using pelvic lift devices (hip lifters)
When to Use: For patients who are weight bearing and cooperative and
who need extra security and assistance when ambulating. Increases
patients safety during ambulation and reduces risk of falls (Fig. 8.31).
Fig. 8.31: Ambulation training using a para podium

Points to Ponder
• Usually requires one caregiver.
• The device supports patients as they walk and push it along during
ambulation.
• Ensure height adjustment is correct for resident before ambulation.
• Ensure device is in good working order before use and rated for the
load weight to be lifted.
• Apply brakes before positioning patients in or releasing patients from
device.
TRAINING FOR ACTIVITIES OF DAILY LIVING

Depending on others to perform most intimate and personal activities
like toilet is the biggest demoralizing factor for a paralyzed patient.
Inability to feed, dress, do other activities of ones own choice further
complicates the issue. Once the patient is able to move on his own in the
bed, the emphasis of rehab should shift to training of ADL. Following
illustrations give a few essential tips to this end (Figs 8.32 and 8.33).
When to Use: For toileting partially weight-bearing patients who can sit
up unaided, use upper extremities (have upper body strength), are able
to bend hips, knees, and ankles, and are cooperative. Independent patients
can also use these devices.
Points to Ponder
• Risers decrease the distance and amount of effort required to lower
and raise patients.
• Grab bars and height-adjustable legs add safety and versatility to the
device.
• Ensure device is stable and can accommodate patient’s weight and
size.
Fig. 8.32: Bath tub, shower, and toileting activities using toilet seat risers
the Spinal Cord 241
When to Use: During feeding, dressing, personal hygiene tasks, vital

sign assessment, and other bedside assistance.
Bedside Assistance
• Lower bed rails, position resident as close to edge as safely possible.
• Sit or stand as close as possible to resident’s side and face resident.
• Adjust tables and electric beds to a height to allow caregivers to
work at waist level and place supplies close by to avoid back flexion
and twisting.
• Gather supplies in advance and place them on a table that is
positioned perpendicular to the resident.
• Avoid reaching across resident, rather, walk to other side.
• Carry objects close to the body.
• Provide adaptive equipment for resident use when appropriate to
increase independence and reduce assistance from caregiver.
Feeding: Cut food before placing in front of resident.
Bathing aids – washer and scrubber Dressing aid – reacher
Fig. 8.33: Various activities of daily living and bedside

assistance for work practices
Dressing and Grooming

• Ensure that resident’s feet are flat on the floor or a stool for balance
when sitting.
• Place weaker limb in pant or sleeve first.
• Use appropriate adaptive equipment for bathing and dressing.
Disorders of the Peripheral
9 Nerves
INTRODUCTION
Disorders of peripheral nerves are said to occur when the spinal nerves
originating from the spinal cord and the cranial nerves originating from
the brain are damaged, causing symptoms such as tingling and numbness,
lack of sensation, pain, and muscle weakness.
BASIC PATHOLOGY
Peripheral nerves may be affected by following distinct types of
pathological processes.
• Wallerian degeneration takes place usually following a blunt trauma
or a clean cut or prolonged impingement of the axon of a nerve. It
leads to degeneration of the axon fibers and the myelin sheath distal
to the site of the lesion. Chromatolysis occurs in the neuron but the
endoneurium or the axon sheath usually remains intact, which can
later guide the regenerating axon fibers to their end organs.
• Segmental demyelination is said to have happened when patches of
myelin sheath degenerates, leaving the underlying axons exposed.
The axons are preserved, i.e. no Wallerian degeneration takes place.
The nerve is still able to conduct impulses but at a much reduced
velocity than normal. Remyelination usually takes place to restore
function to the nerve, though some amount of efficiency of nerve
conduction may be lost, e.g. Guillian-Barre syndrome.
• Axonal degeneration is said to have taken place when the axon
fibers along with its myelin cover degenerates from distal to proximal
in a “dying back pattern”, e.g. peripheral neuropathy due to diabetes,
alcohol abuse, heavy metal poisoning etc.
• Neuronal degeneration is said to have occurred when the motor
neuron cells located in the anterior horn and the sensory neurons
located in the dorsal root ganglions of the spinal cord and their axonal
pathways degenerate, e.g. motor neuron disease (ALS), tabes dorsalis,
etc.
A Primer to the Anatomy ofofthe
Disorders theNervous
PeripheralSystem
Nerves 243
NOMENCLATURE
In broad sense, any damage to peripheral nerves can be called a
neuropathy. However by convention, depending on the cause or
presentation of the disorder following nomenclature is used to describe
a peripheral nerve disorder:
a. Peripheral neuropathy: Peripheral nerve lesions arising out of causes
like alcohol abuse, heavy metal poisoning, infection or deficiency disorder or
systemic diseases such as diabetes, where predominant symptoms are
numbness, anesthesia of skin and muscle weakness.
b. Neuritis or Neuralgia: When peripheral nerve lesion is accompanied
by severe pain and tingling sensation.
c. Nerve injuries or traumatic neuropathies: Direct trauma to the nerves
result in wallerian degeneration of the axon. According to Seddon’s
classification, there may be three types of nerve injuries:
1. Neuropraxia, a temporary impingement (pinching) of a peripheral
nerve axon that usually recovers spontaneously as soon as the
impingement is relieved. However if the pressure on the axon is
not relieved for sufficient length of time, wallerian degeneration
may occur, e.g. Bell’s palsy, Carpal tunnel syndrome, Crutch
palsy, Saturday night palsy, etc.
2. Axonotenesis results when the axon of a peripheral nerve is
subjected to a blunt trauma, which does not divide the nerve but
contuses the axon fibers, leading to wallerian degeneration distal
to the site of the lesion, e.g. blow on the radial groove in upper
arm resulting in Radial nerve damage causing wrist drop.
3. Neurotemesis follows a clean cut or laceration of a peripheral
nerve axon, resulting in loss of continuity of the nerve, e.g. glass
cut injuries at the wrist resulting in transection of median or
ulnar or both nerves creating claw hand.
The peripheral nerve damage may also be classified depending upon
the number of nerves involved and site of the lesion on the nerve.
• Mono-neuropathy or neuritis is the lesion involving a single
nerve;
• Multiple mono-neuropathy or mono-neuritis multiplex is the lesion
involving two or more nerves.
• Poly-neuropathy or neuritis is the lesion involving many nerves
throughout the body.
• Radiculopathy is the lesion involving a nerve root, at the point of its
origin from the spinal cord.
• Neuronopathy is the lesion involving the nerve cell, usually the motor
neuron or anterior horn cell in the spinal cord.
• Bulbar palsy refers to the motor weakness or paralysis of muscles of
tongue, larynx and pharynx due to involvement of cranial nerve
nuclei located in the brainstem.
MANAGEMENT APPROACH TO SOME COMMON PERIPHERAL

NERVE LESIONS
Peripheral Neuropathy
When peripheral nerves are damaged, communication between the central
nervous system and the rest of the body is disrupted. The nature of
damage to the nerves influences the types of symptoms that will occur.
For example, if the sensory nerve fibers are damaged, one may experience
altered sensation such as tingling, numbness or pain. However, if the
motor fibers are damaged, skeletal muscles may be affected, causing
weakness, wasting, hypo tonicity and loss of function. Since most
peripheral nerves are mixed nerves, i.e. consisting of both motor and
sensory fibers, peripheral neuropathies usually result in loss of motor
and sensory functions.
Symptoms of Peripheral Neuropathies

Most Peripheral neuropathies usually start with numbness and tingling
in the feet or hands (Table 9.1). Symptoms appear and progress gradually
over a period of months or years.
However, neuropathies caused by acute infective disorders like
Guillain-Barré syndrome that may develop and worsen in a matter of
days or weeks.
Symptoms of peripheral neuropathies usually begin in the extremities,
in the toes or fingertips and then spread upwards towards the trunk. The
symptoms of numbness, prickling, or tingling first appear in the distal
most part of the limb, which may then spread proximally. Symptoms
usually occur and progress in a symmetrical fashion, so that both hands
and both feet are affected in similar pattern.
Patient may experience burning, coldness or shooting pain worsening
at night, along with gradual muscular weakening and skin that is
extremely sensitive to touch. In extreme conditions, the patient may lose
the ability to stand, walk, or hold objects.
Table 9.1: Symptoms of peripheral neuropathy

Numbness
Tingling or prickling
Sharp pain
Burning or freezing sensations
Decreased sensation
Lack of sensation
Extreme sensitivity to touch
Muscle weakness
Lack of muscle control
Loss of balance or coordination
PeripheralSystem
Nerves 245
Peripheral neuropathy can also affect the nerves that control automatic
functions such as heartbeat, bladder control, or bowel function. The patient
may experience diarrhea or constipation, incontinence, sexual impotence,
and high or low blood pressure. The skin may become dry, scaly and
pale, or there may be excessive sweating. The patient may also develop
blurred vision, dizziness or stomach upset.
The loss of sensation and numbness caused by peripheral neuropathy
can lead to self inflicted injuries and infections. This happens because the
patient is unaware of an injury such as a burn while handling hot objects
or a cut while trimming nails. The untreated wound may then become
infected.
Risk Factors
Peripheral neuropathy affects men and women equally. Older adults
above 55 to 60 years are most likely to develop peripheral neuropathy.
Some inherited conditions that cause nerve damage can strike even during
childhood.
Types of Peripheral Neuropathy

1. Diabetic Neuropathy: Nerve damage is a frequent complication of
diabetes mellitus. Peripheral neuropathy occurs in 5-10% of patients
newly diagnosed with diabetes, and may affect more than 50% of
patients who have had diabetes for more than 25 years. In diabetic
neuropathy, the numbness and diminished sensation in the feet and
legs may prevent one from noticing an injury or infection until it
becomes an ulcer. Diabetic neuropathy can also cause weakness of
the eye, face, and skeletal muscles.
Diabetic neuropathy is more likely to develop in patients whose
blood glucose levels have been poorly monitored. If one has diabetes,
he can reduce the risk of developing diabetic neuropathy by keeping
the blood sugar at a normal level and maintaining normal blood
pressure. The patient should also have regular physical exams and
blood and urine tests, stop smoking, limit alcohol consumption, and
exercise regularly.
2. Neuropathy in AIDS: Neuropathy is commonly associated with HIV
infection and AIDS. An estimated one-third of AIDS patients
experience the typical symptoms of neuropathy, such as loss of feeling
in the feet or hands, and other sensations, including prickling or
burning. The type of neuropathy that occurs typically varies with the
stage of the disease. The most common condition is a type of poly-
neuropathy that develops during the late stages of HIV infection.
In patients with HIV, peripheral neuropathy can be caused by
the viral infection itself, or as a side effect of drugs taken to fight the
infection, or due to vitamin deficiencies or concurrent diabetes.
AIDS drugs associated with peripheral neuropathy include

stavudine, didanosine, and zalcitabine. Although neuropathy can
affect anyone with HIV, it is more likely to occur if the patient is
taking one or more of these drugs. The symptoms may improve on
discontinuing the medication. In such cases alternative drugs may be
prescribed.
3. Alcoholic Neuropathy: Alcoholism is a leading cause of neuropathy.
The symptoms of alcoholic neuropathy are numbness, abnormal or
painful sensations, and muscular weakness. Habitual, heavy drinking
increases the risk for developing this disorder.
4. Neuropathies Arising from Systemic Diseases: Rheumatoid arthritis,
lupus, scleroderma, atherosclerosis, sarcoidosis, leprosy, and
polyarteritis nodosa are different diseases which may cause peripheral
neuropathy.
Guillain-Barré Syndrome, rheumatoid arthritis, and lupus are
examples of autoimmune diseases—diseases in which the body’s
immune system attacks organs, organ systems, or tissues instead of
protecting them.
5. Toxic Neuropathy: Exposure to toxic chemicals can cause neuropathy,
which include industrial agents such as solvents; heavy metals such
as lead, arsenic, and mercury; pesticides; and nitrous oxide, sniffing
glue (Dendrite) or other toxic compounds.
6. Deficiency Neuropathy: Nutritional deficiencies can cause peripheral
neuropathy, commonly in vitamin B12. Poor diet is the cause for
peripheral neuropathy in India and developing nations.
7. Drug Induced Neuropathy: Certain medications can damage the
nerves and cause changes in sensation seen in peripheral neuropathy,
for example:
• Heart or blood pressure medications such as amiodarone,
hydralazine, and perhexiline
• Cancer drugs such as vincristine and other vinca alkaloids,
cisplatin, suramin, and paclitaxel
• Antibiotics, such as metronidazole, nitrofurantoin, thalidomide,
isoniazid, emetine, chlorobutanol, and sulfonamides
• Drugs that treat skin conditions, such as dapsone
• The anticonvulsant, such as phenytoin
• The anti-alcohol drug, such as disulfiram
• Sedatives such as hexobarbital and barbital
8. Genetic Neuropathy: Peripheral neuropathy can be inherited. The
most common inherited peripheral neuropathy, seen in both adults
and children is Charcot-Marie-Tooth disease. People with this
condition have progressive muscular degeneration and a mild loss of
limb sensation. A condition known as Friedreich’s ataxia or spino-
cerebellar degeneration can also cause damage to multiple nerves.
PeripheralSystem
Nerves 247
Diagnosis – Checklist for the Therapist

Primary diagnosis of a neuropathy is done from the history and confirmed
by the presenting symptom.
• Ask about what symptoms the patient is experiencing, when they
began, and where they are occurring.
• Note the medications the patient is routinely taking, other health
problems such as diabetes or AIDS, work habits that may have
affected the nerves, e.g. prolonged use of computer or any repetitive
motion tasks,
• Ask about recent illnesses or injuries, level of nutrition, history of
drug and alcohol abuse, exposure to heavy metals and solvents, and
any family history of neuropathy.
During the physical examination, you should check for signs of:
• Muscle cramping or twitching, and test the muscular strength.
• Sensitivity of the skin to temperatures, vibration, touch, and pinpricks.
• Ask patient to walk a few steps to see if nerve damage has affected
your gait.
• Examine the eyes for abnormalities that suggest vitamin B12 deficiency
or certain types of inherited brain disorders.
Specialized nerve function tests may be run to help make a diagnosis.
These tests are useful for diagnosing poly-neuropathy as well as mono-
neuropathy.
• Nerve function tests can determine whether the patient has
neuropathy and, if so, the extent and possible cause of the nerve
damage.
• Look for a pattern of nerve damage such as lack of sensation in both
feet and both hands, which is characteristic of peripheral neuropathy.
• You may order an electromyography (EMG) test, which measures
the electrical activity of affected muscles. The muscle’s electrical
activity at rest and during contraction will be recorded, and view a
display of the activity on a screen.
• A nerve conduction study is often conducted at the same time as an
EMG. This test measures the speed of conduction of nerve impulses,
and gives an idea of the state of health of the nerves that are supplying
muscles and sensory nerve endings.
• A nerve biopsy is another test that may be used to diagnose peripheral
neuropathy. A nerve biopsy is usually done only if tests such as the
EMG and nerve conduction study have been inconclusive. The biopsy
can also help to learn what type of nerve damage has occurred.
During the test, a small portion of a nerve from ankle or wrist will
be removed under local anesthesia. The sample will be examined
under a microscope to check for abnormalities like demyelination,
axonal degeneration etc.
The primary care physician or neurologist may order laboratory

studies of blood, urine, and spinal fluid to detect underlying medical
problems that could lead to neuropathy. The results of blood tests may
reveal an underlying health problem such as pernicious anemia
(suggested by vitamin B12 deficiency) or lead poisoning. Elevated blood
sugar levels suggest poorly managed diabetes, while kidney failure
would be suspected if the test results showed elevated blood creatinine
levels. Heavy metal poisoning or multiple myeloma could be detected
from urine tests. A thyroid function test would determine whether a
thyroid disorder is responsible for the nerve damage. Analysis of spinal
fluid can reveal signs of certain types of neuropathy, such as Guillain-
Barré syndrome.
Prevention and Screening

Since peripheral neuropathy can be caused by so many factors, prevention
is difficult. However, one can reduce the risk for neuropathy by avoiding
some of the known causes of the disorder. For example:
• One can avoid contact with solvents or pesticides.
• Follow a balanced diet to prevent vitamin deficiencies.
• In a heavy drinker, one may be able to reduce the risk of developing
alcoholic neuropathy by drinking less, or by abstaining from alcohol.
• A diabetic should follow the doctor’s advice for proper management
of diabetes.
• If a patient is prescribed a drug that may affect the nervous system,
one should be informed accordingly by the doctor and asked to
promptly report any possible symptoms of peripheral neuropathy.
TREATMENT OF PERIPHERAL NEUROPATHIES: GOALS AND

INTERVENTIONS
Self-care Instructions to the Patient
• Taking good care of your feet may relieve sensory symptoms, improve
circulation and obtain temporary pain relief. As peripheral neuropathy
often affects the feet, you can take some simple precautions to alleviate
symptoms.
• Avoid tight-fitting shoes and socks that can aggravate pain and
tingling. Instead, choose comfortable, padded shoes and loose, cotton
socks.
• Soaking your feet in cool water for 15 minutes twice a day can alleviate
burning foot pain. You can also massage your calf, feet and hands
for relief of cramps.
• Examine your feet and your hands daily for signs of wounds and
infection.
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• Walk with a cane or another form of support if neuropathy has

affected your balance.
• Wheelchairs, braces, and splints may help to improve your mobility
or enhance your ability to use an extremity that has been affected by
nerve damage.
• If you have a bathtub, you may want to install rails next to it for
safety.
• Activity can enhance your quality of life if you live with neuropathy.
Physical activity such as walking can improve your circulation. It
can also help take your mind off of your health problems, and reduce
your stress level.
Medical Management
The physician is the best source of information on the drug choices
available to the patient for treatment of the condition. Treatment for
peripheral neuropathy may require addressing an underlying cause, such
as poorly controlled diabetes, alcoholism, or exposure to toxic substances
or infections. If the patient has been taking a routine medication that has
triggered the neuropathy, the physician should be able to prescribe another
drug. Nutritional supplements may be helpful if a poor diet is the cause
of the disorder.
Alternative Medicine
• Physical therapy, starts with detailed evaluation of the motor and
sensory deficits resulting from the neuropathy. Functional evaluation
is done to assess the ability of the patient to perform independent
mobility and perform ADL. The goal of functional evaluation is to
identify the key functions that are not possible and the key parameters
responsible for such deficits. Once the target parameters have been
identified, therapy in the form of graded exercises, massage and
electrical stimulation may help maintain or increase muscle strength
and control, and improve the ability to perform daily activities. The
nature of physiotherapy will depend on the type of neuropathy and
the presenting symptoms of motor and sensory loss. Education of
the patient in energy saving strategies, protection of the insensitive
skin and contracture prophylaxis is also the responsibility of the
physiotherapist.
• An occupational therapist can suggest aids, appliances and ways in
which the patient can adjust the lifestyle to continue his daily activities
despite the adverse effects of neuropathy. One of the key area in
which the occupational therapist has significance is in prescription,
fabrication and training the use of splints.
• Acupuncture, massage therapy, chiropractic care, meditation, and
various types of movement therapy (including yoga and tai chi)
may help to relieve the symptoms of peripheral neuropathy.
Acupuncture, a traditional Chinese medical technique, is widely used

in many conventional hospitals and clinics, and may provide relief
from the pain and weakness associated with peripheral neuropathy.
• Other alternative therapies that have been mentioned in connection
with neuropathy include magnets, herbs, and vitamins. Little scientific
information is available on the effectiveness of most of these
approaches. However, taking B-complex vitamins and other nerve
specific substances could be beneficial, since such deficiency is one of
the causes for neuropathy. One should talk to the physician if planning
to take herbal supplements, as they may cause harmful interactions
with other medications.
Prognosis
The outcome of peripheral neuropathy varies considerably. If the cause
for the condition can be identified, and if damage to the nerve is limited,
one may make a complete recovery. The recovery time will vary from a
few weeks to over a year. However in most circumstances, the patient
may face chronic disability due to loss of sensation and partial or complete
loss of movement. Medication and changes in lifestyle may enable the
patient to cope better with the symptoms of neuropathy, even if a complete
recovery is not possible. Research is under way on therapies that may
repair or slow the pace of nerve damage.
Follow-up
Since peripheral neuropathy is often a persistent condition, it may need
monitoring periodically. The doctor must be informed if the symptoms
worsen despite treatment. If the neuropathy has been successfully treated,
there should be no need to see a physician unless symptoms recur.
COMMON NEUROPATHIES/PERIPHERAL NERVE LESIONS AND

THEIR MANAGEMENT
Guillian-Barre‘ Syndrome
It is a classical example of acute polyneuropathy, with sudden onset and
rapidly progressive muscular weakness, usually preceded by a infectious
episode. The suspected cause of GB syndrome is autoimmune dysfunction,
triggered by a viral/bacterial infection causing the febrile episode along
with gastrointestinal or respiratory illness.
Pathophysiology
GB syndrome is characterized by acute demyelination of cranial and
spinal nerves, creating LMN type dysfunction. Presenting symptoms of
the disorder include:
• Beginning with distal symmetrical involvement of muscles of both
lower extremities.
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• Progressing in an ascending pattern to involve the muscles of upper

extremities.
• Culminating in involvement of proximal muscles of both extremities.
• Finally resulting in full tetraplegia, sometimes with respiratory failure.
• Autonomic dysfunctions such as tachycardia, arrhythmia and
vasomotor symptoms may be seen.
• The symptoms evolve over a few days up to few weeks. Recovery is
usually spontaneous but slow, taking over a month up to a year. It
is important to note that the faster the onset and progression of the
disorder, faster is the rate of recovery and vice versa.
• Recovery of muscle power is usually complete in faster onset- recovery
type of presentation. Some residual weakness and therefore mild
disability is common in the slower onset-recovery variety of the
disorder.
Key Points of Assessment

• Assess the cardiac status through records of vital signs such as the
pulse rate, BP and ECG in the bedside patient ticket. This should be
verified every time you attend the patient in ICU.
• Assess the respiratory status daily through available records of the
SaO2, PaO2, blood pH. Auscultation of the chest should be done daily
to check the quality and distribution of the air entry in the lungs and
the status of the airway. Chest expansion must be measured and the
breathing pattern be recoded during first visit and repeated at weekly
intervals till the patient is out of ICU.
• Assess for motor loss through manual muscle testing (MMT) of major
muscle groups at the outset. However MMT should be done only
when the vital signs of the patient has stabilized. MMT should be
repeated at weekly intervals to keep track of the progression of the
disorder. While doing MMT keep a record of muscle tone and deep
tendon reflexes.
• Assess for sensory changes, such as paresthesia, hyperasthesia,
anesthesia, aching pain of muscles and burning sensation. The patient
may typically have loss of sensation (anesthesia) extending from the
tip of toes and fingers up to middle of extremities, in the pattern as
if the patient is wearing long gloves and stockings.
• Assess functional status, starting from rolling, bridging, shifting and
turning in bed, supine to sit, sit to stand, and walking.
Goals and Interventions

• Maintain respiratory competence: GB patients with acute respiratory
failure due to bulbar involvement may require endotracheal
intubations, tracheostomy and mechanical ventilation. Since the
patient may not be able to cough effectively, intubation/tracheostomy
provides an easy access for endotracheal suctioning to remove excess

secretions from the airway. Such cases may require mechanical
ventilation. Regular chest physiotherapy consisting of chest vibration,
gentle percussion and endotracheal suction can be done while the
patient is under mechanical ventilation. Vigorous breathing exercises
and postural stimulation of respiration will be needed during weaning
of ventilatory support.
• Medical management: Consists of plasmapheresis, intravenous
immunoglobulins and analgesics, along with nutritional support
through Ryles tube feeding.
• Physiotherapy: Primary goal of the physiotherapist is to prevent
secondary complications arising out of prolonged immobility and
muscle paralysis.
1. Regular passive movements, done through full range of motion
to the extremities and preventing positioning of vulnerable joints
with rolls and pillows will prevent deep vein thrombosis and
soft tissue contracture.
2. Regular inspection of the skin, particularly over bony prominences
and two hourly change of position will prevent pressure sores.
3. Splinting and postural corrections will prevent overstretching of
paralyzed muscles.
4. Provide muscle power maintenance and prevent disuse atrophy
with moderate active assisted exercises done on bed progressing
to resisted exercises done in and out of bed, mat exercises, sitting
and standing balance training progressing to gait training.
Functional electrical stimulation to assist in strengthening of key
muscles may be done using simple surged faradic current or
sophisticated software based stimulating currents wherever
available.
5. The patient must be taught energy conservation techniques to
avoid overuse and fatigue. Regular exercise programme should
be given to the patient to continue at home. This will help improve
the fitness level of the patient for reconditioning of the
cardiovascular system after prolonged bed rest.
Amyotrophic Lateral Sclerosis

