Acute Neurologic Disorders

Review of the NS

Brain
I. Definition
The communication and control center of the body
Receives, processes and evaluates many kinds of input ; decides on the
response to be taken ; and then initiates the response
Responses :
o Involuntary activity regulated by autonomic ns
o Voluntary actions regulated by somatic ns
II. Protection for the Brain

Protected by :
o Skull
o 3 membranes / meninges
o CSF
Sutures :
o Immovable joints consisting of fibrous tissue
o Cranial and facial joints are connected by this
o If pressure inside the skull increases in infants before sutures
fuse or ossify , cranial bones may separate causing the head to
enlarge
Foramina :
o Cavities /Openings in skull
o Canals through which nerves and blood vessels pass
o Largest opening is the Foramen magnum , located in the
occipital bone @ the base of the skull where the spinal cord
emerges

Meninges

Consists of 3 connective tissue membranes covering the brain and

spinal cord

Invaginate @ 4 points forming a supportive partition bet portions of

brain :
o Falx cerebri
- extends downward into the longitudinal fissure (deep
groove) bet the cerebral hemispheres
o Tentorium cerebelli
- separates the cerebral hemispheres from the cerebellum

Dura mater
o Outer layer
o Tough, fibrous, double-layered membrane that separates @
specific points to form the dural sinuses w/c collect venous
blood and CSF for return to the general circulation

Subdural space
o Lying beneath the dura
o A potential space i.e normally empty, could fill with blood
after an injury

Arachnoid
o Middle layer
o Loose, web-like covering

Subarachnoid space
o Contains the CSF and cerebral arteries and veins
o Lies beneath the arachnoid

Arachnoid villi
o Projections of arachnoid into the dural sinuses @ several
places around brain through w/c CSF can be absorbed into
the venous blood

Pia mater
o Inner layer
o Delicate connective tissue
o Adheres closely to all convolutions on the surface of the brain
o Many small blood vessels can be found
CSF

Provides a cushion for the brain and spinal cord

Clear, almost colorless liquid
Concentrations of electrolytes, glucose and protein remain relatively
constant

Characteristics :
o Appearance clear and colorless
o Pressure 9 to 14 mm Hg or 150 mm H20
o RBC - None
o WBC Occasional
o Protein 15 to 45 mg/dL
o Glucose 45-75 mg/dL
o Sodium 140 mEq/L
o Potassium 3 mEq/L
o Sp. gravity 1.007
o pH 7.32 to 7.35
o Volume in the system @ one time 125 to 150 mL
o Volume formed in 24 h 500 to 800 mL
Change in the characteristic is a useful diagnostic tool
Formed constantly in the choroid plexuses in the ventricles and then
flows into the subarachnoid space where it circulates around the
brain and spinal cord and eventually passes through the arachnoid
villi , returning into the venous blood
To maintain a relatively constant pressure within the skull
(intracranial pressure) , it is important for equal amt of CSF to be
produced and reabsorbed @ the same rate
Present throughout the brain except where the presence of sensory
receptors for regulation of body fluids requires normal diffusion (eg.
osmoreceptors in hypothalamus)

Blood-brain barrier

Protective mechanism provided primarily by relatively impermeable

capillaries in the brain

Endothelial cells of the capillaries are tightly joined together rather

than possessing pores

Limits the passage of potentially damaging materials into brain and

controls delicate but essential balance of electrolytes, glucose, and
proteins in brain

Poorly developed in neonates and therefore substances such as

bilirubin , Rh factor incompatibility or other toxic materials can pass
easily into infants brain , causing damage

When fully developed , it can be a disadvantage because it does not

allow the passage of many essential drugs into brain

Lipid-soluble substances including some drugs and alcohol , pass

freely into brain
Blood-CSF barrier

@ choroid plexus

Control constituents of CSF

III. Functional Areas
Cerebral hemispheres

Make up the largest and most obvious portions of the brain

Outer surface is covered by elevations (gyri) that are separated by

grooves (sulci)

The longitudinal fissure separates the 2 hemispheres

The surface (cortex) consists of gray matter / nerve cell bodies

White matter :
o Beneath the gray matter
o Composed of myelinated nerve fibers bundled into tracts
w/c :
- connect the hemispheres (corpus callosum)
- occur as projection fibers , connecting the cortex to the
spinal cord
- occur as association fibers, connecting diff gray areas in
the brain

Each hemisphere
o Divided into 4 major lobes , each of w/c has some specific
functions
o Concerned with voluntary movements and sensory function in
the opposite (contralateral) side of the body

Upper motor neurons (UMNs)

o Cells of the motor cortex of the frontal lobe w/c initiate
specific voluntary movements
o Their axons form the corticospinal tracts in the spinal cord

Because the crossover of most of these tracts occurs in

medulla, damage to the motor cortex in L frontal lobe
adjacent to the longutidinal fissure (on top of head) results
paralysis / paresis of muscles of the R leg
Each special sensory area of the cortex has an association area
surrounding primary cortex in w/c sensory input is recognized and
interpreted
o Primary visual cortex receives stimuli from the eye
o Surrounding association cortex identifies the object seen
o If primary cortex is damaged :
- person is blind
o If association area is damaged :
- person can see the object but cannot comprehend its
significance
Basal nuclei
o Sometimes called the basal ganglia
o Clusters of cell bodies or gray matter
o Located deep among the tracts of the cerebral hemispheres
o Part of the extrapyramidal system (EPS) of motor control
w/c controls and coordinates skeletal muscle activity,
preventing excessive movements and initiating accessory and
often involuntary action
o 2 additional nuclei located in the midbrain : (also connected
to basal nuclei and EPS)
- substantia nigra
- red nucleus
Limbic system
o Consists of many nuclei and connecting fibers in the cerebral
hemispheres that encircle the superior part of the brain
stem
o Responsible for emotional reactions or feelings and for this
purpose, it has many connections to all areas of the brain
o Part of hypothalamus is involved with limbic system , it
provides link for autonomic responses such as altered BP or
nausea that occur when one experiences fear, excitement,
or an unpleasant sight or odor
o Any cognitive (intellectual) decision arising from higher
cortical centers may be accompanied by an emotional aspet
mediated through limbic system
o

Dominant hemisphere / L hemisphere

Side of the brain that controls language

2 special areas involved in language skills :

o Brocas area
- the motor or expressive speech area
- the output of words, both verbal and written is
coordinated in an app and understandable way
- located @ the base of the premotor area of the L frontal
lobe
o Wernickes area
- comprehends language received , both spoken and written
- located in the posterior temporal lobe
- has connecting fibers to the prefrontal, visual, and
auditory areas

Also responsible for :

o Mathematical
o Problem-solving
o Logical reasoning
Right Hemisphere

Has greater influence on :

o Artistic abilities
o Creativity
o Spatial relationships
o Emotional and behavioral characteristics
4 major Lobes of each hemisphere

Frontal Lobe
o Prefrontal area intellectual function and personality
o Premotor cortex skilled movements
o Motor cortex voluntary movements
o Brocas area speech (expression)

Parietal Lobe

o Somatosensory area sensation

Occipital Lobe
o Visual cortex - vision
Temporal Lobe
o Auditory cortex - hearing
o Olfactory cortex smell
o Wernickes area - comprehension of speech ; memory

Diencephalon

Central portion of the brain

Surrounded by the hemispheres

Contains the thalamus and hypothalamus

Thalamus

Consists of many nerve cell bodies

Serve as a sorting and relay station for incoming sensory impulses

Connecting fibers transmit impulses to the cerebral cortex and

other app areas of brain
Hypothalamus

Has a key role in maintaining homeostasis

o Controlling autonomic NS and much of endocrine system
through hypohysis / pituitary gland
o Regulation of body temp
o Intake of food and fluid
o Regulation of sleep cycles

Also key to the :

o Stress response
o Emotional responses through limbic system
o Biologic behaviors (eg. sex drive [libido])
Brainstem

Inferior portion of the brain

Connecting link to the spinal cord

Pons

Composed of bundles of afferent (incoming) and efferent (outgoing)

fibers
Several nuclei of cranial nerves are also located here

Medulla oblongata

Contains the :
o Vital control centers that regulate respiratory and
cardiovascular function
o Coordinating centers that govern cough reflex, swallowing and
vomiting

Location of the nuclei of several cranial nerves

Distinguished by 2 longitudinal ridges on the ventral surface termed

pyramids , marking the site of crossover (decussation) of the
majority of fibers of corticospinal (pyramidal) tracts w/c results in
contralateral control of muscle function
Reticular formation

