Case Closed Neuroanatomy

CASE CLOSED!
NEUROANATOMY
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CASE CLOSED!
NEUROANATOMY
WARREN BERGER BSc BESc MD
JOHN BERGER BA
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CRC Press
Taylor & Francis Group
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Boca Raton, FL 33487-2742
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v
Contents
Preface vi
Acknowledgements vii
Abbreviations viii
Part One
1 Introduction to the Nervous System 3
2 The Cortex and Associated Structures 23
3 The Cranial Nerves and the Brainstem 55
4 The Spinal Cord 97
5 The Peripheral Nervous System 119
6 Localization Primer 153
Part Two
7 The Cases 177
Index 329
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vi
Preface
Neuroanatomy texts typically fall into two distinct groups. The more traditional text is
usually in excess of 1000 pages and covers every esoteric detail of this already challenging
subject. At the other end of the spectrum are short texts, typically less than 150 pages, that
succinctly summarize material and may be useful for review studies but don’t actually
teach neuroanatomy.
Neither of these is particularly useful for the beginning student. Indeed, a straightforward
text designed exclusively for novice studies in neuroanatomy has remained elusive.
Appropriately frustrated, many students have shunned the subject. This phenomenon
has been coined “Neurophobia” in three international studies of medical students.
It doesn’t need to be this way. That’s where Case Closed! Neuroanatomy comes in. We know
students can’t afford the inefficiency of sifting through pages and pages of a tome of a text,
trying to determine whether what they are reading is or isn’t relevant. Conversely, the blunt
memorization encouraged by short review texts leads to a poor understanding of the art
of localization; localization is the skill that neuroanatomy texts try to impart and involves
determining where in the nervous system the dysfunction is located.
In Chapters 1–5 we present the core fundamentals of neuroanatomy as we work through

the nervous system at all its levels: the cortex, brainstem, spinal cord and finally the
peripheral nervous system. An uncluttered, concise figure is worth more than a thousand
words, so we accompany each figure with an entire page of explanatory text. Key points
are then summarized in our Take Home Message.
In Chapter 6 we introduce how to localize, and also present a Localization Key. This is
designed to serve as a quick reference for all the common localizations you should be
familiar with.
Finally, in Chapter 7 we present 25 cases for you to practice and master the art of
localization. Each case is complemented with a detailed step-by-step solution and a
Clinical Pearl, which supplements the case with practical clinical points.
Case Closed! Neuroanatomy is everything you need and nothing you don’t. “Neurophobia”
exists because of a lack of restraint from instructors, not a lack of enthusiasm from
students. We hope that this text remedies that.
Warren Berger
John Berger
February 2016
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vii
Acknowledgements
When undertaking an enterprise of this size, one finds that the list of people to thank
nearly becomes the size of the original text itself. The following is by no means exhaustive
and we are indebted to the many students who have contributed their thoughts and
desires as to what a neuroanatomy text should be.
Firstly, we’d like to thank our parents for teaching us the value of divergent thinking and
instilling in us the tenacity to see an idea through to its conclusion.
To our wives, Anna and Allison, we’d like to thank you for your love and support during
this challenging time. You have had to do more than your fair share; thank you for
cancelling countless weekend plans to allow us to work on this project.
Warren Berger would like to thank the faculty and residents of the Department of
Clinical Neurological Sciences at the University of Western Ontario for their inspiration
and instruction over the years. In addition, he would like to thank Drs. Jorge Burneo,
Alex Fraser and Shannon Venance for (patiently) teaching him how to localize. Deep
appreciation also goes to Drs. Ian Taylor and Mike Wiley of the University of Toronto for
introducing him a passion for teaching anatomy.
He would also like to thank Drs. Nicholas Cothros, Nevena Markovic and Miljan Tripic
for joining him on this residency adventure. It has been said that your friends are the
ones you consider your equals, but your closest friends are the ones you consider your
betters. The latter is certainly the case here. A finer group of residents could not be found.
Finally, we would like to thank our editor Dr. Joanna Koster and everyone at CRC Press.
Without your guidance and gentle redirections on this adventure we would have veered
far off course!
Warren Berger
John Berger
February 2016
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viii
Abbreviations
Abd abduct EF elbow flexor
ABP abductor pollicis EHB extensor hallucis brevis
ACA anterior cerebral artery EHL extensor hallucis longus
Ach acetylcholine EMG electromyogram
ACOM anterior communicating artery EWN Edinger–Westphal nucleus
Add adductors EP extensor pollicis
ADF ankle dorsiflexion EV eversion (ankle)
ADP adductor pollicis FE finger extensors
AF arcuate fasciculus FEF frontal eye fields
AHC anterior horn cell FF finger flexors
AICA anterior inferior cerebellar artery FP flexor pollicis
AIDP acute inflammatory GBS Guillain–Barre syndrome
demyelinating polyneuropathy HE hip extensors
ALS amyotrophic lateral sclerosis HF hip flexors
AP anterior – posterior HIV human immunodeficiency virus
APF ankle plantar flexion IAM internal acoustic meatus
B Broca’s area ICA internal carotid arteries
BIPAP bilevel positive airway pressure ICP intracranial pressure
C conception tract ICU intensive care unit
CN cranial nerve INO internuclear ophthalmoplegia
CNS central nervous system INV inversion (ankle)
CSF cerebrospinal fluid IO inferior oblique muscle
CT computed tomography IR inferior rectus muscle
CTS carpal tunnel syndrome IV intravenous
DC dorsal column(s) KE knee extensors
DI dorsal interossei KF knee flexors
DRG dorsal root ganglion LGN lateral geniculate body
EC extensor carpi LHH left sided homonymous
ECR extensor carpi radialis hemianopsia
ECU extensor carpi ulnaris LMN lower motor neuron
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Abbreviations ix
LOC level of consciousness RAS reticular activating system

MCA middle cerebral artery RAPD relative afferent pupillary defect
MCAT medical college admissions test RHH right sided homonymous
MGN medial geniculate nucleus hemianopsia
ML medial lemniscus, also medial – SACD subacute combined

lateral (plane) degeneration
MLF medial longitudinal fasciculus SCA superior cerebellar artery
MMA middle meningeal artery SCM sternocleidomastoid
MRC Medical Research Council SO superior oblique muscle
MRI magnetic resonance imaging SR superior rectus muscle
MS multiple sclerosis ST spinothalamic tract
NE norepinephrine SUP supinator
NMJ neuromuscular junction TCM transcortical motor (aphasia)
OP opponens (short for opponens TCS transcortical sensory (aphasia)

pollicis) TIA transient ischemic attack
PCA posterior cerebral arteries UMN upper motor neuron
PCOM posterior communicating VA ventral anterior nucleus
arteries VLN ventral lateral nucleus
PICA posterior inferior cerebellar VPL ventral posterior lateral nucleus
artery
VPM ventral posteromedial nucleus
PNS peripheral nervous system
W Wernicke’s area
PPRF paramedian pontine reticular
formation WE wrist extensor
PRO pronator (short for pronator WF wrist flexor

teres)
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Part One
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Chapter 1
Introduction to the
Nervous System
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4 Chapter 1 Introduction to the Nervous System
Figure 1.1 Divisions of the Nervous System
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Divisions of the Nervous System 5
Let’s begin by examining the divisions of the nervous system.
The human nervous system is first divided into the central nervous system (CNS) and
the peripheral nervous system (PNS). The CNS is made up of the brain and spinal cord.
The PNS is made up of cranial nerves (CN), which innervate the head, and spinal nerves,
which innervate the body. The function of the PNS is to transmit information to and from
the CNS. Since many nerves feed into the spinal cord, it is sometimes called the “bridge”
between the PNS and CNS.
The PNS can be further subdivided into the autonomic nervous system, and the somatic
nervous system. The autonomic nervous system is not under conscious control; it auto-
matically controls all of the functions needed to sustain life (i.e., blood pressure, respiratory
rate, digestion and excretion). The autonomic nervous system can be further subdivided
into the sympathetic nervous system, which readies you for an impeding conflict, and
the parasympathetic nervous system, which conserves energy and regulates growth.
The somatic nervous system, by contrast, is under conscious control. It is responsible for
conscious sensation (such as feeling something is cold, or that something is sharp) as
opposed to the unconscious sensation of the autonomic nervous system (such as your
carotid bulbs sensing decreased blood perfusion to the brain). It is also responsible for
the voluntary control of muscles. The autonomic and somatic systems act through the
CN in the head as well as the spinal nerves in the body.
The autonomic system and the somatic system should be thought of as distinct entities.
However, they can both travel together in the same nerve. For example, CN III is con-
sidered to have a somatic and autonomic component. However, this is usually for just
a short part of the nerve pathway, and the components soon separate. We will examine
this further in Chapter 3.
Take Home Messages
The CNS is made up of the brain and spinal cord.

The PNS is composed of the somatic nervous system, under conscious
control, and the autonomic nervous system, which is not under conscious
control.
The somatic system and the autonomic system act both through cranial
nerves and spinal nerves.
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Figure 1.2 Anatomy of a Neuron
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Anatomy of a Neuron 7
Before we continue, it is useful to go over the anatomy of a neuron. A neuron is a single