A classical example of gradual onset neuronopathy, amyotrophic lateral
sclerosis (ALS), sometimes called Lou Gehrig’s disease or motor neuro
disease (MND) is a progressive and frequently fatal neuromuscular disease
that is characterized by degeneration of a select group of motor neuron
cells and their axons located in the spinal cord and cranial nerve nuclei.
The disease affects
• Anterior horn cells located in the spinal cord creating LMN type
motor dysfunction.
• Descending corticospinal tracts with UMN presentation.
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This gradual degeneration of motor neurons and the descending tracts

leads to progressive paralysis of the voluntary muscles, some which may
be hypotonic, hyporeflexic and wasted whereas others may be
hyperreflexic, hypertonic or spastic.
The heart muscles are not voluntary and are therefore spared by the
disease. However, since the respiratory muscles control breathing are
voluntary, death usually occurs due to respiratory muscle fatigue.
ALS may also have bulbar presentation, where the muscles for
speaking, swallowing or breathing are affected. The term “bulbar” refers
to the motor neurons located in the cranial nerve nuclei located in the
brainstem, that control the muscles used for chewing, swallowing, and
speaking. Symptoms and the order, in which they develop, vary from
person to person. In general there is no impairment of the cerebral higher
functions or of the sensorium.
Cause
Cause of the disease is not known. Suspected causes for ALS may be
genetic predispositions, viral or infectious agents, environmental toxins
and immunological changes.
Prognosis
Prognosis of ALS is poor. Approximately 80% of the patients lose their
lives within two to five years of diagnosis and only 10 and 20% may live
for ten years or more.
Diagnosis
ALS is difficult to diagnose. There is no specific test available that will
either rule out or confirm the presence of ALS. Diagnosis is usually made
through a diagnosis of exclusions. Neurologists conduct a number of tests,
thereby ruling out other disorders that may cause similar symptoms,
such as strokes or multiple sclerosis and if nothing else is positive and
yet the symptoms continue to worsen, ALS is often the reason.
Symptoms
1. Muscular weakness in ALS usually becomes apparent either in the
legs, the arms, the throat or the upper chest area.
2. Atrophy, cramping and muscle twitching (fasciculation) of mostly
upper limb muscles are the typical LMN symptoms.
3. Frequent stumbling and fall along with spastic ataxic gait are the
typical UMN features.
4. The patient may find it hard to swallow, choke while drinking fluids
and may slur their speech. Dysarthria, dysphagia and dysphonia are
all caused by bulbar palsy.
5. Sensory loss may be seen in 20% and autonomic dysfunctions in 30%

of the cases.
6. Higher functions, bladder and bowel functions are typically not
affected.
Key Assessment Areas

The purpose of assessment is to identify the short-term problems as
enumerated by the patient in his complaint and to identify long-term
problems that are likely to develop as a result of existing respiratory,
motor and sensory deficit.
1. History must elicit varied patterns of onset- most commonly seen is
gradual onset and insidious progression of loss of motor function
involving the distal muscles of extremities, along with twitching
(fasciculation) of abductor/flexor policis brevis and deltoid muscles.
2. Respiratory functions, such as ability to deep breathe, hold breath,
swallow and cough must be checked. In the short-term any deficit in
respiratory reserve may mean shortness of breath on exertion,
however in the long-term it may mean impending respiratory failure
on slightest respiratory infection.
3. Assess cranial nerve function, specifically for VII, IX, X, XI and XII
th cranial nerves. All of these nerves have significant input into key
bulbar functions like swallowing, coughing, etc.
4. Motor function – Diminished or lost DTR with symmetrical wasting
and weakness of extremities is common in MND. Power of the affected
muscles must be graded using serial MMT at intervals of 3-6 weeks
to assess progression of the disease.
5. Sensory changes, if any, must be identified and recorded on a body
diagram.
6. Functional status- Exercise intolerance and fatigue, exacerbation of
weakness following activity, self-limitation on ADL must be identified
and recorded in an activity log.
There is no known cure at this time and very little in the way of
treatment that will have an effect on the disease itself. However, there is
much that the physiotherapist does to ensure better quality of life for the
person with ALS.

Techniques of PT as stated above under GB syndrome will then apply in
most cases of ALS.
• Maintaining respiratory function: Vibration and gentle percussion to
the chest wall helps re-inflate collapsed alveoli as well as shake loose
secretions sticking to the walls of the airway. Postural drainage and
cough facilitation helps to remove the secretions. Breathing execises,
breathe holding at end inspiration and incentive spirometry helps
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stretches the lung tissue for better ventilation. In the long-term ALS
patients may need mechanical ventilation due to progressive bulbar
involvement at the last stage of the disease.
• Prevent secondary complications, such as contracture through PROM
exercises splinting and positioning, pressure sores with skin care,
DVT with pressure hoses etc, the target being to maintain function
for as long as possible.
• Provide muscle power maintenance and prevent disuse atrophy with
moderate active assisted execises done on mat, sitting and standing
positions. Always be alert to avoid fatigue.
• Functional electrical stimulation to assist in strengthening of key
muscles may be done using simple surged faradic current or
sophisticated software based stimulating currents wherever available.
• Prescribe and train the use of mobility aids such as orthosis, crutches
and walker. Teach the caregiver the proper use of the aids and
appliances prescribed to the patient.
• Teach energy conservation techniques, such as using crutches and
sticks for mobility, reorganizing home environment, handrails in
passages and toilet, reachers and grippers to compensate for lost
reach or grip, to avoid overuse and fatigue of recovering muscles.
Try to anticipate the need of the patient in advance and take
preventive rather than corrective measures.
• Improve cardiovascular fitness to overcome creeping disability using
graded aerobic exercises such as swimming, etc.
• Manage muscle spasticity, spasm, and cramps as appropriate
with simple modalities such as moist heat, cold packs etc.
Bulbar Palsy in GB/ALS/Lower Brainstem Lesions

Bulbar palsy or bulbar paralysis, as it is commonly known, refers to
weakness or loss of function of the muscles of tongue, larynx and pharynx.
It occurs due to a disorder of the motor nuclei of some cranial nerves
located in the lower brainstem, caused by tumor, vascular impairment,
and degeneration or due to effect of diseases like ALS or GB syndrome.
The glossopharyngeal and the vagus nerve are the primary sites of
damage, leading to loss of phonation, articulation, movement of the soft
palate, gag reflex, and swallowing. There may be dysphonia or changes
in voice quality, i.e. nasal or hoarse voice. Severe bilateral involvement
may result in loss of cough reflex, frequent aspiration of saliva into the
airway resulting in pneumonia, severe breathlessness and finally
respiratory failure.
Pseudobulbar Palsy
It is a bilateral dysfunction of the cortico-bulbar innervations of the
brainstem nuclei due to an UMN lesion, similar to corticospinal lesions
affecting the function of anterior horn cells. Clinically it presents as a

bulbar palsy, with key distinguishing UMN signs like increased jaw jerk
and snout reflex, i.e. pouting when the lips are tapped. Line of
management is the same in both cases.

• Medical treatment should focus on treating the underlying cause.
• Frequent oro-pharyngeal suctioning should be done to remove saliva
from the bucal cavity and prevent aspiration.
• Naso-gastric tube (Ryle’s tube) must be introduced for feeding,
without the risk of aspiration.
• Patient should be propped up on bed at 30-45 degrees of inclination
and positioned in high side-lying position.
• The patient may be intubated to keep an unobstructed airway and
mechanically ventilated in case of respiratory failure.
• The role of physiotherapy is mostly passive, being limited to
maintenances of airway hygiene, prophylactic positioning, prevention
of DVT, pressure sores, and joint contractures.
Common Entrapment Neuropathies (Pinched Nerve Syndrome) and

their Management
The peripheral nerves are actually bundles of millions of nerve fibers
encased in an outer sheath that leave the spinal cord and branch to their
target muscles to make them move or go to the skin to provide sensation.
In simple terms, each individual fiber is like a microscopic water hose.
The outer part of the hose is the nerve membrane, upon which a nerve
impulse, which is a static electrical charge, can travel from the brain to
the distal most part of the nerve. The inside of the nerve transports fluid
from the nerve cell body to nourish and replenish the lower part of the
nerve fiber. If a nerve gets “pinched” the flow of this life giving fluid, up
and down the inside of the hose is reduced or blocked. Eventually the
membrane starts to loose its ability to transmit the nerve impulses and
the nerve fiber may eventually die. When enough fibers stop working,
the skin may feel numb or a muscle may not contract.
• A nerve can be pinched as it leaves the spine, at the lateral foramen,
(radiculopathy) by a herniated disc or by osteophyte as in case of
cervical or lumbar spondylosis.
• When one has a pinched nerve in the low back or neck, pain is
usually perceived as radiating down the leg or arm along the
distribution of the nerve.
• Muscle spasm commonly accompanies pinched nerves and can be
quite painful.
• Sometimes, nerves can be pinched and the only symptoms may be
weakness in muscles without any pain or loss of sensation, e.g. Bells
palsy or vice versa, e.g. carpal tunnel syndrome.
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A pinched nerve may be treated with medication, physical therapy,

cortisone injection or surgery. All of these aims to improve the room
available for the nerve by either shrinking swollen tissue around the
nerve, mobilizing the nerve through scar tissue that may have built up
around it from chronic inflammation, or by removing the disc or bone
spurs pressing upon it. Following are some examples of common
entrapment neuropathies encountered in clinical practice.
Sciatica Sciatic Nerve Compression

Sciatica is not a disease or a condition, but a set of symptoms caused by
irritation and/or compression of the sciatic nerve. If the sciatic nerve is
irritated, it causes intense pain along the nerve pathway, extending from
the buttocks to the toes. If the nerve is compressed by bulging or herniated
disc or tumor, symptoms may include a loss of reflexes, weakness and
numbness besides severe pain. Sciatic nerve pain can make everyday
activities such as walking, sitting and standing very difficult. Although
very painful, it is rare for the sciatica to cause permanent nerve damage.
Most sciatic pain syndromes resulting from inflammation usually get
better within a few weeks.
Symptoms of Sciatica
• Pain in the rear or leg that is worse when sitting.
• Burning or tingling down the leg, particularly on straight leg raising.
• Weakness, numbness or difficulty moving the leg or foot.
• A constant pain on one side buttocks and posterior aspect of upper
thigh.
• A shooting pain that makes it difficult to stand up straight and this
makes the patient lean towards the affected side. This is known as
sciatic list.
Sciatica usually affects only one side lower limbs. Often, the pain
extends from the lower back all the way through the back of the thigh
and down through the leg, foot or toes.
What Causes Sciatica?

Any condition that causes irritation to the sciatic nerve can cause sciatica.
In many cases, sciatica is caused by pressure from a herniated or slipped
or ruptured disc.
Additional causes of sciatica include:
• Lumbar spinal stenosis or narrowing of spinal canal in the lower
back.
• Degenerative disc disease or breakdown of discs between the
vertebrae.
• Spondylolisthesis, a condition in which one vertebra slips forward
over another.
• Pregnancy.
Factors that may make back pain worse include being overweight, wearing
high heels, or sleeping on a mattress that is too soft.
How is Sciatica Diagnosed?

In diagnosing sciatica, one should take the history and perform an
examination of the back, hips, and legs in order to test for muscle strength,
flexibility, sensation, and reflexes, along with:
• X-rays
• MRI scans
• CT scans
• Nerve conduction studies.
General Principles of Treatment

Treatment for sciatica focuses on relieving pressure and inflammation.
Typical treatments include:
• Non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, oral
steroids, or epidural steroid injections help to relieve inflammation.
• Epidural steroid injections where steroids, with their strong anti-
inflammatory effects, are delivered at the origin of the inflamed sciatic
nerve roots.
• Physical therapy usually starts after adequate pain control and has
an essential role both for the acute episode as well as long-term
avoidance of further episodes.
• Surgery for sciatica may be warranted if the sciatic nerve pain is
severe and has not been relieved with appropriate physical or medical
treatments, particularly with any symptoms of progressive lower
extremity weakness, loss of bladder or bowel control.
Acute spinal nerve pain may require more aggressive types of treatment.
Combination of therapies usually gives maximum pain relief, which may
include:
• Chiropractic medicine providing many conservative, non-invasive
and drug-free therapies to reduce sciatic nerve symptoms.
• Stronger medication like a more potent NSAID, a muscle relaxant
and/or anti-depressant medication. Certain anti-seizure and anti-
depressant medications are effective in blocking pain messages sent
to the brain. Some of these drugs may enhance the body’s production
of natural pain killers—endorphins.
• Epidural steroid injection, a type of spinal injection that places
corticosteroid near spinal nerve roots. Steroids reduce inflammation
and can help to ease back and leg pain. An epidural steroid injection
may provide pain relief for several months or longer.
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Physical therapy and rehabilitation include electrotherapy and therapeutic
exercises customized to meet the patient’s individual needs.
Physiotherapists work one-on-one with the patient to reduce pain, increase
flexibility, and build strength.
• Electrotherapy includes application of intermittent spinal traction,
SWD, ultrasound, trans-cutaneous electrical stimulation (TENs),
Interferential therapy (IFT) and cold/heat therapies. Such therapies
usually are administered to reduce pain and concurrent muscle spasm,
before exercise and movement therapies.
• Therapeutic exercise helps the patient to increase flexibility, spinal
range of motion, and build a stronger body. Patients are urged to
continue a regular flexibility and strengthening program at home.
• Manual techniques like myofascial release or deep tissue massage
are very effective in reducing tenderness at the trigger points.
• The physical therapist should provide an easy-to-follow plan to enable
continued progress outside of the rehab facility. In addition, exercise
enhances the production of endorphins. Endorphins help to reduce
pain and improve mood.
• A structured physical therapy program should also educate the patient
about proper posture and body mechanics, which help to prevent
recurrence of sciatica.
Instruction to Patient on Self-care

Most patients with sciatica can be helped by self-care. Some of these self-
help measures include:
• Being aware of and avoiding activities or movements that trigger or
aggravate sciatica. Avoid activities that require bending forward at
the waist or stooping.
• When coughing or sneezing, try to stand up, bend slightly backwards
to increase the curve in your spine when you cough or sneeze.
• Avoiding prolonged bed rest. Although sciatica is painful, some
activity is better than none. Inactivity can make symptoms worse.
Lifting Objects
• Avoid lifting objects at all if possible.
• If you must lift objects, do not try to lift large objects or are heavier
than 5 kg.
• Before you lift a heavy object, make sure you have firm footing.
• To pick up an object that is lower than the level of your waist, keep
your back straight and bend at your knees and hips. Do not bend
forward at the waist with your knees straight.
• Stand with a wide stance close to the object you are trying to pick up
and keep your feet firm on the ground. Tighten your stomach muscles
and lift the object using your leg muscles. Straighten your knees in
a steady motion. Don’t jerk the object up to your body.
• Stand completely upright without twisting. Always move your feet
forward when lifting an object.
• If you are lifting an object from a table, slide it to the edge to the
table so that you can hold it close to your body. Bend your knees so
that you are close to the object. Use your legs to lift the object and
come to a standing position.
• Avoid lifting heavy objects above waist level.
• Hold packages close to your body with your arms bent. Keep your
stomach muscles tight. Take small steps and go slowly.
• To lower the object, place your feet as you did to lift, tighten stomach
muscles and bend your hips and knees.
Reaching Overhead
• Use a foot stool or chair to bring yourself up to the level of what you
are reaching.
• Get your body as close as possible to the object you need.
• Make sure you have a good idea of how heavy the object is you are
going to lift.
• Use two hands to lift.
Sleeping
• Select a firm mattress and box spring set that does not sag. If
necessary, place a board under your mattress. You can also place the
mattress on the floor temporarily if necessary.
• If you’ve always slept on a soft surface, it may be more painful to
change to a hard surface. Try to do what’s most comfortable for you.
• Use a back support (lumbar support) at night to make you more
comfortable. A rolled sheet or towel tied around your waist may be
helpful.
• Try to sleep in a position which helps you maintain the curve in your
back (such as on your back with a lumbar roll or on your side with
your knees slightly bent). Do not sleep on your side with your knees
drawn up to your chest.
• When standing up from the lying position, turn on your side, draw
up both knees and swing your legs on the side of the bed. Sit up by
pushing yourself up with your hands. Avoid bending forward at
your waist.
New Technologies for Treating Sciatica and Back Pain

Two as yet unproven minor procedures are available that may help with
the treatment of back pain and sciatica:
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Intradiscal electrothermoplasty (IDET): This procedure involves the

insertion of a needle into the affected disc with the guidance of an X-ray
machine. A wire is then threaded down through the needle and into the
disc until it lies along the inner wall of the annulus. The wire is then heated
which destroys the small nerve fibers that have grown into the cracks and
have invaded the degenerating disc.
Radiofrequency discal nucleoplasty (Coblation nucleoplasty): Nucleoplasty
is similar to the IDET procedure, a needle is inserted into the disc. Instead
of a heating wire, a special radiofrequency probe is inserted through the
needle into the disc. This probe generates a highly focused plasma field
with enough energy to break up the molecular bonds of the gel in the
nucleus, essentially vaporizing some of the nucleus. The result is that 10-
20% of the nucleus is removed which decompresses the disc and reduces
the pressure both on the disc and the surrounding nerve roots.
Carpal Tunnel Syndrome

Carpal tunnel syndrome is caused when the median nerve that extends
from the forearm to the hand, going through a “tunnel” in the wrist
formed by the carpal bones, becomes compressed. This is a bottleneck
area in the wrist through which all of the finger flexor tendons and the
median nerve must pass on to the hand.
Symptoms
When the median nerve becomes compressed, it can cause numbness,
tingling, and pain in the hands. Patient may experience decreased feeling
in thumb, index finger, and middle finger. Mild numbness and faint
tingling may exacerbate to excruciating pain, but generally only burning,
tingling, or numbness in the thumb and first three fingers persist.
Crippling atrophy of the thumb can result. Symptoms are often worse at
night or in the morning. The pain may eventually spread to the arm and
shoulder. Symptoms normally affect only one hand, but may be present
in both.
Cause
Carpal tunnel syndrome (CTS) is a repetitive stress disorder of the median
nerve that develops over time, due to repeated stressful movements of
the hands and wrist. It affects menial workers such as hairstylists,
musicians, writers, drivers, athletes, restaurant servers, and jack hammer
and chain-saw operators.
The occurrence of CTS has greatly increased since the 1980s, when
personal computers came into use. Women between 29 and 62 experience
CTS more often than anyone else.
Physiological causes such as Raynaud’s disease, pregnancy,
hypothyroidism, diabetes, and menopause, inflammatory arthritis or
tendonitis or water retention increase the risk of developing CTS.

Instruction to Patient on Self-care
• As soon as the tingling begins, begin doing some gentle hand
exercises. Rotate the wrist in a circle for 2 minutes. This exercises all
the muscles of the wrist, restores circulation, and gets your wrist out
of the position that usually causes the trouble.
• Raise your hands above your head and rotate your arms while rotating
your wrists at the same time. Also do some neck turns, look over
your right, then left, shoulder. Learn to exercise and relax as you
work.
• Vitamin B6 helps eliminate the problem.
• Eat half a fresh pineapple daily, for 1-3 weeks. The bromelain in it
will reduce swelling and pain.
• Eat only moderate amounts of food containing oxalic acid such as
beets, green peas, spinach, cabbage, and sea fish. Avoid salt and all
sodium rich food, for they promote water retention.
• Try to reduce the impact of repetitive mechanical tasks on your wrists
and hands. If possible, stop all such movements for several days and
see if improvement occurs. If so, try to do these functions less
frequently. If possible, rotate your duties, so you do not do those
repetitive tasks every day.
• Keep your arms close to your body and your wrists straight while
sleeping. If the hand drop over the edge of the bed while sleeping,
the pressure on the median nerve is increased.
• Use a neutral wrist splint at night. This helps keep the wrist straight.
Avoid crepe bandage as this could cut off the circulation.
• If you have to carry something, make the sure the handle is the right
size. If it is too small or large, it could hurt the wrist.
• Use a tool instead of flexing your wrists forcibly. Use the whole hand
and all the fingers when gripping an object. In doing a task, use the
whole arm, not just your wrist. For example, when hammering, swing
your arm rather than just the wrist.
• Maintain good posture while working at the office desk or computer
work station. What is the ideal position? Keep the elbows bent when
typing or writing. Extend the wrist slightly, so that the thumb is
parallel to the forearm and the fingers as if it were holding a pen.
This position keeps the carpal tunnel as open as possible. Place a
wrist pad on the table, just in front of the keyboard.
• Take a break every hour. Shake out your hands ever so often
throughout the day.
Physiotherapy: Goals and Interventions

• UST to carpal tunnel helps relive inflammation and swelling of the
soft tissue in the area.
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• IR laser is also effective in reducing inflammation and pain.

• TENS also has some role in relieving pain.
Surgery
Surgery for carpal tunnel syndrome is typically performed under local
anesthesia at an OPD. After the anesthesia has taken effect, the doctor,
usually an orthopedic or hand surgeon will make an incision on the
volar surface of the wrist and cut the ligament that forms the roof of the
carpal tunnel. This will relieve pressure on the median nerve. The incision
is then closed with stitches. Recovery takes about four weeks, during
which time the patient may have to wear a resting splint to hold the
wrist in neutral position.
Brachial Neuralgia or Neuritis

Brachial neuralgia (BN) is a syndrome of unknown etiology affecting
mainly the lower motor neurons of the brachial plexus and its branches.
BN usually is characterized by the acute onset of excruciating unilateral
shoulder pain, which may sometimes be followed by flaccid paralysis of
shoulder and para-scapular muscles. The syndrome can vary greatly in
presentation and nerve involvement.
Pathophysiology
BN is generally thought to be due to impingement or an inflammatory
reaction of the brachial plexus nerve roots. Axonopathy, with subsequent
wallerian degeneration appears to predominate.
Age: The prevalence is highest in young to middle-aged adults. A male
predominance exists with BN, with a male-to-female ratio ranging from
2:1 to 4:1
Symptoms
One to three hours after falling asleep, there is a sense of pins, needles,
numbness, and pain in one or both hands. The discomfort generally
wakes the person. There may be wasting in the small muscles in the
hands, as well as coldness or swelling. It generally occurs among adults,
not children.
The symptoms can eventually include the lower arm, upper arm,
and even the shoulder, and are generally worse after a day of heavy
lifting. During the day few symptoms are present, unless heavy lifting
occurs.
Pain: Usually localized to the right shoulder region, the pain may be
bilateral in 10-30% of cases. Onset of pain is often sudden and may
follow recent illness, surgery, immunization, or even trauma. Up to two
thirds of cases begin during the nighttime. Intensity of pain is very high
(9+/10) and is maximal at onset. Usually, the pain is described as sharp
or throbbing in nature. Pain usually is constant, but it is exacerbated by
movements of the shoulder. Movements of the neck, coughing, and/or

sneezing usually do not worsen the pain. Intense pain can last a few
hours to several weeks and requires opiate analgesia. Low-grade pain
may persist for up to a year.
Weakness: In some cases, as the pain subsides, weakness becomes
apparent. In most cases, this weakness manifests within about 2 weeks
of onset. Weakness is maximal at onset but can progress over 1 or more
weeks. The supraspinatus, infraspinatus, serratus anterior, and deltoid
muscles are particularly affected, with marked atrophy and wasting, as
well as a deep aching in the affected muscles (Figs 9.1 and 9.2).
Other symptoms include:
Fig. 9.1: The patient is a 43-year-old farmer, shown 6 months after presenting with
severe right shoulder pain and weakness. Note severe wasting of the right
infraspinatus and deltoid and winging of the scapula
Fig. 9.2: This is the same patient as in Figure 9.1. Note again severe
supraspinatus and infraspinatus wasting on the right
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• Numbness may occur, corresponding to the maximal muscle

weakness.
• Phrenic nerve involvement occurs in up to 5% of cases and can result
in significant shortness of breath due to involvement of the
diaphragm.
• In 25-50% of patients, the medical history indicates a viral illness or
vaccination that occurred days or weeks prior to the onset of
symptoms. Rest of the patients may give H/O recent whiplash trauma
of the cervical spine, sudden traction to arm, vigorous exercise etc.
Causes
• This is to the shoulder girdle, what sciatica is to the pelvic girdle.
• Any nerve, originating from brachial plexus and leading to the
shoulder girdle, may be inflamed or pinched as it exits the spine.
• It can be caused by viral infections, overworking of the arms, carrying
excessively heavy weights, slumped posture, and letting the arms
and hands get cold at night with exposure to Air conditioners.
• In some cases there may be an abnormality in the transverse process
of the seventh cervical vertebrae, known as cervical rib.
• The lower branch of the brachial plexus exits from the lower cervical
vertebrae then passes underneath the clavicle and over the enlarged
transverse process of the seventh cervical vertebrae, on into the arm.
This may causes compression of the nerves. This affliction is called
the cervical rib or thoracic outlet syndrome. It occurs more often in
younger people, and produces pain or numbness soon after heavy
lifting, wearing a heavy coat, etc. The symptoms occur in the day,
not at night.
Assessment
• Due to the extreme pain, physical examination of brachial neuralgia
may be difficult in acute stage.
• Typically, the patient holds the affected arm supported by the
uninvolved arm in adduction and internal rotation.
• Atrophy of the affected muscles becomes noticeable after
approximately 2 weeks.
• Considerable muscle pain and tenderness (myalgia) may be noted
on palpation.
• Passive and active movements of the shoulder and scapula result in
significant increase in pain.
• Movements of the neck are relatively pain-free.
• Muscle strength in affected muscles often is reduced to Grade 2 or
less on the MRC grading scale.
• Reflexes may be reduced or absent, depending on which nerves are
involved.
• Sensory loss is not prominent but may be detectable, depending on

the specific nerves affected (in particular, loss of axillary nerve
sensation).
Investigations
• MRI or CT scan of cervical spine should be considered initially to
rule out cervical radiculopathy (particularly C5/C6) and impingement
due to cervical rib.
• MRI of the brachial plexus can help to rule out carcinomatous
infiltration, if clinically indicated.
• A shoulder radiograph may be indicated to rule out shoulder
subluxation.
Other Tests
• Electrodiagnosis should be considered to confirm neuropathic
diagnosis and to rule out various other conditions, e.g. amyotrophic
lateral sclerosis, as well as for specific localization. Loss of sensory
and motor amplitudes with relatively normal conduction velocity is
frequent after approximately 1 week. Needle electromyogram (EMG)
shows denervation potentials (fibrillations, positive sharp waves, and/
or motor unit potential changes) in affected muscles 2-3 weeks after
onset; however, clinically uninvolved muscles also may show
abnormalities. Approximately 50% of patients with unilateral clinical
involvement demonstrate bilateral EMG abnormalities.