Network of nuclei and neurons scattered throughout the brainstem

Has connections to many parts of the brain

RAS/ Reticular-activating system

o Determines the degree of arousal or awareness of the
cerebral cortex
o Neurons decide w/c of the incoming sensory impulses the
brain ignores and w/c it notices
o Many drugs can affect the activity of the RAS thus
increasing or decreasing input to the brain
Cerebellum

Located dorsal to the pons and medulla , below the occipital bone

Functions to coordinate movement and maintain posture and

equilibrium by continuously assessing and adjusting input from:
o Pyramidal system
o Prorioceptors in joints and muscles
o Visual pathways and vestibular pathways from inner ear

IV. Blood Supply to the Brain

Blood is supplied to the brain by the internal carotid arteries and

vertebral arteries
Each internal carotid artery is a branch of a common carotid artery (R
or L) and includes the carotid sinus
Carotid sinus :
o Location of pressoreceptors/Baroreceptors that signal
changes in BP
o Also of chemoreceptors that monitor variations in blood pH
and O2 levels
At the base of brain, each internal carotid artery divides into an
anterior and middle cerebral artery
o Anterior cerebral artery supplies the frontal lobe
o Middle cerebral artery supplies the lateral part of cerebral
hemispheres ,primarily temporal and parietal lobes
Posteriorly , the vertebral arteries join to form :
o Basilar artery supplies branches to brainstem and cerebellum
as it ascends
At the base of the brain , basilar artery divides into :
o R and L posterior cerebral arteries - supply blood to the
occipital lobe
Anastamoses bet. the major arteries at the base of brain are provided
by the :
o Anterior communicating artery bet. the anterior cerebral
arteries
o Posterior communicating arteries bet. the middle cerebral
and posterior cerebral arteries
Circle of Willis
o The arrangement of arteries and anastamoses
o Provides an alternative source of blood when internal carotid or
vertebral artery is obstructed
o Surrounds the pituitary gland and optic chiasm
Blood flow in cerebral arteries is relatively constant because brain
cells constantly use O2 and glucose and have little storage capacity
Autoregulation
o Mechanism by w/c increased CO2 levels or decreased pH in
blood or decreased BP in an area of brain results in immediate
local vasodilation
o The pressoreceptors and chemoreceptors protect brain from
damage r/t abnormal BP or pH levels in systemic flow
Venous blood from brain collects in dural sinuses and then drains into R
and L internal jugular veins, to be returned to the heart

V. Cranial Nerves

There are 12 pairs

Originate from the brainstem
Pass through the foramina in the skull to serve structures in the head
and neck
The vagus nerve :
o Serves a more extensive area
o Branching to innervate many of the viscera
May consist of :
o Motor fibers
o Sensory fibers
o Mixed nerve (both motor and sensory)
4 cranial nerves (III, VII, IX, X) include parasympathetic fibers

Spinal Cord and Peripheral Nerves

I. Spinal cord

Protected by :
o Bony vertebral column
o Meninges
o CSF
Continuous with medulla oblongata
Ends @ the level of first lumbar vertebra
Cauda equina
o Beyond the end of spinal cord extends a bundle of nerve roots
Arrangement of spinal cord is significant because there is little risk of
damaging the cord when a needle is inserted into the SA space below
the 1st lumbar level (usually space bet. L3-L4) to obtain a sample of CSF

Consists of nerve fibers / tracts :

White matter
o Surrounding an internal butterfly-shaped core of gray matter
or nerve cell bodies
o Composed of afferent (sensory) and efferent (motor) fibers
that are organized into tracts and communicating fibers that
run bet the 2 sides of spinal cord
o Each tract is assigned a unique position in the white matter
o Ascending tracts
- conduct sensations w/c are relayed from spinal nerves and
receptors on opposite side of body to thalamus
o Descending tracts
- 2 types : pyramidal /corticospinal tracts and extrapyramidal
tracts
o Pyramidal tracts
- conduct impulses concerned with voluntary movement from
motor cortex (upper motor neurons) to lower motor neurons in
anterior horn @ app level of spinal cord
- most of these tracts cross in medulla
o Extrapyramidal tracts
- carry impulses that modify and coordinate voluntary
movement and maintain posture
Gray matter
o Anterior horns
- consist of cell bodies of motor neurons whose axons leave the
spinal cord through the ventral root of spinal nerves to
innervate skeletal muscles
o Posterior horns
- contain association (interneuron) neurons
II. Spinal Nerves

31 pairs of spinal nerves emerge from spinal cord carrying motor and
sensory fibers to and from organs and tissues of body
Named by loc in the vertebral column where they emerge and are
numbered within each section (eg. C1-C8)
Each is connected to the spinal cord by two short roots
o Ventral /anterior root
- made up of efferent or motor fibers from lower motor
neurons in anterior horn
o Dorsal/ posterior root
- made up of afferent or sensory fibers from dorsal root
ganglion (collection of nerve cell bodies) where sensory fibers
from peripheral receptors have already synapsed
Dermatome
o Area of sensory innervations of skin by a specific spinal nerve
o Can be drawn on a map of the body surface
o Assessment of sensory awareness using dermatome map can be
essential to determine level of damage to spinal cord
Plexuses
o Four :
- cervical
- brachial
- lumbar
- sacral
o Fibers from several spinal nerves branch and then re-form in
diff combinations to become specific peripheral nerves

Phrenic nerve
- consists of fibers from spinal nerves C3-C5
Sciatic nerve
- contains fibers from spinal nerves L4-L5 and S1-S3
The dispersal pattern can minimize the effects on a muscles
contraction of damage to one spinal cord segment

III. Reflexes

Automatic , rapid, involuntary responses to a stimulus

Involves a sensory stimulus from a receptor that is conducted along an
afferent nerve fiber , a synapse in spinal cord and an efferent impulse
that is conducted along a peripheral nerve to elicit a response
Acquired /learned reflexes such as those developed when learning to
ride a bicycle
Patellar/knee-jerk reflex or oculocephalic (dolls head eye response)
reflex are useful in diagnosis
Absent, weak or abnormal responses may indicate presence of
neurologic problem and sometimes can show location of spinal cord
damage

Neurons and Conduction of Impulses

I. Neurons

Neurons / nerve cells

Highly specialized, nonmitotic cells that conduct impulses throughout
CNS and PNS
Require glucose and O2 for metabolism
Dendrite
o Receptor site
o Conduct impulses toward the cellbody
Cellbody
o Contains the nucleus
Axon
o Conducts impulses away from cellbody toward an effector site
or connecting neuron where it can release neurotransmitter
chemicals @ its terminal point
Myelin sheath
o Insulates the fiber and speeds up the rate of conduction
o Formed by schwann cells
o Nucleus and cytoplasm of schwann cell form the neurilemma or
sheath of schwann, around the myelin
Nodes of Ranvier
o Axon collateral branches may emerge and stimuli may affect
the axon
Glial (neuroglial) cells
o Support and protect the neurons
o Astroglia /Astrocytes
- provide a link bet neurons and capillaries for physical and
prolly metabolic support as well as contributing to the bloodbrain barrier
o Oligodendroglia
- provide myelin for axons in the CNS
o Microglia
- Have phagocytic activity
o Ependymal cells
- line the ventricles and neural tube cavity
- form the part of choroid plexus
Regeneration of neurons
Neurons cannot undergo cell division
If the cellbody is damaged, neuron dies
In PNS, axon may be able to regenerate if cellbody is viable
After damage to the axon occurs :
o The section distal to injury degenerates because it lacks
nutrients and is removed by macrophages and schwann cells
o Schwann cells then attempt to form a new tube @ the end of
remaining axon
o Cellbody becomes larger and synthesizes addt'l proteins for
the growth of replacement axon
o The new growth does not always occur appropriately or make
its original connections, because the surrounding tissue may
interfere

II. Conduction of Impulses

Depolarization
A stimulus increases permeability of neuronal membrane allowing Na
ions to flow inside cell thus depolarizing it and generating an action
potential
The change to a + electrical charge inside the membrane results in
increased permeability of adjacent area and the impulse moves along
the membrane
Decrease in electrical charge across a membrane due to inward flow
of Na ions
Repolarization / Recovery
Reestablishment of the resting membrane potential after
depolarization occurred
Potassium ions move outward
Normal permeability of membrane is restored
Sodium-Potassium pump :