cell composed of three main parts – dendrites, a single cell body and a single axon.
Dendrites transmit information signals toward the cell body of the neuron. Axons transmit
information away from the cell body, in the form of an electrical impulse called an action
potential. Action potentials are caused by transient changes in the voltage measured
between a neuron’s cell membrane and the exterior environment. The cell body contains
the nucleus and all the cellular machinery necessary to sustain the neuron.
An axon is covered in myelin, which is produced in the PNS by the Schwann cell. In the
CNS, myelin is produced by another kind of cell, the oligodendrocyte. Nodes of Ranvier
are small areas along the axon that do not contain myelin. Myelin allows for much more
rapid transmission of action potentials, as they can jump between Nodes of Ranvier as
shown in Fig. 1.2.
Many dendrites can feed into one cell body, but each cell body has only one axon. Even
though most books draw the dendrites as being quite short, they can be very long, even
longer than the axon. It is important to note that one neuron spans the entire length of
any individual nerve. Thus, the neurons of the sciatic nerve are over 1 meter (over 3 feet)
long!
The nomenclature of neuron cell bodies is important and can be a cause of confusion.
In the CNS a collection of cell bodies is called a nucleus. In the PNS a collection of cell
bodies is called a ganglion (pl. ganglia). This difference is illustrated nicely by the auto-
nomic nervous system, as we will see in a few pages.
Take Home Messages
Dendrites transmit information towards the cell body and axons transmit
information away from the cell body.
Axons are covered in myelin, which is made by Schwann cells in the PNS
and oligodendrocytes in the CNS.
A collection of cell bodies is called a nucleus in the CNS and a ganglion in
the PNS.
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Figure 1.3 Overview of the Central Nervous System
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Overview of the Central Nervous System 9
As we saw earlier, the CNS is composed of the brain and spinal cord. The brain itself is
made up of the cerebrum, brainstem and cerebellum.
The cerebrum is what most people picture when they think of the brain. It is divided into
two identical hemispheres: one on the left side and one on the right side. The outer layer
of the cerebrum is called the cortex and made up of folded layers of tissue called gray
matter. Gray matter houses neuronal cell bodies and initiates neuronal impulses. The
other type of tissue in the CNS is white matter, which contains the axons that transmit
the impulses initiated from the gray matter.
If you examine the cerebrum shown in Fig. 1.3, you will see it is composed of many ridges
and valleys. A ridge is called a gyrus and a valley is called a sulcus. The central sulcus is
important because the gyrus anterior to it is the primary motor cortex, which initiates all
motor functions. The gyrus posterior to the central sulcus is the primary sensory cortex,
which receives all sensory input.
The cerebrum is divided into lobes by various anatomical landmarks. The frontal lobe ex-
tends back to the central sulcus, and inferiorly until the Sylvian fissure. The frontal lobe is
responsible for thinking, planning and all motor control. The parietal lobe is posterior to the
central sulcus but doesn’t have a specific defining landmark between it and the temporal or
occipital lobes. The parietal lobe receives and integrates all sensory information. The tempo-
ral lobe sits inferior to the Sylvian fissure, but doesn’t have a defined posterior border; it cre-
ates and stores new memory and is involved in emotional regulation. It also contributes to the
understanding of language. Finally, the occipital lobe serves as the visual processing center.
The brainstem sits just inferior to the cerebrum, and is divided into three sections called
the midbrain, pons and medulla. The brainstem regulates all life preserving functions and
controls consciousness. It also provides all innervation to the head via the CN. Just inferior to
it sits the cerebellum, which is responsible for coordinating smooth, voluntary movement.
Just as the brainstem provides all innervation to the head via the CN, the spinal cord
provides all innervation to the body via the spinal nerves.
Take Home Messages
The brain is made up of the cerebrum, brainstem and cerebellum.

The cerebrum is divided into four lobes: frontal, parietal, temporal and occipital.
The brainstem is divided into the midbrain, pons and medulla.
The brainstem provides all innervation to the head, and the spinal cord
provides all innervation to the body.
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Figure 1.4 Overview of the Peripheral Nervous System
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Overview of the Peripheral Nervous System 11
The PNS consists of the CN and the spinal nerves. We will discuss the CN in detail in
Chapter 3. In order to understand the spinal nerves, we need to briefly discuss their
relation to the spinal cord.
A total of 31 paired spinal nerves exit the spinal cord. Because of morphological differ-
ences that occur in the spinal cord, the spinal cord and its associated nerves are divided
into four different sections: cervical, thoracic, lumbar and sacral. There are 8 cervical
nerves, 12 thoracic nerves, 5 lumbar nerves and 5 sacral nerves (in addition there is one
coccygeal nerve, but it serves no clinically relevant purpose so it is usually ignored).
Nerves are named by stating which group they belong to, and the relative position of
the nerve in the group; for example the 6th nerve of the cervical group is called Cervical 6
(abbreviated C6).
If we take a closer look at the spinal cord we will see that a total of four nerve roots exit
the spinal cord (two on each side). There is an anterior nerve root, which carries motor
signals to muscle, and a posterior nerve root, which carries sensory information to the
brain. The nucleus for the motor neuron lies in a special area of the gray matter, called
the anterior horn cell (AHC). The cell body for the sensory neuron lies outside the cord
in what is called the dorsal root ganglion (DRG).
Just distal to the DRG, the nerve roots merge to form a spinal nerve. The spinal nerves
destined for the arm or the leg travel a short distance and then enter a mesh-like
network called a plexus. In the plexus, the spinal nerves mix together and ultimately
form individual peripheral nerves. The peripheral nerves travel throughout the body to
their end target, which is a muscle or a sensory organ (usually skin). The plexus in the
upper limb is called the brachial plexus and the plexus in the lower limb is called the
lumbosacral plexus.
Take Home Messages
31 paired spinal nerves exit the spinal cord: 8 cervical, 12 thoracic,

5 lumbar, 5 sacral and 1 coccygeal (often ignored).
The nucleus for the motor neuron lies in the AHC of the spinal cord. The
cell body of the sensory neuron lies outside the cord, in the DRG.
The anterior nerve root carries motor signals and the posterior nerve root
carries sensory signals.
Spinal nerves mix together in the plexus to form peripheral nerves.
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Figure 1.5 Long Tracts of the Central Nervous System
LMN: lower motor neuron; UMN: upper motor neuron.
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Long Tracts of the Central Nervous System 13
There are three different pathways, or tracts, that the CNS uses to transmit and receive
information, as shown in Fig. 1.5. Collectively, these three pathways are often referred
to as the long tracts because they run longitudinally throughout the entirety of the CNS.
Let’s consider each of these.
The motor pathway is made up of two neurons; an upper motor neuron (UMN) and
a lower motor neuron (LMN). The UMN travels in the corticospinal tract, which runs
from the motor cortex to the AHC in the spinal cord. As the corticospinal tract passes
through the medulla it crosses over, or decussates, to the contralateral side. The UMN
continues downward and eventually exits the corticospinal tract to synapse with the
LMN in the AHC. The LMN exits the spinal cord, and travels as part of the peripheral
nerve until it reaches its end muscle. As we will examine further later, lesions of the UMN
produce very different symptoms than lesions of the LMN.
The sensory pathway is made up of three neurons called the 1st order, 2nd order and 3rd
order neurons. The CNS has two different sensory tracts and they carry different types
of information. The spinothalamic tract (ST) carries pain and temperature information.
The dorsal columns (DC) carry vibration and proprioception. Proprioception is the
innate knowledge of where your body is in space (i.e., if your eyes are closed and you put
your hand in front of your face, you are still are aware that your hand is in front of your
face). Unfortunately the DC undergo a needless name change once it synapses with its
2nd order neuron, and is afterwards known as the medial lemniscus (ML).
The 1st order neuron for both paths begin in the PNS and travel into the spinal cord;
as they do, they pass their cell body, which is housed in the DRG. If the neuron carries
vibration/proprioceptive it enters the DC. It continues up the DC into the medulla where
it synapses with its 2nd order neuron, decussates and is now known as the ML. The 2nd order
neuron travels into the thalamus where it synapses with the 3rd order neuron and then
terminates in the sensory cortex. If the 1st order neuron carries pain/temperature signals,
it synapses with its 2nd order neuron upon entering the spinal cord and decussates to enter
the contralateral ST. It then continues up the ST, through the brainstem and synapses
with its 3rd order neuron in the thalamus before finally terminating in the sensory cortex.
Take Home Messages
Motor information is transmitted by the UMN (motor cortex to AHC) and

the LMN (AHC to muscle). The UMN travels in the corticospinal tract and
decussates at the medulla.
The ST decussates upon entering the cord. The DC decussate at the level
of the medulla.
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Figure 1.6 Somatotopy of the Central Nervous System
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Somatotopy of the Central Nervous System 15
Unlike the PNS, the CNS displays an important property called somatotopy. This is a
fundamental, defining characteristic of the CNS and its importance cannot be overstated.
Somatotopy is the point mapping of body part to a precise neuroanatomical area. Figure 1.6
shows a distorted person, called a homunculus, who appears to be lying on top of the
cortex. The homunculus is a pictorial representation that shows which neuroanatomical
area controls what part of the body. For example, we see that the lateral part of the motor
cortex innervates the face and mouth, whereas the medial part innervates the leg. Note
that somatotopic representation is proportional; as the more precise control needed over
a part of the body, the more neuroanatomical area is required. For example, the hand,
with its fine, highly evolved, intricate movements, requires more neuroanatomical area
than the foot, with its relatively primitive, easy to perform movements. This is also true
between individuals. Anatomical studies show, for example, that musicians, with the
need for extremely precise dexterity, will have a larger section of the brain devoted to
finger and hand control then their nonmusician equivalents.
Figure 1.6 shows that somatotopy continues as we move down the CNS. The internal
capsule is an important area of white matter; once again parts of the body are mapped to
precise, defined, neuroanatomical areas. The same is true of the spinal cord.
Another way to think of it is that the CNS is analogous to a computer. Each specific
motor or sensory function (equivalent to a computer program) is stored in a specific,
defined neuroanatomical area (equivalent to an area of memory). Damage to one area
of memory will cause the corresponding program to be unable to run. Neuroanatomical
damage will cause symptoms in the corresponding somatotopic area of the body. This is
why understanding the somatotopy of the CNS at each level is so important.
As mentioned, somatotopy does not exist in the PNS. If one were to examine a cross
section of a nerve, there would be no 1:1 mapping of body function to neuroanatomical
area.
We will revisit the concept of somatotopy as we explore each part of the CNS.
Take Home Message
The CNS exhibits somatotopy. All parts of the body are mapped 1:1 to a
distinct and precise neuroanatomical area.
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Figure 1.7 Arterial Supply to the Central Nervous System
ACA: anterior cerebral artery; ACOM: anterior communicating artery; AICA: anterior inferior cerebellar
artery; ICA: internal carotid arteries; MCA: middle cerebral artery; PCA: posterior cerebral arteries; PCOM:
posterior communicating arteries; artery; SCA: superior cerebellar artery.
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Arterial Supply to the Central Nervous System 17
Two distinct circulations, the anterior circulation and the posterior circulation, supply
blood to the brain. The anterior circulation is ultimately derived from the internal carotid
arteries (ICA), and supplies the anterior two-thirds of the brain. The posterior circulation
is ultimately derived from the vertebral arteries, and supplies the posterior one-third of
the brain, including the brainstem and cerebellum. The carotid arteries branch from the
aorta itself, whereas the vertebral arteries come off the subclavian artery.
The common carotid artery divides into the external carotid artery, which supplies the
face, and the ICA. The ICA travels into the skull and, once it reaches the base of the brain,
bifurcates into the anterior cerebral artery (ACA), and the middle cerebral artery
(MCA). The ACA supplies the medial aspect of the cerebral hemispheres while the MCA
supplies the lateral aspect.
The vertebral arteries travel up into the head through the foramen of the vertebral bones.
Once they have passed through the skull they unite to form the basilar artery. Before they
do so, however, they each give off a branch called the posterior inferior cerebellar artery
(PICA). The basilar artery gives rise to two other cerebellar arteries: the superior cerebellar
artery (SCA), and the anterior inferior cerebellar artery (AICA). The cerebellar arteries
supply the brainstem, and cerebellum. Finally, the basilar bifurcates into two posterior
cerebral arteries (PCA). The PCA supplies the occipital lobe and a small part of the midbrain.
If we had the arterial system just described, strokes and other vascular events would be
much more common since each part of the brain has its own, sole, independent vascular
supply. One single artery (left ICA, right ICA, or basilar) would supply one single part of the
brain. However, we have evolved “backup collaterals” that tie the blood supply of the left
hemisphere and right hemisphere to each other, as well as tying the anterior and posterior
circulations together. This is achieved through “communicating arteries,” and include the
anterior communicating artery (ACOM), which link the two ACA together, thus joining
the left and right circulation together, and the posterior communicating arteries (PCOM),
which join the MCA to the PCA, effectively linking the anterior and posterior circulation
together. The communicating arteries help form a continuous circle of circulation that
supplies the entire brain, called the Circle of Willis after the physician that first described it.
Take Home Messages
The common carotid artery becomes the ICA which bifurcates into the ACA
and MCA.
Two vertebral arteries unite to become the basilar artery. The basilar artery
gives off AICA and SCA branches and bifurcates to become two PCA arteries.
The ACOM joins the left and right circulation together, and the PCOM joins
the anterior and posterior circulation together to form the Circle of Willis.
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Figure 1.8 The Meninges
CSF: cerebrospinal fluid.