• Tips to Patients
– Keep the hands and arms warm at night.
– Improve the diet. A good, nourishing diet which will build the
nerves and bones is important. Raw green vegetables are needed,
along with daily vitamin/mineral supplements.
– Maintain an ongoing exercise program, to strengthen the muscles
of the shoulders and arms and improve the posture: arm lifts,
neck exercises, shoulder shrugs, horizontal upper trunk push-
ups, etc. Also helpful: swimming, ball throwing, and similar
activities.
– Avoid heavy lifting. When you have to lift, shrug first, and remain
in a semi-shrugged position while you lift. This will ward off
nerve compression.
• Physical therapy (PT) should be focused on the
– Maintenance of full range of motion (ROM) in the shoulder and
other affected joints. Passive range of motion (PROM) and active
range of motion (AROM) exercises should begin as soon as the
pain has been controlled adequately, followed by regional
conditioning of the affected areas.
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– Strengthening of the rotator cuff muscles and scapular

stabilization may be indicated.
– Passive modalities, e.g. dry heat, cold, transcutaneous electrical
nerve stimulation [TENS]) may be useful as adjunct pain relievers.
– Surged faradic stimulation, if started early, to susceptible muscles
can slow down or prevent wasting,
• Occupational Therapy: Functional conditioning of the upper extremity
may be helpful. Assistive devices may be used, depending on the
particular disabilities present. The occupational therapist (OT) may
be involved in maintaining ROM and strengthening, particularly if
the hand and wrist are involved.
• Medical Issues: Treatment is largely symptomatic, and opiate analgesia
often is necessary in the initial period. Steroids may be prescribed
with indifferent results.
Prognosis
Eighty percent of patients recover functionally by 2 years; 90% recover
functionally by 3 years. Bilateral disease has a less favorable outcome
than unilateral disease. Lower trunk lesions have a less favorable
prognosis than upper trunk lesions.
Bells Palsy (VIIth Cranial Nerve Palsy)

Other Names: Facial Palsy
It is a LMN type lesion resulting in paralysis of muscles of facial
expressions. Only one side of the face is generally affected.
Symptoms
• Onset is sudden. Pain and ache behind the ear are the first symptoms.
The paralysis may reach its peak within few hours or days.
• There is pain, weakness, and a sensation of pricking, tingling, or
creeping on the skin of the face.
• Muscles of one side of the face are paralyzed, resulting in deviation
of the facial midline towards the sound side due to the unopposed
pull of intact muscles.
• There may excessive salivation and flowing of tears from the affected
eye.
• In most cases the recovery is spontaneous and complete within few
weeks.
Cause
It is be caused by an acute inflammatory process due to viral infection,
exposure to cold or a decayed tooth resulting in compression of the facial
nerve at the point it leaves the bone.
Treated properly, there can be as much as 80% chance of significant

recovery in those with partial palsy and 75% of those with complete
palsy recover with no treatment of any kind. But severe taste impairment
and/or reduced tear forming in the eyes are bad signs, especially in
older people.
Bell’s palsy can occur in anyone at any age, but most frequently
occurs between 20 and 40. The younger the person, greater the chance of
a full recovery.

• Medical management: Tapered dose of cortico-steroid (Prednisolone)
is often given to reduce the inflammation, but it has negative side
effects. Vitamin B12 @ 1000 mcg/day, for a total of 20,000 mcg;
calcium @ 2,000 mg/day, magnesium @ 800 mg/day, and essential
fatty acids are the medications recommended for bell’s palsy.
• Make sure that the patient does not sleep so that a current of cold air
from an AC is blowing across the uncovered face while the rest of
the body is covered under the blankets. When this happens, the
chilled part does not receive adequate blood supply. A nerve in the
face or neck can become chilled and cause problems.
• Apply moist heat with a steaming towel to the face twice a day, for
20 minutes at a time, to relieve pain and tenderness. Follow with
gentle massage to face with both backward and upward strokes from
the tip of the chin up to the temples. UST may be applied to the
tender points located just in front or behind the ear.
• Splash cool clean water to the affected eye 4 times a day, to keep it
moist and free from dust. Wearing sunglasses will reduce evaporation
from that eye. Occasionally ask the patient to close that eye with the
finger, to rest it. Wear an eye patch at night to protect it.
• A few days later, as the muscles begin functioning again, the patient
should be taught to exercise his facial muscles: Standing before a
mirror, wrinkle the forehead, close the affected eye, purse the lips,
move the mouth to one side and then the other, blow out the cheeks,
and try to whistle. Chewing gum helps in improving the tone of
facial muscles.
• Electrical stimulation with IG current may be given to the facial
muscles, starting after the nerve irritation has ceased. The purpose of
ES is exercising the delicate muscles of the face, to maintain its
nutrition and physiological properties of the paralyzed muscles, till
the nerve regains function. In the beginning the muscles may respond
to long duration IG impulses (100 msec). As the neural status improves
the muscles will require progressively lower duration impulses to
evoke a response, till a time comes when they begin to respond to
impulses of 1 msec or less. At this stage, the stimulating current may
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be changed to faradic type of current. The patient may be asked to

attempt volitional contraction along with surged faradic stimulation.
This will lead to faster gain of power in these muscles.
• In chronic cases, if recovery has not started in more than 3 months
of onset (as seen in Ramsay Hunt Syndrome), a facial support splint
may be provided to prevent the sound side muscles pulling the
paralyzed side away from the midline, accentuating the facial
asymmetry.
Common Peripheral Nerve Injuries and their Management
Erb-Duchenne Palsy Lesions of the Upper Brachial Plexus
Lesions of the upper brachial plexus are usually the result of a traction
injury to the upper extremity, tearing the C5 and C6 roots of the brachial
plexus away from the spinal cord during birth (Fig. 9.3). This usually
occurs in infants during a forceps delivery and is called Obstritic Brachial
Plexus Injury (OBPI) and occasionally in adults following a fall on or a
blow to point of the shoulder.
The lateral rotation of the humerus is lost and the arm remains
medially rotated, due to the suprascapular nerve lesion leading to paralysis
of supraspinatus, infraspinatus and teres minor muscles.
Due to the lesion of musculoskeletal nerve, there is loss of flexion of
forearm, supination of the forearm and weakness of flexion of shoulder,
due to involvement of biceps brachii and brachialis (Fig. 9.4).
Abduction of shoulder is lost due to the lesion of the axillary nerve
which causes paralysis of deltoid.
Klumpke’s Palsy: Lower brachial plexus lesion

Lower brachial plexus lesions are usually injuries by excessive abduction
of the arm as a result of someone clutching for an object when falling
from a height. Such injury results in damage to the T1 segment, which
innervates those fibers of median and ulnar nerve that supply the small
muscles of the hand, i.e. the interossei and lumbricals (Fig. 9.5). The
hand has a clawed appearance due to hyperextension of the metacarpo-
phalangeal joints and flexion of the inter-phalangeal joints. The extensor
digitorum is unopposed by the lumbricals and interossei resulting in
hyperextension of the metacarpo-phalangeal joints. Since the action of
flexor digitorum superficialis and profundus are unopposed by the
lumbricals and interossei, the middle and terminal phalanges are flexed,
leading to a claw hand. There is also sensory loss along the medial side
of the forearm, hand and medial 2 fingers. Lower brachial plexus lesions
may also be the result of malignant metastases from the lungs in the
lower deep cervical lymph nodes and an aberrant cervical rib.
Fig. 9.3: Lesions of the upper brachial plexus involves injury to the upper
extremity, tearing the C5 and C6 cervical roots
Fig. 9.4: The typical posture of the upper limb seen in Erbs
palsy is called the ‘Policeman’s tip’
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Fig. 9.5: Lower brachial plexus injury
Goals and Interventions in Brachial Plexus Injuries

• Regular physical therapy and occupational therapy play an important
role in rehabilitation of all types of brachial plexus lesion.
• Early intervention is the key to successful recovery of some function
in Erb’s palsy, particularly if the onset is due to peri-natal trauma,
i.e. traction injury to the brachial plexus during forceps delivery.
Thankfully this mode of injury is now relatively rare due to advent
and popularity of cesarean sections.
• In an infant, the most important treatment is the Prophylactic
Positioning and Passive Range of Motion (PROM) exercises that
parents can do at home. This must be demonstrated carefully by the
therapist.
• Airplane splints is a popular choice for acute brachial plexus injuries,
however no study has been done to demonstrate it’s superiority over
simple shoulder sling for resting the injured plexus.
• Surgical intervention may be necessary if spontaneous recovery is
not fast and complete enough. There has been a great deal of
discussion regarding the timing of surgical intervention in infants.
• At one end of the spectrum, those with an aggressive approach to
treating this injury favor operating at the age of three months if there
has been no sign of biceps and deltoid contraction. More conservative
authors have suggested that one can wait for recovery until the fifth,
sixth or even ninth month of life before surgical intervention is
recommended.
• When there is global lesion, possibly with Horner’s syndrome, most
authors favor earlier reconstruction at the age of 1-3 months. There
is little hope of spontaneous recovery in global lesions and early
timing of the surgery can lead to better hand function.
• In the adult version, physiotherapy in the form of electrical
stimulation, massage, bio-feed back of the paralyzed muscles and
corrective splinting play an important role.
• Serial MMT is necessary to monitor the progress and assess the
effectivity of the intervention.
Deformities
Sequelae deformities are due primarily to muscle imbalance and
contractures in the upper extremity. The most common sequelae
deformities may include:
1. Subluxation of shoulder due to imbalance in the muscles of the
shoulder area.
2. Forearm deformities – pronation or supination contractures,
dislocations of the radial head.
3. Winging of the scapula.
4. Hypoplasia of the bones in the upper extremity.
5. In OBPI limb length differences between the upper extremities may
be observed.
Some of these deformities may need surgical correction.
Aims of Surgical Repair of Brachial Plexus

• Priorities are for functional improvement: elbow flexion, shoulder
abduction, finger flexion, wrist extension, shoulder rotation.
• Proximal muscle gain power can occur after careful rehab. Distal
recovery is much more difficult to achieve.
Preoperative Workup
• MRI, CT-myelogram
• EMG: documents the degree and pattern of denervation, and any
signs of reinnervation.
Root Avulsion
• No spontaneous recovery is expected. Grafting not yet feasible
(experimental). Most treatment is by nerve transfer.
• Intra-operatively some dissect the nerve root into the foramina to
prove avulsion.
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Neurotization (Nerve Transfer)

• Spinal accessory nerve (CN11) works best for suprascapular nerve,
less for axillary or musculotaneous nerves (where interposed grafts
are necessary).
• Intercostal-musculotaneous nerve restores biceps in 70%.
• Medial pectoral-musculo cutaneous nerve works if these branches
are substantial.
• Oberlin procedure: fascicle of ulnar nerve co-opted to distal
musculocutaneous nerve.
Preferred by some to restore biceps in patients presenting over
8 months after injury.
Thoracic Outlet Syndrome

Thoracic outlet syndrome is actually a collection of syndromes brought
about by abnormal compression of the neurovascular bundle by bony,
ligamentous or muscular obstacles between the cervical spine and the
lower border of the axilla. The neurovascular bundle which can suffer
compression consists of the brachial plexus plus the C8 and Tl nerve
roots and the subclavian artery and vein (Fig. 9.6).
Signs and Symptoms of Thoracic Outlet Syndrome

It is important to understand that the presenting symptoms listed below
in no way indicate a definitive diagnosis for thoracic outlet syndrome.
Therapists must understand the importance of coupling diagnostic testing
Fig. 9.6: The bony, ligamentous, and muscular obstacles that define the cervico-
axillary canal or the thoracic outlet and its course from the base of the neck to the
axilla
skills with the patient’s complaints of what hurts and what doesn’t seem
to be working properly.
Vascular Symptoms Include

1. Swelling or puffiness in the arm or hand.
2. Bluish discoloration of the hand.
3. Feeling of heaviness in the arm or hand.
4. Pulsating lump above the clavicle.
5. Deep, boring toothache – like pain in the neck and shoulder region
which seems to increase at night.
6. Easily fatigued arms and hands.
7. Superficial vein distention in the hand.
Neurological Symptoms Include
1. Paresthesia along the inside forearm and the palm (C8, T1

dermatome).
2. Muscle weakness and atrophy of the gripping muscles (long finger
flexors) and small muscles of the hand (thenar and intrinsics).
3. Difficulty with fine motor tasks of the hand.
4. Cramps of the muscles on the inner forearm (long finger flexors).
5. Pain in the arm and hand.
6. Tingling and numbness in the neck, shoulder region, arm and hand.
What Causes the Neurovascular Compression at the Thoracic Outlet?

Compression occurs when the size and shape of the thoracic outlet is
altered. The size of the outlet can be altered by exercise, trauma,
pregnancy, a congenital anomaly, a bony exostosis, postural weakness or
changes. Principal anatomical causes are:
Anterior scalene tightness: Compression may occur in the inter-scalene
space between the anterior and middle scalene muscles; probably from
muscle spasm due to nerve root irritation, cervical spondylosis or facet
joint inflammation.
Costo-clavicular approximation: Compression may occur in the space
between the clavicle and the first rib or between the muscular and
ligamentous structures in the area, probably due to postural deficiencies
or from carrying heavy objects.
Pectoralis minor tightness: Compression may occur beneath the tendon
of the pectoralis minor under the coracoid process, which may result
from repetitive movements of the arms above the head (shoulder elevation
and abduction).
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What Sorts of Activities are likely to Cause these Compression Syndromes?

Thoracic outlet syndrome has been described as occurring in a diverse
population. It is most often the result of poor or strenuous posture but
can also result from trauma or constant muscle tension in the shoulder
girdle.
• Static postures such as those sustained by assembly line workers,
cash register operators, students, e.g. those who do needle work often
result in a drooping shoulder and forward head posture. This position
of the shoulders and head is also indicative of poor upper body
posture. Middle aged and elderly women who suffer from
osteoporosis often display this type of posture as a result of increased
thoracic spinal kyphosis.
• Carrying heavy loads, such as briefcases and shoulder bags, can also
lead to neurovascular compression. Humans are not well adapted as
beasts of burden and heavy loads hung form the shoulders and arms
can stress the supporting structures of the shoulder girdle which is
basically suspended by the clavicle and all of the component ligaments
and muscles.
• Occupations, which require repetitive overhead arm movements, can
also produce symptom of compression. Electricians, painters and
plasterers may develop hyper-abduction syndrome. Compression of
the neurovascular structures also occurs in athletes who repetitively
hyper-abduct their arms. Swimmers, volleyball players, tennis players
and baseball pitchers may suffer compression of the neurovascular
structures as well.
• Compression of these structures may also be caused by stretching or
micro-trauma to the muscles that support the scapula.
• Some people are born with an extra rib right above the first rib. Since
this intersection of nerves, vessels, muscles, bones and ligaments is
already quite narrow one can imagine what the presence of an extra
rib in the region might do.
• A fibrous band extends from this cervical rib to the first rib causing
an extra bend in the lower part of the brachial plexus may produce
a compression in this region.
Assessment
• Make a list of all of the symptoms, which seem to be present even
if the sensations are vague.
• Make a note of what activities and positions produce or alleviate the
symptoms and the time of day when symptoms are worst.
• Also, note when the symptoms first appeared. This list is important
and should also include any questions the patient may have. Due to
overlapping in terms of symptoms it’s difficult to make a definitive
diagnosis; this is why a list is so important.
Certain diagnostic tests have been designed which are very useful
for examination of the thoracic outlet. These tests involve maneuvers of
the arms and head and can help the practitioner by providing information
as to the cause of the symptoms and help in designing an approach to
treatment. These tests, accompanied by a thorough history help in ruling
out other causes which may produce similar symptoms. The other causes
of similar symptoms may include pancoast tumor, neurofibromas, cervical
spondylosis, cervical disk herniation, carpal tunnel syndrome and cubital
tunnel syndrome.
Here are a few commonly applied provocation tests used in the
diagnosis of thoracic outlet syndrome. These tests may or may not
momentarily reproduce symptoms but as was mentioned earlier are
important in ruling out other causes which may produce similar
symptoms (Figs 9.7 to 9.11).
Figs 9.7A and B: EAST test or “Hands-up” test. The patient brings his arms up as
shown with elbows slightly behind the head. The patient then opens and closes his
hands slowly for 3 minutes. A positive test is indicated by pain, heaviness or profound
arm weakness or numbness and tingling of the hand
Fig. 9.8: Adson or scalene maneuver. The examiner locates the radial pulse. The
patient rotates their head toward the tested arm and lets the head tilt backwards
(extends the neck) while the examiner extends the arm. A positive test is indicated
by a disappearance of the pulse
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Fig. 9.9: Costoclavicular maneuver. The examiner locates the radial pulse and
draws the patient’s shoulder down and back as the patient lifts their chest in an
exaggerated “at attention” posture. A positive test is indicated by an absence of a
pulse. This test is particularly effective in patients who complain of symptoms while
wearing a back-pack or a heavy jacket
Fig. 9.10: Allen’s test. The examiner flexes the patient’s elbow to 90 degrees while
the shoulder is extended horizontally and rotated laterally. The patient is asked to
turn his head away from the tested arm. The radial pulse is palpated and if it
disappears as the patient’s head is rotated the test is considered positive
Figs 9.11A and B: Provocative elevation test. This test is used on patients who
already present with symptoms. The patient sits and the examiner grasps the
patient’s arms as shown. The patient is passive as the shoulder girdles are elevated
forward and into full elevation. The position is held for 30 seconds or more. This
activity is evidenced by increased pulse, skin color change (more pink) and increased
hand temperature. Neurological signs go from numbness to pins and needles or
tingling as well as some pain as blood flow to the nerve returns. Similar to what is
felt after an arm “falls asleep” and circulation returns
Goals and Interventions in TOS
• Once a diagnosis is decided, every effort is made for a conservative

treatment approach consisting mainly of physiotherapy, medications
and ergonomic advice.
• Should symptoms persist over 3 or 4 months or if there is intractable
pain, vascular loss or neuralgic loss, then surgery should be
considered.
• Surgery is consistent in relieving pain but muscle weakness and
atrophy do not usually improve significantly.
• Conservative treatment usually includes local heat and a program
which address postural retraining, shoulder strengthening and
stretching exercises. The practitioner will create a treatment program
specific to the presenting symptoms. Below are a few self-stretching
exercises. All of these exercises should be performed slowly and
carefully. Each position is assumed smoothly to the point where a
stretch is felt intensely but with no pain. There should be no bouncing
in any of these positions. Hold the stretch for 30 seconds and then
gently and slowly release it. Wait 10 seconds and repeat the stretch
3-5 times. If the stretches increase the symptoms do not continue.
(Figs 9.12 to 9.17).
Figs 9.12A and B: A. Stretching the muscles at the back of the neck. Using the
arm, which is on the side of the tightness, assume the position, which is
demonstrated in the picture above, the head turning away from the pain. The hand
behind the head helps stabilize the head position. Take a deep breath, exhale
slowly while keeping the elbow where it is against the wall.
B. Another method for stretching the back of the neck can be accomplished by
sitting down in a sturdy chair. Turn the head away from the tight side, look down
until a slight stretch is felt. Reach down with the hand on the tight side and hold
onto the chair. With the other hand pull the head forward, gently
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Figs 9.13A and B: Stretching the chest muscles. Above-sit in a sturdy backed
chair with the hands clasped behind the back of the head as demonstrated. Bring
the elbows back as far as possible during a slow, deep breath in. While exhaling
slowly bring the elbows together letting the head bend forward slightly
Fig. 9.14: Stretching the chest muscles. Fig. 9.15: Stretching the muscles and
Another method for stretching the chest other soft tissue on the side of the neck.
area is to stand facing a corner or a Sit in a sturdy chair. Hold the underside
doorway with the arms in a “U” or a “V” of the chair with the hand of the tight
against the wall or door posts (see above side. Bend the head away from the tight
image). With the knees bent lean slightly side and turn the face toward the tight
forward from the ankles side. It won’t go very far. Lean away from
the arm holding onto the chair and reach
with the opposite arm to the top of the
head and gently pull to increase the
stretch
Figs 9.16A to C: Stretching the shoulder and the chest muscles

A. There are three exercises for this region: Sit in a sturdy chair next to a table
with the arm placed as demonstrated, palm down. Slide the arm forward while
bending at the waist as far as is possible without pain. Eventually the head
should be in level with the side of the table.
B. Stand with back to the table and grasp the edge with the fingers facing forward.
Bend the knees and lower the body allowing the elbows to bend. Let the knees
do the work.
C. Sit on a firm and sturdy surface with the hand of the tight side grasping the
edge. Lean away slowly.
These stretches are not cures. They may help in alleviating some of
the symptoms of thoracic outlet syndrome but as with any exercise
program one should always consult a physician before beginning
particularly when symptoms persist for any length of time.
Other physiotherapy measures include application of ultrasound
therapy at the thoracic outlet tender points and/or TENS/IFT along the
track of radiation of pain in the arm.
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Figs 9.17A and B: Mobilization of the first rib. Use a large bath towel and grasp it
at opposite corners. Sling it across the shoulder of tightness and bring both ends
across to the opposite hip or waist. With the arm on that side pull gently downward
then release slowly
Scapular bracing exercises, such as elevation of both upper girdles

against resistance as indicated for offloading the neurovascular bundle
in the thoracic outlet. Application of cervical traction is usually counter
productive.
Winged scapula: Long Thoracic Nerve Lesion (Nerve to Serratus

Anterior)
Blows or pressure in the posterior triangle of the neck or during a radical
mastectomy may result in winging of scapula due to injury to this nerve.
The serratus anterior muscle pulls the medial border of the scapula
to the posterior thoracic wall and stabilizes it there (Fig. 9.18). A way to
check to see if this muscle is working properly is to have a person push
against a wall. On the side that has the lesion of the nerve, the medial
border of the scapula will be pushed away from the thoracic wall, and
protrude like a wing would. Thus, the name ‘winged scapula’. Nothing
much can be done with physiotherapy.
Wrist Drop: Radial Nerve Lesion

• If the radial nerve is compressed/injured, the final results will depend
on where along its path it is injured. The most complete injury is one
that occurs in the axilla, usually caused as a result of poor positioning
of the axillary pad of a crutch, inferior shoulder dislocation or fractures
of the upper portion of the humerus.
• The high radial injury results in paralysis of the triceps, anconeus
and the long extensors of the wrist. The patient is unable to extend
Fig. 9.18: Winged scapula
the elbow joint, the wrist joint and the fingers. Even though the
brachioradialis and supinator muscles are paralyzed, supination can
still be performed. Do you know by which muscle this is done?
• The radial nerve may be injured as it passes along the spiral groove
of the humerus following factures of the humerus. The nerve may
also be injured due to prolonged pressure on the posterior-inferior
aspect of the arm, draped over the edge of a hard-back chair in a
drunken state or the arm hanging out and pressing against edge of
the operating table in an unconscious patient. This mode of injury to
the radial nerve is called “Saturday night palsy”. The branches to the
triceps are spared in this injury so that extension of the elbow is
possible (Fig. 9.19).
Fig. 9.19: Wrist drop. The long extensors of the forearm are paralyzed and this will
result in a “wrist drop”. This is a very disabling injury, since a person can’t flex the
fingers strongly for gripping an object (loss of tenodesis action). There is a small
loss of sensation over the dorsal surface of the hand and the dorsal surfaces of the
lateral three fingers