System of coupled ion pumps that actively tranports Na ions

out of a cell and K ions into cell @the same time
Returns the Na and K ions to their normal locations

Saltatory conduction
Propagation of an action potential (nerve impulse) along the exposed
portions of a myelinated nerve fiber
action potential appears @ successive nodes of Ranvier and therefore
seems to jump or leap from node to node
Synapase
Provides connection bet :
o 2 or more neurons
o neuron and an effector site
EEG/ encephalogram
Measure brainwaves
III. Synapses and Chemical Neurotransmitters
Typical synapse consists of :
- Terminal axon of presynaptic neuron
- Vesicles in terminal axon with neurotransmitter
- Receptor site on membrane of postsynaptic neuron
- Axon and Receptor site are separated by fluid-filled synaptic cleft

Neurotransmitters (few examples) :

1. Acetylcholine (ACh)
- Present @ neuromuscular junctions and in ANS, PNS and less commonly in
CNS
2. Catecholamines
- Norepinephrine (SNS) ,Epinephrine, Dopamine
3. Serotonin
4. Histamine
5. Gamma-aminobutyric acid (GABA)

Stimulus reaches the axon

Neurotransmitter is released
from vesicles

Taken up by presynaptic axon

to prevent continued
stimulation

Neurotransmitter flows
across the synaptic cleft

Neurotransmitter act on
receptor in postsynaptic
membrane

Stimulus / Response

Inactivated by enzymes

Autonomic Nervous system

Incorporates the Sympathetic and Parasympathetic NS

Generally have antagonistic effects thereby providing a fine balance
that aids in maintain homeostasis in body
Provides motor and sensory innervations to smooth muscle, cardiac
muscle and glands
Although individual is largely unaware of the involuntary activity , it is
integrated with somatic activity by the higher brain centers
Neural pathways in motor fibers of ANS differ from somatic nerves
because each involves 2 neurons and a ganglion
o
Preganglionic fiber is located in brain and spinal cord
o
Axon then synapses within the second neuron in the ganglion
outside CNS
o
Postganglionic fiber continues to the effector organ or
tissue

II. Parasympathetic NS

I. Sympathetic NS
Thoracolumbar NS
Increases the general level of activity in the body
Necessary for fight-or-flight or stress response
Augmented by the increased secretions of adrenal medulla in response
to SNS stimuli
Preganglionic fibers
o Arise from the thoracic and the 2 lumbar segments of the
spinal cord
Ganglia
o Located in 2 chains or trunks , one on either side of spinal cord
o Preganglionic fibers synapse with postganglionic fibers or
connecting fibers to other ganglia in the chain
Neurotransmitters and Receptors
o Important in ANS because they are closely linked to drug
actions
o Cholinergic fibers / Acetylcholine
- the neurotransmitter released by preganglionic fibers at the
ganglion
- the postganglionic fibers to sweat glands and blood vessels in
skeletal muscle
o Adrenaline fibers/ norepinephrine
- released by most SNS postganglionic fibers
Adrenergic receptors :
o Norepinephrine
- acts primarily on alpha receptors
o Epinephrine
- acts on both alpha and beta receptors
o An organ or tissue may have more than 1 type of receptor but
one type is usually present in greater numbers and exerts
dominant effect
o Drugs may be used to stimulate receptors or to prevent
stimulation :
- beta adrenergic blocking agents (beta blockers) may be used
to block beta receptors
- beta adrenergic drug to stimulate beta receptors
- the best drugs are specific for 1 type of receptor in one
organ or tissue and do not alter function in other areas of the
body
- the more specific the drug action is the milder the adverse
effects of the drug

Craniosacral NS
Dominates the digestive system
Aids in the recovery of the body after sympathetic activity
2 locations of PNS Preganglionic fibers :
o Cranial nerves III, VII, IX, and X @ the brainstem level
o Sacral spinal nerves
Vagus nerve :
o Provides extensive innervations to the heart and digestive
tract
Ganglia are scattered and located close to the target organ
Neurotransmitter @ both Preganglionic and postganglionic synapses is
Ach
2 types of cholinergic receptors :
o Nicotinic receptors
- always stimulated by Ach
- located in all postganglionic cholinergic neurons in the PNS
and SNS
o Muscarinic receptors
- located in all effector cells
- may be stimulated or inhibited by ACh depending on the
organ
Cholinergic blocking agents
o Reduce PNS activity
Cholinergic / Anticholinesterase agents
o Prevent the enzyme cholinesterase from breaking down Ach
o Increases PNS activity

General Effects of Neurologic Dysfunction

Local (Focal) effects

Signs r/t the specific area of the brain or spinal cord w/c the lesion
is located
o Paralysis of R arm that results from damage to a section of L
frontal lobe
o Loss of vision that results from damage to the occipital lobe
o With an expanding lesion (eg. growing tumor/ hemorrhage) ,
addtl impairment is noted as the adjacent areas become
involved

Supratentorial and Infratentorial Lesions

Supratentorial Lesion
Occur in cerebral hemispheres above tentorium cerebelli
Leads to a specific dysfunction in a discrete area, perhaps numbness
in a hand
Must become very large before it affects consciousness
Infratentorial Lesion
Located in the brainstem / below tentorium
May affect motor and sensory fibers resulting in widespread
impairment because nerves are bundled together when passing
through the brainstem
Resp and circulatory function and LOC may also be impaired

Motor dysfunction

L and R hemispheres

L sided brain damage impairs :

Logical thinking ability
Analytical skills
Intellectual abilities
Communication skills
R sided brain damage impairs :
Appreciation of music and art
Behavior
Spatial orientation
Recognition of relationships

Cerebral cortex and RAS in brainstem determine the LOC

Information must be processed in the association areas of cortex
before one is conscious of the info
Extensive Supratentorial lesions must be present in the cerebral
hemisphere to cause loss of consciousness
Relatively small lesions in the brainstem / Infratentorial lesions can
affect the RAS
The ff can also cause reduced LOC :
o Space-occupying masses in cerebellum can also compress
brainstem and RAS
o Systemic disorders (eg. acidosis / hypoglycemia) can depress
CNS
Various levels of reduced consciousness may present as :
o Lethargy
o Confusion
o Disorientation
o Memory loss
o Unresponsiveness to verbal stimuli
o Difficulty of arousal
Coma
o Most serious level of loss of consciousness
o Affected person does not respond to painful or verbal stimuli
o Body is flaccid although some reflexes are present
Deep coma
o Terminal stage
o Loss of all reflexes
o Fixed and dilated pupils
o Slow and irregular pulse and resp
Vegetative state

Damage to the upper motor neurons:

o In the cerebral cortex (frontal lobe) or to the corticospinal
tracts in brain
o Interferes with voluntary movements causing weakness or
paralysis on the opposite (contralateral) side of the body
The contralateral effect is determined by the crossover of the
corticospinal tracts in the medulla
Hyperreflexia
o Muscle tone and reflexes may be increased because the
intact spinal cord continues to conduct impulses with no
moderating or inhibiting influences sent from brain (spastic
paralysis)
o Frequently leads to contractures in the affected limbs

LOC

Loss of awareness and mental capabilities resulting from

diffuse brain damage
o Appears to be a sleep-wake cycle (eyes are open or closed)
but person is unresponsive to stimuli
o Some may in time recover consciousness but often survive
with significant neurologic impairment
Locked-in syndrome
o Person with brain damage is aware and capable of thinking
but is paralyzed and cannot communicate
o Some can move their eyes in a yes or no response
Brain death (criteria)
o Cessation of brain function (eg. a flat or inactive EEG)
o Absence of brainstem reflexes
o Absence of spontaneous respirations when ventilator
assistance is withdrawn
o Establishment of the certainty of irreversible brain damage
by confirmation of the cause of dysfunction
Drug overdose or hypothermia can cause loss of brain activity
temporarily thus a longer time period and addtl testing are required
before brain death can be confirmed in this case
o

Damage to the lower motor neurons :

o In the anterior horns of the spinal cord
o Causes weakness or paralysis on the same side of the body
and below level of damage
In the area of damage :
o Muscles are usually flaccid (lack tone)
o Reflexes are absent (flaccid paralysis)
If the cord distal to the damage is intact , some reflexes in that area
may be present and hyperactive (hyperreflexia)
Lower motor neurons are also located in nuclei of cranial nerves in
brainstem :
o Ipsilateral weakness (same side) or flaccid paralysis may
result from damage to any cranial nerves containing motor
fibers