Top Figure: Adapted from Blumenfeld H. Neuroanatomy Through Clinical Cases. Sinauer Associates Inc,
Sunderland, 2002.
Bottom Figure: Redrawn with permission from Waxman SG. Clinical Neuroanatomy. Lange, New York, 2013.
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The Meninges 19
The CNS is surrounded by several layers of tissue, collectively called the meninges,
that separate it from the skull bone. The deepest layer of tissue, the pia mater (Latin
for “tender mother”), directly covers the brain and spinal cord. The next layer is called
the arachnoid mater, for its spider-like appearance. The area in between the arachnoid
mater and the pia mater is called the subarachnoid space. The blood vessels of the Circle
of Willis lie in the subarachnoid space. Cerebrospinal fluid (CSF), which acts as a shock
absorber for the brain, also fills the subarachnoid space. CSF is produced by the choroid
plexus in the ventricles and is eventually absorbed by the arachnoid granulations in the
subarachnoid space.
The outermost layer of tissue is called the dura mater (Latin for “tough mother”) and
lies on top of the arachnoid mater and directly below the bone of the skull. It is actually
composed of two layers on top of each other; meningeal dura mater, which lies directly on
top of the arachnoid mater, and the periosteal dura mater, which abuts the skull bone. Two
potential spaces exist: the epidural space, which is the area between the periosteal dura
and the skull, and the subdural space, between the meningeal dura and the arachnoid
mater. They are called potential spaces because they normally should not exist but, as we
will see, can be filled with pathologic material, such as blood or pus, and become realized.
Note also that at times the periosteal dura is not always in direct contact with the meningeal
dura, which creates a channel. These channels are referred to as venous sinuses and help
to drain venous blood from the brain. We will discuss them further in Chapter 2.
Take Home Messages
Working our way in from the skin, the layers encountered on the way to
the brain are:
• Skin;
• Skull bone;
• Epidural space (potential space);
• Periosteal dura mater;
• Meningeal dura mater;
• Subdural space (potential space);
• Arachnoid mater;
• Subarachnoid space (containing blood vessels bathed in CSF);
• Pia mater;
• Brain tissue.
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Figure 1.9 Overview of the Autonomic Nervous System
CN: cranial nerve.

Adapted from Freeman S, et al. Biological Science. Pearson, Boston, 2013.
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Overview of the Autonomic Nervous System 21
Figure 1.9 displays an overview of the autonomic nervous system, which you’ll recall is
divided into the sympathetic nervous system and parasympathetic nervous system. Both
systems use two neurons. The first neuron lies in the CNS and is called the preganglionic
neuron. It synapses in various ganglia (which, remember, are neurons whose cell bodies
are located in the PNS) with the postganglionic neuron.
We’ll begin with the parasympathetic system, which, remember, acts to conserve energy
and anabolically build tissue. The nuclei for preganglionic neurons arise from two
locations: the brainstem (specifically, CN III, CN VII, CN IX and CN X) and the sacral
part of the spinal cord (specifically, spinal levels S2–S4). These neurons travel into the
periphery where they synapse with their ganglia, and the postganglionic neurons con-
tinue into their effector organs. It’s important to note that the parasympathetic ganglia
are located very close to the organs they innervate, in contrast to the sympathetic system,
as we’ll see now.
The sympathetic nervous system acts to mobilize energy for survival purposes. The
nuclei for preganglionic neurons of the sympathetic system are housed in spinal cord
levels T2–L3. The preganglionic neuron has two sets of ganglia it can synapse with. The
first is located in the sympathetic chain, which is a bundle of neural tissue that lies
just adjacent to the spinal cord. The second set is located at various points throughout
the body. Each preganglionic neuron synapses with only one postganglionic neuron,
whether it is located in the sympathetic chain or elsewhere.
Take Home Messages
The autonomic nervous system employs two neurons: the preganglionic

neuron and the postganglionic neuron.
The parasympathetic system conserves energy for growth. The nuclei of
the preganglionic neurons originate in the brainstem or sacral spinal cord.
The postganglionic neurons are near their effector organs.
The sympathetic system uses energy for survival. The nuclei of the
preganglionic neurons originate in the spinal cord from levels T2 to L3. Its
postganglionic neurons begin either in the sympathetic trunk or at other
various ganglia.
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Chapter 2
The Cortex and
Associated Structures
Immediate Localization – Higher Functions

As we will see, the patterns of motor and sensory dysfunction produced
by lesions of the cortex are quite diverse, but typically involve one side of
the body (face, arm, and leg). However, problems of any higher cognitive
functions can only be produced by lesions of the cortex. These Higher
Functions include:
• Aphasia – the inability to perceive and use language
• Agnosia – the inability to interpret sensory information to recognize
objects
• Apraxia – the inability to perform learned tasks
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24 Chapter 2 The Cortex and Associated Structures
Figure 2.1 Specialized Areas of the Cortex
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Specialized Areas of the Cortex 25
Earlier we saw that the cerebrum can be divided into four lobes: frontal, parietal,
temporal and occipital. We also saw that the motor cortex is located in the precentral
gyrus, and the sensory cortex is located in the postcentral gyrus. There are several other
important functional areas of cortex and we will cover them now.
Just anterior to the motor cortex lies the premotor cortex and the supplementary motor
area. These structures are involved in the planning of complex movements, such writing,
or playing the piano, before they are initiated by the motor cortex.
Anterior to the supplementary motor area is the frontal eye field (FEF). The FEF controls
voluntary eye movement in the horizontal plane. Activation of the FEF in one hemisphere
drives the eyes in the contralateral direction; the left FEF will drive the eyes to the right
and vice versa.
On the other side of the central sulcus lies the sensory association cortex. This area of
the brain integrates various sensory information to make sense of the object providing
the stimulus. For example, it determines that the small, round, cold object that you are
holding in your hand likely represents a coin.
Near the anterior portion of the frontal lobe lies Broca’s area. This part of the brain produces
language; written or verbal. Note that Broca’s area lies right beside the part of the motor
cortex that controls lips, tongue and the larynx. Wernicke’s area resides in the temporal
lobe and is the part of the brain responsible for language comprehension. Note its proximity
to the primary auditory cortex, which receives and processes auditory information.
On the medial side of the hemispheres lies the cingulate gyrus, which plays an important
role in memory and behavior.
Recall from Chapter 1 that the motor and sensory cortices are somatotopically organized
according the homunculi shown in Fig. 2.1. The homunculi extend to the medial aspect
of the hemispheres, which is a fact of great importance, as we will soon see.
Take Home Messages
The premotor cortex is located adjacent to the motor cortex and plans
complex movement.
The FEF drive the eyes to the contralateral side.
The sensory association cortex makes 3D sense of sensory input from the
sensory cortex.
Wernicke’s area is responsible for the understanding of language, and
Broca’s area is responsible for generating language.
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Figure 2.2 The Basal Ganglia and Associated Structures
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The Basal Ganglia and Associated Structures 27
The basal ganglia are a group of gray matter structures located near the base of the
cerebrum*. They can be thought of as gatekeepers, modulating motor and sensory signals
sent back and forth between the rest of the cerebrum and the brainstem and spinal cord.
The main components of the basal ganglia are the caudate, putamen, globus pallidus,
and substantia nigra. Knowing the functions of each component is neither practical nor
needed at this stage in learning. Dysfunction of the basal ganglia as a whole can give rise
to a variety of movement disorders, by far the most common being Parkinson’s disease.
The egg shaped structure that lies posterolateral to the basal ganglia is the thalamus,
which we explore shortly.
Several white matter tracts separate the basal ganglia from each other. Framing the
basal ganglia at the anterior and posterior poles are the genu and splenium of the cor-
pus callosum, respectively. These tracts serve to connect the left hemisphere and right
hemisphere. In between the basal ganglia lies the internal capsule, which is an important
white matter tract that carries both descending motor neurons from the cortex, and
ascending sensory neurons from the brainstem and spinal cord.
The insula lies just lateral to the putamen, and is a part of the cortex that is buried at the
base of the Sylvian fissure. The functions of the insula are not completely understood, but
it is believed to play a role in autonomic function and emotional regulation.
* Note: If you’ve been paying attention, the opening sentence of this page will give you pause; ganglia are a group
of neuron cell bodies in the peripheral nervous system (PNS). A group of nerve cell bodies in the central nervous
system (CNS) are called nuclei. Well right you are, and the basal ganglia should really be referred to as the basal
nuclei, but for historical reasons the name basal ganglia sticks.
Take Home Messages
The basal ganglia are involved in helping make sure that motion is smooth
and regulated.
The internal capsule is a white matter tract that conveys all motor
neurons from motor cortex as well as ascending sensory neurons from the
brainstem and spinal cord.
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Figure 2.3 Nuclei of the Thalamus
LGN: lateral geniculate body; MGN: medial geniculate nucleus; VA: ventral anterior nucleus; VLN: ventral
lateral nucleus; VPL: ventral posterior lateral nucleus; VPM: ventral posteromedial nucleus.
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Nuclei of the Thalamus 29
The thalamus can be thought of as a large relay center made up of many different nuclei.
Not all of these nuclei are completely understood. We have listed some of the most
relevant and well understood ones in Fig. 2.3, but a complete discussion of the thalamus
is beyond this text.
There are many different ways to classify the nuclei of the thalamus and this diversity
is a frequent source of frustration for students. One of the simplest methods is to group
them according to anatomical region. Examining Fig. 2.3 you will see that a “Y-shaped”
white matter tract called the internal medullary lamina separates the thalamus into
three anatomical regions; anterior, medial and lateral. There are also nuclei, called the
intralaminar nuclei, embedded in the internal medullary lamina, which is sometimes
referred to as the fourth anatomical region.
Functionally, the nuclei of the thalamus can be classified into two groups: specific nuclei,
which project to one single, precise neuroanatomical area and nonspecific nuclei, which
have projections to many different areas. All of the specific nuclei are located in the lateral
section of the thalamus. (These nuclei tend to pop up on exams and should be committed
to memory.) Nuclei in the anterior and medial section are involved in processing both
emotion and memory. The intralaminar nuclei are responsible for regulating the sleep–
wake cycle and plays a critical role in consciousness. Bilateral lesions of the thalamus
involving the intralaminar nuclei often result in coma.
Two very important nuclei include the ventral posterior lateral nucleus (VPL nucleus)
and the ventral posteromedial nucleus (VPM nucleus). These nuclei receive neurons
from the spinothalamic tract (ST) and dorsal columns (DC). The VPL is the relay site for
sensory neurons from the body (arms and legs) and the VPM is the relay site for sensory
neurons from the face.
Take Home Messages
Anatomically, the thalamus is divided into four regions: anterior, medial,