• Conservative management includes static cock up/resting splint in
the acute stage to give rest to the paralyzed wrist and finger extensors.
(Fig. 9.20).
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Nerves 283
Fig. 9.20: Static cock up/resting spint
• Application of interrupted galvanic stimulation to the extensors of

wrist and fingers in the paralytic stage to maintain physiological
properties of these muscles.
• As the muscle start getting re-innervated one can switch to Surged
Faradic stimulation in conjunction with active wrist and finger
extension exercises to gain power and function.
• If recovery does not occur within three months of conservative
management, a dynamic cock up splint may be considered to prevent
contracture and retain active participation of finger flexors for hand
grip (Fig. 9.21).
Fig. 9.21: Dynamic cock up splint to assist extension at the wrist
Claw Hand: Ulnar Nerve Lesion

The ulnar nerve is a branch of the medial cord of the brachial plexus
from C8 and T1 segments of the spinal cord. It passes into the anterior
compartment of the forearm after passing behind the medial epicondyle
of the humerus. It is at this site that the nerve can be injured following
fractures of the medial epicondyle. The muscles paralyzed are the flexor
carpi ulnaris, medial half of the flexor digitorum profundus, medial two
lumbricals, all interossei and the adductor pollicis (Fig. 9.22). Principle of
physiotherapy management is the same in radial nerve injury. Splintage
may be prescribed to prevent hyperextension at MCP and flexion at PIP
and DIP of medial two fingers (Fig. 9.23).
Figs 9.22A and B: Ulnar claw hand. The appearance of the hand is indicative of
the muscles involved. The thumb is abducted and extended with the distal phalanx
flexed. The first two fingers are fully extended with a slight flexion of the distal
phalanges. The medial two fingers are hyperextended at the metacarpophalangeal
joints but flexed at the distal phalangeal joints. The hand resembles a “claw” and is
called a claw hand
Figs 9.23A to C: Static splints for ulnar nerve injury. Ulnar claw hand corrected by
static ulnar splints that maintains the MCP of the medial two fingers in flexion and
the IP joints in extension
Foot Drop
Foot drops usually result from weakness and inadequate contraction of
the dorsiflexors of the ankle, the muscles in the antero-lateral compartment
of the leg, i.e. tibialis anterior, extensor hallux and digitorum longus,
supplied by the common peroneal nerve (Fig. 9.24). As a result the person
has loss of heel strike during the gait cycle and foot slaps to/drags on the
floor during stepping forward while walking. To compensate, a person
may increase the extent of hip and knee flexion during the swing phase
of the gait. Patients with painful sole of the feet or the heel may have a
similar gait but do not have foot drop. Because of the extreme pain
evoked by even the slightest pressure on the feet or the heel, the patient
walks on tip toes as if walking barefoot on hot sand. This type of gait is
called steppage gait (Fig. 9.25).
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Nerves 285
Fig. 9.24: Foot drop. A dropped foot is caused by weakness of the muscle that lifts
the foot up at the ankle (the dorsiflexors-tibialis anterior, EHL and EDL muscle). The
foot drop may be temporary or permanent, typically characterized by steppage gait
Figs 9.25A and B: Steppage gait in foot drop—when the person with foot drop
walks, the foot slaps down onto the floor. To compensate for the toe drop, and to
avoid dragging of toes on the floor, the patient must flex the hip joint excessively,
as if walking upstairs. Individuals with foot drop are unable to walk on their heel
and walk with the normal heel-toe pattern. Correction of foot drop is done most
easily by a static moulded shoe insert AFO (Ankle foot orthosis)
Cause
• Foot drop is most frequently caused by injury to the L5 nerve root.
The L5 nerve is usually injured by a bad L4-L5 disc.
• Occasionally, a foot drop can be caused by an injury to the common
peroneal nerve. The common peroneal nerve is a branch of the sciatic
nerve and can be injured during hip or knee surgery or by a deep

bruise or a bad laceration.
• Foot drop can also be caused by poliomyelitis, amyotrophic lateral
sclerosis (ALS) and multiple sclerosis (MS).
• The cause for foot drop can be determined by history taking and
confirmed by electro diagnosis, MRI, and EMG.
Goals and Intervention

The type of treatment is dependent on the cause of the drop foot. The
underlying disorder must be treated.
• If the cause is a prolapsed disc in lumbar spine impinging on the
sciatic nerve causing symptoms of foot drop, then the herniated disc
should be treated.
• Unstable ankles in foot drop can be stabilized by lightweight splints
and shoes fitted with springs to prevent foot drop, known as
dorsiflexion assisst, while walking (Fig. 9.26).
• Regular exercise under supervision of a physiotherapist is usually
prescribed. Stretching the tendo achilis helps prevent heel cord
tightness, caused by unopposed pull of plantarflexors.
• Electrical stimulation of the dorsiflexor muscles is recommended if
the common peroneal nerve is expected to get back function in near
future.
• The latest treatments include functional electrical stimulation of the
peroneal nerve that lifts the foot during heel strike of the gait cycle.
Such stimulation is given through small stimulators worn by the
patient on the waist belt. Many stroke and multiple sclerosis patients
with foot drop have had success with it.
Fig. 9.26: Foot drop support strap with dorsiflexion assist device in the front of
the ankle joint
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Nerves 287
• Devices have also been designed to regulate walking. An ankle foot

orthosis (AFO) can prevent falls.
• The damaged nerve should, however, be repaired as soon as possible.
If a disc is the problem, it should be corrected immediately. If the
nerve is damaged by a knife wound, repairing it is also urgent. Till
such time the nerve function is not restored, the ankle and foot should
be rested in a static foot drop splint (Fig. 9.27), as a night splint,
particularly during sleeping.
Fig. 9.27: A foot drop night splint
SUMMARY
Peripheral nerves are the most superficial and under protected
components of the nervous system. Being exposed to the vagaries of the
environment, the peripheral nerves are most often susciptible to infections
and inflammations. Further, due to their wide spread network and often
being placed in close proximity of very hard objects like bones these
structures are prone to compression, contusion and laceration, leading to
loss of motor and sensory faculties. However, peripheral nerves are blessed
with capacity for significant recovery and are thus amenable to
conservative and surgical repair, which more often than not, yield
satisfactory results.
Disorders of Balance, Coor-
10 dination and Equilibrium
INTRODUCTION
Human being is the highest primate, the most successful species on the
planet earth. One of the reasons behind his success in the evolutionary
ladder, apart from a large and well-developed brain, is the ability to
stand freely on two feet, leaving the upper extremities free for all sorts
of manipulative activity. This is a mixed blessing, because the two-
legged posture inevitably reduces the base of support on which the
human has to hold the center of mass of his body against the force of
gravity. Any movement of the center of mass away from the base of
support tends to upset the equilibrium, to which a human body adjusts
with rapid and complex interplay of various skeletal muscles during
any static or dynamic situation. The skeletal muscles of posture and
movement are controlled by an array of nervous mechanisms, mediated
through master organs like the cerebellum and the vestibular apparatus,
which renders the posture stable and the movements smooth and
coordinated. Any disorder in these regulatory components of posture
and movement leads to disorders of Balance, Coordination and
Equilibrium. In the following chapter I have detailed the afflictions of
the cerebellum resulting in disorders of balance and coordination under
the section of “Ataxia” and the vestibular disorders under the section
of “Disorders of equilibrium”. Apart from the cause, effect and general
management of these disorders I have also focused on the goals and
interventions of a physiotherapist for treatment of these disorders. Most
of the physiotherapy techniques of assessment and management
discussed herein have developed since the 1990s and are now accepted
world wide as standard operating procedures. A conscious attempt has
been made to empower the patient to participate in the treatment
through notes on “instructions to patient”.
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SECTION 1
ATAXIA-DISORDERS OF BALANCE AND
COORDINATION
INTRODUCTION
Ataxia describes a lack of muscle coordination when one performs
voluntary movements, such as walking or picking up or manipulating
objects. It’s a sign of an underlying condition, not a disease itself. Ataxia
can affect any part and function of the body—such as movements, speech,
ability to focus the eyes and ability to swallow, etc.
Drinking too much alcohol may cause temporary ataxia, affecting
speech, eye-hand coordination and ability to walk. However, persistent
ataxia is usually the result of damage to that part of the brain that controls
coordination of voluntary movements, i.e. the cerebellum. Many
conditions, such as stroke, head injury, tumor, cerebral palsy and multiple
sclerosis may affect the cerebellum causing ataxia (Fig. 10.1). An individual
may also inherit a defective gene that may cause one of many variants
of ataxia.
Treatment for ataxia depends on the underlying cause. Adaptive
devices, such as walkers or canes, might help maintain functional
independence in movement despite the ataxia. Ataxic patients may also
benefit from physical therapy, occupational therapy and speech therapy.
Figs 10.1A and B: MRI at the right shows a normal cerebellum, compared to the
plate at the left showing cerebellar degeneration. Presence of cerebellar
degeneration usually indicates incurable ataxia
SIGNS AND SYMPTOMS

The cerebellum comprises of two ping-pong-ball-sized portions of folded
tissue situated on either side at the base of the brain, near the brainstem.
The right half of the cerebellum is responsible for coordination of
movements occurring in the right side of the body and vice versa.
Ataxia usually results from damage to the cerebellum from disease,

infection or injury. It can develop over time or come on suddenly,
depending on the cause. Signs and symptoms of ataxia include:
• Unsteady walk
• Tendency to stumble
• Slurred speech
• Difficulty with fine-motor tasks, such as eating or buttoning a shirt
• Slow eye movements and inability to focus on an object
• Difficulty swallowing.
CAUSES
The most common cause of ataxia is damage to the cerebellum, which
may be the result of any number of conditions mentioned above. Diseases
that damage the spinal cord and peripheral nerves that connect the
cerebellum to skeletal muscles may also cause ataxia. Major causes for
cerebellar ataxia include:
• Trauma: Damage to the brain or upper end of the spinal cord from
a blow to the head, might occur in a car accident, can cause sudden
onset ataxia, also known as acute cerebellar ataxia.
– Stroke: When the blood supply to a part of the brain is interrupted
or severely reduced, depriving brain tissue of oxygen and
nutrients, brain cells begin to die. If the cerebellum is affected by
the stroke it may cause acute cerebellar ataxia.
– Transient ischemic attack (TIA): Caused by a temporary decrease
in blood supply to a part of the brain, may cause transient loss
of consciousness, coordination and other symptoms. TIA are
temporary, mostly lasting for only a few minutes.
– Cerebral palsy: This is a general term for a group of disorders
caused by damage to a child’s brain during early development;
before, during or shortly after birth; that may affect the child’s
ability to coordinate body movements.
– Multiple sclerosis (MS): MS is a chronic, potentially debilitating
disease that affects the central nervous system, sometimes affect
the cerebellum.
– Chickenpox: Ataxia can be an uncommon complication of
chickenpox and other viral infections. It may appear in the healing
stages of the infection and last for days or weeks. Normally, such
ataxia resolves completely over time.
– Paraneoplastic syndromes: These are rare, degenerative disorders
triggered by the immune system’s response to a cancerous tumor
(neoplasm), most commonly from lung, ovarian, breast or
lymphatic cancer. Ataxia may appear months or years before the
cancer is diagnosed.
– Tumor: A growth on the brain, malignant or benign, can damage
the cerebellum.
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– Toxic reaction: Ataxia is a potential side effect of certain

medications, such as phenobarbital and sedatives such as
benzodiazepines. Alcohol and drug intoxication heavy metal
poisoning, such as with lead or mercury and solvent poisoning,
such as with paint thinner, also can cause ataxia.
Hereditary Ataxias
Some ataxias are hereditary. In these conditions, a defect in a certain
gene produces abnormal proteins. The abnormal proteins hamper the
ability of nerve cells, primarily in the cerebellum and spinal cord, to
function properly and cause them to degenerate over time. As the disease
progresses, coordination problems worsen.
One can inherit a genetic ataxia in different ways. Genes occur in
pairs, one receives half of each pair from the mother, and the other half
from the father. Genes are either dominant or recessive, with the effects
of a dominant gene in a pair taking precedence over the effects of the
recessive gene.
If the dominant gene carries a defect, that mutation will control the
gene’s expression, sometimes resulting in disease. Diseases that are caused
by dominant gene mutations are called autosomal dominant disorders.
Some mutations that cause ataxias occur in recessive genes. Diseases
that are caused by recessive gene mutations are called autosomal recessive
disorders. For one to inherit such a disorder, both parents must carry the
associated recessive genetic mutation, even if they don’t have the disorder
themselves (silent mutation). In this case, they are only “carriers” of the
disorder, so there may be no apparent family history of the disorder.
Different gene defects cause different types of ataxia, most of which
are progressive in nature. Each type causes poor coordination, but each
has specific signs and symptoms by which they can be identified.
Ataxia may result from either an autosomal recessive disorder or an
autosomal dominant disorder.
Autosomal Recessive Ataxias

These include:
• Friedreich’s ataxia: This neurological disorder involves damage to
the cerebellum, spinal cord and peripheral nerves. It was once believed
to be a childhood disease, with onset occurring before age 15.
However, with the identification of the gene defect that causes the
disease, experts now recognize that there is an adult-onset Friedreich’s
ataxia. In most cases, however, signs and symptoms appear between
the ages of 5 and 15. The rate of disease progression varies. If one has
Friedreich’s ataxia, however, one is likely to rely on a wheelchair by
30s, and the life span may be affected.
The first indication generally is difficulty walking (gait ataxia).

The condition typically progresses to the arms and trunk. Muscles
weaken and waste away over time, causing deformities, particularly
in the feet, lower legs and hands. Other signs and symptoms that
may develop as the disease progresses include slow, slurred speech
(dysarthria), fatigue, rapid, involuntary eye movements (nystagmus),
spinal curvature (scoliosis) and heart disease, including heart
enlargement (cardiomegaly) and heart failure.
• Ataxia-telangiectasia: This rare, progressive, childhood disease causes
degeneration in the brain and other body systems. The disease causes
the immune system to break down (immunodeficiency disease),
making one susceptible to diseases. It affects various organs.
Telangiactasias are tiny red “spider” veins that may appear in
the corners of the child’s eyes or on the ears and cheeks. Although
they’re characteristic of the disease, the child may or may not develop
them. Delayed motor skills development, poor balance and slurred
speech are typically the first indications of the disease. Recurrent
sinus and respiratory infections are common. About one in five
children with ataxia-telangiectasia develop leukemia or lymphoma.
Most people with the disease need a wheelchair by their teens and
die in their 20s.
• Congenital cerebellar ataxia: This type refers to ataxia resulting from
damage to the cerebellum at birth.
• Wilson’s disease: People with this condition accumulate copper in
their brains, livers and other organs, which can cause neurological
problems, including ataxia.
Autosomal Dominant Ataxias

Till date, researchers have identified 28 autosomal dominant ataxia genes.
These include:
• Spino-cerebellar ataxias: Cerebellar ataxia and cerebellar
degeneration are common to all types, but other signs and symptoms,
as well as age of onset, differ depending on the specific gene mutation.
The most common of the autosomal dominant ataxias is known
as Machado-Joseph disease. Onset can occur at any age, but most
commonly occurs in the 30s and 40s. Signs and symptoms generally
include speech and swallowing difficulties; eyelid retraction, which
gives the impression of staring fixedly; and verbal and visual memory
defects.
• Episodic ataxia. There are two types of hereditary ataxias that are
episodic rather than progressive.
– Type 1 involves brief ataxic episodes that may last seconds or
minutes. Getting startled or exercising may bring on an episode.
– Type 2 involves longer episodes, which may last days. One also
experience dizziness (vertigo), nausea, vomiting, headache and
weakness during the episodes.
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Both types of episodic ataxia may respond to treatment with

acetazolamide, which also is used to treat seizures. Type 1 also may
respond to the anticonvulsant phenytoin.
In an autosomal dominant disorder, the mutated gene is a dominant
gene located on one of the non-sex chromosomes (autosomes). One only
needs single mutated gene to be affected by this type of disorder.
To have an autosomal recessive disorder, one inherits two mutated
genes, one from each parent. Two healthy carriers can usually pass on
these disorders to their offspring.
SCREENING AND DIAGNOSIS

• History: Ask about when and how the ataxia developed and what
signs and symptoms the patient is having, ask about drug and alcohol
use and potential exposure to toxins.
• Exams: Conduct a physical exam and a neurological exam. A
neurological exam includes checking the memory and concentration,
vision, hearing, balance, coordination and reflexes.
• Laboratory tests
– Blood tests: The specific tests will depend on the suspected cause,
but most likely will include a complete blood count (CBC), which
helps evaluate overall health and detect a range of disorders,
including infection and heavy metal poisoning.
– Urine tests: Urine analysis may suggest certain systemic
abnormalities that can be related to some forms of ataxia. If
Wilson’s disease is suspected, a 24-hour urine collection to
determine the amount of copper in the system may be done.
– Imaging studies: A computerized tomography (CT) scan or
magnetic resonance imaging (MRI) of the brain may help
determine potential causes.
– Genetic testing: You may recommend genetic testing to determine
whether a patient, particularly a child has the gene mutation
that causes one of the hereditary ataxic conditions.
TREATMENT
• Treatment for ataxia depends on the underlying cause. There’s no

treatment specifically for ataxia. However, in some cases, such as
ataxia that follows chickenpox or other viral infection, it’s likely to
resolve on its own over time.
• For ataxia caused by conditions such as multiple sclerosis or cerebral
palsy, ataxia might not be treatable. In that case, recommend adaptive
devices that help with the affected movements, such as a cane for
walking or modified utensils for eating.
• The patient also might benefit from certain therapies, such as physical
therapy and occupational therapy to help in walking. If slurred speech
is a problem, speech therapy may help. If the slurred speech is severe,
therapist may recommend communication aids, such as a speech
synthesizer, an electronic device that turns written text into speech.
MANAGEMENT – SPINO-CEREBELLAR AND OTHER DEGENERA-

TIVE CEREBELLAR ATAXIA’S
Management of patients with spino cerebellar ataxia and other
degenerative types of cerebellar ataxia remains supportive as there is
currently no known therapy or medication which can delay or halt the
progression of the disease.
• Although no dietary factors have been shown to affect symptoms.
Vitamin supplements are recommended and should stop patients
from feeling ‘run down’ or tired. It is often reported that when you
are feeling ‘run down’ or tired that your symptoms will seem to be
much worse.
• Affected individuals should avoid alcohol and medications known
to affect cerebellar function.
• Weight control is particularly important because fatness/obesity can
exacerbate any difficulties with movement and mobility (especially
in association with muscle wasting/weakness).
• In addition, patients should attempt to remain as fit and active as
possible in order that they can retain some degree of movement or
mobility for the longest time. Swimming is a highly recommended
activity which is usually possible even with poor co-ordination and
muscle strength and will exercise many of the bodies muscle group,
the cardiovascular system and the respiratory system.
• As the symptoms of the disease progress patients may find that they
become more easily fatigued and tired. Tiredness will cause the
symptoms to seem worse.
• As movement/mobility becomes more difficult canes and walkers
can be a useful aid. It is important to encourage patients and to
provide any assistance or physical aids that might help them to
function by themselves. This will help them to maintain a sense of
independence and to feel ‘able’.
• Modifications to the home with such conveniences as grab bars, raised
toilet seats and ramps to accommodate motorized chairs may also be
helpful.
• Hand and finger dexterity (co-ordination and grip) will become
increasingly difficult and tremors may present additional problems.
Hand writing will become increasingly difficult. Using thicker
diameter pens may help control writing.
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• Weighted eating utensils (Fig. 10.2) with enlarged handles can help
patients at meal time.
• Slip-on shoes or footwear with ‘Velcro’ fixings can be much easier to
put on.
• Buttons will become very difficult for patients to use, but clothing
with large zips or ‘Velcro’ fixings can be much easier. (Key rings
fitted through the zip pulls also make operation much simpler).
Dressing hooks can also be helpful.
• Speech therapy and communication devices such as writing pads
and computer-based devices may be helpful for patients suffering
with dysarthria (speech difficulties).
• Travel type mugs with a screw-able lid and open/close aperture can
be very helpful to avoid spillages and to make drinking easier.
• Sufferers may experience problems with frequent peeing and this
can often be helped with medication.
• Dysphagia [choking] can be a significant problem that is caused by
gradual loss of reflex actions such as swallowing. Certain foods and
thinner liquids can go down the throat quickly. When reflexes have
slowed, food or liquid may sometimes enter the airway by accident.
It will initially cause the emergency reflex of choking but, more
significantly, if the food or liquid isn’t choked back out, it may be
able to enter the lungs where it is likely to cause pneumonia. Early
stage choking problems may be helped by looking down when you
swallow. When the chin is in a down position the muscles of the
larynx may help to block access to the windpipe. As choking problems
progress the only way to avoid this problem is to drink specially
thickened liquids and to avoid certain foods (like crisps and nuts).
• Sufferers who find that they choke often should consult a nutritionist.
A ‘nutritionist should be able to identify the consistency of food/
liquid least likely to trigger choking. (Dysphagia can be checked by
swallowing a radioactive drink/food and monitoring its progress
through the body by ‘Video esophagram’. In severe cases intravenous
feeding is necessary.
Fig. 10.2: Weighted cutleries

• A ‘gastroscopy’ or jejunostomy operation which inserts a liquid

nutrient feed tube directly into the upper or lower stomach and avoids
the risk of oral feeding.
• The use of simple anti-depressant drugs can be extremely helpful
and effective.
Instructions to Patients: Coping Skills

Living with ataxia can be extremely frustrating. The challenges ataxia
represents, such as loss of independence, may lead to depression and
anxiety. Talking to a counselor or therapist can help cope better. Or one
may find encouragement and understanding in a support group, either
for ataxia or for the underlying condition, such as cancer or multiple
sclerosis.
Although support groups aren’t for everyone, they can be good
sources of information. Group members often know about the latest
treatments and tend to share their own experiences.
Cerebellar Re-education – Goals and Interventions

• With ataxia, the cerebellum no longer plays its role in the adjustment
of the movements necessary for coordination and contraction and
relaxation of the muscles. It no longer permits one to accomplish the
automatisms learned in our young years, e.g. walking.
• This is why, with ataxia, we meet problems on the level of balance,
posture, the voluntary and automatic movements creating a deficit
in control and adjustment of posture as well as in the movements
necessary for respiration, chewing, swallowing, the voice, the
articulation of speech and writing.
• We cannot cure these problems linked to ataxia, but we can treat
the symptoms which follow from it.
• Treatments by speech therapists (speech) and physiotherapists
(motor troubles) are offered by health professionals who will intervene
with persons afflicted with cerebellar ataxia by accompanying them
in doing exercises, especially designed for their respective needs.
• The regular practice of these exercises will have as its goal to maintain
their knowledge and to improve certain functions.
• The efficiency of the treatments will depend, among others, on their
frequency, the motivation of the beneficiaries, their physical ability
and the seriousness of the affliction.
• The treatments sessions are lengthened on the long run. The exercises
program is based on regular repetition of the exercises to further the
learning.
• The persons treating them guide the patient all along their
performance. They explain, counsel, encourage, correct and plan the
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contents of each session depending on the evolution of the ataxia

and the results. They also prepare the program of exercises at home.
• The goal of the therapist is to diminish their efforts and bad habits
and to procure a better quality of life.
These treatments must complement each other well for the ataxic
patients to gain from them.
The Role of the Speech Therapist

1. Improvement in the movements of respiration.
2. Mastering of the mechanism of swallowing.
3. Control of articulation.
4. Control of the rate of language (speed).
5. Control of the voice (tone).
6. Control of the gestures of the hands accompanying language.
7. Mastering the movements of writing.
The Role of the Physical Therapist

1. Strengthening, stretching, relaxation of the muscles.
2. Improvement of posture in all positions.
3. Improvement in the pattern of walking.
With the goal of:
1. Diminishing back pains, spasms, muscular retractions.
2. Preventing deformations of the bones.
3. Making traveling easier.
4. In short, improving all the motor system, therefore the whole physical
stat.
Occupational Therapy (For Autonomy in Activities of Daily Living)