-Two involuntary motor responses that occur in persons with severe brain
trauma :
Decorticate posturing
o Rigid flexion in the upper limbs
o Adducted arms and internal rotation of hands
o Lower limbs are extended
o May occur in persons with severe damage in cerebral
hemispheres
Decerebrate posturing
o Occur in persons with brainstem lesions and CNS depression
caused by systemic effects
o Both the upper and lower limbs are extended

Sensory deficits

May involve :
o Touch
o Pain
o Temp
o Position
o Special senses of vision, hearing , taste and smell
Somatosensory cortex in parietal lobe

Recieves and localizes basic sensory input from body

Mapped to correspond to receptors in skin and skeletal
muscles of various body regions
o Specific site of damage determines deficit
Dermatomes
o Mapping assists in evaluation of spinal cord lesions
o
o

Seizures

Visual Loss : Hemianopia

Loss of visual field depends on site of damage in visual pathway
@ the optic chiasm (crossover)
o Fibers in each optic nerve come together and then divide
o If optic chiasm is totally destroyed , vision is lost in both
eyes
Partial loss can result in variety of effects depending on particular
fibers damaged
Fibers from medial (inner) half of each retina (cells receive visual
stimuli)
o Cross over to the other hemisphere
Fibers from lateral (outer) half of each retina
o Remain on the same side
Optic tract coursing from optic chiasm to the occipital lobe on one
side includes fibers from half of each eye
Homonymous hemianopia
o If optic tract or occipital lobe is damaged , vision is lost from
medial half of one eye and lateral half of other eye
o Overall effect is loss of visual field on the side opposite to
that of damage
o Damage to L occipital lobe = loss of R visual field
- because L half of both retinas receives light waves from R
side of visual field

Language Disorders

Aphasia
o Inability to comprehend or to express language
o Main types :
- expressive
- receptive
- global
Expressive /motor aphasia
o Impaired ability to speak or write fluently
o Person may be unable to find any intelligible words or
construct a meaningful senstence
o Occurs when Brocas area in dominant frontal lobe (usually L
lobe) , inferior motor cortex is damaged
Receptive /sensory aphasia
o Inability to read or understand the spoken word
o Does not include hearing or visual impairment
o Source of problem is inability to process info in brain
o Person may be capable of fluent speech , but frequently it is
meaningless
o Damage to Wernickes area in L temporal lobe
Global aphasia
o Combination of expressive and receptive aphasia
o Results from major damage to the brain including Brocas
area, Wernickes area and many communicating fibers
throughout brain

Other types
Dysarthria
o Words cannot be articulated clearly
o Motor dysfunction that usually results from cranial nerve
damage or muscle impairment
Agraphia
o Impaired writing ability
Alexia
o Impaired reading ability
Agnosia
o Loss of recognition or association
o Visual Agnosia indicates inability to recognize objects

Convulsions
Caused by spontaneous excessive discharge of neurons in the brain
May be precipitated by :
o Inflammation in brain
o Hypoxia
o Bleeding
Can be focal or generalized
Frequently manifested by involuntary repetitive movements or
abnormal sensations

Increased Intracranial Pressure

Definition
Any increase in fluid (blood / inflammatory exudate) or any addtl
mass (tumor) causes an increase pressure in brain
Result is less arterial blood can enter the high-pressure area in
brain
Eventually brain tissue itself is compressed
Effects decrease function of the neurons both locally and generally
and eventually brain tissue dies
Pressure increases @ the site of problem initially but gradually is
dispersed throughout the CNS by means of continuous flow of CSF
and blood leading to widespread loss of function
Changes in ICP can be monitored by :
o Instruments placed in ventricles (invasive procedure) (direct)
o Methods such as radiologic examinations or assessment of
LOC and v/s (indirect)
Common in many neurologic problems including :
o Brain hemorrhage
o Trauma
o Cerebral edema
o Infection
o Tumors
o Accumulation of excessive amt of CSF
Early Signs
Compensation mechanisms when ICP increases :
o Body initially shifts more CSF to the spinal cavity
o Increasing venous return from brain
o Resulting hypoxia triggers arterial vasodilation in the brain
through local autoregulatory reflexes in an attempt ot
improve blood supply to brain but this adds to fluid volume
inside skull so it is effective for only a short time
Decreased LOC is the first indication of increased ICP
Addtl early indications :
o Severe headache
- occurs from stretching of dura and walls of large blood
vessels
o Projectile Vomiting
- result of pressure stimulating the emetic center in medulla
o Papilledema
- caused by increased ICP and swelling of the optic disc
- can be observed by looking through the pupil of the eye @
the retina , where the optic disc provides a window into the
brain
- optic nerve (cranial nerve II) is a projection of brain tissue
that is surrounded by CSF and meninges and enters the eye
@ the optic disc where it reflects the effects of increased
ICP of brain
Vital Signs

Cerebral ischemia develops

o Stimulates a powerful response (Cushings reflex) from the
vasomotor centers in an attempt to increase arterial blood
supply to the brain
Systemic vasoconstriction occurs
o Increase systemic BP
o Force more blood into the brain to relive ischemia
Baroreceptors in carotid arteries
o Respond to the increased BP by slowing the HR
Chemoreceptors

Respond to the low CO2 levels that accompany accelerated

systemic circulation by reducing RR
Reflex vasoconstriction momentarily ceases
o As improved cerebral circulation relieves ischemia
o Increasing ICP causes ischemia to recur in a very short time
and cycle is repeated
As ICP continues to rise, so does systemic BP
An increasing pulse pressure
o Results from the slow HR and intermittent but rapid on-off
cycle of Cushings reflex controlling systemic
vasoconstriction
Severe ischemia and neuronal death prevent any circulatory control
and BP drops
Varous abnormal resp patterns develop
o

Visual Signs
Papilledema
Pressure on oculomotor nerve (cranial nerve III) affects size and
response of pupils
o One pupil ipsilateral to the lesion becomes fixed
(unresponsive to light) and dilated as PNS fibers in affected
oculomotor nerve become nonfunctional
o With an addtl pressure increase, both pupils become fixed
and dilated
Ptosis / droopy eyelid
o Another effect of pressure on cranial nerve III
o Innervation to the muscle of upper eyelid is impaired
Nystagmus
o Abnormal or excessive eye movements
Changes in CSF
A specimen may be procured with a lumbar puncture by inserting a
fine needle bet vertebrae @ L3-4 , into SA space and withdrawing a
small sample of CSF
A manometer may be attached to the syringe to measure pressure
Pressure of CSF is elevated in pt with increased ICP (above 20 mm
Hg)
Composition of CSF may vary with the cause of problem ;
o Pinkish in color and contain erythrocytes = hemorrhage
o Cloudy, yellowish fluid and contains numeours WBCs =
infection
o Abnormal CHON levels in CSF = neoplasm

Herniation

Displacement of brain tissue due to enlarge mass such as blood clot

or tumor
Types :
o Transtentorial (central) herniation
- cerebral hemispheres, diencephalon and midbrain are
displaced downward
- the resulting pressure affects flow of blood and CSF , RAS
and respiration
o Uncal (uncinate) herniation
- uncus of temporal lobe is displaced downward past the
tentorium cerebelli
- creates pressure on 3rd cranial nerve , posterior cerebral
artery and RAS
o Cerebellar/ tonsillar (infratentorial) herniation
- cerebellar tonsils are pushed downward through foramen
magnum
- compresses the brainstem and vital centers
- causes death

Diagnostic Tests

CT scans
MRI
Cerebral angiography
Doppler utz (assess patency of carotid and intracerebral vessels)
EEG
Radionuclide/ technetium (tract movement in CNS)
Lumbar puncture (check pressure and analyze CSF for altered
components)
Glasgow coma scale (assess LOC)
Checklist of normal reflexes


Acute Neurologic Problems

Brain tumors
I. Definition
Space-occupying lesions that cause increased ICP because of space
constraints within rigid skull
Benign or malignant tumors can be life-threatening unless they are in
an accessible superficial location where they can be removed
Gliomas
o Form the largest category of primary malignant tumors
o Arise from one of the glial cells , the parenchymal cells in CNS
o Further classified acc to :
- cell of derivation (astrocytomas are most common)
- location of tumor
May develop from meninges (meningioma) or pituitary gland (adenoma)
Primary malignant tumors
o Rarely metastasize outside CNS
o Multiple tumors may be present within CNS
Secondary brain tumors
o Quite common
o Usually metastasizing from breast or lung tumors
o Cause effects similar to those of primary brain tumors
Diagnosis is made by :
o MRI
o Stereotactic biopsy
II. Pathophysiology