lateral, and intralaminar.
A white matter tract called the internal medullary lamina divides the
thalamus into the above regions.
Functionally, the thalamic nuclei can be classified into specific and
nonspecific.
The intralaminar nuclei play a critical role in consciousness.
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Figure 2.4 The Internal Capsule

Redrawn with permission from Waxman SG. Clinical Neuroanatomy. Lange, New York, 2013.
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The Internal Capsule 31
As we mentioned, the internal capsule is a white matter tract that cuts through the center
of the basal ganglia. Descending neurons from the motor cortex and ascending sensory
neurons from the brainstem and spinal cord both pass through this small area. Given
the extreme density of the neuroanatomical real estate found here, small lesions, such as
strokes, can have devastatingly large effects.
The internal capsule is divided into three sections. The anterior limb sits between
the putamen and caudate. It carries fibers running from the thalamus to cortex, the
thalamocortical fibers, as well as fibers back from the cortex to the thalamus, the
corticothalamic fibers. These fibers carry various types of information. The posterior
limb of the internal capsule lies between the putamen and thalamus. The first part of
the posterior limb carries the arm and leg neurons of the corticospinal tract. The second
part of the posterior limb carries sensory neurons from the VPM and VPL nuclei of
the thalamus, en route to the sensory cortex. Note that the somatotopy of the sensory
information is identical to its motor counterpart, repeating the same “face, arm, leg”
pattern.
In between the anterior and posterior limb lies the genu, which represents the “bend,” or
“knee” of the internal capsule. The motor neurons destined for the face travel here and
continue on in the corticobulbar tract. The corticobulbar tract is a white matter tract that
carries neurons from the motor cortex to the CN that innervate the face; it is the facial
equivalent of the corticospinal tract.
Take Home Messages
The components of the internal capsule are as follows:

• Anterior limb: thalamocortical fibers and corticothalamic fibers.
• Genu: motor neurons to the face (travelling in the corticobulbar tract).
• Posterior limb motor neurons to the arm and leg (travelling in the
corticospinal tract), followed by sensory neurons from face, arm and
leg.
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Figure 2.5 The Motor Pathways
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The Motor Pathways 33
We are now in a position to trace out the motor and sensory pathways in the CNS, with
an emphasis on the somatotopic arrangement at several keys levels. In doing so, we will
continue to employ our “face”, “arm” and “leg” nomenclature, which refers to either a)
motor neurons travelling to these areas, or b) sensory neurons travelling from these areas.
We will begin with the motor system. As we just learned, the motor system is subdivided
into a corticobulbar tract, which innervates the muscles of the face via the brainstem and a
corticospinal tract, which innervates the muscles of the rest of the body via the spinal cord.
The tracts begin in the motor cortex and descend through the white matter. Initially, the
neurons were oriented in the medial–lateral (M – L) plane, with face neurons lateral and
leg neurons medial. As the tracts enter the internal capsule, however they twist 90° to
run in the anterior–posterior (A – P) direction. Now face neurons are anterior and leg
neurons are posterior, as we saw in Fig. 2.4.
They continue to twist another 90° as they enter the midbrain such that they again run in
the M – L direction, however now the face neurons are the most medial and leg neurons
are the most lateral. As we descend through the pons and medulla, the upper motor
neurons (UMN) of the corticobulbar tract exit and synapse with the lower motor neuron
(LMN) nuclei in the brainstem.
At the level of the medulla the corticospinal tract both decussates and twists 180°, so
that the somatotopic arrangement is maintained. Prior to decussation leg neurons were
lateral and arm neurons were medial; by both decussating and twisting, the leg remains
lateral, and the arm remains medial, but on the opposing side.
The UMNs of the corticospinal tract continue down the lateral part of the spinal cord. At
the level of the cervical spine, arm neurons synapse with their LMN in the anterior horn
cell (AHC). Leg neurons continue down the cord and eventually synapse with their LMNs
at the level of the lumbar spine.
Take Home Messages
The motor system is made up of two tracts: the corticobulbar tract and
the corticospinal tract.
Just before entering the internal capsule, motor neurons twist 90° to run
in the A – P direction.
They then twist another 90° just before entering the midbrain, to run in
the M – L direction.
Just before entering the cervical cord, motor neurons decussate and twist
180°.
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Figure 2.6 The Sensory Pathways
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The Sensory Pathways 35
We’ll now turn our attention to the ST, which carries pain and temperature, and the DC,
which carries proprioception and vibration. Remember, once the DC synapses with its
2nd order neuron, it is renamed the medial lemniscus.
Let’s begin with the ST tract. Neurons from the leg enter the lumbar cord. They decussate
immediately and enter the contralateral ST, which ascends up the cord. At the cervical
level it is joined by neurons from the arm, which travel medial to neurons from the leg. In
the pons, neurons from the face join the ST tract and now occupy the most medial spot.
The neurons travel up into the VPM (facial neurons) and VPL (arm and leg neurons)
nuclei of the thalamus, where they synapse with their 3rd order neurons.
We’ll now move onto the DC pathway. Neurons from the leg enter the lumbar cord
and travel up the ipsilateral DC. At the cervical level it is joined with neurons from the
arm, which travel lateral to neurons from the leg, as shown in Fig. 2.6. At the level of the
medulla, the neurons decussate without twisting, making the leg neurons lateral and
arm neurons medial. As they travel up through the pons, they are joined by neurons from
the face, which now occupy the most medial spot. They continue into the VPM and VPL
of the thalamus, where they synapse with their 3rd order neurons.
Note that as the medial lemniscus ascends up the brainstem it moves laterally until it
merges with the spinothalamic tract at the level of the midbrain. Beyond this point, both
tracts share the same somatotopy; face neurons are medial and leg neurons are lateral.
The two tracts continue into the thalamus, where they have neighboring synapses. The
paths of the 3rd order neurons for both tracts are identical. They leave the thalamus, twist
90° to run in the A – P direction and travel in the posterior limb of the internal capsule, as
shown in Fig. 2.4. They then twist another 90° to run in the M – L direction, but now face
neurons are lateral and leg neurons are medial. The tracts then synapse in the sensory
cortex.
Take Home Messages
The ST tract decussates upon entering the cord; neurons are added
medially as the tract travels into the brain.
The DC initially have the opposite somatotopy; neurons are added
laterally. However, once the DC becomes the medial lemniscus, the
neurons are added medially, as in the ST.
3rd order neurons for both tracts share the same path and somatotopy.
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Figure 2.7 The Language Circuit
AF: arcuate fasciculus B: Broca’s area; C: conception tract; W: Wernicke’s area.
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The Language Circuit 37
Having reviewed the motor and sensory systems, we will now study the function of
several key areas of the cerebrum. We will begin with one of the most fundamental, the
language circuit.
By definition, the language circuit of the brain is located in the dominant hemisphere.
There are many different models for language, but the best one is the Wernicke–
Lichtheim model, shown in Fig. 2.7. Broca’s area, represented as B, is responsible for
language production, and Wernicke’s area, W, is responsible for the reception and
understanding of language. They are connected directly together by another tract, called
the arcuate fasciculus (AF); this tract allows for repetition. Wernicke’s area understands
the command to repeat, and sends the signal through the AF to Broca’s area. The
anatomical location of Broca’s area, Wernicke’s area and the AF are known and shown in
the second part of Fig. 2.7.
The AF is a direct connection between Wernicke’s area and Broca’s area. As such, it does
not allow for any thinking about or processing of language received by Wernicke’s area,
nor does it allow for the creation of new language. Another tract must exist. The exact
anatomical location of this “conception tract,” called C, is unknown. It is theoretical
and used by the Wernicke–Lichtheim model to illustrate the different types of language
problems, which we will discuss in a moment.
Aphasia is defined as the inability to comprehend and/or express language. It can