• Because of the evolution of ataxia, the person will sustain a loss of
the ability to execute daily tasks, such as to dress, to wash, to prepare
his meals or to participate in recreations and pastimes.
• Occupational therapists can help ataxic persons to keep an
autonomous way of life. They analyze their level of autonomy, their
skills to carry out their occupations, evaluate their life environment,
take note of the tasks which the person must accomplish daily, his
habits, the presence of physical help, the milieu in which he lives
and the accessibility of the place.
• Occupational therapists work to discover solutions to functional
problems. They help these persons to live in their lodging or residence,
to perform daily tasks, to go about, to work and to enjoy receiving
personal care. The beneficiary is perceived as a global being with
needs, tastes and habits which are susceptible of changing. One must
never forget, however, that autonomy must come first for autonomy
is a liberty.
A Few of the Interventions of the Occupational Therapist

• Suggest changes in the residence to make it more accessible and safe
(eliminate architectural barriers).
• Find solutions to save on the expense of energy in the execution of
daily tasks, in a way that what is left to them is sufficient to do other
things.
• Recommend the use or the replacement of an apparatus which is
more advantageous for movement and autonomy.
• Obtain information by means of questionnaires, interviews, and
concretely set it up.
• Guide the person toward the identification of difficulties.
• Research support services.
Goals and Interventions in Friedreich’s Ataxia

• This disease involves nervous degeneration which results in loss of
balance and inability keep the body in an optimum position in the
space.
• Friedreich’s ataxia generally causes serious loss of sensibility of the
position of the body in space. That is to say the ataxic patient must
compensate by vision to remember where and how are his hands
and his legs situated.
• This deficiency produces improper adjustments during movements
of the trunk and arms and induces loss of balance and difficulties in
walking and changing positions.
• The movement control of the arms may also be affected by gradual
muscular weakness, spasticity and involuntary tremor during hand
movements.
• Nystagmus adds to mobility and coordination difficulties.
• Friedreich’s ataxia may be characterized by deformities such as Pes
cavus and Kypho-scoliosis which may induce further loss of mobility
and balance.
Frenkel’s Exercises for Ataxic Conditions

This program consists of a planned series of exercises designed to help
the patient compensate for the inability to tell where his arms and legs
are in space without looking.
The exercise routine takes about 1/2 hour and should be done 2
times daily.
1. Exercises are designed primarily for coordination, they are not
intended for strengthening.
2. Commands should be given in an even, slow voice, the exercises
should be done to counting.
3. It is important that the area is well lit and that the patients are
positioned so that they can watch the movement of their legs.
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4. Avoid fatigue. Perform each exercise not more than four times. Allow
rest between each exercise.
5. Exercises should be done within normal range of motion to avoid
over-stretching of muscles.
6. The first simple exercise should be adequately performed before
progressing to more difficult patterns.
Exercises While Lying

Starting position: Lie on bed or couch with a smooth surface along
which the feet may be moved easily. The head should be raised on a
pillow so that the patient can watch every movement.
1. Bend one leg at the hip and knee sliding the heel along the bed.
Straighten the hip and knee to return to the starting position. Repeat
the same with the other leg.
2. Bend one leg at the hip and knee as in #1. Then slide the leg out to
the side leaving the heel on the bed. Slide the leg back to the center
and straighten the hip and knee to return to the starting position.
Repeat the same with the other leg.
3. Bend one leg at the hip and knee with the heel raised from the bed.
Straighten the leg to return to the starting position. Repeat the same
with the other leg.
4. Bend and straighten one leg at the hip and knee sliding the heel
along the bed stopping at any point of command. Repeat the same
with the other leg.
5. Bend the hip and knee of one leg and place the heel on the opposite
knee. Then slide the heel down the shin to the ankle and back up to
the knee. Return to starting position and repeat with the other leg.
6. Bend both hips and knees sliding heels on the bed keeping ankles
together. Straighten both legs to return to starting position.
7. Bend one leg at the hip and knee while straightening the other in a
bicycling motion.
Exercises While Sitting

Starting position: Sit on a chair with feet flat on the floor.
1. March in sitting, raising just the heel. Then progress to alternately
lifting the entire foot and placing the foot firmly on the floor upon
a traced footprint.
2. Make two cross marks on the floor with chalk. Alternately glide the
foot over the marked cross: forward, backward, left and right.
3. Learn to rise from the chair and sit again to a counted cadance. At
one, bend knees and draw feet under the chair; at two, bend trunk
forward; at three, rise by straightening the hips and knees and then
the trunk. Reverse the process to sit down.
Exercises While Standing

Starting position: Stand erect with feet 4 to 6 inches apart.
1. Walk sideways beginning with half steps to the right. Perform this
exercise in a counted cadance: At one, shift the weight to the left
foot; at two, place the right foot 12 inches to the right; at three, shift
the weight to the right foot; at four, bring the left foot over to the
right foot. Repeat exercise with half steps to the left. The size of the
step taken to right or left may be varied.
2. Walk forward between two parallel lines 14 inches apart placing the
right foot just inside the right line and the left foot just inside the left
line. Emphasize correct placement. Rest after 10 steps.
3. Walk forward placing each foot on a footprint traced on the floor.
Footprints should be parallel and 2 inches from a center line. Practice
with quarter steps, half steps, three-quarter steps and full steps.
4. Turn to the right. At one, raise the right toe and rotate the right foot
outward, pivoting on the heel; at two, raise the left heel and pivot
the left leg inward on the toes; at three, completing the full turn, and
then repeat to the left.
5. Walk up and down the stairs one step at a time. Place the right foot
on one step and bring the left up beside it. Later practice stair climbing
with alternate steps. At first use the railing, then as balance improves
dispense with the railing.
Upper Extremity Exercises

When the arms are affected use a blackboard and chalk. Change a minus
sign to a plus sign; copy simple diagrams (straight lines, circles, zig-zag
lines, etc.) Various coordination boards may be used to improve eye-
hand coordination.
SECTION 2
DISORDERS OF EQUILIBRIUM—
DIZZINESS AND IMBALANCE
INTRODUCTION
Dizziness and Imbalance is an Extremely Common Problem in the
Older Population
Jonsson et al (2004) found that the overall prevalence of balance problems
at age 70 was 36% (women) and 29% (men). Balance symptoms were
more common among women than men, and increased with increasing
age. At ages 88-90 years the corresponding values were 51-45%.
As can be seen from the Table 10.1, the main two sources of dizziness
in older people are the ear (peripheral vestibular canals) and the brain.
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Table 10.1: Causes of dizziness in the elderly

Causes Of Dizziness in Older People (Davis, 1994)
System Contribution
Peripheral vestibular (otologic) 56
Brainstem/cerebellum (central) 22
Proprioceptive (peripheral neuropathy) 7
Visual 1
Psychological 3
Unknown 14
The following causes of dizziness is divided into five main categories:

A) Otologic; B) Central; C) Proprioceptive D) Medical; E)
Psychogenic; and F) Unlocalized.
Otologic Dizziness
Otologic dizziness is the most common type of dizziness in the elderly.
This is mainly due to an increased tendency for the elderly to develop:
1. Benign paroxysmal postural vertigo (BPPV)
• About 50% of dizziness is caused by BPPV by the age of 80, compared
to about 20% for all ages considered together.
• With BPPV, patients complain of brief bouts of vertigo provoked by
changing the orientation of the head to gravity.
• BPPV is presently felt to be caused by dirigible otoconial debris
(Figure 10.3)
• BPPV is diagnosed by performing a Dix-Hallpike maneuver, a
positional test.
• Vertigo and a typical twisting type of nystagmus ensue after a latency
of two seconds and last about ten seconds.
• BPPV almost always responds to the Brandt-Daroff exercises
performed over a three-week period. Other physical treatments such
as the Epley or Semont maneuvers are also highly effective.
• Treatment with vestibular suppressants (Table 10.2), or anti-emetics
is also helpful in the week after onset before the exercises have had
a chance to work, in patients too physically limited to perform the
exercises, or in patients who do not respond to the exercises. Meclizine
is the most helpful of these agents.
2. Meniere’s disease is also a significant cause of dizziness in the older
population and has its highest incidence above fifty years of age.
• Meniere’s disease usually presents as spells of rapid decline in
hearing, a roaring tinnitus, vertigo, and monaural fullness.
• In acute stage, vestibular suppressants (Table 10.3) and anti-
emetics are used.
• Over the long-term, a two gram salt diet combined with a mild
diuretic may reduce the frequency of attacks.
Fig. 10.3: In Benign Paroxysmal Positional Vertigo (BPPV) dizziness is generally

thought to be due to debris which has collected within a part of the inner ear. This
debris can be thought of as “ear rocks”, although the formal name is “otoconia”.
Ear rocks are small crystals of calcium carbonate derived from a structure in the
ear called the “utricle” (Fig. 10.1). While the saccule also contains otoconia, they
are not able to migrate into the canal system. The utricle may have been damaged
by head injury, infection, or other disorder of the inner ear, or may have degenerated
because of advanced age
Table 10.2: Vestibular suppressants (arranged in order of preference)

Drug Dose Adverse Reactions
Meclizine antihistamine 12.5-25 mg Sedating
(antivert, bonine) PO q4-6h
anticholinergic
Lorazepam benzodiazepine 0.5 mg PO Mildly sedating
(ativan) BID addictive
Clonazepam benzodiazepine 0.5 mg PO Mildly sedating
(klonapin) BID addictive
Diazepam benzodiazepine 2 mg PO Sedating
(valium) BID respiratory depressant
addictive, long acting
• Recently, a treatment for Meniere’s involving injections of

gentamicin through the eardrum has been rapidly gaining
popularity. It is about 90% effective for unilateral disease.
3. Vestibular neuritis is a monophasic self-limited condition typified
by vertigo, nausea, ataxia and nystagmus.
• Both vertigo at rest and positional vertigo are often present.
• Spontaneous nystagmus differentiates this disorder from BPPV.
• Severe vertigo usually only lasts two to three days.
• An anti-emetic, such as phenergan, may be used acutely.
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• Vestibular suppressants (Table 10.3) should be used sparingly as

they may delay central compensation to the lesion.
• Older patients with prior central disease, peripheral neuropathy,
visual troubles, or difficulties that restrict ambulation may not
recover as quickly and may benefit from vestibular physical
therapy.
4. Bilateral Vestibular Paralysis
• It is most commonly caused by exposure to ototoxic medications,
particularly courses of gentamicin lasting 2 weeks or longer.
• Other causes include spirochaete infections of the inner ear,
autoimmune processes, and age-related changes.
• Symptoms include oscillopsia (Fig. 10.4) and ataxia, often without
vertigo.
• In such a case, it is important to advise the patient to avoid any
agents that may suppress the vestibular system.
• It is also important for them to avoid anti-cholinergic agents
such as many of the tricyclic antidepressant medications.
• Ototoxic agents must be avoided above all, particularly
gentamicin.
• Vestibular rehabilitation physical therapy is usually helpful, but
full recovery is never attained in many patients.
• Recovery depends on the degree of vestibular loss and on the
individual patient’s ability to compensate.
Central Dizziness
• Central dizziness is relatively less common than otologic dizziness
but, as it is most often secondary to vascular events (strokes) involving
the cerebellum and the brainstem, it may be a warning sign of
dangerous underlying conditions.
• Many neurological disorders may cause vertigo by disruption of the
brainstem/cerebellar pathways. Patients with central vertigo are often
distressed by ataxia, nausea, and illusions of motion for many years.
Fig. 10.4: Blurred stop sign demonstrating oscillopsia

• Multiple white matter lesions, such as multiple sclerosis or

periventricular leukomalecia are a common source of unsteadiness.
• Parkinsonism has also become a common cause for dizziness in older
persons.
• Although it is uncommon for patients with history of seizures to
present as dizziness, epileptic vertigo deserves a special mention
because it responds well to treatment with anticonvulsant medication.
Epileptics may give a history of very brief spinning sensations or
“quick spins”.
• For treatment of central dizziness one must first treat the cause. In
the case of vascular events, e.g. vascular risk factors should be treated.
A patient with “quick spins” should have an electroencephalogram.
Vestibular physical therapy is often helpful in these patients.
• Dizziness caused by vertebro-basilar insufficiency is common in mid-
adulthood, but is much less prevalent in the elderly.
Proprioceptive Problems
Sensory loss in the feet, due to diabetes, vitamin B12 deficiency, cervical
spondylosis, or just peripheral neuropathy may contribute to unsteadiness
in the older population.
Medical Dizziness
Medical causes of dizziness mainly include postural hypotension
(Fig. 10.5), cardiac events, infection, low blood glucose, and drug induced.
In postural hypotension, dizziness interfaces with syncope. Both occult
Fig. 10.5: Blood pressure should be measured first in sitting and then in standing
position. A fall in BP > 10 mm of Hg indicates presence of postural hypotension
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cardiac arrhythmias and acute myocardial infarctions may manifest as

dizziness. Medications are a common contributor to dizziness and ataxia
(Table 10.3) as elderly patients are often on multiple drugs, which place
them at high risk for these adverse side effects.
Table 10.3: Drugs that can cause ataxia

Miscellaneous drugs Cimetidine
Anticonvulsants Phenytoin, carbamazepine
Antihypertensive and Adrenergic blockers (e.g., propranolol,
drugs with hypotension terazosin) Diuretics (e.g., furosemide)
as side effects Vasodilators (e.g., isosorbide, nifedipine)
Tricyclic antidepressants (e.g., nortriptyline)
Phenothiazines (e.g., chlorpromazine)
Dopamine agonists (e.g., L-dopa/carbidopa)
Ototoxic drugs and Some of the mycin antibiotics (e.g., gentamicin)
vestibular suppressants Anticholinergic (e.g., trans-dermal scopolamine,
promethazine, amitriptyline, meclizine)
Loop diuretics (furosemide)
Psychotropic agents Sedatives (e.g., barbiturates and benzodiazepines)
Drugs with Parkinsonism as side effects (e.g.,
phenothiazines)
Drugs with anti-cholinergic side effects (e.g.,
amitriptyline)
It may be noted that, medications causing symptomatic orthostatic

hypotension as well as hypoglycemia are the most common cause of dizziness in
the elderly. Treatment begins by removing any unnecessary agents and
drug “tuning”, or substituting similar, but better tolerated, medications.
Psychogenic Dizziness
It is common and includes entities such as anxiety disorders, panic attacks,
agoraphobia, somatization syndrome, and malingering. This group is
difficult to diagnose because organic dizziness is often accompanied by
considerable and often appropriate anxiety.
Unlocalized Dizziness
At all ages, in general, about one-third of patients with dizziness will go
undiagnosed. These patients usually need to be followed more closely
than patients in whom a clear diagnosis is available. Empirical trials of
medication and vestibular physical therapy may be helpful options.
Summary
Dizziness is common in older adults and has diverse causes. The
diagnostic process must distinguish between otologic, central, medical,
and psychogenic etiologies. Furthermore, in a substantial fraction of

patients, a clear etiology may not be determined. Medications must be
used with greater caution in older adults as they may be more sensitive
to side effects. Vestibular physical therapy is often helpful and should be
utilized in many situations1.
REFERENCE
1. Jonsson R, E Sixt, S Landahl, et al. “Prevalence of dizziness and vertigo
in an urban elderly population (2004).
VESTIBULAR REHABILITATION THERAPY (VRT)

Rationale for Vestibular Rehabilitation
Here we will consider the “generic” type of vestibular rehabilitation in
which ataxic or vertiginous individuals are provided with a series of
tasks to perform that require them to use their eyes while their head is
moving, and possibly when their body is also moving. There are many
processes that might be usefully influenced by experience and motion:
• Plasticity – Adaptations in CNS connections to compensate for
peripheral disturbances.
• Formation of internal models – A cognitive process where one learns
what to expect from ones actions. Internal models are critical for
predictive motor control, which is essential when one is controlling
systems that have delays. Much of the benefit of vestibular physical
therapy may depend on internal models.
• Learning of limits – Another cognitive process involved with learning
what is safe and what is not. Someone who does not know their
limits may be overly cautious and avoid dangerous situations.
Someone who does not realize that, e.g. they can’t figure out which
way is up, may drown in a swimming pool.
• Sensory weighting – A cognitive process in which one of several
redundant senses is selected and favored over another. Classically,
selection occurs between vision, vestibular and somatosensory inputs
when one is attempting to balance. People with unreliable vestibular
systems, such as those in Meniere’s disease, sometimes seem to unable
to switch off their visual reliance, causing them distress in certain
situations where vision is an incorrect reflection of body movement.
Vestibular physical therapy has been reported to cause no change in
the risk of falling or the use of assistive devices.
General Interventions
Cawthorne-Cooksey Exercises
One of the first “general” interventions for vestibular problems were the
Cawthorne-Cooksey exercises, as shown below. These are a one page
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handout of activities that progress from simple head movement to

complex activities such as throwing a ball.
Position: Lying in Bed

1. Eye movements — at first slow, then quick
1. Up and down
2. From side to side
3. Focusing on finger moving from 3 feet to 1 foot away from face.
2. Head movements at first slow, then quick, later with eyes closed
1. Bending forward and backward
2. Turning from side to side.
Position: Sitting
3. Eye movements and head movements as above.
4. Shoulder shrugging and circling.
5. Bending forward and picking up objects from the ground.
Position: Standing
6. Eye, head and shoulder movements as before.
7. Changing from sitting to standing position with eyes open and shut.
8. Throwing a small ball from hand to hand (above eye level).
9. Throwing a ball from hand to hand under knee.
10. Changing from sitting to standing and turning around in between.
Position: Moving about (in class)

11. Circle around center person who will throw a large ball and to whom
it will be returned.
12. Walk across room with eyes open and then closed.
13. Walk up and down slope with eyes open and then closed.
14. Walk up and down steps with eyes open and then closed.
15. Any game involving stooping and stretching and aiming such as
bowling and basketball.
Diligence and perseverance on the part of the patient are required,
but the earlier and more regularly the exercise regimen is carried out, the
faster and more complete will be the return to normal activity. Ideally
these activities should be done with a supervised group. A friend or
relative who also learns the exercises should accompany individual
patients.
Group Therapy
Recreational activities done in a group can also be excellent for vestibular
rehabilitation. In general, activities should involve using the eyes while
the head and body are in motion. Of course, many such activities require
this—golf, bowling, tennis, racquetball, ping-pong, etc. The trick is to

find one that is fun, safe, and somewhat stimulating. Dancing is of course,
an excellent vestibular rehabilitative activity. Martial arts activities are
also beneficial, as long as physical injury is avoided.
“Alternative” balance activities. Yoga and martial arts (Fig. 10.6) are
the activities that have been considered in the literature. Tai Chi and Yoga
both incorporate some relaxation which may be helpful for those who
have anxiety accompanying their dizziness or imbalance. Usually done
in groups, these activities are intrinsically lower in cost than individualized
therapy, but their efficacy has not been compared in a head-on fashion
to individualized therapy. They are probably most appropriate for those
who no longer need individual physical therapy.
Individualized Physical Therapy

• Since the 1990’s physical therapists begun an effort, to advocate
exercises customized to individual diagnoses or at least functional
patterns of disorders of equilibrium.
• Therapists perform an “specific evaluation”, which allowed them to
adjust their treatment program. This was an important development
as prior to this, therapists often used treated all dizzy patients with
the same protocol, e.g. the Cawthorne-Cooksey exercises.
• The major advantage of this individualized approach is greater
efficiency of treatment.
• The disadvantage of individualized physical therapy is the higher
cost compared to the Cawthorne-Cooksey or other “do it yourself”
regimes.
Fig. 10.6: Slow martial art dance form popular in South-East Asia is an effective
alternative balance activity
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• Usually eight sessions of therapy are prescribed, but sometimes as

many as 16 sessions or ongoing treatment is recommended. This
approach can be compared to working out with a personal trainer.
The trainer is likely to be helpful, but the experience will cost the
patient a bit more than doing it himself.
Assessment of Vestibular Dysfunction

Vestibular rehabilitation therapists also often rely on a physical
examination that uses a “foam and dome” to destabilize individuals, as
well as more conventional devices such as Frenzel’s goggles for diagnosis
of BPPV.
• The “foam” is a slab of spongy material (Fig. 10.7) that makes it more
difficult to balance as it gives way, reducing and delaying torques
related to changes in the center of pressure. Persons who become
more unstable on foam are said to be more dependent on
somatosensory feed back from their receptors in ankles and feet for
stability than others in the same age group. The result of the “foam”
paradigm is difficult to interpret. The input—perturbation to stance—
is an uncontrolled variable. A person who has very little postural
shifts—such as a person with early Parkinsonism—might not sway
at all on foam. A person, who is fidgety, might sway more. The
output is also difficult to calibrate. Whether or not a person takes a
step might depend on their stability, their level of anxiety, etc. Whether
or not use of the “foam” paradigm for evaluation is associated with
better outcomes is presently unclear. It seems likely that using “foam”
might be useful for persons with abnormally high somatosensory
dependence (see below).
• The “dome” is a lamp-shade like device that obscures vision without
eliminating it completely. Total elimination of vision can obviously
be done by closing the eyes, but in this situation people might switch
Fig. 10.7: Balance foam

off their visual processing. The logic of the dome is that it might
select out persons who are visually dependent. Again, the input to
this test is uncontrolled (postural sway), and the output is somewhat
difficult to quantify.
• Moving platform posture evaluation shares most of the same problems
as the “foam and dome”, but does have a better outcome measure
(sway), as well as a better quantified input. When available,
posturography is preferable to use of the “foam and dome” (Fig. 10.8).
Fig. 10.8: Moving platform posture evaluation
Points to Ponder
• The foam/dome examination reflects an attempt to separate out
persons who are dependent on vision or somatosensory input for
their stability.
• When vision or somatosensory feedback becomes unreliable, people
switch over to a vestibular balance strategy.
• Those that cannot make this switch, become visually or somatosensory
dependent.
Diagnosis of BPPV
The diagnosis of BPPV can be made with history and Dix-Hallpike test.
History of the Disorder

• The key observation is that dizziness is triggered by lying down, or
on rolling over in bed.
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• Most other conditions, such as in orthostatic hypotension positional

dizziness get worse on standing rather than lying down.
• There are some rare conditions that have symptoms that mimic BPPV.
Patients with vertigo from spino-cerebellar ataxia may have “bed
spins” and prefer to sleep propped up in bed. Such conditions can
be detected on a careful neurological examination and by a positive
family history.
Dix-Hallpike Maneuver for Testing BPPV

• In this test, a person is brought from sitting to a supine position, with
the head turned 45 degrees to one side and extended about 20 degrees
backward (Fig. 10.9).
• A positive Dix-Hallpike test consists of a burst of nystagmus (jumping
of the eyes).
• The eyes jump upward as well as twist so that the top part of the eye
jumps toward the down side.