Primary malignant tumors (particularly astrocytomas)

o Do not usually have well-defined margins
o Invasive and have irregular projections into adjacent tissue
that are difficult to totally remove
The ff increases ICP :
o Obstruction of CSF or of venous sinuses
o An area of inflammation around tumor
As the mass expands , it compresses and distorts the tissue around it
eventually resulting in herniation

III. Etiology

Brainstem and cerebellar tumors are common in young children

Tumor occur in adults most often in mid-life
Adults are affected more frequently by tumors in cerebral
hemispheres

IV. Signs and Symptoms

Specific site of tumor determines the focal signs

If tumor grows rapidly, signs of increased ICP develop quickly , often
beginning with morning headaches ; overtime headaches increase in
severity and frequency
Vomiting occurs
Lethargy and irritability may develop along with behavioral changes
In some cases, focal or generalized seizures are the first sign, as the
tumor irritates surrounding tissue
Brainstem or cerebellar tumors may affect several cranial nerves
possibly causing unilateral facial paralysis or visual problems
Brain tumors unlike other forms of cancer do not cause the usual
systemic signs of malignancy because they do not metastasize outside
CNS and they will cause death before they are large enough to cause
gen effects
Pituitary adenomas in brain usually cause endocrinologic signs
depending on type of excess secretion
Visual disturbances resulting from compression of adjacent optic
chiasm , nerves or tract
Headaches and visual signs may result from increased ICP

V. Treatment

Surgery is the treatment of choice if tumor is reasonably accessible

Chemotherapy is often accompanied by radiation

In some cases, surgery and radiation may cause substantial damage to

normal tissue in CNS

Vascular Disorders (3)

Transient Ischemic Attack (TIAs)

I. Definition
Results from a temporary localized reduction of blood flow in the
brain
Recovery occurs within 24 h
II. Pathophysiology

May be caused by :
o Partial occlusion of an artery caused by atherosclerosis
o Small embolus
o Vascular spasm
o Local loss of autoregulation
Advantageous if it serve as a warning and lead to early diagnosis and
treatment of a problem before the occurrence of stroke
Brain must have a constant source of glucose and O2 or suffer
permanent damage
Not all strokes are preceded by TIAs

III. Signs and Symptoms

Directly r/t location of ischemia

Pt remains conscious
The ff may occur :
o Muscle weakness in an arm or leg
o Visual disturbances
o Numbness
o Paresthesia in face
o Transient aphasia
o Confusion
Attack may last a few min or longer but rarely lasts > 1-2 h and then
signs disappear
Repeated attacks are frequently a warning of the development of
obstruction r/t atherosclerosis

Cerebrovascular Accidents (CVA)

Total occlusion of a cerebral
blood vessel by atheroma or
embolus

Ruptured
cerebral vessel

Lack of blood in
brain tissue

Tissue
necrosis/Infarction

Central area of necrosis develops

surrounded by an area of inflammation
and function in the area is lost
immediately

Tissue liquefies

Cavity in brain
I. Pathophysiology

Development and effects of stroke vary with cause:

Occlusion of an artery by an atheroma
o Most common cause of CVA
o Atheromas often develop in large arteries (eg. carotid
arteries)
o Causes gradual narrowing of arterial lumen by plaque and
thrombus
o Leads to possible TIAs and eventually infarction
Sudden obstruction caused by an embolus lodging in cerebral artery
o Thrombi may break off of an atheroma or
o Mural thrombi may form inside the heart after a MI and
then break away
o Can also result from other materials : tumors, air , infection
(eg. endocarditis)
Intracerebral hemorrhage / Hemorrhagic strokes
o Usually caused by rupture of a cerebral artery in pt with
severe HTN
o Frequently more severe and destructive than other CVAs
because they affect large portions of brain
o Because of the greater increase in ICP with hemorrhage,
effects are evident in both hemispheres and are
complicated by secondary effects of bleeding
o Presence of free blood in interstitial areas affects the cell
membrane and can lead to secondary damage such as :
- vasospasm
- electrolyte imbalances
- acidosis
- cellular edema
- Five min (or less) of ischemia causes irreversible cell damage
Cerebral edema and an increasing area of infarction in first 48-72 h
tend to increase the neurologic deficits
Inflammation and pressure in brain must be minimized as quickly as
possible and therapy instituted to dissolve thrombi and maintain
adequate perfusion adequate perfusion to limit area of permanent
damage
Collateral circulation may have already developed in areas gradually
affected by atherosclerosis

Because neurons do not regenerate , an area of residual scar tissue

and often cysts remains, with a permanent loss of neurons in that area
In many cases, because specific functions result from integrated
output from many areas, it is possible with intensive therapy for a
person who has experienced a stroke to develop new neural pathways
in brain or to relearn a task thus recovering some lost function
Complications are common :
o Recurrent CVA
o Secondary problems r/t immobility : pneumonia, aspiration,
constipation
o Contractures r/t paralysis

II. Etiology

Risk factors :
o DM
o HTN
o Systemic lupus erythematosus
o Elevated cholesterol levels
o Hyperlipidemia
o Atherosclerosis
o History of TIAs
o Increasing age
o Heart disease
Combination of oral conctraceptives and cigarette smoking has been
well documented as an etiologic factor
Emboli may arise from ;
o Atheromas in large arteries (eg. carotid)
o Cardiac disorders of L ventricle (eg. MI, atrial fibrillation,
endocarditis)
o Implant (eg. prosthetic valve)
Risk of intracerebral hemorrhage increase in :
o Pt with long term HTN
o Pt with arteriosclerosis

III. Signs and Symptoms

Depend on :
o Location of obstruction
o Size of artery involved
o Functional area affected
Presence of collateral circulation may diminish the size of affected
area
Silent areas of brain
o In w/c dysfunction resulting from small infarctions is not
obvious
Obstruction of small arteries may not lead to obvious signs until
several small infarctions have occurred
Evolving stroke
o Effects of a stroke develop slowly over a period of hours
Initially flaccid paralysis is present
Spastic paralysis develops several weeks later as NS recovers from
initial insult
Generally , functional deficits increase the first 48 h as inflammation
develops @ the site and then subside as some neurons around
infracted area recover
Occlusion of large arteries / hemorrhage may cause :
o Coma
o Loss of consciousness
o Death almost immediately
Hemorrhagic strokes usually begin suddenly with a blinding headache
and increasingly severe neurologic deficits
Specific local signs
o Depend on area affected (eg. occlusion of an anterior
cerebral artery affects frontal lobe)
o Common signs :
- contralateral muscle weakness / paralysis
- sensory loss in leg
- confusion
- loss of problem-solving skills
- personality changes
Middle cerebral artery
o Supplies a large portion of cerebral hemisphere
o Lack of blood supply to this artery leads to contralateral
paralysis and sensory loss primarily of upper body and arm
Aphasia occurs when dominant hemispheres of brain is affected
Spatial relationships may be more severely impaired if R side is
damaged
Posterior cerebral artery
o Supplies the occipital lobe
o Visual loss is likely if it is occluded

o
o
o
o

o
o
o
o

Often results from a sudden increase in BP during exertion

Bleeding occurs into the SA space (location of circle of Willis)
and CSF
May be a small leak or a massive tear
Blood is irritating to the meninges and causes an inflammatory
response and irritation of the nerve roots passing through
the meninges
The free blood also causes vasospasm in cerebral arteries,
further reducing perfusion and leading to addtl ischemia
Hemorrhage from ruptured vessels causes increased ICP and
its associated signs
No focal signs are present because addtl blood is dispersed
through the system
SA hemorrhages may be classified acc.to their clinical
effects

II. Signs and Symptoms

Enlarging aneurysm :
May cause pressure on surrounding structures
Small leak :
Headache as tension increases on blood vessel wall and meninges
Photophobia
Intermittent periods of dysfunction :
o Confusion
o Slurred speech
o Weakness
Nuchal rigidity
o A stiff, extended neck
o Often develops because the escaped blood irritates the spinal
nerve roots and causes muscle contractions in neck
Massive rupture/ SA hemorrhage :
Immediate, severe , blinding headache
Vomiting
Photophobia
Seizures
Loss of consciousness
Death may occur shortly after rupture
III. Treatment
Before rupture :
Can be treated surgically ASAP by clipping or trying it off
While pt is waiting for surgery, sudden increases in BP must be
prevented