sometimes be confused with dysarthria, which is the mispronunciation of words, usually
due to facial or mouth weakness. The distinction between the two can be remembered as
aphasia is saying incorrect words (language problem), whereas dysarthria is saying words
incorrectly (pronunciation problem).
Take Home Messages
Wernicke’s area is connected to Broca’s area by the AF, which allows for
repetition.
Wernicke’s area is connected to Broca’s area by an alternative connection,
the conception tract, which allows for processing of received language
and the formation of new language.
Aphasia is saying incorrect words; dysarthria is saying words incorrectly.
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Figure 2.8 The Aphasias
AF: arcuate fasciculus; B: Broca’s area; C: conception tract; TCM: transcortical motor; TCS: transcortical
sensory; W: Wernicke’s area.
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The Aphasias 39
The examination for aphasia evaluates three cardinal abilities. They are:
• the ability to understand a vocal or written command
• the ability to repeat a sentence
• observation of the fluency of the patient’s spontaneous speech.
Fluency is notoriously difficult to define, and is best thought of as both the rate and
syntax of speech.
The lesions shown in Fig. 2.8 produce five distinct aphasias. A Broca’s aphasia (lesion
1) results in a patient with decreased fluency; they struggle even to say a few words,
meaningful or not. Language understanding however, is largely intact. They understand
the command to repeat a sentence but cannot do so. A Wernicke’s aphasia (lesion 2)
results in a patient that does not comprehend language including the command to repeat
a sentence. They also do not understand language of their own creation; we think in words
and phrases, and patients with Wernicke’s aphasia lose the ability to do this. This extremely
frustrating condition results in a speech that is fluent, but is random and nonsensical.
A conduction aphasia is the result of a lesion to the AF (lesion 3). The patient can
understand language and produce language correctly, but cannot repeat a sentence.
A lesion to the conception tract (lesion 4 and 5), results in a transcortical motor (TCM)
aphasia or transcortical sensory (TCS) aphasia, respectively. A TCM aphasia impairs
fluency, as the patient cannot think about what to say, but the patient is still able to
understand and repeat. A TCS aphasia results in a patient who is fluent and can repeat,
but is unable to think about the speech they have heard.
Note that a TCM aphasia is identical to a Broca’s aphasia except that the TCM aphasia
patient retains the ability to repeat. Similarly, a TCS aphasia is identical to a Wernicke’s
aphasia except that the TCS aphasia patient retains the ability to repeat.
A large insult to the brain can knock out the entire language circuit, resulting in a global
aphasia, where the patient cannot understand, repeat and is not fluent.
Take Home Messages
Broca’s aphasia patients retain the understanding of language. Wernicke’s

aphasia patients retain the fluency of language.
A conduction aphasia results in impaired repetition.
A TCM aphasia results in impaired fluency but intact comprehension and
repetition. A TCS aphasia results in impaired understanding but intact
fluency and repetition.
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Figure 2.9 Dominant Higher Functions
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Dominant Higher Functions 41
If you study the cortex closely you will note that each primary sensory modality (auditory
cortex, visual cortex, or primary sensory cortex) has beside it an association cortex, as
depicted in Fig. 2.9. The association cortex is involved in pattern recognition and allows
us to perceive objects, based on the sensory information received by the corresponding
primary cortex. For example, the primary sensory association cortex recognizes that
the small, cold, irregularly shaped object in your pocket is a key. Difficulties with this
perceptive ability is called agnosia. Interestingly, as one studies progressively higher
order mammals the association areas take up an increasingly large amount of brain
tissue, with humans having the largest area.
Tactile agnosia is a failure to recognize objects despite having intact tactile sensation. It
is the most common type of agnosia evaluated at the bedside. It is examined by asking
the patient to close their eyes and placing an object (usually a coin, paperclip or key) in
their hand. They then must identify the object by manipulating it with the fingers alone.
The inability to do this is specifically referred to as astereognosis, as seen in Fig. 2.9.
Closely related is agraphesthesia, which is the inability to recognize symbols traced on
one’s skin (typically a number or a letter traced out on the hand).
Visual agnosia is the inability to recognize visual objects, despite having intact primary
vision; for example, despite normal vision, a patient cannot recognize simple objects
(such as a cup or a pen). An extreme of visual agnosia is prosopagnosia, which is the
inability to recognize faces, as was famously popularized in the book by Oliver Sacks,
“The Man that Mistook His Wife for a Hat.”
Auditory agnosia is the inability to recognize the meaning of sound despite having intact
hearing; this can either involve language (hearing words, but not knowing what they
mean, called pure word deafness) or nonlanguage (interpretation of simple sound, for
example, recognizing the ‘clicking’ of high heeled shoes, or the bang of a gunshot).
Another type of agnosia is anosognosia, which is the inability to recognize that one is ill.
Despite demonstration of significant neurological deficit, such as having hemi-paresis,
the patient states she is perfectly well.
Interestingly, depending on the type of agnosia, the lesion can be located in either the
dominant or nondominant lobe.
Take Home Messages
Lesions to an association area will produce agnosia, which is the inability

to integrate sensory information to recognize objects.
This can manifest as tactile, visual, or auditory agnosia.
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Figure 2.10 Nondominant Higher Functions
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Nondominant Higher Functions 43
Apraxia can be thought of as the motor equivalent of agnosia. It is the inability to perform
learned motor tasks, despite having intact motor power and coordination.
Just as with agnosia, there are many different types of apraxia. The most common is
ideomotor apraxia, which is difficulty using the limbs for complex tasks. This is tested
at the bedside with simple commands, such as “show me how you would salute a
soldier”, or “ show me how you would brush your teeth”. While patients retain the motor
ability to perform the task, they have lost the cognitive ability to plan out and execute it.
Reflexively, they are still able to perform the task; for example, if a soldier were to walk
into the exam room, the patient would reflexively salute. This is known as voluntary-
automatic dissociation.
Other types of apraxia include geographic apraxia (inability to plan a route to a known
destination), buccofacial apraxia (the inability to carry out movements of the face, such
as whistling or blowing out a match), and constructional apraxia (inability to draw
complex patterns, such as intersecting pentagons).
Apraxia is often seen in lesions to the nondominant hemisphere, and has many potential
localizations, including premotor cortex, supplementary motor area, corpus callosum
and parietal lobe.
Another phenomenon that localizes to the nondominant hemisphere is hemi-neglect,

which is a defect in the registration of, and attention to, space. Patients have no awareness
of anything occurring in that half of space, including themselves. This was demonstrated
in an episode of Seinfeld when the character Kramer, after receiving a head injury, did not
shave or dress one side, and was unaware that he had failed to do so. Neglect is not due
to any sort of primary sensory defect such as vision or proprioception. Patients simply do
not process information from that side of the space, do not move limbs on the affected
side and may even deny that their body exists on that side. This can be tested for clinically
by asking patients to perform the “line bisection task.” Patients are given a full sheet of
paper, as in Fig. 2.10, and asked to draw dashes through all the lines they see. Patients
with neglect will often demonstrate a definitive and marked inability to fill in the lines
beyond midline.
Take Home Messages
Apraxia and hemi-neglect are due to lesions of the nondominant

hemisphere.
The most common type of apraxia is ideomotor, which is a defect in using
limbs for complex motor tasks.
Hemi-neglect is the inability to process information from one half of the
world.
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Figure 2.11 The Cerebellum and Ataxia
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The Cerebellum and Ataxia 45
The cerebellum lies just posterior to the brainstem and is responsible for coordinating
all voluntary movement initiated by the motor cortex. Lesions of the cerebellum result
in irregular, uncoordinated movements called ataxia.
The cerebellum can be divided into three parts. Two hemispheres surround a central
structure, called the vermis. As we’ve seen, the CNS is organized somatotopically, and
the cerebellum is no exception. Its somatotopy is extremely simple, which is a true rarity
for neuroanatomy. The central structure, the vermis, is responsible for coordination
of the central part of the body, the trunk. A lesion to the vermis causes truncal ataxia;
the patient would involuntarily rock their body back and forth as they constantly try to
stabilize themselves about their center of gravity. A lesion to a cerebellar hemisphere
results in ataxia of the ipsilateral limb: the cerebellar tracts do not decussate.
Testing for limb ataxia is often carried out by having a patient trace out a path. This is
depicted in Fig. 2.11; here the patient is asked to run his heel down the contralateral shin
(often abbreviated clinically as “heel to shin” testing).
Consider for a moment what happens as the patient traces the path. His hip is flexed and
externally rotated while his knee is flexed. As he traces out the path he simultaneously
extends and internally rotates his hip and extends his knee; the result is smooth, coordinated
movement that stays on the target path. It is this simultaneous coordination of muscle
movement that is impaired in cerebellar ataxia. A patient with ataxia can only do one muscle
movement at once. If observed carefully, you would note the patient extending the hip, then
internally rotating it and then finally extending the knee. The patient then must do a series
of correction movements in order to realign the foot with its target path and destination.
Contrast this with tremor, which is often confused with ataxia. A tremor is a rhythmic
oscillation about a central point. Unlike ataxia, a tremor is symmetric about its midpoint.
The amplitude of the oscillation can change over the length of the movement, but it
remains symmetric.
Patients with ataxia of the lower limbs have an unsteady gait. Due to the inability to
coordinate muscle movements, when they walk their center of gravity shifts significantly,
causing falls to the same side as the lesion. To compensate for this, patients will lower
their center of gravity by moving their feet further apart creating a wide based gait.
Take Home Messages
The cerebellum coordinates voluntary movement and is made up of a