BPPV has often been described as “self-limiting” because symptoms often
subside or disappear within 2 months of onset. BPPV is not intrinsically
life-threatening. One can certainly opt to just wait it out.
Fig. 10.9: Dix-Hallpike test

No Active Treatment (wait/see): Instructions to Patients

• Certain modifications in daily activities may be necessary to cope
with dizziness.
• Use two or more pillows at night.
• Avoid sleeping on the “bad” side.
• In the morning, get up slowly and sit on the edge of the bed for a
minute.
• Avoid bending down to pick up things, and extending the head,
such as to get something out of a cabinet.
• Be careful when at the dentist’s office, the beauty parlor when lying
back having ones hair washed, when participating in sports activities
and when you are lying flat on your back.
• Symptoms tend to wax and wane.
• Motion sickness medications are sometimes helpful in controlling
the nausea associated with BPPV but are otherwise rarely beneficial.
BPPV should nearly always be treated with vestibular rehabilitation, using
specific maneuvers for the type of dizziness that the patient experiences,
such as:
Balancing exercises
These exercises basically involve moving and balancing at the same time.
One practices ones balance. Typical activities involve standing heel-toe,
walking with the head moving back and forth, combining these activities
with eyes closed, or on spongy surfaces. Walking, running, sports, Yoga
or Tai Chi offer similar benefits to these patients.
• Gaze stabilization exercises
Figs 10.10A to C: Gaze stabilization exercises; Ask the patient to look forward at a
fixed point, say a card held in front. Now slowly turn the head to the right and left,
keeping the gaze focused on the card. Repeat 5-10 times in each direction in one
sitting, 3 sittings a week
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Visual dependence exercises

Therapists might ask patients to smear their glasses with Vaseline. The
rationale is to reduce “visual dependency”, which is an inappropriate
reliance on visual input, in situations where it might be better to use
somatosensory or vestibular inputs.
Other forms of exercises include
• Otolith recalibration
• Ocular tracking
• Axial weight loading
• Virtual reality
• Somatosensory dependence training
• Habituation training.
The Epley and Semont Maneuvers

• There are two treatments of BPPV that are usually performed in the
clinic.
• Both treatments are very effective, with roughly an 80% cure rate.
• The maneuvers, named after their inventors, are both intended to
move debris or “ear rocks” out of the sensitive part of the ear (posterior
canal) to a less sensitive location.
• Each maneuver takes about 15 minutes to complete.
• The Semont maneuver (also called the “liberatory” maneuver)
involves a procedure whereby the patient is rapidly moved from
lying on one side to lying on the other, holding each position for 30
seconds. It is a brisk maneuver that is 90% effective after 4 treatment
sessions (Fig 10.11).
• The Epley maneuver is also called the particle repositioning or canalith
repositioning procedure. It was invented by Dr John Epley (Fig 10.12).
Fig. 10.11: The Semont maneuvers

Fig. 10.12: The Epley maneuvers
• It involves sequential movement of the head into four positions,

staying in each position for roughly 30 seconds. The recurrence rate
for BPPV after these maneuvers is about 30 percent at one year, and
in some instances a second treatment may be necessary.
• Use of an anti-emetic prior to the maneuver may be helpful if nausea
is anticipated.
• When performing the Epley maneuver, caution is advised should
neurological symptoms (e.g. weakness, numbness, visual changes
other than vertigo) occur.
• Occasionally such symptoms are caused by compression of the
vertebral arteries and if one persists for a long time, a stroke could
occur.
After doing either of these maneuvers, the patient should follow the
instructions listed below, which are aimed at reducing the chance that
debris might fall back into the sensitive back part of the ear.
After doing Epley or Semont Maneuvers Ask the Patient to:

1. Wait for 10 minutes after the maneuver is performed before going home.
2. Sleep semi-recumbent for the next night. This means sleep with the head
at 45 degree angle. This is most easily done by using a recliner chair
or by using pillows arranged on a couch (Fig. 10.13).
3. During the day, try to keep the head vertical. Do not go to the hairdresser
or dentist. Activities which requires head movement, for shaving
under their chins, bend the body forward in order to keep the head
vertical. If eye-drops are required, try to put them in without tilting
the head back. Shampoo only under the shower.
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Fig. 10.13: Brandt - Daroff Exercises

Suggested schedule for Brandt Daroff exercises
Morning 5 repetitions 10 minutes
Noon 5 repetitions 10 minutes
Evening 5 repetitions 10 minutes
4. For at least one week, avoid provoking head positions that might bring
BPPV on again.
• Use two pillows when you sleep.
• Avoid sleeping on the “bad” side.
• Don’t turn your head far up or far down.
• Be careful to avoid head-extended position, especially with the
head turned towards the affected side.
• Try to stay as upright as possible.
• Exercises for low-back pain should be stopped for a week.
• No “sit-ups” and no “crawl” swimming should be done for at
least one week. Breast stroke is OK.
• Also avoid far head-forward positions which might occur in
certain exercises (i.e., touching the toes).
• Do not start doing the Brandt-Daroff exercises immediately or 2
days after the Epley or Semont maneuver, unless specifically
instructed.
5. After one week of the treatment, put yourself in the position that
usually makes you dizzy. Position yourself cautiously and under
conditions in which you can’t fall or hurt yourself.
Home Management of BPPV Brandt – Daroff Exercises

• The Brandt-Daroff exercises are a home method of treating BPPV,
usually used when the side of BPPV is unclear.
• They succeed in 95% of cases but are more tiring and take longer
than the other maneuvers.
• These exercises are performed in three sets per day for two weeks.
In each set, one performs the maneuver as shown five times.
• Starting position- Sitting upright on bed (Position 1).
• Then move into the side-lying position (Position 2). Stay in the side-
lying position for 30 seconds, or until the dizziness subsides.
• Then go back to the sitting position (Position 3). Stay sitting for 30
seconds.
• Then go to the opposite side lying (position 4) and follow the same
routine (Fig. 10.13).
These exercises should be performed for two weeks, three times per day,
or for three weeks, twice per day. This adds up to 42 set in total. In most
persons, complete relief from symptoms is obtained after 30 sets, or about
10 days. When performing the Brandt-Daroff maneuver, caution is advised
should neurological symptoms, such as weakness, numbness, visual
changes other than vertigo occur. Occasionally such symptoms are caused
by compression of the vertebral arteries. In this situation stop the exercises
and consult ones physician.
11 Cerebral Palsy
INTRODUCTION
Cerebral palsy is a congenital disability that affects movement and body
posture. It occurs due to brain damage that may have happened before
the baby was born, at birth, or immediately after birth. The whole brain
is not damaged, only parts of it, mainly parts that control movements
and posture may be affected. Once damaged, the parts of the brain do
not recover, nor do they get worse. However, the movements, body
positions, and related problems can be improved or made worse
depending on how we treat the child and how damaged his or her brain
happens to be. The earlier we intervene, the more improvement can be
made.
Cerebral palsy is the most frequent cause of physical disability, second
only to polio. About 1 of every 300 babies worldwide is born with or
develops cerebral palsy.
CAUSES
The causes for CP are often difficult to find.
• Prenatal causes before birth:
– Infections of the mother while she is pregnant. These include
German measles and shingles (herpes zoster).
– Differences between the blood type of mother and child (Rh
incompatibility).
– Physiological disorders of the mother, such as diabetes or toxemia
of pregnancy.
– Inherited causes, rare ‘familial spastic paraplegia’.
– Idiopathic: No cause can be found in about 30% of the children.
• Perinatal causes around the time of birth:
– Birth asphyxia or lack of oxygen (air) at birth. The baby does not
breathe soon enough and becomes blue and limp. In some areas,
misuse of hormones (oxytocin) to speed up birth narrows the
blood vessels in the womb so much that the baby does not get
enough oxygen. The baby is born blue and limp-with brain
damage.
– Birth injuries from difficult births. These are mostly large babies
of mothers who are small or very young. The baby’s head may
be pushed out of shape, blood vessels torn, and the brain
damaged.
– Premature birth: Babies born before 9 months and who weigh
under 2 kilos (5 pounds) are much more likely to have cerebral
palsy. In rich countries, over half the cases of cerebral palsy
happen in babies that are born early.
• Postnatal causes after birth:
– Very high fever due to infection or dehydration (water loss from
diarrhea). It is more common in bottle-fed babies.
– Brain infections (meningitis, encephalitis). There are many causes,
including malaria and tuberculosis.
– Head injuries.
– Lack of oxygen from drowning, gas poisoning, or other causes.
– Poisoning from lead glazes on pottery, pesticides sprayed on
crops, and other poisons.
– Bleeding or blood clots in the brain, often from unknown cause.
– Brain tumors cause progressive brain damage in which the signs
are similar to cerebral palsy but steadily get worse.
DETECTION – HOW TO RECOGNIZE CEREBRAL PALSY?

• At birth a baby with cerebral palsy is often limp and floppy, or may
even seem normal (Fig. 11.1).
• Slow development compared to other children in the village, the
child is slow to hold up his head, to sit, or to move around. He may
not use his hands. Or he only uses one hand and does not begin to
use both.
• Feeding problems. The baby may have difficulties with sucking,
swallowing and chewing. She may choke or gag often. Even as the
child gets bigger, these and other feeding problems may continue.
Fig. 11.1: Normal and floppy child

Cerebral Palsy 319
• Difficulties in taking care of the baby or young child. Her body may
stiffen when she is carried, dressed, or washed, or during play
(Fig. 11.2). Later she may not learn to feed or dress herself, to wash,
use the toilet, or to play with others. This may be due to sudden
stiffening of the body, or to being so floppy she ‘falls all over the
place’.
• The baby may cry a lot and seem very fussy or ‘irritable’. Or she may
be very quiet (passive) and almost never cry or smile.
Communication difficulties: The baby may not respond or react as other
babies do. This may partly be due to floppiness, stiffness, or lack of arm
gestures, or control of face muscles. Also, the child may be slow in
beginning to speak. Later some children develop unclear speech or other
speaking difficulties. Although parents find it hard to know exactly what
the child wants, they gradually find ways of understanding many of his
needs. At first the child cries a lot to show what he wants. Later he may
point with his arm, foot or eyes.
Intelligence: Some children may seem dull because they are so limp and
slow moving. Others move so much and awkwardly they may appear
stupid. Their faces twist, or they may drool because of weak face muscles
or difficulty swallowing. This can make an intelligent child appear
mentally slow.
Fig. 11.2: The baby may be so limp that her head seems as if it will fall off. Or she
may suddenly stiffen like a board, so that no one feels able to carry or hug her
About half of the children with cerebral palsy are mentally retarded,
but this should not be decided too soon. The child needs to be given help
and training to show what she is really like. Parents can often tell that
she understands more than she can show (Fig. 11.3).
Hearing and sight are sometimes affected. If this problem is not
recognized, the family may think that the child lacks intelligence. Observe
the child carefully and test him to find out how well he can hear and see
(Fig. 11.4).
Fig. 11.3: Communication with a CP child
Fig. 11.4: Testing the hearing of a CP child
Fits (convulsions) may occur in some children with cerebral palsy.

Restless behavior: Sudden changes of mood from laughing to crying,
fears, fits of anger, and other difficult behavior may be present. This may
partly be due to the child’s frustration of not being able to do what he
wants with his body. If there is too much noise and activity the child can
become frightened or upset. The brain damage may also affect behavior.
These children need a lot of help and patience to overcome their fears
and other unusual behavior.
Sense of touch, pain, heat, cold, and body position are not lost. However,
the children may have trouble controlling movements of their bodies
and trouble with balance. Because of their damaged brains they may
have difficulty learning these things. Patient teaching with lots of
repetition can help.
Abnormal reflexes: Babies have certain ‘early reflexes’ or automatic body
movements that normally go away in the first weeks or months of life.
In children with brain damage, they may last much longer. However,
these are only important if they affect how the child moves.
Cerebral Palsy 321
TYPES OF CP
Cerebral palsy is different in every child. Different experts have worked
out different ways of describing it. But labeling a child’s particular type
of cerebral palsy does not usually help his treatment. It is helpful, however,
to recognize three main forms that cerebral palsy may appear in a
particular child- but usually in some sort of combination.
Spastic CP
The spastic child is rigid, or stiff. Movements are slow and awkward. A
change in the position of the head triggers abnormal positions of the
whole body. The stiffness increases when the child is upset or excited, or
when his body is in certain positions. The pattern of spasticity varies
greatly from child to child (Fig. 11.5).
Fig. 11.5: Typical spastic CP postures

Athetoid CP
Athetosis are slow, writhing, or sudden quick (Choric) movements of the
child’s feet, arms, hands, or face muscles. The arms and legs may seem
jumpy and move nervously, or just a hand or the toes may move for no
reason. When he moves by choice, body parts move too fast and too far.
Spastic movements or positions like those shown above may continually
come and go (constantly changing muscle tension). His balance is poor
and he falls over easily (Fig. 11.6).
Most children with athetosis have normal intelligence, but if the
muscles needed for speech are affected, it may be hard for them to
communicate their thoughts and needs.
Typical athetoid arm and hand movements may be as a regular shake
or as sudden ‘spasms’. Uncontrolled movements are often worse when
the child is excited or tries to do something.
Fig. 11.6: Athetoid CP
Ataxic CP (Fig. 11.7)

The child who has ‘ataxia’, or poor balance, has difficulty beginning to
sit and stand. She falls often, and has very clumsy use of her hands. All
this is normal in small children, but in the child with ataxia it is a bigger
problem and lasts longer (sometimes for life).
Because children who have mainly a balance problem often appear
clumsier than disabled, other children are sometimes cruel and make fun
of them.
Many children who have spasticity or athetosis also have problems
with balance. This may be a major obstacle in learning to walk. However,
much can often be done to help a child improve her balance.
Cerebral Palsy 323
Fig. 11.7: Ataxic CP
Pattern of Involvement in CP
Three typical patterns of involvement or presentation may be seen in
children with cerebral palsy. These are hemiplegic, diplegic or quadriplegic
presentation (Fig. 11.8).
Although majority of cerebral palsy children fit one or another of
these patterns, check also for minor deviations like focal hypotonia or
similar such problems in other body segments resulting in a mixed or
atypical presentation.

• The damaged parts of the brain cannot be repaired, but often the
child can learn to use the undamaged parts to do what she wants to
do.
• It is important for parents to know more or less what to expect.
Families can do a lot to help these children learn to function better.
Fig. 11.8: Typical involvement patterns in CP
• Generally, the child who is more intelligent will learn to adapt

successfully to her condition. However, intelligence is not always a
blessing. In fact, some intelligent children become more easily
frustrated and discouraged, so they stop trying. Extra effort is needed
to find new and interesting ways to keep them progressing.
• Even severely retarded children can often learn important basic skills.
Only when mental damage is so great that the child does not respond
at all to people and things is there little hope for much progress.
• However, before judging the child, who does not respond, be sure to
check for deafness or loss of eyesight.
Points to Ponder
• Rather than try to treat the symptoms of cerebral palsy, we can do
more for the child if we help her with development of movement,
communication, self-care and relationships with others.
• Sometimes we can partly correct the symptoms through helping the
child develop basic skills.
• Family members can learn to play and do daily activities with the
child in ways that help her both to function better and to prevent
secondary problems such as contractures and deformities.
• Most important lesson for the parents is not to do everything for the
child. Help should be just enough so that the children can learn to
do more by themselves.
Learning to Walk
• Most children with cerebral palsy do learn to walk, although often
much later than normal.
Cerebral Palsy 325
• In general, the less severely affected the child is and the earlier she
is able to sit without help, the more likely she is to walk. If she can
sit without assistance by age 2, her chances for walking may be
good-although many other factors are involved. Some children begin
to walk at age 7, 10, or even older.
• Hemiplegic and diplegic children usually do learn to walk, although
some may need crutches, braces, or other aids.
• Many severely affected children may never walk. Parents need to
accept this, and aim for other important goals like other modes of
ambulation. Whether or not the child may someday walk, he needs
some way to get from place to place.
When a child with severe brain damage is held like this, her legs
may automatically stiffen and her feet point down-the so-called ‘tip-toe
reflex’. Because the feet sometimes take jerky ‘steps’, parents think the
child is ‘almost ready to walk’. This is a common mistake that may give
rise to false hope (Fig. 11.9). The tip-toe reflex must be overcome before
the child can begin to learn to walk. One should not hold the child in this
position or make her try to walk. It will only strengthen this disabling
equines reaction.
Points to Ponder
• There are many different ways to help children who cannot walk, or
who walk with difficulty, get where they want to go.
• These include scoot boards, wagons, wheelchairs, special walkers,
and hand-pedal tricycles.
Guideline to Parents
Functional mobility and ADL: Parents must first carefully observe what
the child can do with her body. Such observation is best done in the
presence of trained professional, such as a therapist, to identify the
following:
Fig. 11.9: Tip-toeing reaction – commonly mistaken for readiness to bear weight
Can the child:

• Lift her head? Hold it up? Sit and roll over?
• Creep along the floor in any way possible or crawl or walk?
How does the child use her hands?
• Can she grasp things, hold on to it and let go at will, use both hands
simultaneously or only one hand at a time?
• Can she use her fingers to pick up small stones or pieces of food?
How much can the child do for herself in ADL?
• Can she feed herself, wash herself, dress herself? Is she ‘toilet trained’?
What can the child do in the home or in the fields to help the family?
After observing and discussing what the child can do, we must expect
him to do these things. If the parents are used to doing almost everything
for the child, at first this may be difficult for both parents and child. But
soon it will help the child to have more confidence. The parents, also,
will be encouraged by seeing what he can do for himself, and they will
think less about what he cannot do.
Abnormal Postures in CP
Due to abnormal pull of muscles, children with cerebral palsy often spend
a lot of time in abnormal posture. These postures include abnormal
positions of the limbs and the trunk and should be corrected at the
earliest and avoided as much as possible, failing which the child can
become permanently deformed (Fig. 11.10).
Fig. 11.10: Common postural abnormalities seen in CP children

Cerebral Palsy 327
PRINCIPLES OF CORRECTIVE POSITIONING IN CP

Imp: Whenever possible the child should be positioned in a way that
prevent rather than cause these problems. Whatever the child is doing
(lying, sitting, crawling, standing) try to encourage correct posture with
the use of specifically designed CP chair, logs or bolsters, walkers or
simple positioning (Fig. 11.11).
The basic principle of correct posture of the CP child should be such
that:
• Her head remains straight up, looking forward.
• Her trunk remains straight, with shoulders level. Avoid rotation,
lateral flexion, flexion or hyperextension of spine.
• Both arms should be straight and abducted slightly away from the
sides.
• Both hands should be in use, in front of her eyes.
• She should bear weight equally on both sides of her body – through
the pelvis, both hips, both knees, both feet or both arms.
Encourage positions that the child can manage at her stage of
development. Parents may play with her, talk with her, and give her
interesting things to do in these positions. Not all children will be able
to stay in these positions without some kind of support. Special CP chairs,
tables, wedges, pads, or bags of clean sand may be needed to keep a
good position.
Fig. 11.11: Proper positioning of a CP child

WARNING: Never leave a child in any one position for long as his
body may gradually stiffen into that position. Change his position
frequently and encourage him to do so with out assistance. If she is able
to change her posture effectively, then chairs, seats, and other aids must
not prevent the child from moving freely. Any aid should not restrict the
movement of the child.
Reeducation of Dynamic Posture

When the child with cerebral palsy moves she may do so in a very
strange or abnormal way. To some extent this should be allowed, as long
as the child is able to do things as best she can. But also show the child
other ways to move in order to correct some of the abnormal positions
that she repeats again and again. For example,
If her arm repeatedly bends up, encourage her to reach out and hold
objects or a post to hold on to (Fig. 11.12).
If she bends backward a lot, she needs actions that bend her head,
body, and shoulders forward (Fig. 11.13).
Fig. 11.12: Correction of abnormal involuntary reflex stance of right upper limb
Fig. 11.13: Specific activity correcting involuntary stance of right upper limb and
hyperextension of the spine
Cerebral Palsy 329
CORRECTIVE POSITIONING FOR ABNORMAL STATIC POSTURES

Lying and Sleeping
The therapist must try to find ways for the child to be in positions that
are correct or are opposite to his abnormal reflex postures, such as
scissoring of legs in supine posture (Fig. 11.14).
If the child’s body often arches backward, try positioning him to lie
and play on his side. Look for ways to ‘break the spasticity’ by bending
him forward, lying in a hammock or over a barrel (or beach ball or big
rock, etc.), or in a car tire swing (Fig. 11.15).
If the child does not have enough control to reach out in this position,
help position him so he can lift his head using his arms. (Fig. 11.16).
Fig. 11.14: Correction of scissoring of lower limbs
Fig. 11.15: Correction of arching (hyperextension) of trunk
Fig. 11.16: Position to gain head-neck control

If the child’s head always turns to the same side, do not have him lie
so that he turns his head to that side to see Instead, have him lie so that
he has to turn his head to the other side to see the action (Fig. 11.17).
Fig. 11.17: Correct positioning to stimulate the child’s brain
Rolling and Twisting

A child with cerebral palsy is often very stiff when it comes to twisting
or rotating her trunk. However, trunk rotation is necessary for learning
to walk. Rolling also helps develop trunk rotation. If the child is very
stiff, first help her ‘loosen up’ by swinging her pelvis and legs back and
forth. Then help her learn to twist her body and roll. Figure out games
so that the child wants to twist, and does it without help (Fig. 11.18).
Fig. 11.18: Stimulation of rotation of the trunk
Sitting
The way that you help position a child for sitting also depends on the
type of abnormal posture he has. For example, if his legs are adducted,
shoulders depressed and arms internally rotated, as demonstrated in the
picture at the left, sit him with his legs abducted and externally rotated,
his shoulders elevated and turn his arms externally rotated as in the
picture at the right (Fig. 11.19). Playing with a water hose, trying to
water garden plants focuses his eyes and mind to a meaningful and
pleasurable activity, ensuring far better cooperation from the child rather
than simple corrective positioning.
Therapists should look for simple ways to help the CP child maintain
correct sitting and play in the improved position without help. Sitting in
a corner seat, with the legs in a ½ ring helps rotate hips outward. For the
child with spasticity who has trouble sitting due to internal rotation and
Cerebral Palsy 331
Fig. 11.19: Correction of sitting
extension at the hips, you can control his legs like this. This leaves your
hands free to help him control and use his arms and hands in play
activity (Fig. 11.20).
Fig. 11.20: Using a corner seat
The positions demonstrated below helps inhibit scissoring of legs

and tip-toeing reflex in CP while training to gain sitting balance. In the
first picture the therapist may sit facing the child, with his hips abducted
and knee straight, held in position by the legs of the therapist. Further,
as shown in the second picture, you may sit the child on your belly with
his hips abducted, knee flexed and feet flat on the ground. Give support
to the trunk of the child with your knees as needed. As he begins to
reach for his face, help his shoulders, arms, and hands take more natural
positions. Make a game out of touching or holding parts of his face.
Make it fun! (Fig. 11.21).
Fig. 11.21: Teaching correct sitting

Children, who have trouble with balance due to cerebral palsy, polio,
or other musculoskeletal or neuromuscular disability, often sit with their
legs in a ‘W’ in order not to fall over (Fig. 11.22). Sitting in a “W” should
usually be discouraged because it can increase contractures of hip and
knee muscles and lead to subluxation of hip and knee. However, if it is
the only way a child can sit and use her hands, it should be allowed.
Fig. 11.22: “W” sitting
Standing
Many children with cerebral palsy stand and walk in strange positions.
A child’s unsure balance often increases the uncontrolled spasm of certain
muscles and makes balance even more difficult. As a result the child
stands in an awkward position that can lead to frequent falls, deformities
and contractures (Fig. 11.23).
Fig. 11.23: Typical standing posture of a CP child

Cerebral Palsy 333
If the child can maintain her balance without the fear of falling, she
is less tense and can stand straighter. Holding a stick with both hands in
front of the body helps the child keep much straighter standing posture
(Fig. 11.24).
Fig. 11.24: Standing with a forward hand hold
Therapist should look for ways to provide similar assistance during

play and other activities. Here a rolator or cart provides easier balance
and keeps the arms straight (Fig. 11.25).
Fig. 11.25: Using a rolator or a cart for standing training
Two sticks can help the child once she develops some standing
balance. At first the child can hold the tops of the sticks. But let go as
soon as possible. Be sure sticks are taller than child so that she will not
injure herself if she falls (Fig. 11.26).
Fig. 11.26: Standing and walking with two sticks

The child who cannot yet stand alone can be placed in a standing
frame for an hour or 2 each day.
Even for the child who may never stand alone or walk, standing in
a frame helps prevent deformities. It also helps the leg bones grow and
stay strong. Start such training at about the age normal children begin to
stand, i.e. around one year old (Fig. 11.27).
Fig. 11.27: Standing training in a standing frame
CONTRACTURES IN CEREBRAL PALSY

Abnormal muscle tightness often leads to contractures (muscle shortening
and reduced motion of joints). In time, the muscles that keep a limb
flexed become shortened so that the limb cannot straighten even when
the muscles relax. But with care, contractures can often be prevented.
The typical contractures of cerebral palsy are similar to the abnormal
positions of cerebral palsy are demonstrated in Fig. 11.28.
Restriction of ROM in CP is caused by combined effect of spasticity and
contractures decreased range of motion may be caused partly by spasticity
and partly by contractures. Therefore, whenever a child has spasticity, check
to see if contractures are also forming, and if so, how much.
Fig. 11.28: Typical contractures in CP

Cerebral Palsy 335
Prevention of Contractures
In cerebral palsy, it is important that steps to prevent contractures be
included in activities that help the total development of the child. Many
of the corrective positions I have already suggested for activities such as
lying, sitting, and standing about are helpful in preventing contractures.
When there are signs of developing contractures, give even more time
and care to corrective positions.
• Range-of-motion exercises
Although the reasons contractures form in cerebral palsy and polio are
different, many of the stretching and holding exercises will be helpful.
However, in cerebral palsy, take care to do exercises in ways that do not
increase spasticity, but help to relax the spastic muscles.
• Relaxation of spastic muscles
To help relax spastic muscles, before beginning range-of-motion exercises
try the following to see what works best for the child:
– Moist heat: The child may sit or lie in warm water in a tub or
hydrotherapy pool (Fig. 11.29).
– Slow stretch: Slowly rotate the trunk passively or assist the child to
rotate his trunk from side to side. This reduces spasticity throughout
the body, and is a good first stretching exercise (Fig. 11.30).
Fig. 11.29: Warm water soaking in a tub
Fig. 11.30: Trunk rotation for slow stretch

Massage
Therapists sometimes use massage, or rubbing, to try to relax spastic
muscles. Although massage often helps relax muscle spasms, cramps, or
tight muscles from other causes, in CP spasticity, massage usually
increases the muscle tightness. As a general rule, Do not massage spastic
muscles.
• Reflex Inhibiting Postures