IV. Treatment

Clot-busting agents eg. Tissue plasminogen activator (tPA)

Surgical interventions to relieve carotid artery obstruction
Glucocorticoids may reduce cerebral edema
O2 supply to maximize cerebral circulation
Assisting pts return to a sitting or standing passion as soon as v/s are
stable to maintain muscle tone and minimize perceptual deficits
Correct positioning , frequent changes of position, and passive
exercises to prevent muscle atrophy, contractures and skin
breakdown

Cerebral Aneurysms
I. Pathophysiology
An aneurysm is a localized dilation in an artery
Frequently multiple
Usually occur @ the points of bifurcation on the circle of Willis
Develop where there is a weakness in the arterial wall where
branching occurs
Force of blood leads to bulging in the wall, w/c is often aggravated by
HPN
Initially, are small and asymptomatic
Tend to enlarge over years until compression of the nearby structures
(eg. a cranial nerve) causes clinical signs or rupture occurs
Rupture

After rupture :
Surgical clipping may also be done
There is substantial risk of rebleeding @ the site of repair or from
other aneurysms
Addtl therapeutic measures focus on reducing effects of :
Increased ICP
Cerebral vasospasm

Infections (5)

Meningitis
I. Definition

An infection , usually bacterial , of the meninges of CNS

Many microbes can infect CNS
All age groups are susceptible

II. Pathophysiology

Microorganisms reach the brain :

o Via blood
o By extension from nearby tissue
o By direct access through wounds
Meningococcus
o Can bind to nasopharyngeal cells in an individual
o Cross mucosal barrier , attach to the choroid plexus and
enter CSF
Infection spreads rapidly through coverings of brain because :
o Membranes are continuous around CNS
o CSF flows in SA space
Focal signs are absent because there is no localized mass of infection
Inflammatory response to infection leads to :
o Increased ICP
o Pia and Arachnoid layers become edematous
Common bacterial infections lead to :
o Purulent exudate that covers surface of brain and fills the
sulci, causing surface to appear flat
o Exudate is present in CSF
o Blood vessels on surface of brain appear dilated

III. Etiology

In some categories, vaccines have reduced the risk

Diff. age groups are susceptible to diff. organisms that cause meningitis
Neisseria meningitidis / meningococcus
o Classic meningitis pathogen in children and young adults
o Frequently carried in nasopharynx of asymptomatic carriers
o Spread by resp. droplets
o Any close contacts of affected persons should be given
prophylactic treatment
o Epidemics are common in schools or institutions where close
contact bet. children is likely to spread the organism
Escherichia coli
o Most common causative organism in neonates
o Usually seen in conjunction with :
- a neural tube defect
- premature rupture of amniotic membranes
- a difficult delivery
Haemophilus influenza
o Meningitis results most often from bacterial infections in
young children
Streptococcus pneumoniae
o Major cause of meningitis in elderly persons and young
children
Other cause :
S/t other infections (sinusitis, otitis)
Abscess located where the infection can spread through bone to
meninges (eg. an abscessed tooth)
Any form of head trauma or surgery from a variety of microorganisms
Aseptic /viral meningitis
Results from an infection (eg. mumps, measles)
IV. Signs and Symptoms

Sudden onset of meningitis is common

Meningeal irritation leads to :

Severe headache
Back pain
Photophobia
Nuchal rigidity (hyperextended , stiff neck)
2 other clinical signs of meningeal irritation
Kernigs sign
o Resistance to leg extension when lying with hip flexed
Brudzinskis sign
o Neck flexion causes flexion of hip and knee
Early indicators of increased ICP
Vomiting
Irritability
Lethargy
Stupor
Seizures
Indicators of infection
Fever
Chills
Leukocytosis (increased WBC production)
Meningococcal infections
Petechial rash
Extensive ecchymoses over body
Potential complications :
Hydrocephalus
o If CSF flow is blocked by pus or adhesions
Cranial nerve damage
Damage to cerebral cortex resulting in :
o Mental retardation
o Seizures
o Motor impairment
In fulminant (rapidly progressive, severe) cases caused by highly virulent
organisms (frequently meningococcal)
Disseminated intravascular coagulation develops with associated
hemorrhage of adrenal glands or meningococcal septicemia may
directly cause adrenal hemorrhage (Waterhouse-Friderichsen
syndrome)
Usually result in vascular collapse or shock and death
V. Diagnostic tests

Examination of CSF obtained by lumbar puncture , confirms the

diagnosis
If present :
o CSF pressure is elevated
o CSF will appear cloudy
o CSF usually contains an increased # of leukocytes
Causative organism in CSF or blood must be identified to ensure
effective treatment

VI. Treatment

Aggressive antimicrobial therapy (eg. ampicillin)

Specific treatment measures for ICP and seizures
Glucocorticoids reduce cerebral inflammation and edema
Vaccines are available as a preventive measure
Carriers should be identified in institutional epidemics

VII. Prognosis

With prompt dx and treatment , majority of pt survive

Mortality rate in neonatal meningitis is high
There is some risk of permanent brain damage in young children

Brain Abscess

A localized infection , frequently occurring in frontal or temporal

lobes
There is usually necrosis of brain tissue and a surrounding area of
edema
Usually result from :
o Spread of organisms from ear, throat, lung or sinus
infection
o Multiple septic emboli from acute bacterial endocarditis
o Directly from a site of injury or surgery
Common organisms :
o Staphylococci
o Streptococci
o Pneumococci
Onset tends to be insidious
Focal signs indicating neurologic deficits and increasing ICP develop
The ff are required :
o Surgical drainage
o Antimicrobial therapy
Mortality rate : 10 %

Encephalitis

An infection of the parenchymal or connective tissue in the brain and

cord (particularly basal ganglia)
May include the meninges
Necrosis and inflammation develop in brain tissue, often resulting in
some permanent damage
Early signs of infection :
o Severe headache
o Stiff neck
o Lethargy
o Vomiting
o Seizures
o Fever
Usually of viral origin but may be r/t other organisms

I. Western equine encephalitis

An arboviral infection spread by mosquitoes
Occurs more frequently in summer months
Common in young children
II. St. Louis encephalitis
Affects older persons more seriously than younger ones
III. West Nile fever
Originated in northeastern US
Caused by a flavivirus, spread by mosquitoes w/ certain birds as an
intermediate host
Focus for control has been to track the spread and reduce risk of
mosquito bites in affected areas
Initally causes flu-like sx w/ low grade fever and headache , sometimes
followed by confusion and tremors
IV. Neuroborreliosis (Lyme disease)

Caused by a spirochete, Borrelia burgdorferi , transmitted by tick

bites in summertime
Site of tick bite :
o Red
o With a pale center
o Gradually increasing in size to form the unique marker lesion,
a bulls eye
Microbes disseminate through circulation , causing :
First :
o Sore throat
o Dry cough
o Fever
o Headache
Followed by :
o Cardiac arrhythmias

Neurologic abnormalities (eg. facial nerve paralysis) r/t

meningoencephalitis

Lastly ..
o
Pain and Swelling may develop in large joints
o Sometimes progressing to chronic arthritis
Prolonged therapy w/ antimicrobials such as doxycycline is prescribed

V. Herpes simplex encephalitis

Occurs occasionally and is dangerous
Arising from spread of herpes simplex virus type 1 (HSV-1) from the
trigeminal nerve ganglion
The virus causes extensive necrosis and hemorrhage in brain , often
involving frontal and temporal lobes
Early treatment w/ an antiviral drug such as acyclovir may control
infection ; otherwise treatment is supportive
Other Infections

Rabies (hydrophobia)

Caused by a virus that is transmitted by the bite of a rabid animal

Virus travels along peripheral nerves to the CNS , where it causes
severe inflammation and necrosis, particularly in the brainstem and
basal ganglia
Incubation period :
o Often 1-3 months
o Depends on the distance bet. the bite and access to the CNS
Onset is marked by :
o Headache
o Fever
o Nervous hyperirritability
o Sensitivity to touch
o Seizures
Virus also travels to salivary glands
Difficulty swallowing caused by muscle spasm and foaming @ the mouth
are typical
Resp.failure causes death
Necessary treatments :
o Immediate cleansing of bite area
o Prophylactic immunization