central vermis and two lateral hemispheres.
The vermis coordinates the trunk, and each hemisphere coordinates the
ipsilateral limbs.
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Figure 2.12 The Anterior Circulation
ACA: anterior cerebral artery; ACOM: anterior communicating artery; ICA: internal carotid arteries; MCA:
middle cerebral artery; PCA: posterior cerebral arteries; PCOM: posterior communicating arteries.
Bottom figure redrawn with permission from Blumenfeld H, Neuroanatomy Through Clinical Cases. Sinauer
Associates, Inc, Sunderland, 2002.
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The Anterior Circulation 47
As we saw in Chapter 1, the internal carotid artery (ICA) supplies the anterior two-thirds
of the brain. We will now review the ICA’s path and branches in more detail.
The ICA travels up the neck and enters the petrous bone of the skull through the carotid
canal. It then travels through a structure called the cavernous sinus. This sinus is actually
filled with venous blood and contains several important CN: we will revisit it in Chapter 3.
Just before the ICA bifurcates into the anterior cerebral artery (ACA) and the middle
cerebral artery (MCA), it gives off two important branches. The first is the ophthalmic
artery, which supplies many structures of the eye, including the retina. The second is
the anterior choroidal artery, which travels posteriorly and supplies part of the basal
ganglia.
The ACA continues anteriorly between the cerebral hemispheres and bifurcates into the
callosomarginal artery and the pericallosal artery. These arteries continue posteriorly
and supply roughly two-thirds of the medial aspect of the hemisphere. Remember, the
two individual ACA are connected to each other through the anterior communicating
artery (ACOM), which provides emergency collateral flow.
The MCA continues laterally to the Sylvian fissure. Along its way it gives off many little
arteries that supply the basal ganglia and internal capsule: these are collectively called
the lenticulostriate arteries. At the Sylvian fissure the MCA bifurcates into a superior
branch and an inferior branch. Overall, the MCA supplies most of the temporal lobe,
and also the lateral parts of the parietal and frontal lobes.
Take Home Messages
After the ICA passes through the cavernous sinus, it gives off two
important branches, the ophthalmologic artery and the anterior choroidal
artery, before bifurcating into the ACA and MCA.
The ACA travels in between the hemispheres.
The MCA travels laterally and gives off tiny perforating branches called
the lenticulostriates arteries, before bifurcating at the Sylvian fissure.
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Figure 2.13 The Posterior Circulation
AICA: anterior inferior cerebellar artery; CN: cranial nerve; PCA: posterior cerebral arteries; PICA: posterior
inferior cerebellar artery; SCA: superior cerebellar artery.
Bottom figure redrawn with permission from Blumenfeld H, Neuroanatomy Through Clinical Cases. Sinauer
Associates, Inc, Sunderland, 2002. (Figure 14.17b).
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The Posterior Circulation 49
The posterior circulation of the brain originates from the vertebral arteries. They
travel up to the medulla and once they reach the pons, unite to form the basilar artery.
However, just before doing so, they each give off a branch that merges to become the
anterior spinal artery, which travels back down the body to supply the anterior portion
of the spinal cord, as we will see in Chapter 4.
As the basilar artery travels up the belly of the pons, it gives off many small arteries, simply
called the basilar perforators. These small arteries are analogous to the lenticulostriates
of the MCA.
Despite their name, the superior cerebellar artery (SCA), the anterior inferior cere-
bellar artery (AICA) and the posterior inferior cerebellar artery (PICA) supply both
the cerebellum as well as part of the brainstem. The SCA and AICA come off the basilar
artery. The PICA comes off the basilar in about 50% of individuals; in the other half it
comes off the vertebral artery.
Finally, just over the midbrain, the basilar artery terminates and branches into the
posterior cerebral artery (PCA). The PCA helps supply circulation to the entirety of
the occipital lobe and the inferior part of the temporal lobe. It also supplies most of the
midbrain. The PCA is joined to the anterior circulation by the posterior communicating
arteries (PCOM), completing the Circle of Willis.
Note the close proximity between the PCA and CN III. This is important because the first
sign of a ruptured aneurysm of the PCOM is usually dysfunction of CN III, as we will
examine again in the next chapter.
Take Home Messages
At the brainstem, the vertebral arteries unite to form the basilar artery,
which eventually bifurcates to become the PCAs.
Important branches from the basilar include the basilar perforators, and
the SCA, AICA and PICA (in 50% of individuals the PICA comes off the
vertebral arteries).
The posterior circulation is joined to the anterior circulation by the PCOM.
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Figure 2.14 Vascular Territories of the Brain
ACA: anterior cerebral artery; MCA: middle cerebral artery; PCA: posterior cerebral arteries.
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Vascular Territories of the Brain 51
Knowledge of the vascular supply of the brain is critical to predicting and understanding
cerebral strokes and hemorrhages. We’ll now examine Fig. 2.14 in detail.
Beginning with the ACA, we can see it supplies the medial two-thirds of each hemisphere.
Somatotopically, this includes the leg, bowel and bladder area of both the motor and
sensory cortices. Thus, a stroke involving the ACA would only produce weakness and
numbness of leg. The ACA also supplies the genu of the corpus callosum, which connects
the two hemispheres.
The MCA supplies a tremendous amount, including a large part of the motor and sensory
cortices. What would happen if the MCA were to be occluded? Now you might be tempted
to examine the homunculus and see that the face and arm area of the cortex would be
affected. That is true. But note also that the MCA supplies the subcortical white matter
tracts that funnel into the internal capsule, including those from the area of cortex
supplied by the ACA. Thus, an MCA stroke will produce whole body weakness on one
side, but through two different mechanisms. Face and arm weakness is produced by
infarction of the gray matter, and leg weakness is caused by infarction of the subcortical
white matter. White matter is more robust than gray matter so strokes affecting the white
matter are typically less severe and carry a better prognosis. Thus, in MCA strokes, leg
weakness is typically less severe than face/arm weakness, and recovers better.
The PCA supplies part of the temporal lobe and the majority of the occipital lobe. As we
will see in Chapter 3, PCA strokes will cause characteristic patterns of visual loss.
While the ACA, MCA and PCA all contribute branches to supply the components of
the basal ganglia, the most important branch is the anterior choroidal artery because it
supplies the posterior limb of the internal capsule, which, you’ll recall from Fig. 2.4, acts
as a funnel for all motor and sensory neurons.
We will examine the brainstem vascular territories in the next chapter once we get a
better sense of the CN and their nuclei.
Take Home Messages
ACA territory: medial aspect of each hemisphere, including the leg, bowel
and bladder areas of the motor and sensory cortex.
MCA territory: arm and face area of the motor and sensory cortex, as well
as virtually all the subcortical white matter.
PCA territory: visual cortex.
Anterior Choroidal territory: posterior limb of the internal capsule, which
is a narrow funnel for all motor and sensory neurons.
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Figure 2.15 Venous Drainage of the Head
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Venous Drainage of the Head 53
The venous system of the brain is actually composed of more than just veins. In addition
to regular veins, the brain also contains venous sinuses. As we saw in Fig. 1.8, these
channels are created when the periosteal dura separates from the meningeal dura and
are filled with venous blood.
The size and placement of cortical veins differs greatly between individuals but the
sinus formation is usually quite consistent. Typically, cortical veins are very small and
superficial, and usually drain into the larger sinuses before ultimately leaving the skull
via the internal jugular vein.
The superior sagittal sinus runs along the entire length of the skull, and drains the veins
that lie in the superficial aspect of the cortex. Inferior to this lies the inferior sagittal
sinus and the Great vein of Galen. Both work together to drain the basal ganglia and
midbrain. The Great vein of Galen and the inferior sagittal sinus join together to form the
straight sinus.
The superior sagittal sinus, straight sinus, and the two transverse sinuses (which run
along the base of the skull) make up the confluence of sinuses.
The internal jugular veins are the ultimate destination of all venous blood in the head.
They are composed of venous blood from the transverse sinus and also the cavernous
sinus. Remember, the cavernous sinus is unique as it contains not only venous blood,
but also a small portion of the ICA, as well as several CN, which we’ll re-examine in
Chapter 3.
Take Home Message
Venous drainage of the brain is carried out by both veins and sinuses
(which are channels created by the separation of the layers of dura).
Suggestions for further reading:

Blumenfeld H. Neuroanatomy Through Clinical Cases. Sinauer Associates, Inc, Sunderland, 2002.
Lindsay, KW, Bone I, and Fuller G. Neurology and Neurosurgery Illustrated. Churchill Livingstone:
Elsevier, Edinburgh, 2010.
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Chapter 3
The Cranial Nerves
and the Brainstem
Immediate Localization
Only a lesion in the brainstem can produce the pattern of long tract dysfunction
known as Crossed Signs.
Crossed Signs – refers to a loss of long tract function on the ipsilateral side of
the face, and the contralateral side of the body. This occurs in two different
patterns. If the lesion involves the lateral part of the brainstem, the patient
has ipsilateral loss of pain and temperature in the face and contralateral loss
in the body. If the lesion involves the medial brainstem, the patient will have
ipsilateral loss of motor function in the face, and contralateral loss of motor
function and vibration/proprioception in the body.
The important point is that patients experience ipsilateral loss in the face, and
contralateral loss in the body.
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56 Chapter 3 The Cranial Nerves and the Brainstem
Figure 3.1 Overview of the Cranial Nerves
CN: cranial nerve.
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Overview of the Cranial Nerves 57
The human head is innervated by 12 cranial nerves* (CN) as shown in Fig. 3.1. In the
same way as spinal nerves insert into the spinal cord, CN insert into the brainstem.
Cranial nerves can have motor function, sensory function and parasympathetic function,
and can thus be composed of motor neurons, sensory neurons and parasympathetic
neurons. CN I is responsible for smelling, also called olfaction, and is virtually never
tested clinically. CN II transmits visual information to the occipital lobe, where it is
processed and interpreted. Together, CN III, CN IV and CN VI control eye movements.
CN III also helps to keep the eye open and plays a role in determining pupillary size. CN
V provides sensory innervation of the face, and controls muscles involved in chewing,
also called mastication. CN VII controls all the other muscles in the face, receives taste
from anterior two-thirds of the tongue and innervates many glands in the head. CN VIII
is involved in both hearing and balance. CN IX and X both provide sensory and motor
innervation to the throat. In addition, CN X provides much of the parasympathetic
innervation to the body. CN XI controls turning of the head and shrugging the shoulders.
Finally, CN XII controls the tongue.
Like their spinal nerve equivalents, a CN is actually composed of thousands of individual