To correct abnormal postures, therapists may use inhibitory postures to
release or ‘break’ the muscle spasms. Muscle tone in any part of the body
is affected by the position of the head and body. Spasms that straighten
the legs and pull the knees together can be partly relaxed by bending the
head and back forward. Whatever you do with the child, look for ways
that will help relax and stretch the tight muscles.
• Correct Handling
Never pick up the CP child as demonstrated in the picture at the left. Her
head and spine will extend and her whole body and legs stiffen in
extension. If you roll her a little to one side, it will be easier to bend her
head and back forward as shown in the picture at the right. This relaxes
her hips and legs so that they also bend (Fig. 11.31).
Fig. 11.31: Correct handling technique
• Correct carrying techniques

Teach the parents to carry a CP child in positions that work to correct
abnormal posture. If the child usually lies with arms bent and legs straight,
do not carry him like shown at the left. Carry him in ways that straighten
his arms and bend his knees and hips as shown in the middle. As the
child gains more control, he can be carried with less support as shown
at right (Fig. 11.32).
Cerebral Palsy 337
Fig. 11.32: Carrying techniques – do and don’t
Activities of Daily Living in CP

A child with cerebral palsy will get abilities later than other children-but
she will eventually get them in majority of the cases. Of course, the
child may not achieve everything, and may not always walk. But make
sure the child achieves what she can in each important area of
development.
The CP child will often need a lot of help with language and
communication skills. Develop these skills in whatever way seems
possible: using words, gestures, pointing (with hand, foot, head, or eyes),
or with communication boards. Help the child become as independent as
possible in eating, dressing, washing, toileting, and in meeting other
daily needs. Do this by guided practice, imitation, and step-by-step
learning.
• Toilet activities
To wash between the legs, do not try to pull the child’s legs apart at the
ankles as shown in extreme left. This will increase the adductor spasm
and make the legs pull together more tightly. Instead, put a rolled towel
under the head and shoulders to bend them forward as shown in the
middle. This helps to relax the muscle hypertonia in the whole body.
Then bend the legs and slowly separate them. If you hold them above
the knees, they will open more easily as seen in the extreme right. Washing
will be much easier with her knees bent. After washing with warm water,
you can stretch the tight muscles by slowly abducting her legs as wide
as they will go, and then gradually straighten her knees (Fig. 11.33).
Fig. 11.33: Proper bathing and cleaning technique

• Feeding
When feeding the child, her head and shoulders may extend backward
as seen in the picture at the left. Do not try to pull her head forward. It
will push back even more as seen in the picture in the middle. Her head
and shoulder relaxes more easily if you put your arm across the back of
her neck and push her shoulders forward as depicted in the picture at
extreme right (Fig. 11.34).
Fig. 11.34: Proper feeding technique
• Dressing
When dressing the child, if her arms press against her chest as seen in
the picture at the left, do not try to pull them straight as seen in the
picture at the middle. They will stiffen more. Try holding her arms above
her elbows, and gently turning her arms out and straighten them at the
same time as shown in the picture at the right (Fig. 11.35).
Fig. 11.35: Proper dressing technique
With care and patience, the therapist can learn to handle a CP child
successfully. It is even more important for the therapist to pass on this
knowledge to the parents since they are the primary caregivers. Together
they can often achieve the seemingly impossible task of reintegrating the
CP child in the society.
Annexures
ANNEXURE 1
GLASGOW COMA SCALE
Characteristic Response Score
Opening eyes Spontaneous 4

To verbal command 3
To pain 2
No response 1
Motor response Obeys commands 6

Localizes painful stimuli and pushes away 5
Flexes and withdraws 4
Abnormal reflex flexion 3
Abnormal reflex extension 2
No response 1
Verbal response Oriented and appropriate 5

Disoriented, converses 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Scoring and Interpretation of GCS

Score for best response in each of these areas are added together. The total score
may range from 3 to 15; the higher the score the better the level of consciousness.
A score of 8 or lower usually indicates coma. An awakened person, who has
orientation to person, time and place, and can also follows simple commands,
such as “squeeze my hand”, has a Glasgow score of 15. A patient, oriented to
self, but not to time and place, yet follows all simple commands, has a score of
14. An aphasic person may score a 2 on verbal response, but then total a twelve,
as he will follow simple commands and open eyes spontaneously.
ANNEXURE 2
ASSESSMENT OF MOTOR DYSFUNCTION
A. Spasm Frequency Scale1

Definitions of Spasms:
1. Spasm is a twitching or sustained contraction of a muscle without voluntary
control.
2. A spasm can be a “shooting” of the body part into a position without control;
like sudden withdrawal of the lower limbs.
3. A rapid series of “spasms” without significant pausing/resting is defined as
one spasm.
How many spasms has the patient had in the last 24 hours in affected muscles or
extremity?
0 = No spasms
1 = One spasm or fewer per day
2 = between one and five spasms per day
3 = between five and nine spasms per day
4 = Ten or more spasms per day
B. Manual Muscle Testing

[Medical Research Council Scale2]
With the patient in bed, assess motor strength of all major segments bilaterally
using MRC grading. As far as possible, the action of each muscle should be
observed separately.
0 = No contraction
1 = Flicker or trace of contraction
2 = Active movement through full range of motion, with gravity
eliminated
3 = Active movement against gravity through full range of motion
4 = Active movement against gravity and resistance through full range
of motion
5 = Normal power
(Note: Grades 4 –, 4 and 4 + may be used to indicate movement against slight,
moderate and strong resistance respectively)
C. Modified Ashworth Scale3

0 = No increase in muscle tone
1 = Slight increase in muscle tone, manifested by a catch and release or
by minimal resistance at the end range of motion when the part is
moved in flexion or extension/abduction or adduction, etc.
1+= Slight increase in muscle tone, manifested by a catch, followed by
minimal resistance throughout the remainder (less than half) of the
ROM
2 = More marked increase in muscle tone through most of the ROM, but
the affected part is easily moved
3 = Considerable increase in muscle tone, passive movement is difficult
4 = Affected part is rigid in flexion or extension (abduction or adduction,
etc.)
Annexures 341
D. Adductor Tone Rating Scale1

0 = No increase in tone
1 = Increased tone, hips easily abducted to 45º by one person
2 = Hips abducted to 45º by one person with mild effort
3 = Hips abducted to 45º by one person with moderate effort
4 = Two people required to abduct the hips to 45º
Rate the total amount of pain the patient has had in the last 24 hours.
REFERENCES
1. Snow BJ, Tsui JKC, Bhart MH, Varelas M, Hashimoto SA, Calne DB.
Treatment of spasticity with botulinum toxin: A doubleblind study. Ann
Neurol 1990;28:512-15.
2. Medical Research Council of the UK. Memorandum No. 45. London,
Pendragon House, 1976;6-7.
Aids to the Investigation of Peripheral Nerve Injuries.
3. Bohannon RW, Smith MB. Interrater reliability of a modified Ashworth scale
of muscle spasticity. Phys Ther 1986;67:206-07.
ANNEXURE 3
ASSESSING DEEP TENDON AND PLANTAR REFLEXES
Deep tendon reflexes are tested with a reflex hammer, as shown in Figures. Test
each of the following, grading them from 0 to 5 +, with 0 being no reflex, 2 +
being normal, and 5 + being hyper-reflexia with clonuses (repeated rhythmic
contractions):
Biceps Jerk (Fig. A3.1)

The patient’s arm should be flexed slightly with the palm facing up. Hold the
arm with your thumb in the ante-cubital space over the biceps tendon. Strike
your thumb with the hammer; the arm should flex slightly.
Fig. A3.1: Biceps jerk
Triceps Jerk (Fig. A3.2)

The patient’s arm should be flexed 90 degrees. Support the arm and strike it just
above the elbow, between the epicondyles, on the triceps tendon; the arm should
extend at the elbow.
Fig. A3.2: Triceps jerk

Annexures 343
Brachioradialis Jerk
The patient’s arm should be flexed slightly and resting on your forearm with the
palm facing down. Strike the outer border of forearm about two inches above the
wrist; the palm should turn upward as the forearm rotates laterally.
Knees (Patellar Tendon) Jerk (Fig. A3.3)

With the patient supine on the bed flex the knee, place your hand under the calf
just below the knee and strike the patellar tendon just below the kneecap; the leg
should jerk to extend at the knee.
Fig. A3.3: Knee (patellar tendon) jerk
Ankle (Achilles Tendon) Jerk (Fig. A3.4)

With the patient supine on bed, bend one knee to cross the leg to be tested over
the shin of the sound limb. Stretch the foot in slight dorsiflexion, lightly strike
the heel cord of the leg to be tested, just above the heel- the foot jerk towards
plantar flexion.
Fig. A3.4: Ankle (Achilles tendon) jerk

Plantar Response (Fig. A3.5)

Patient supine on bed, stimulate the outer border of the sole, with a pointed
object like a key, drawing it with firm pressure from heel towards the little toe.
Normal response will be indicated by curling of the toes- Plantar flexor response.
Fig. A3.5: Plantar response

Annexures 345
ANNEXURE 4
Testing of Superficial Sensations

• Light touch- Expose the part to be tested. Use a wisp of cotton to brush
against the skin of the part to be tested to elicit a response from the patient.
You may ask the patient to close his eyes and count aloud every time he
feels the touch. Mark the response on a body diagram as illustrated above.
Response to touch may be graded as Normal/Dullness/Absent.
• Thermal- Use two test tubes, one containing hot and the other cold water.
Touch the skin of the part to be tested alternately with the two test tubes
and record the response on a body diagram as illustrated above. Response
to touch may be graded as Normal/Aberrant/Absent.
ANNEXURE 5
Cranial nerves, their function and the method of testing
Nerve Type Major functions Assessment
I. Olfactory Sensory Sense of smell Ask patient to identify a familiar scent
with eyes closed.
II. Optic Sensory Acuity and field of Ask patient to read from a card or
vision; pupil newspaper, one eye at a time. Test
reactivity to light and visual fields by having patient cover one
accommodation eye, focus on your nose, and identify
the number of fingers you’re holding up
in each of four visual quadrants.
III. Oculomotor Motor Eyelid elevation; Check pupillary responses by shining a
most EOMs; pupil bright light on one pupil; both pupils
size and reactivity should constrict. Do the same for the
(efferent impulse) other eye. To check accommodation,
move your finger toward the patient’s
nose; the pupils should constrict and
converge. Check EOMs by having
patient look up, down, laterally, and
diagonally.
IV. Trochlear Motor EOM (turns eye Have patient look down and in.
downward and
laterally)
V. Trigeminal Both Chewing; facial and Ask patient to hold the mouth open while
mouth sensation; you try to close it and to move the jaw
corneal reflex laterally against your hand. With
(sensory) patient’s eyes closed, touch her face
with cotton and have her identify the
area touched. In comatose patients,
brush the cornea with a wisp of cotton;
the patient should blink.
VI. Abducens Motor EOM (turns eye Have patient move the eyes from side
laterally) to side.
VII. Facial Both Facial expression; Ask patient to smile, raise eyebrows,
taste; corneal reflex and keep eyes and lips closed while you
(motor); eyelid and try to open them. Have patient identify
lip closure salt or sugar placed on the tongue
(usually deferred).
VIII. Acoustic Sensory Hearing; equilibrium To test hearing, use tuning fork or rub
your fingers, place a ticking watch, or
whisper near each ear. Equilibrium
testing is usually deferred.
IX. Glossop- Both Gagging and Touch back of throat with sterile tongue
haryngeal s w a l l o w i n g depressor or cotton-tipped applicator.
(sensory); taste Have patient swallow.
X. Vagus Both Gagging and Assess gag and swallowing with CN IX.
swallowing (motor); Assess vocal quality.
speech (phonation)
XI. Spinal Motor Shoulder movement; Have patient shrug shoulders and turn
accessory head rotation head from side to side
XII. Hypoglossal Motor Tongue movement; Have patient stick out tongue and move
speech (articulation) it internally from cheek to cheek. Assess
articulation.
Annexures 347
ANNEXURE 6
Spinal nerve plexus, their function and signs of dysfunction

Spinal Nerve Function Neuritis/compression or
Transection signs
Cervical Plexus
Phrenic Controls diaphragm, breathing “Hiccups”/inability to breath
Brachial Plexus
Musculocutaneous Biceps Inability to flex forearm
Axillary/circumflex Deltoid Inability to raise arm
(Watch deltoid
injection location!!!)
Radial Triceps, bends thumb, “Wrist drop”
extends hand
Median Flexes hand Carpal tunnel syndrome-
inability to flex wrist
Ulnar Abducts and adducts fingers Inability to abduct/adduct
innervates little finger fingers
Lumbar Plexus
Genitofemoral Scrotum and labia Loss of scrotal elevation
Femoral Flexors of thigh, Inability to flex thigh, extend
extensors of leg leg
Obturator Adductors of thigh Inability to adduct thigh
Sacral Plexus
Gluteal Gluteus muscles Inability to abduct, adduct or
rotate thigh
Sciatic Hamstrings extend thigh, “Foot drop,” inability to extend
flex leg thigh
Branches of
Sciatic
Tibial Plantar flexes foot, gastronomies, Inability to plantar flex,
Post. leg compartment inability to stand on toes
Common peroneal Evertors of foot, peroneus Inability to evert or dorsiflex
muscles, tibialis anterior, foot.
dorsiflex foot Foot drop and
equinovarus (inversion).
Pudendal Penis, clitoris Inability to erect either
ANNEXURE 7
Specific branches of brachial plexus and their muscle innervations

Arises from Nerve formed Root value Muscles supplied
Primary roots Dorsal scapular nerve C5 Rhomboidius major and minor,
levator scapulae
Primary roots Nerve to the subclavius C5, C6 Subclavius
Primary roots Long thoracic nerve C5, C6, C7 Serratus anterior
Main trunk Suprascapular nerve C5, C6 Supraspinatus and
Infraspinatus
Lateral cord Lateral pectoral nerve C5, C6, C7 Pectoralis major and minor
Lateral cord Musculocutaneous C5, C6, C7 Coracobrachialis, brachialis
nerve and biceps brachi. It then
becomes the lateral cutaneous
nerve of the forearm.
Lateral cord Lateral root of the C5, C6, C7 Muscles on the flexor aspect of
median nerve forearm and thenar eminence
of hand
Posterior cord Subscapular nerve C5, C6 Subscapularis and Teres major
Posterior cord Thoracodorsal nerve C6, C7, C8 Latissimus Dorsi
Posterior cord Axillary nerve C5, C6 Anterior branch: Deltoid and a
small area of overlying skin
posterior branch: Teres major
and deltoid muscles. It then
becomes the upper lateral
cutaneous nerve of the arm.
Posterior cord Radial nerve, the C5, C6, C7, Triceps brachi, Anconeus and
largest nerve of the C8, T1 muscles of the extensor
bracial plexus compartment of the forearm
and sensory supply to the skin
of the posterior arm as the
posterior cutaneous nerve of
the arm.
Medial cord Medial pectoral nerve C8, T1 Pectoralis major and minor
Medial cord Medial root of the C8, T1 Muscles on the flexor aspect of
median nerve forearm and thenar eminence
of hand
Medial cord Medial cutaneous C8, T1 front and medial skin of the arm
nerve of the arm
Medial cord Medial cutaneous C8, T1 Medial skin of the forearm
nerve of the forearm
Medial cord Ulnar nerve C8, T1 Flexor carpi ulnaris, the medial
2 bellies of flexor digitorum
profundus, most of the small
muscles of the hand and the
sensory supply of the medial
side of the hand and medial one
and a half fingers on the palmar
side and medial two and a half
fingers on the dorsal side.
Annexures 349
ANNEXURE 8
Sympathetic Functions
• Diverts blood flow away from the gastrointestinal (GI) tract and skin via
vasoconstriction.
• Blood flow to skeletal muscles, the lungs are not only maintained, but
enhanced.
• Dilates bronchioles of the lung, which allows for greater alveolar oxygen
exchange.
• Increases heart rate and the contractility of cardiac cells, thereby providing
a mechanism for the enhanced blood flow to skeletal muscles.
• Dilates pupils and relaxes the lens, allowing more light to enter the eyes.
Para-sympathetic Functions
• Dilates blood vessels leading to the GI tract, increasing blood flow. This is
important following the consumption of food, due to the greater metabolic
demands placed on the body by the gut.
• The parasympathetic nervous system can also constrict the bronchiolar
diameter when the need for oxygen has diminished.
• During accommodation, the parasympathetic nervous system causes
constriction of the pupil and lens.
• The parasympathetic nervous system stimulates salivary gland secretion,
and accelerates peristalsis, in keeping with the rest and digests functions;
appropriate PNS activity mediates digestion of food and indirectly, the
absorption of nutrients.
• Is also involved in erection of genitals.
ANNEXURE 9
Exercise programme recommendations for Stroke Patients

Mode of exercise Major goals Intensity/frequency/duration
Aerobic training
• Large-muscle activities with • Increases 20–60 min session per day
walking, treadmill, stationary independence in ADLs or multiple 10 min sessions
cycle, cross trainer, shoulder • Increase walking as per tolerance
wheel, seated stepper speed/efficiency To be done 3–7 days/wk
• Improve tolerance for
prolonged physical
activity
Additional benefits • Reduce risk of
cardiovascular disease
Strength training • Increase independence 1–3 sets of 10–15 repetitions
• Circuit training in ADLs each of 8–10 exercises,
• Weight machines involving the major muscle
• Free weights groups
• Isometric exercise To be done 2–3 days/wk
Flexibility training
• Stretching • Increase ROM of 2–3 days/wk before or after
involved extremities aerobic or strength training
• Prevent contractures Hold each stretch for 10–30
seconds
Neuromuscular coordination Improve level of safety 2–3 days/wk; consider
and balance training during ADLs performing on same day as
strength activities
Recommended intensity, frequency, and duration of exercise depend on each individual
patient’s level of fitness. Intermittent training sessions may be indicated during the initial
weeks of rehabilitation.
Annexures 351
ANNEXURE 10
Comprehensive Spinal Cord Lesion Evaluation Chart
Name.................................................................Age.............................Sex............................
Address......................................................Referred by......................................................
Date of onset...................................................
Date of admission...........................................
Date of discharge............................................
History: Trauma/fever/nothing specific
Onset: Sudden/Gradual/Episodic
X- ray/Scan shows: # spine/# dislocation of spine/osteoporosis/TB spine/SOL
spine/non-compressive myelopathy changes
Diagnosis:..........................................................................................................................
..............................................................................................................................................
MOTOR LOSS:
Main involvement below: Neck/Nipple/Naval/Groin/Knee/Ankle on Right/
Left/Bilateral
Tone: Hypertonia in UE/LE/Trunk; Hypotonia in UE/LE/Trunk
Reflexes: Abdominal ....................; Knee jerk R ..................../L .................... Ankle
jerk R ..................../L .................... Planter R ..................../L ....................
Muscle Power:
Neck flexor ....................; Extensors ....................; Scapular Elevators R ..................../
L ....................; Depressors R ..................../L....................
Shoulder: Flexor R ..................../L ....................; Extensors R ..................../L
....................; Abductors R ..................../L .................... Adductors R ..................../L
....................
Elbow-flexors R ..................../L....................; Extensors R ..................../L ....................;
Wrist-extensors R ..................../L ....................; Flexor R ..................../L ....................
Upper trunk flexors ..................../Extensors ....................
Lower abdominals ....................; Lower trunk extensors ....................; Quadratus
lumborum: R ..................../L ....................
Hip-flexors: R ..................../L ....................; Extensors: R ..................../L ....................;
Abductors: R ..................../ L ....................; Adductors: R ..................../ L ....................
Knee extensors: R ..................../L ....................; Flexors: R ..................../L ....................;
Ankle dorsiflexor R ..................../Planter-flexors R ..................../L ....................;
Toe: extensors R ..................../L ....................; Flexors R ..................../L
Spinal nerve R Tick Motor loss

Phrenic Nr (C3) “Hiccups”/inability to breath
Axillary (C5-6) Can’t raise arm
Musculo-cutaneous (C5-6) Can’t flex forearm
Radial (C5-8) Wrist drop
Median (C5- T1) Can’t flex wrist and fingers
Ulnar (C7- T1) Can’t abduct or adduct fingers
Thoracic (T1-L1) Can’t control trunk
Femoral (L2-4) Can’t flex hip or extend knee
Obturator (L2-4) Can’t adduct hip
Glutei (L5- S2) Can’t extend, abduct, adduct or rotate hip
Sciatic (L3- S3) Foot drop, can’t extend hip
Tibial (L5- S2) Can’t plantar flex ankle invert foot or curl toes
Common peroneal (L3- S1) Can’t dorsiflex ankle, evert foot or extend toe
Pudendal (S3) No sensation of genitals
SENSORY LOSS (DESCRIPTION)

Bladder and Bowel Function
• Type of bladder ........................................
• Type of incontinence ..................................
• Residual volume ........................................
• Type of catheter ........................................
• Bowel frequency ........................................
• Bowel day .................................................
Mobility Aids being Used

Wheel chair/Walker/Crutches/Para
podium/None
Functinal Mobility
Motor: Able to turn on bed/sit up on bed/sit
with legs out of bed/stand with support/
Stand without support/Walk with support/
Walk without support
Sensory: Able to feel below neck/nipples/
naval/groin/knee/ankle/bladder/bowel/
Pain
ADL: Able to feed/dress/brush teeth/bath/
toilet activities/move indoor/move outdoor
Short-term goals
Long-term goals
Management plan:
Annexures 353
ANNEXURE 11
Check list for Proper Positioning for the Prevention of Pressure Sores and Soft
Tissue Contracture.
Patients who are confined to bed or wheelchair due to any debilitating condition
like CVA, TBI, SCI/D or GB syndrome resulting in motor paralysis and/or
sensory loss may develop complications; such as pressure sores (or decubitus
ulcer) and soft tissue contracture. All these complications are related to improper
positioning, poor nursing and hypo mobility. Caregivers can improve their
nursing skills and assist patients in changing their positions regularly and perform
prophylactic movements to minimize their risk of developing these complications.
I. Pressure Sores
Pressure sore is an ulcerated area of skin over bony prominences. When localized
parts of the body are under continuous pressure, blood supply to that area is
hindered and a pressure sore develop as a consequence.
High-risk Patients
• Chronically ill and bedridden patients, with sensory loss in particular
• Urinary or fecal incontinent leading to most, contaminated skin
• Overweight or underweight
Prevention of Pressure Sores

1. Reduce localized pressure
• Adopt proper positioning to minimize pressure over bony prominences.
• Change positions frequently and turn every 2 hours.
• Avoid friction between the body and the bed during lifting and transfer of
the elderly.
• Choose the suitable type of chair and teach a chair-bound elder, if possible,
to change posture every 30 min with the help of their upper limbs.
• Consult health professionals regarding use of pressure-relieving devices, e.g.
sheep skin and air mattress.
Sheep skin Air mattress
2. Other measures
• Keep clothing and bed linen clean and dry.
• Avoid placing hot or heavy objects, e.g. hot-water bottle and beddings
over the body.
• Wound dressings or bandages should not be too tight.
• Carers should keep their nails short and avoid wearing jewellery that may
cause injury to the patient’s skin.
3. Personal hygiene of the patient
• Keep skin clean and dry; change napkins frequently to decrease risk of skin
infection in elders who suffer from incontinence.
• Inspect the skin condition daily and check for signs of pressure sores, seek
medical advice when necessary.
4. Balanced diet
• Maintain a nutritious and high protein diet, e.g. meat, eggs, milk and beans
to keep skin healthy.
II. Soft Tissue Contractures

Soft tissue contracture is the result of prolonged immobility and improper
positioning leading to joint stiffness and decreased range of movement, especially
in patients with paralytic conditions such as Stroke, Parkinson’s disease, SCI/D
or those who are bedridden.
Prevention of Soft Tissue Contracture

• Adopt proper positioning and change positions every two hours.
Supine Lying
• Support the affected side with pillows, elbow and fingers should be straight
with palm facing upwards
• Place a pillow under the knee of the affected side, keep knee slightly bent.
Annexures 355
Side Lying
• Use a pillow to keep the knees from direct contact with each other in order
to prevent deformity.
• Use a pillow to support the affected side with elbow straight and knee
slightly bent.
Prone Lying
• Turn the head to one side to allow normal breathing.

• Place both arms by each side of the head.
• Support the shoulders, chest and ankles with thin pillows in relaxed position.
Sitting
• Sit straight with the back well supported.