Tetanus (lockjaw)

Caused by Clostridium tetani, a spore-forming bacillus

Spores survive for years in soil
The vegetative form is an Anaerobe , thriving deep in tissues ,for ex. in
a puncture wound
Exotoxin enters the NS , causing tonic muscle spasms
Sx :
o Jaw stiffness
o Difficulty swallowing
o Stiff neck
o Headache
o Skeletal muscle spasm
o Eventually ..resp. failure
Mortality rate is 50 %
Immunizations are advised w/ boosters as needed or ff injury

Poliomyelitis (infantile paralysis)

Polio virus
o Highly contagious through direct contact or oral doplet
o Reproduces in lymphoid tissue in oropharynx and digestive
tract , then enters blood and eventually CNS
o Attacks the motor neurons of the spinal cord and medulla ,
causing minor flulike effects in many cases, but paralysis and
resp. failure in other cases , depending on level of destruction
Sx :
o Fever
o Headache
o Vomiting
o Stiff neck
o Pain
o Flaccid paralysis

Postpolio syndrome (PPS)

Has been occurring 10-40 years after recovery from the original
infection w/ progressive and debilitating fatigue, weakness , pain and
muscle atrophy

Infection-Related Syndromes

Reyes syndrome
I. Pathophysiology
Unknown cause but is linked to a viral infection such as influenza in
young children that have been treated with aspirin (ASA)
Depending on particular virus, signs appear 3-5 days after the onset
of viral infection
Acetaminophen is now used to treat fever in children
Major pathologic changes occur in the brain and liver
o A noninflammatory cerebral edema develops leading to
increased ICP
o Brain function is severely impaired by cerebral edema and
effects of high ammonia levels in serum r/t liver dysfunction
o Liver enlarges, develops fatty changes in the tissue and
progresses to acute failure
o Jaundice is not present, but serum levels of liver enzymes are
elevated
o Resultant metabolic abnormalities : hypoglycemia and
increased lactic acid in blood and body fluids w/c also
contribute to acute encephalopathy
II. Signs and Symptoms

Vary in severity
Encephalopathy initially causes :
o Lethargy
o Headache
o Vomiting
w/c are quickly followed by :
o disorientation
o Hyperreflexia
o Hyperventilation
o Seizures
o Stupor
o Coma

III. Treatment

No immediate cure
Treatment is supportive and symptomatic , managing the metabolic
imbalances and cerebral edema

Guillain-Bare syndrome
I. Definition

Also known as :
o Post-infectious polyneuritis
o Acute idiopathic polyneuropathy
o Acute infectious polyradiculoneuritis
An inflammatory condition of the PNS

II. Pathophysiology

Cause is unknown
Evidence indicates that an abnormal immune response, perhaps an
autoimmune response , precipitated by a preceding viral infection or
immunization may be responsible
Local inflammation accompanied by :
o Accumulated lymphocytes
o Demyelination
o Axon destruction

The above changes cause impaired nerve conduction particularly in

efferent (motor) fibers although afferent (sensory) and autonomic
fibers may also be involved
If the cell body remains alive through the acute period, the axon can
regenerate
Initially, the inflammatory and degenerative processes affect the
peripheral nerves in legs ; then the inflammation ascends to involve
the spinal nerves to the trunk and neck and frequently includes cranial
nerves as well
Critical period :
o Ascending paralysis involves the diaphragm and respiratory
muscles
Recovery :
o Usually spontaneous with the manifestations diminishing in
reverse order i.e motor function is regained first in the
upper body and then gradually improves in trunk and lower
extremities

III. Signs and Symptoms

Progressive muscle weakness and areflexia beginning in the legs lead

to an ascending flaccid paralysis w/c may be accompanied by
Paresthesia or pain and gen muscle aching
As paralysis advances upward, vision and speech may be impaired
If swallowing and resp are affected , a life-threatening situation
develops
Many pt sustain ANS impairment manifested as :
o Cardiac arrhythmias
o Labile (fluctuating) BP
o Loss of sweating capability

IV. Treatment

Treatment is primarily supportive

Ventilator is required in many cases
Use of immunoglobulin therapy or plasmapheresis in w/c IgG is
separated and removed from pts blood in early stage may shorten the
acute period of disease in some pt and hasten recovery
Physiotherapy throughout recovery period is essential to maximize
restoration of function
About 30 % of pt exp residual weakness

Head Injuries

III. Pathophysiology

I. Definition
May involve :
o Skull fractures
o Hemorrhage
o Edema
o Direct injury to brain tissue
Can be :
o Mild causing only bruising of tissue
o Severe causing destruction of brain tissue and massive
swelling of brain
Skull can also destroy brain by means of :
o Bone fragments that penetrate or compress the brain tissue
o Inability of skull to expand to relieve pressure

Primary brain injuries

Direct injuries
May involve laceration or compression of brain tissue by :
o Piece of bone or foreign object
o Rupture or compression of the cerebral blood vessels
Because brain is not held tightly in place :
o Application of unusual force may rotate or shift it inside the
skull
o Brain tissue may be damaged by the rough and irregular inner
surface of the skull
o It may also be damaged by movement of lobes of brain against
each other (shearing injury)
Any trauma to the brain tissue causes loss of function in the part of
the body controlled by that specific area of brain
Cell damage and bleeding :
o Lead to inflammation and vasospasm around site of injury
increasing ICP and creating further gen ischemia and
dysfunction
o After bleeding and inflammation subside, some recovery of
neurons in the area surrounding direct damage may occur
o Central area of damage undergoes necrosis and is replaced by
scar tissue or a cyst

II. Types
Concussion
Reversible interference with brain function
Usually resulting from a mild blow to the head w/c causes sudden
excessive movement of brain , disrupting neurologic function and
leading to loss of consciousness
Amnesia / memory loss and headaches may follow a concussion
Recovery with no permanent damage usually occurs within 24 h
Contusion
Bruising of brain tissue with rupture of small blood vessels and edema
Usually results from a blunt blow to the head
Possibility of residual damage depends on force of blow and degree of
tissue injury
Closed head injury
Skull is not fractured but brain tissue is injured and blood vessels
may be ruptured by force exerted against skull
Extensive damage may occur when head is rotated with considerable
force
Open head injury
Fractures or penetration of brain by missiles or sharp objects
Linear fractures
Simple cracks in the bone
Comminuted fractures
Several fracture lines but may not be complicated
Compound fractures
Trauma in w/c brain tissue is exposed to environment
Likely to be severely damaged because bone fragments may penetrate
the tissue
Risk of infection is high
Depressed skull fractures
Displacement of a piece of bone below the level of the skull thereby
compressing the brain tissue
Blood supply to the area is often impaired
Considerable pressure is exerted on the brain
Basilar fractures
Occur @ the base of the skull
Often accompanied by leaking of CSF through ears / nose
May occur when forehead hits a car windshield with considerable
force
Cranial nerve damage and dark discoloration around eyes are common
Contrecoup injury
Area of brain contralateral to the site of direct damage is injured as
brain bounces off the skul
May be secondary to acceleration or deceleration injuries
Skull and brain hit a solid object w/c causes brain to rebound against
opposite side of skull usually causing minor damage

Secondary brain injuries

Result from addtl effects of :
o Cerebral edema
o Hemorrhage
o Hematoma
o Cerebral vasospasm
o Infection
o Ischemia r/t systemic factors
Hematoma (Classification in relation to meninges)
Epidural (extradural) hematoma
o Bleeding bet dura and skull
o Usually caused by tearing of middle meningeal artery in
temporal lobe
o Signs of trouble usually arise within a few h of injury when
person loses consciousness after a brief period of
responsiveness
Subdural hematoma
o Bleeding bet dura and arachnoid
o Frequently , there is small tear in a vein w/c causes blood to
accumulate slowly
o May be acute (signs present in 24 h) or subacute (increasing
ICP develops over a week or so)
o Chronic subdural hematoma may occur in an elderly person , in
whom brain atrophy allows more space for a hematoma to
develop
o A tear in the arachnoid can allow CSF to leak to into subdural
space (hygroma) creating addtl pressure
Subarachnoid hemorrhage
o Bleeding bet arachnoid and pia
o Associated with traumatic bleeding from blood vessels @ the
base of brain
o Because blood mixes with circulating CSF , a localized
hematoma cannot form
Intracerebral hematoma
o Results from contusions or shearing injuries
o May develop several days after injury
In all types of hematomas bleeding leads to :
o Local pressure on adjacent tissue
o General increase in ICP
Blood may be partially coagulated, forming a solid mass
When blood accumulates slowly :
o Blood cells undergo hemolysis
o Fluid in area of cell breakdown exerts osmotic pressure ,
drawing more and more H2O into the area, increasing size and
pressure of mass and raising ICP
Herniation may result from untreated mass