• Support the upper limbs with a pillow or table; place the feet on the floor
or footrest with the knee flexed at 90 degree (right angle).
Passive/Assisted Exercise
Caregivers should encourage and assist patients in performing regular active or
passive stretching exercise in order to maintain good circulation, joint flexibility,
and prevent muscle contracture.
Other Measures
• Use firm pillow with a suitable thickness of approximately 5 to 10 cm
• Use firm mattress to provide adequate support
• Choose wheelchair with back and neck rests
• An ideal chair must have the width of seat = width of pelvis + 5 cm; the
height of seat = 39 to 50 cm; the depth of seat = the length of client’s thigh
– 5 cm; the seat should be firm and well supported.
An ideal chair
Annexures 357
ANNEXURE 12
Urinary Incontinence
Incontinence, the inability to restrain the discharge of urine, is an extremely
common and highly treatable disorder. There are two types:
1. Acute, often related to a disease
2. Chronic persistent incontinence.
Acute Incontinence
Acute incontinence appears suddenly and is not rare in older individuals. It is
usually associated with an underlying disease. The causes of acute incontinence
are best remembered by the mnemonic, DRIP:
Drugs, delirium
Retention of urine, Restricted mobility
Impaction, Infection
Polyuria, Prostatism
The treatment of acute incontinence includes frequent toileting and treatment
of the underlying cause. Catheterization should be avoided as it increases the
likelihood of hospital-acquired infections.
Chronic Incontinence
The types of chronic incontinence are:
• Urge incontinence, the most common form of incontinence, is characterized
by loss of small or large volumes of urine when the individual has insufficient
warning, following the first urge to void, to allow him or her to reach the
toilet.
• Stress incontinence occurs in women who usually have had children and is
characterized by loss of small volumes of urine following coughing, sneezing
or other maneuvers that increase intra-abdominal pressure. It happens
because the internal urethral sphincter, the circular band of muscle that
surrounds the bladder opening, has lost muscle tone and pushed outside of
the abdominal cavity.
• Reflex incontinence occurs in persons with spinal cord damage. Their
bladders do not receive, via the spinal cord, the message to stop urination.
• Functional incontinence occurs when either a person’s physical or mental
state deters the person from urinating in the toilet, i.e., the person lacks the
physical ability to reach the toilet or lacks an adequate thought process to
go to the toilet when having the urge to urinate. Causes include strokes,
dementia and depression.
• Overflow incontinence is of two types:
1. Neurogenic - The individual does not receive a message that the bladder
is full and a signal to urinate is not transmitted. This occurs in persons
with autonomic neuropathy.
2. Obstructive - Prostate enlargement is the usual cause.
Diagnosis
A careful history and step by step bedside investigation of urine flow
(urodynamics) is done as follows:
• The patient empties their bladder and then, lying on the examination table
with a bedpan underneath them, is asked to cough. Loss of urine indicates
stress incontinence.
• The patient is then catheterized and urine drained. If there is more than 100
cc, the person has overflow incontinence.
• A 50 cc syringe is then attached to the catheter and the bladder is filled with
normal saline. The patient is asked to indicate when the first urge to urinate
is felt. If this occurs before 300 cc or if it is accompanied by immediate,
vigorous movement of the bubble in the syringe, the diagnosis is urge
incontinence.
• When 400 cc of saline has been instituted into the bladder, the catheter is
removed and the person is asked to cough again. Loss of urine indicates
stress incontinence.
The patient is then asked to void into a container. If greater than 100 cc, then
overflow incontinence is diagnosed.
Management of Incontinence
Fig. A12.1 below provides a useful summary of the treatments for various types
of incontinence.
Fig. A12.1: Management of incontinence

Annexures 359
Many older persons develop DHIC (detrusor hypercontractibility and

impaired contraction), a combination of urge and neurogenic incontinence.
Treatment depends on needs of patient, e.g. if being wet during the day is
unacceptable, then oxybutynin is given in the morning and bethanechol in the
evening.
Conclusion
Urinary incontinence is a straightforward condition, its cause easily identified
and treated. Treatment can have a major impact on the older person’s quality of
life. Proactive preventive Kegel exercises may be helpful.
Kegel Exercises
Kegel exercises are for the treatment of stress incontinence:
A. During urination try to stop and start the urine flow. At the end of the
exercises make sure you empty your bladder totally.
B. Tighten your anal muscles as if stopping gas from coming out. Then shift
tightness from the rear to the front (vaginal) area.
C. Tighten your vaginal muscles around two fingers inserted into the vagina
or a tampon inserted halfway into the vagina.
Contract these muscles 50 to 100 times daily.
Before coughing or sneezing, contract these muscles.
Expect results after eight weeks of exercising.
Be patient!
ANNEXURE 13
Glossary of Common Terms

• Anisocoria: Describes pupils that are unequal in size. Though pupils may
appear to open (dilate) and close (constrict), it is really the iris that is the
prime mover; the pupil is merely the absence of iris. The size of the pupil
determines how much light is let into the eye. With anisocoria, the larger
pupil lets more light enter the eye.
• Ataxia: Lack of coordination and steadiness in movements and gait.
• Atrial Fibrillation: An ineffective atrial contraction, resulting from
disorganized atrial electrical activity. Atrial fibrillation may lead to a CVA
as blood pools in the heart vessels secondary to lack of ineffective pump,
and then the pooled blood coagulates, breaks off and is expelled toward the
brain.
• Cerebral Vascular Accident (or stroke): A broad term including various
disorders influencing the blood flow to the brain; cerebral ischemia is an
inadequate flow of blood to the brain, perhaps from a blood clot; hemorrhage
is an accumulation of blood, which may displace brain tissue or cause
ischemia to brain cells.
• Consensual Response: A slight constriction in the opposite pupil when
testing pupillary reaction with a flashlight.
• Diplopia: Double vision, the condition whereas a single object appears as
two.
• Edema: The swelling of soft tissues as a result of excess water accumulation.
• Decorticate Posturing: Arms are adducted and flexed, with the wrists and
fingers flexed on the chest, the legs may be internally rotated and stiffly
extended, with plantar flexion of the feet. Illustrated below:
– Decerebrate Posturing: Arms are adducted and extended with the wrists
pronated and the fingers flexed; the legs may be internally rotated and
stiffly extended, with plantar flexion of the feet.
• Head Injury Home Care Instructions: A set of guidelines for the family of
a head injury victim to indicate signs and symptoms which must be reported
immediately to the physician, such as: increased drowsiness, confusion,
nausea and vomiting, seizures, stiffening of neck, sensory disturbances,
behavior changes or motor problems. Someone must stay with the victim to
monitor for these changes. Advise the victim to avoid alcohol, driving, and
to check with the physician before taking any medications that may increase
drowsiness.
• Infarction: The formation of an infarct, an area of tissue death due to a local
lack of oxygen.
• Pernicious Anemia: A blood disorder caused by inadequate vitamin B12 in
the blood, existing because the stomach does not produce the substance that
allows the body to absorb vitamin B12.
• Retrograde Amnesia: The lack of memory relating to events occurring around
a traumatic incident.
• Widening Pulse Pressure: Increasing systolic pressure, along with decreasing
diastolic pressure.
• Hemiplegia: Involvement of both limbs on one side of the body.
• Paraplegia: Involvement of both legs.
• Quadriplegia (tetraplegia): Involvement of all four limbs.
Annexures 361
• Diplegia: Involvement of all four limbs with more involvement in the lower
limbs than upper limbs.
• Paresis: Partial weakness to one or more limbs.
• Spasticity: An involuntary increase in muscle tone.
• Muscle Tone: Amount of tension in a resting muscle or muscle group.
• High Tone (spasticity or hyper-tonicity): Excessive amount of tone in a
resting muscle or muscle group.
• Low Tone (Hypotonia): Decreased amount of tone in a resting muscle or
muscle group.
• Functional Muscle Mass: Muscle mass that can be improved in a training
program.
• Contracture: Shortening of a muscle group and tendon usually seen in persons
with spasticity.
• Progressive Disorder: Condition that gets worse over time.
• Exacerbation: A flare-up in which symptoms deteriorate in a particular
condition.
• Remission: Symptoms stabilize or slightly improve.
Index
A Botulinum toxin block 82

Brachial neuralgia or neuritis 263
Abnormal posturing 31 Brain death 138
Amyotrophic lateral sclerosis 252 Brainstem gliomas 149
Analgesia 89 Brainstem syndrome 91
Aneurysm 109 Brain tumors 145
Anterior cord syndrome 90, 191 causes 145
Anterior horn cells disorder 194 diagnosis 147
Aphasia 130, 141 general considerations 145
Aquatic therapy programs 207 long-term outlook 152
Arterial-venous malformation 109 symptoms 146
Astrocytomas 148 treatment 150
Ataxia 44, 85, 288, 289 anti-seizure medication 151
causes 290 chemotherapy 151
classification 291 radiation therapy 151
autosomal dominant 292 steroids 151
autosomal recessive 291 surgery 150
hereditary 291 ventriculo-peritoneal shunt 151
management 294 Broca’s aphasia 141
cerebellar re-education 296 Brown-Séquered syndrome 90, 192
Frenkel’s exercises for ataxic Brunstrom’s technique 96
conditions 298 Bulbar palsy 255, 243
instructions to patients: coping
skills 296 C
interventions in Friedreich’s
ataxia 298 Carpal tunnel syndrome 261
occupational therapy 297 Cauda equina syndrome 197
screening and diagnosis 293 Central cord syndrome 90, 191
signs and symptoms 289 Central nervous system 11
treatment 293 embryology 11
Ataxia-telangiectasia 292 Cerebellar function 41
Autonomic dysreflexia 204, 220 Cerebral edema 134
Autonomic nervous system 25 Cerebral palsy 290, 317
function 26 abnormal postures 326
Axonal degeneration 242 activities of daily living 337
Axonotenesis 243 dressing 338
feeding 338
B toilet 337
assessment 340
Bell’s palsy 267 deep tendon and plantar reflexes
Benign paroxysmal postural vertigo 342
301 motor dysfunction 340
Bilateral vestibular paralysis 303 causes 317
Bladder management program 216 perinatal 317
postnatal 318 problems with thinking and

prenatal 317 memory 130
contractures in 334 sensory disturbances including
massage 336 pain 129
prevention 335 thalamic pain syndrome 129
corrective positioning for abnormal understanding language 130
static postures 329 diagnosis 110
lying and sleeping 329 specific tests 111
rolling and twisting 330 general caring tips 118
sitting 330 adopting proper posture 118
standing 332 affected side of the body 118
detection 318 good personal hygiene 120
difficulties 319 injury 118
abnormal reflexes 320 mobility of affected limbs 118
communication 319 proper lifting and transferring
intelligence 319 technique 120
restless behavior 320 swelling of extremities 120
functional mobility and ADL 325 goals of rehab in CVA 127
learning of walk 324 long-term problems of stroke
pattern of involvement 323 patients 126
principles of corrective positioning management of post-stroke sequel
327 121
reeducation of dynamic posture medical management 112
328 acute care stroke 112
scoring and interpretation of GCS ICU management 112
339 physiotherapy in acute care of CVA
types 321 117
ataxic 322 caring goal 118
athetoid 322 essential observation 117
spastic 321 physiotherapy in long-term care of
Cerebrospinal fluid 187 CVA 121
Cerebrovascular accidents 106 prevention 114
assessment of post-stroke sequel principles of nursing care 115
122 prevention of secondary
assessment of gait 125 complications 116
changes in behavior 122 simple tips for the caregiver 116
deficits in balance reactions and prognosis 114
postural control 124 risk factors 107
deficits in motor control 123 general 109
functional mobility skills 124 hemorrhagic CVA 108
sensory deficits 123 ischemic CVA 107
speech and communication 122 pathophysiology 107
categories 106 route map to stroke rehab 128
hemorrhagic 106 signs and symptoms 109
ischemic 106 specific 110
complications 114 specialized stroke assessment tools
complications following stroke 129 125
bladder and bowel incontinence staging of recovery in CVA 122
130 surgical interventions 113
emotional disturbances 131 Cerebro-vascular lesions 140
hemiplegic’s shoulder pain 129 Chest infection 117
Chickenpox 290 Dermatome chart 345

Choking 117 Dermatomes 20
Circle of Willis 14 Disorder of control micturition 195
Cranial nerves 16 Disorder of control of respiration 194
Claw hand 283 Disorders of equilibrium 288, 300
Cognitive impairment 141 Disorders of peripheral nerves 242
Coma 138 basic pathology 242
Computed tomography 49 management approach 244
Cortico-basal degeneration 157 nomenclature 243
Coup injury 133
Disorders of the brain 105
Cranial nerves 41
Dizziness and imbalance 300
Craniopharyngioma 150
main categories 301
central dizziness 303
D medical dizziness 304
Deep brain stimulation 161 otologic dizziness 301
common DBS procedures 161 psychogenic dizziness 305
coping with Parkinsonism 179 unlocalized dizziness 305
family concerns 181 Dorsal (posterior) column syndrome
lifestyle changes 179 192
seeking help 181 Drug-induced Parkinsonism 156
telling the employer 181 Dysarthria 142
discharge instructions 178 Dysphasia 44
home safety 175 Dystonia 37, 46
maintain mental well-being 177
prevent complications in bed- E
ridden patients 177
safety in bathroom and toilet Electro-diagnostic studies 60
176 Electroencephalogram 60
setting up living spaces 176 Electromyogram 65
teaching communications skills Electromyography 68
177 Entrapment neuropathies 256
teaching safety in home Ependymomas 149
environment 175 Erb-Duchenne palsy 269
principles of physical care and Erectile dysfunction 225
nursing 164 Evoked potentials 69
exercise plan 164 brainstem auditory 70
exercises in lying position 165
somatosensory 70
ten-point maintenance exercise
visual 69
program 164
technique 161
tips to maintaining optimum F
wellness 182 Flaccidity 83
Deep tendon reflexes 342 Foot drop 284
ankle (Achilles tendon) jerk 343
biceps jerk 342
G
brachioradialis jerk 343
knees (patellar tendon) jerk 343 Gaze palsy 45
plantar response 344 Glasgow coma scale 30, 136
triceps jerk 342 Gliomas 148
Deep vein thrombosis 204 Guillain-Barre ‘syndrome 250
H Motor aphasia 141

Motor control and motor learning 97
Hematoma 108, 135 Motor deficits 46
Heterotopic (ectopic) bone formation Motor dysfunction 36
204 Multiple infarct dementias 157
Homan’s sign 204
Multiple sclerosis 290
Human brain 12
Multiple system atrophy 157
blood supply 12
Muscle power 39
function 15
Muscle tone 36
protection 14
Myelopathy 184
Hydrocephalus 135
Myotome 20
Hydrotherapy 207
Hypertonia 36, 78, 79
causes 84 N
diagnosis 84 Nerve blocks 81
recovery and rehabilitation 85 Nerve conduction studies 66
symptoms 84 Nervous system 9
treatment 85 autonomic 25
central 11
I peripheral 19
Incoordination 85 Neuritis or neuralgia 243
Intracranial pressure 146 Neuro rehab team 2
Intradiscal electrothermoplasty 261 clinical psychologist 4
Intra-medullary tumors 191 occupational therapist 3
Intrathecal baclofen 82 orthotist 5
physiotherapist 2
rehab nurses 3
K
social and vocational counselors 4
Kegel exercises 359 Neuro-development technique 95
Klumpke’s palsy 269 Neurological disorders 72
behavioral abnormalities 73
L motor abnormalities 73
sensory abnormalities 73
Language and communication Neurological disorders assessment 27
problems 141 areas of lesion 44
Lateral corticospinal tract (LST) brainstem 46
syndrome 192 cortical 44
Level of consciousness 29, 137 spinal cord 46
Locked-in syndrome 138 sub-cortical 45
Lower motor neuron syndromes 75 assessing the cranial nerves 41
Lower motor neuron type bladder 196
assessment of vital signs 34
clinical implication of dominance 47
M evaluating cerebellar function 41
Magnetic resonance imaging 50 general examination 29
photogallery 56, 57 abnormal posturing 31
Mat exercises 98 abnormal pupillary reactions 33
Medulloblastomas 149 decerebrate posturing 32
Meniere’s disease 301 decorticate posturing 32
Meninges 187 level of consciousness 29
Monosynaptic reflex arc 8 orientation 31
history taking 28 Peripheral neuropathy 244

physical evaluation 36 diagnosis 247
assessment of muscle power 39 prevention and screening 248
changes in muscle tone 36 prognosis 250
signs of motor dysfunction 36 risk factors 245
radio imaging 35 symptoms 244
testing reflexes 39 treatment 248
evaluating sensation 40 alternative medicine 249
Neurological dysfunctions 98 medical management 249
Neuron 6 self-care instructions to the
axon 6 patient 248
cell body 6 types 245
dendrites or nerve endings 7 Phenol/alcohol peripheral nerve block
Neuronal degeneration 242 81
Neuropathy 243 Physiotherapy 72
Neuro-physiotherapy 72 Pinched nerve syndrome 256
Neurophysiotherapy 76 Pineal region tumors 150
Neuropraxia 243 Positron emission tomography 52
Neurotemesis 243 Post-concussion syndrome 140
Neurotization (nerve transfer) 273 Pressure-sore 116, 212
Neurovascular compression 274 Primitive neuroectodermal tumors 149
Normal movement 77 Progressive supranuclear palsy 156
Nystagmus 46
Propriceptive stimulation 97
Proprioceptive neuro-muscular
O facilitation approach 92
Olivo-ponto-cerebellar atrophy 157 Pseudobulbar palsy 255
Optic nerve gliomas 149 Psychiatric health 142
Pulmonary hypostasis 205
P
R
Pain management 211
Pallidotomy 163 Radial nerve lesion 281
Paraneoplastic syndromes 290 Radio imaging 35
Paresthesia 45, 87 Radiography 58
Parkinsonism 153 Reflex sympathic dystrophy 129
Parkinson’s disease 154 Reflexes 39
primary Parkinsonism 154 Remediation/facilitation concept 91
age of onset 154 Rigidity 38
clinical features 155
pathophysiology 154 S
secondary Parkinsonism 156
experimental treatments 160 Sacral sparing 198
medications 158 Sciatica sciatic nerve compression 257
neuroprotective treatments 159 Segmental demyelination 242
principles of management 158 Seizures 45
recognizing secondary Sensation 40
Parkinsonism 156 Sensory abnormalities 87
surgical treatments 160 Sensory loss 352
Peripheral nerve injuries 269 Shy-Drager syndrome 157
Peripheral nervous system 19 Sleep apnea 224
Soft tissue contractures 354 pressure sores after spinal cord

Spasticity 37 injury 212
Spect/pet scans 52 cushions 214
Spinal cord 16 pathophysiology 213
embryology 19 prevention 214
injury 19 rehab life after spinal cord damage
segments 18 209
structure 17 adjusting to life 209
Spinal cord injury 184 adjusting to spinal cord injury
assessment of spinal cord lesions damage 210
199 healthy adjustment 210
bladder management program 216 healthy family adjustment 211
condom catheters 217 relevant anatomy of the spinal cord
Foley or suprapubic catheter 186
216 reproductive health for women 226
intermittent catheterization 217 respiratory complications after 222
blood supply of the spinal cord 189 secondary complications 223
bowel management 218 steps to prevent 224
autonomic dysreflexia during sexuality and reproductive heath
bowel program 220 for men 224
stimuli that cause autonomic medicated urethral system
dysreflexia 220 erection 225
clinical features of spinal cord penile injection therapy 225
injury/lesions 190 vacuum pump 225
clinical implication 190 techniques of handling, positioning,
localization of a spinal cord lesion mobility and ADL training 229
185 techniques of progressive
management 201 mobilization 233
acute care of spinal injuries 201 bedside assistance 241
ADL skill training 202 dressing and grooming 241
bed mobility training 202 training for activities of daily living
hydrotherapy 207 240
individual and family counseling urinary tract infections 217
202 causes 217
maintain skin integrity 205 prevention 218
medical care 201 symptoms 218
physical therapy program 203 Spinal nerve plexus 20
respiratory training 202 brachial 23
skin care 202 cervical 22
nutrition and weight control 227 lumbo-sacral 24
fiber 228 Spinal shock 193
water and fluids 228 Spino-cerebellar ataxias 292
weight gain 227 Stimulated voiding 217
pain after spinal cord injury Stress incontinence 357
damage 211 Striatonigral degeneration 157
instructions to patients in Stupor 138
managing pain 212 Superficial sensations 345
pain management 211 Swelling 108
pathophysiology 198 Syringomyelia 191
T Vestibular neuritis 302

Vestibular rehabilitation therapy 306
Thalamic pain syndrome 129
assessment of vestibular
Thoracic nerve lesion 281
dysfunction 309
Thoracic outlet syndrome 273
balancing exercises 312
Transient ischemic attack 108
visual dependence exercises 313
Traumatic brain injury 131
acute care of a TBI patient 135 Epley and Semont maneuvers
causes of head injuries 131 313
complications 139 diagnosis of BPPV 310
disabilities 140 Dix-Hallpike maneuver for
effects of injury to the brain 153 testing BPPV 311
kinds of rehabilitation 143 history of the disorder 310
long-term problems 143 general interventions 306
mechanism of brain damage 133 Cawthorne-Cooksey exercises
prevention 144 306
TBI affect consciousnsess 137 group therapy 307
types 132 home management 316
Traumatic spinal cord lesions 198 individualized physical therapy 308
rationale 306
U VIIth cranial nerve palsy 267
Visual field defects 45
Ulnar nerve lesion 283
Visual impairment 141
Upper motor neuron syndrome 74
Vital signs 34
Upper motor neuron type bladder 195
Urinary incontinence 357
Urinary tract infection 217 W
Wallerian degeneration 242
V Wasting of muscles 83
Vascular Parkinsonism 157 Wernicke’s aphasia 141
Vegetative state 138 Wilson’s disease 292
Ventriculo-peritoneal shunt 151 Winged scapula 281, 282

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HANDBOOK OF

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

First Edition: 2009

Along with time tested methods adopted in dealing with neurological

1. Rehabilitation Process of the Neurological Disorders ....................... 1

Annexures .............................................................................................. 339

• Psychological support and physical rehabilitation go hand-in-hand,

NEURO REHAB TEAM

Physiotherapy—Role and Scope

• Before discharge from a health care institution, a program of exercises

Rehab Nurses—Role and Scope

Occupational Therapist—Role and Scope

Clinical Psychologist—Role and Scope

Social and Vocational Counselors—Role and Scope

• Exhaustive planning and training is necessary to take up a new

Orthotist—Role and Scope

STRUCTURE OF THE BASIC NEURON

Depending upon the type of neuron, axons can be covered with a

• Receptors sense the environment (chemicals, light, sound, touch)

Monosynaptic Reflex Arc

Fig. 2.3: Monosynaptic reflex arc

PARTS OF THE NERVOUS SYSTEM

Fig. 2.5: The layout of the nervous system

Fig. 2.6: Functional organization of the nervous system

CENTRAL NERVOUS SYSTEM (CNS)

Embryology of the CNS—Sequential Development

Being extremely sensitive, the entire CNS is protected by the

ANATOMY OF THE HUMAN BRAIN

Blood Supply to Brain

Fig. 2.8: The blood supply to brain through the vertebral

Protecting the Brain

Why the Volume of CSF should be Limited?

Function of the Human Brain

coloumn. The main function of the spinal cord is transmission of neural

Structure of the Spinal Cord

Spinal Cord Segments

Fig.2.12: Spinal cord segments

PERIPHERAL NERVOUS SYSTEM

Myotome and Dermatomes

Fig. 2.13: Myotome

Spinal Nerve Plexus

• The cervical plexus provides nerve connections to the head, neck,

Fig. 2.15: Nerves formed by the cervical plexus

supply sternocleidomastoid, Trapezius and Levator scapulae muscles.

Injuries to the Brachial Plexus

Fig. 2.16: Brachial plexus

Fig. 2.17: Lumbo-sacral plexus

• Inferior gluteal nerve having root value of L5, S1 and S2 supplies G.

Injury of Lumbo-sacral Plexus

AUTONOMIC NERVOUS SYSTEM (ANS)

functions, but also salivation, perspiration, vasodilatation, vasoconstriction,

Accurate clinical assessment is the key component in the care of a

ASSESSMENT OF NEUROLOGICAL DISORDERS

cardiopulmonary or gastrointestinal crisis. The neurological system is

History Taking: The Art of Interviewing the Patient/Care-giver

While interviewing the patient, be careful not to suggest symptoms,

GENERAL EXAMINATION OF NEUROLOGICAL DISORDERS

Glasgow Coma Scale (See Annexure 1)

Fig 3.1: Decorticate posture

Decorticate posture indicates damage to the corticospinal tract, the

Common Causes of Decorticate Posturing

Common Causes of Decerebrate Posturing

Fig. 3.2: Decerebrate posturing

• It may alternate with decorticate posture, i.e. abnormal posturing