Any bleeding in brain may precipitate cerebral

vasoconstriction/vasospasm leading to further ischemia and more
damage to neurons

IV. Etiology

Sports injuries
Vehicular accidents
Excessive alcohol intake
o High blood alcohol level can impede neurologic assessment by
masking signs of injury
o Alcohol, because of its dehydrating effects , tends to delay
onset of cerebral edema and elevation of ICP but there may be
a greater increase in ICP @ a later time
Falls
o Common cause of head injury
o More often in elderly persons
Boxers and other athletes
o At risk for repeated head injury
Infants
o When violently shaken, can experience severe damage to the
brain and brainstem as the head swings
Objects that fall on head
Blow to he head

V. Signs and Symptoms

Seizures
o Often focal but may be generalized
o Due to irritating quality of blood
o Common sequelae after recovery because of increased
irritability of tissue around the scar
Cranial nerve impairment
o Particularly in persons who have sustained basilar fractures
Otorrhea / Rhinorrhea
o Occurs with fracture and tearing of the meninges w/c allows
fluid to pass out of SA space
o Provides microbes with an entry point into the brain
Otorrhagia
o Blood leaking from ear through a fracture site with torn vessel
and meninges
Fever
o May be a sign of hypothalamic impairment or of cranial or
systemic infection
Stress ulcers
o May develop from increased gastric secretions
The ff are present for some time after recovery :
o Gen fatigue
o Frequent headaches
o Memory loss
Complications of immobility
o Pneumonia
o Decubitus ulcers

VI. Treatment

CT scan determine extent of brain injury

Glucocorticoid decrease edema
Antibiotic reduce risk of infection
Surgery to reduce ICP
Blood products and O2 - to protect the remaining brain tissue
Awakening person periodically to check LOC
Checking for reactive pupils
Watching for vomiting and any change in movement, sensation or
behavior

Spinal Cord injury

I. Definition
Usually results from fracture or dislocation of the vertebrae , w/c
compresses , stretches or tears spinal cord
Supporting ligaments and intervertebral disc may be damaged also
Most injuries occur in areas of spine that provide more mobility but
less support i.e C1-C7 and T12-L2
Immediate appropriate immobilization is essential to prevent
secondary damage
Common types of injuries :
Cervical spine injuries
o May result from hyperextension (upward) or hyperflexion
(downward) of the neck with possible fracture
o Usually damage to the disc and ligaments occurs
o Leads to :
- dislocation
- loss of alignment of the vertebrae
- compression or stretching of the spinal cord
Dislocation of any vertebra
o May crush or compress the spinal cord and compromise blood
supply
Compression fractures
o Cause injury to the spinal cord when great force is applied to
the top of skull or to feet and is transmitted up or down the
spine
o The ff events can cause this injury :
- diving into an empty pool
- jumping from a height and landing on the feet
- object falling on a standing persons head
o The shattered bone is compressed and protrudes , exerting
pressure horizontally against the cord
o Sharp edges of bone fragments may lacerate or tear nerve
fibers and blood vessels
Penetration injuries
o Due to stab or bullet wounds
Vertebral fractures classification :
Simple
o Single line break
Compression
o Crushed or shattered bone in multiple fragments
Wedge
o Displaced angular section of bone
Dislocation
o Vertebra forced out of its normal position

II. Pathophysiology

Damage to the spinal cord may be temporary or permanent

Nerves in the spinal cord do not regenerate
Laceration of nerve tissue by bone fragments usually results in
permanent loss of conduction in the affected nerve tracts
Complete transection
o Severing or crushing of the cord
o Causes irreversible loss of all function @ and below level of
injury
Partial transection
o May allow recovery of some function
Bruising
o Reversible damage when mild edema and minor bleeding
temporarily impair conduction of nerve impulses
Any compression of cord must relieved quickly to maintain adequate
blood supply
Prolonged ischemia and necrosis lead to permanent damage
Bleeding and inflammation develop locally, creating addtl pressure and
further interfering with blood flow
Edema and hemorrhage extend for several segments above and below
level of injury
Damaged to tissues releases mediators w/c cause vasoconstriction
leading to addtl local ischemia and possible necrosis

o Norepinephrine
o Serotonin
o Histamine
Destructive enzymes are released as well causing more inflammation
and necrosis
Initially, loss of function may appear to be extensive because of addtl
compression , but as edema subsides , there may be partial recovery
of function
Regular assessment of movement and sensory response using
dermatome map can determine degree of damage or recovery in
spinal cord
Injury in cervical region :
o Inflammation may extend upward to the level of C3-C5 ,
interfering with phrenic nerve innervatio to the diaphragm
o Affect respiration
o Ventilatory assistance may be required
Spinal shock
o A period where conduction of impulses ceases in the nerve
tracts and in the gray matter
o A form of neurogenic shock
The ff determine the rate and degree of recovery
o Extent of injury
o Amount of resultant bleeding
o Need for surgical intervention
Recovery period :
o Inflammation gradually subsides , damaged tissue is removed
by phagocytes and scar tissue begins to form
o Reflex activity resumes in spinal cord below level of injury
o Any undamaged tracts continue to conduct impulses through
level of damage

III. Etiology

Automobile accidents
Sports
Falls

IV. Signs and Symptoms

2 stages in post-traumatic period :
Early stage of spinal shock and increasing impairment
Initial period of spinal shock :
All neurologic activity ceases @ , below, and slightly above the level of
injury
No reflexes are present
May persist days or weeks
During period of spinal shock :
Flaccid paralysis
Sensory loss @ and below the injured area
Absence of all reflex responses
Loss of central control of autonomic function
In pt with cervical injury :
o Loss of control of vasomotor tone
o BP is low and labile
o Diaphoresis
o Loss of control in body temp and bowel and bladder emptying
o Urinary retention and paralytic ileus
Recovery and recognition of extent of functional loss
Gradual return of reflex activity below the level of injury
No impulses including reflexes can pass through specific area of
damaged neurons
Hyperreflexia develops due to normal inhibitory or dampening
impulses that cannot reach the cord levels below the injury
Spastic paralysis
Sensory deficits
Reflex / neurogenic bladder and bowel function (urinary incontinence
and reflex defecation) are present below level of damage
-Specific effects of permanent damage depend on the level @ w/c the spinal
cord trauma occurred
Quadriplegia

o Paralysis of all 4 extremities

o C1-C8
Paraplegia
o Paralysis of lower part of the trunk and legs
o T1-L4
Partial cord injuries
o Can lead to diff patterns of impairment depending on point of
decussation and loc. of specific injured tracts :
- ipsilateral paralysis
- contralateral loss of pain and temp sensation
Autonomic dysreflexia
o With injury of cervical spine, stimulation of the sympathetic
system may result in this
o A potentially serious complication
o Caused by a sensory stimulus that triggers a massive
sympathetic reflex response that cannot be controlled from
the brain
o Trigger may be any noxious stimulus in the body but most
frequently is a distended bladder or decubitus ulcer
o A sensory stimulus to SNS below level of injury can stimulate
entire chain of SNS ganglia , leading to :
- excessive vasoconstriction
- sudden increase in BP
- severe headache
- visual impairment
o Bradycardia accompanies this syndrome :
- as the Baroreceptors sense the high BP and respond through
the vagus nerve by slowing the HR
o Excessive vasoconstriction cannot be reduced through the
cardiovascular control center
o Finding and removing the cause of stimulus and Administering
meds to lower BP to prevent stroke or heart failure
Complications are common after spinal cord injury due to :
o Immobility
o Loss of function
o Muscle spasms contractures
o Decubitus ulcers
o Resp and urinary infections
Sensory and psychological components of sexual response are usually
blocked by injury
o Men may have neurogenic reflex erections
o Many men , particularly those with high-level cord injuries are
infertile because sperm production in testes is impaired

V. Treatment

Traction / Surgery to relieve pressure and repair tissue

Glucocorticoids (methylprednisolone) to reduce edema and stabilize
vascular system
Ongoing care to prevent complications r/t immobility