neurons. The nuclei for these neurons lie in the brainstem. If a CN is made up of more
than one neuron type (motor, sensory or parasympathetic), then it will have more than
one nucleus in the brainstem; there is one nucleus for every neuron type that makes up
the CN. For example, CN VII has a motor, sensory, and parasympathetic component so
there is a motor nucleus for CN VII, which is distinct from the sensory nucleus for CN VII,
which is distinct from the parasympathetic nucleus for CN VII. The opposite is not true; a
single nucleus can be shared between nerves. For example, CN VII and CN IX both have
a sensory component innervating taste buds in the tongue. The nucleus responsible for
this in CN VII is the nucleus solitarius. The nucleus responsible for this in CN IX is also
the nucleus solitarius. In this way, one nucleus can have input from multiple CN.
* Note: CN I and CN II are not actually nerves at all. They are direct extensions of the central nervous system
(CNS) itself, and so would more accurately be called tracts. For religious reasons, it was important for the total
number of CN to be twelve and historically CN I and CN II have been referred to as such, though it makes little
practical difference.
Take Home Messages
There are 12 CNs, and the nuclei for each nerve lies in the brainstem.
There is one nucleus for each component (motor, sensory or
parasympathetic) that the CN carries.
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Figure 3.2 The Exit of the Cranial Nerves from the Brainstem
CN: cranial nerve.
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The Exit of the Cranial Nerves from the Brainstem 59
Before we get into the details of the CN it is important to have a working knowledge of
the brainstem. As we saw in Chapter 1, the brainstem can be divided into three main
sections: the midbrain, pons and medulla.
Figure 3.2 shows two important white matter connections found in the brainstem; both
are referred to as peduncles. The cerebral peduncle connects the brain to the spinal
cord, and runs throughout the entire brainstem. They can be viewed directly at the level
of the midbrain. The cerebellar peduncle (sometimes divided into superior, middle and
inferior sections) connects the spinal cord and brainstem to the cerebellum. One of the
many tracts that run through the cerebellar peduncle is the spinocerebellar pathway.
It is important to know where each CN leaves the brainstem. All the CN come off the
anterior part of the brainstem, with the exception of CN IV. It leaves the posterior
midbrain and quickly wraps around the brainstem to become anterior.
If you study Fig. 3.2 closely, you will note two very important patterns. First, the CN tend
to spread out equally between the midbrain, pons and medulla. The midbrain contains
CN I to CN IV, the pons has CN V to CN VIII, and the medulla contains CN IX to CN XII.
Second, CN II, CN III, CN VI and CN XII all insert into the brainstem quite medially,
whereas all other CN are quite lateral. Remembering these patterns will become very
important when we examine the anatomy of the brainstem in cross section.
Take Home Messages
The brainstem consists of the midbrain, which houses CN I to CN IV; the

pons, which houses CN V to CN VIII; and the medulla, which houses CN
IX to CN XII.
All CN exit the brainstem anteriorly, except for CN IV.
CN II, CN III, CN VI and CN XII exit the brainstem medially. All other CN
exit laterally.
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Figure 3.3 Parasympathetic Component of the Cranial Nerves
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Parasympathetic Component of the Cranial Nerves 61
Before we examine the individual CN, we should take a moment and familiarize ourselves
with the parasympathetic innervation they provide.
As we have discussed in Chapter 1, all sympathetic innervation originates from the

thoracic and lumbar spinal cord. The analogous parasympathetic innervation is trans-
mitted by select CN. As we just learned, the parasympathetic component of these CN will
have their own specific nucleus.
The following CN have a parasympathetic component:
CN III: responsible for pupillary constriction. The associated nucleus is the Edinger–
Westphal nucleus in the midbrain.
CN VII: responsible for innervating salivary glands as well as lacrimal (tear) glands. The
associated nucleus is the superior salivatory nucleus in the pons.
CN IX: responsible for innervating the parotid gland, which is the largest salivary gland.
The associated nucleus is the inferior salivatory nucleus in the medulla.
CN X: responsible for parasympathetic innervation to internal organs of the trunk,

including the heart, lungs and digestive tract. The associated nucleus is the unfortunately
named dorsal motor nucleus in the medulla.
Recall from Chapter 1 that the autonomic system employs two neurons, a preganglionic
neuron and a postganglionic neuron. Unlike the sympathetics whose ganglia lie very
close to the spinal cord, the parasympathetic ganglia lie very close to the organs they
innervate.
Take Home Messages
Parasympathetic innervation is transmitted by CN III, CN VII, CN IX and

CN X.
Each parasympathetic component has its own nucleus, which lies in the
brainstem.
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Figure 3.4 The Visual Pathway
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The Visual Pathway 63
In practice, CN I is rarely tested, so we will not concern ourselves with it.
The entire area seen by a pair of stationary eyes is termed the visual field. Each eye
independently views the visual field. Contrary to popular belief, the left eye does not
receive input solely from the left hemifield, and the right eye does not receive input
solely from the right hemifield. Rather, as shown in Fig. 3.4, each eye receives input from
both the left and right hemifields. Thus, in Fig. 3.4, EYELeft receives input from the left
hemifield (L1 and L2) and from the right side, R1. Similarly, EYERight receives input from
R1, R2 and L2. Note that the fields are not equal; EYERight receives information from R2,
which EYELeft does not and EYELeft receives information from L1, which EYERight does not.
The important point is that each eye receives information from both the left and right
hemifield, though the amounts are unequal.
Light from the visual field passes through the cornea, then the lens, and finally hits the
retina. Retinal cells are activated by light, and transmit an electrical impulse to CN II, the
optic nerve. The optic nerve travels posteriorly until it reaches the optic chiasm. A very
important decussation of information occurs at the optic chiasm; the fields representing
peripheral vision (L1 and R2) cross over at the chiasm, so that the right brain will interpret
the entire left visual field (L1 and L2) and the left brain will interpret the entire right visual
field (R1 and R2).
Beyond the optic chiasm the optic nerve is referred to as the optic tract. The optic tract
continues until it reaches the lateral geniculate body (LGN) of the thalamus, which,
remember, is a large relay center for sensory information. The fibers terminate, but axons
from the LGN continue as the optic radiations, and travel back through brain cortex until
they reach the occipital lobe, which is the ultimate destination of visual information.
Take Home Messages
Each eye receives input from the left hemifield and the right hemifield.
At the optic chiasm, the visual fields representing peripheral vision
(L1 and R2) decussate, so that one side of the brain interprets one entire
field (i.e., the left interprets L1 and L2).
The visual information pathway:
È retina È lateral geniculate body of thalamus
È optic nerve È optic radiation
È optic chiasm È occipital lobe.
È optic tract
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Figure 3.5 Visual Field Defects
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Visual Field Defects 65
Lesions in the visual pathway will give rise to characteristic visual field defects, in which
the patient will report a complete loss of vision from the affected aspect.
In naming the following defects, many authors utilize “nasal/temporal” nomenclature.

They divide each hemifield into a nasal side representing central vision (in our diagram
L2 and R1) and a temporal side, named after the temporal bone, representing peripheral
vision (in our diagram L1 and R2). This means that information from the temporal aspects
decussate in the optic chiasm.
The lesion in 1) would cause complete vision loss in a single eye, also called monocular
vision loss. Again, note that the patient would still have vision from both the left and right
hemifields.
A lesion at 2) would interrupt the decussation of the temporal fibers, and would result
in a profound loss of peripheral vision. This lesion results in a bitemporal hemianopsia;
“bitemporal” as both temporal aspects are involved, “hemi” for half of the field in each
eye and “anopsia” for defect in a visual field.
A lesion at either 3) or 6) results in a complete loss of vision of either the left or right
hemifields, depending on which side of the brain is affected. This field defect is called a
homonymous hemianopsia; it is called “homonymous” because the loss in each eye is
the same. Because the loss is of an entire hemifield patients often incorrectly report that
they have lost vision in an entire eye.
The somatotopic arrangement of the visual fields continues in the optic radiations. The
more superior optic radiations carry information from the inferior visual field, and vice
versa. Thus a lesion at 4) results in a homonymous superior quadrantanopsia and a
lesion at 5) results in a homonymous inferior quadrantanopsia.
Take Home Messages
The temporal aspects of the visual field decussate in the optic chiasm.
A bitemporal hemianopsia results in a profound loss of peripheral vision.
A homonymous hemianopsia results in a complete loss of either the left
or right hemifield.
A homonymous quadrantanopsia results in a partial loss of either the left
or right hemifield.
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Figure 3.6 Sympathetic and Parasympathetic Control of Pupillary Size
LGN: lateral geniculate body.
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Sympathetic and Parasympathetic Control Pupillary Size 67
The autonomic system controls pupillary size. As with everything in the autonomic
system, the final outcome is determined by the relative contributions of the sympathetic
system, responsible for pupil dilation (easily remembered by reminding yourself that in
“fight or flight” situation, you would want the most visual information possible), and the
parasympathetic system, responsible for pupillary constriction.
Let’s examine the pathways of the two systems, as shown in Fig. 3.6. The sympathetics
originate in the hypothalamus and travel down the lateral part of the brainstem before
synapsing in the spinal cord and exiting at T1. They then travel up the sympathethetic
chain, before synapsing again at the superior cervical ganglion. At this point the
sympathetics embed themselves in the outer walls of the internal carotid artery (ICA).
They continue up the ICA, through the base of the skull and eventually branch off to
innervate the pupillary dilator muscle, as well as Muller’s muscle, which is responsible
for eye opening (not shown).
In contrast to the rest of neuroanatomy, there is no decussation anywhere along the

sympathetic pathway.
The pupillary light reflex activates the parasympathetic pathway. Light enters the eye
and follows the typical pathway to the LGN as in Fig. 3.4. Just before synapsing at the
LGN, a small number of neurons branch off and travel to the pretectal nucleus in the
midbrain. The pretectal nucleus sends signals to the Edinger–Westphal nucleus (EWN)
of CN III. The signal continues from the EWN to the ciliary ganglion and eventually
into the pupillary constrictor muscles. Note that one pretectal nucleus innervates both
the ipsilateral and contralateral EWN, explaining why shining light in one eye results in
constriction of both pupils.
Take Home Messages
Final pupil size is determined by the relative, often unequal, contributions

of the sympathetic pathway (pupillary dilatation) and parasympathetic
pathway (pupillary constriction).
Sympathetic pathway: Parasympathetic pathway:
È hypothalamus È pretectal nuclei
È brainstem È Edinger–Westphal nuclei
È sympathetic chain È ciliary ganglion
È superior cervical ganglion È pupillary constrictor muscle.
È internal carotid
È pupillary dilator muscle.
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Figure 3.7 The Extraocular Muscles
IO: inferior oblique muscle; IR: inferior rectus muscle; SO: superior oblique muscle; SR: superior rectus
muscle.
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The Extraocular Muscles 69
Six extraocular muscles control eye movement. The muscles can be divided into two
different groups: the rectus muscles, which insert into eye in a straight path, and the
oblique muscles, which insert into the eye on an angled path.
Two different muscles control horizontal eye movement. CN VI innervates the lateral
rectus, which abducts the eye away from the nose. CN III innervates the medial rectus,
which adducts the eye toward the nose.
Four different muscles are responsible for vertical eye movement. CN IV innervates the
superior oblique muscle and CN III innervates the superior rectus, inferior rectus, and
inferior oblique muscles.
Vertical eye movements are complicated by two factors. First, different vertical movement
muscles will be activated depending on what horizontal position the eye is in (full
adduction, full abduction or somewhere in between). We will consider this further in a
moment. Second, the actions of the oblique muscles are counterintuitive because they
insert behind the plane of the eye. We will consider that now.
The eye can be approximated as a sphere rotating about an axis. The plane of the eye
(represented by the dashed lines in Fig. 3.7) divides it into two halves. The rectus system
inserts in front of the plane of the eye, and its movements are straightforward. Pulling on
the muscle, we see that if we pull on the upward portion it moves the eye upward, just
as we would expect. Thus the superior rectus moves the eye upward, and the inferior
rectus moves the eye downward.
However, consider what would happen if the muscle inserted behind the plane of the
eye, as in the oblique system. Now, pulling on the upward portion will result in the eye
moving downward. Thus, the actions of the oblique group are the opposite of what you
would expect; the superior oblique moves the eye downward, and the inferior oblique
moves the eye upward.
We’ll now turn our attention to understanding which system, rectus or oblique, is
activated in different horizontal eye positions.
Take Home Messages
CN III innervates: CN IV innervates:

Medial rectus – adduction of eye Superior oblique – downward
Superior rectus – upward movement movement
Inferior rectus – downward
movement CN VI innervates:
Inferior oblique – upward movement Lateral rectus – abduction of eye
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Figure 3.8 Movement of the Eyes
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Movement of the Eyes 71
As mentioned, vertical movements are more complicated because different muscles

will be activated depending on the horizontal position of the eye (full adduction,
full abduction or somewhere in between). There are two different vertical movement
systems: the rectus system, which is activated when the eye is abducted, and the oblique
system, which is activated when the eye is adducted. Anything less than full abduction or
adduction will result in a partial, but unequal, activation of both systems.
Let’s begin with a set of eyes looking to the right. The right eye is abducted and so has its
lateral rectus activated (CN VI). The left eye is adducted so has its medial rectus activated
(CN III).
We will examine upgaze first; if the eye is abducted, the superior rectus will pull the eye
upwards, however if the eye is adducted, the inferior oblique muscle will pull the eye
upwards. Both of these muscles are innervated by CN III.
Now we’ll turn our attention to downgaze; if the eye is abducted, the inferior rectus
will pull the eye downwards. If the eye is adducted, the superior oblique will pull it
downwards. The inferior oblique is innervated by CN III and the superior oblique is
innervated by CN IV.
Note that the oblique muscles pull the eye in the opposite direction compared to the
their rectus equivalents i.e., the superior rectus pulls the eye upwards, whereas the
superior oblique pulls the eye downwards. This is because the oblique muscles wrap
around the eye and insert behind the eye’s plane of section compared to the rectus
system, which inserts in front of the eye’s plane of section.
Take Home Messages
The muscles responsible for vertical movement of the eyes are:

• Superior rectus – upward movement in full abduction.
• Inferior rectus – downward movement in full abduction.
• Inferior oblique – upward movement in full adduction.
• Superior oblique – downward movement in full adduction.
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Figure 3.9 The Medial Longitudinal Fasciculus
PPRF: paramedian pontine reticular formation.

Redrawn with permission from Greenberg D et al. Clinical Neurology. McGraw– Hill Education,
New York, 2015.
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The Medial Longitudinal Fasciculus 73
Certain pairs of extraocular muscles are yoked together. This means that activation
of an extraocular muscle in one eye results in the simultaneous activation of another
extraocular muscle in the opposing eye i.e., to look to the right, the lateral rectus must
move the right eye, whereas the medial rectus must simultaneously move the left eye.
Failure to do so would result in diplopia (double vision), from eyes that are not in perfect
alignment. Such eyes are said to be in dysconjugate gaze.
The pathway that allows for conjugate eye movement is called the medial longitudinal
fasciculus (MLF) and lies in the central part of the midbrain and pons. The MLF is a
white matter tract that allows CN nuclei to be connected to each other. It is responsible
for both conjugate vertical and conjugate horizontal movements, but the vertical path is
quite complex so we will only consider the horizontal one.
It begins with the nucleus of CN VI. This nucleus actually does much more than just control
CN VI, and is better referred to as the horizontal gaze center because it is responsible
for the initiation of horizontal gaze in both eyes. In addition to directly innervating CN
VI, it also innervates the contralateral CN III nucleus via the MLF. Thus, activation of the
CN VI nucleus will cause simultaneous activation of the ipsilateral lateral rectus and the
contralateral medial rectus, resulting in perfectly aligned eye movement and conjugate
gaze.
As we saw earlier, voluntary control of horizontal eye movement is initiated by the frontal
eye field (FEF). How does the FEF, way up in the cerebrum, connect to this pathway
in the brainstem? It turns out that the FEF synapses with a contralateral structure in
the brainstem called the paramedian pontine reticular formation (PPRF). The PPRF
connects the FEF to the CN VI nucleus and in doing so connects voluntary eye movements
to the automatic movements initiated by the brainstem.
Take Home Messages
Yoked extraocular muscles result in perfectly aligned eye movement and

subsequent conjugate gaze.
The MLF is a white matter tract in the brainstem that connects the CN VI
nucleus to the contralateral CN III nucleus. Activation of the CN VI nucleus
will cause contraction of the ipsilateral lateral rectus and, via the MLF, the
contralateral medial rectus.
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Figure 3.10 Facial Sensation and the Muscles of Mastication
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Facial Sensation and the Muscles of Mastication 75
Now that we understand eye movements, we should return to CN V, which we skipped.
CN V has both a sensory and motor component. CN V is called the trigeminal nerve
because it has three major divisions. This includes the ophthalmic or V1 division, the
maxillary or V2 division and the mandibular or V3 division. Their sensory innervation is
shown in Fig. 3.10. V1 and V2 are purely sensory divisions, but V3 has a sensory and motor
component.
CN V leaves the pons and travels into the trigeminal ganglion, located in an area called
Meckel’s cave at the base of the skull. The nerve then trifurcates and passes through
several openings in the base of the skull. Specifically, the V1 division passes through the
superior orbital fissure, the V2 division passes through the foramen rotundum, and the
V3 division passes through the foramen ovale.
Because CN V has a motor and sensory component, we expect one nucleus for the motor
component and another nucleus for the sensory component. The motor nucleus of CN
V is plainly named the trigeminal motor nucleus. This nucleus innervates the muscles
of mastication (chewing), which include the masseter, temporalis, and the medial and
lateral pterygoid muscles.
CN V actually has a set of three nuclei for sensory information, and they are located
throughout the brainstem. Together they are referred to as the trigeminal sensory nuclei
and are each associated with different sensory modalities. They include:
• The mesencephalic trigeminal nucleus, located in midbrain. It encodes

proprioceptive information from the jaw.
• The chief sensory nucleus, located in the central pons. It encodes fine touch and
vibration information from the face.
• The spinal trigeminal nucleus, located in the medulla. It encodes pain and
temperature information from the face.
Take Home Messages
CN V has three branches; the V1 (ophthalmic) division, the V2 (maxillary)

division and the V3 (mandibular) division.
CN V has three sensory nuclei; the spinal trigeminal nucleus, the chief
sensory nucleus and the mesencephalic trigeminal nucleus.
CN V’s motor component controls the masseter, temporalis, medial
pterygoid, and lateral pterygoid, which are the muscles of mastication.
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Figure 3.11 The Cavernous Sinus
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The Cavernous Sinus 77
Before we continue, we should review the pathway taken by CN II to CN VI, as many of

these nerves pass through an area called the cavernous sinus, just before leaving the
base of the skull.
As we saw in Chapters 1 and 2, a sinus is a large venous channel, created by separation

of the periosteal layer of dura mater from the meningeal layer (Fig. 1.8). Most sinuses
simply contain venous blood, however the cavernous sinus is a notable exception as it
contains not only venous blood, but also arteries and nerves.
The cavernous sinus contains the longitudinally running ICA as it ascends to the cortex.
Remember at this point that the sympathetics are still attached to the walls of the ICA
(Fig. 3.6).
In contrast to the longitudinally running ICA, several CN pass through the cavernous
sinus transversely, on their way to the base of skull. This includes CN III, CN IV, CN V1, CN
V2 and CN VI. These nerves leave the brainstem and enter the subarachnoid space. They
then pass over the petrous bone and pierce the dura to enter the cavernous sinus. Most
of the nerves lie quite far away from the ICA, with the exception of CN VI.
The cavernous sinus is located at the base of the skull, just above the air filled nasal
sinuses. Sitting just above the cavernous sinus is the pituitary gland, which is responsible
for the production of many hormones. Just superior to the pituitary lies the optic chiasm.
If a mass lesion, such as a tumor or ruptured aneurysm, occurs in the cavernous sinus
the subsequent swelling can become so great that not only are the CN affected, but also
these surrounding structures.
Take Home Messages
The components of the cavernous sinus include CN III, CN IV, CN V1, CN V2,
CN VI and the ICA (along with the sympathetics).
The pituitary gland and optic chiasm lie directly above the cavernous
sinus.
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Figure 3.12 Cranial Nerve VII and the Types of Facial Droop
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Cranial Nerve VII and the Types of Facial Droop 79
CN VII has a motor component, sensory component and a parasympathetic component.

CN VII leaves the pons and enters the base of skull through the internal acoustic meatus
(IAM). It continues through the bone of the skull and trifurcates once it reaches the
geniculate ganglion. Each branch now leaves the skull through a different opening.
The motor component of CN VII begins with the facial nucleus in the pons. It passes
through the IAM and leaves the base of skull at the stylomastoid foramen. Here it divides
into five branches: the temporal, zygomatic, buccal, mandibular and cervical branch,
as in Fig. 3.12. These branches innervate the many muscles of facial expression.
Lesions of CN VII will cause the face to droop, as the muscles that maintain resting tone
are now weak. The appearance of the facial droop will be quite different depending if
the causative lesion is located in the upper motor neuron (UMN), which travels from
the motor cortex to synapse with the facial nucleus, or the lower motor neuron (LMN),
which travels from the facial nucleus to the muscles. If you look closely at Fig. 3.12, you
will notice that the neuron supplying the forehead is dually innervated from both
the left and right motor cortex! This dual motor innervation is quite unique and only
occurs for one other nerve, CN XII. However, the rest of the face is not dually innervated.
Thus, a facial droop from an UMN lesion will spare the forehead (as it would still receive
innervation from the other motor cortex), whereas a facial droop from a LMN lesion will
cause the entire face to droop.
The parasympathetic component of CN VII is controlled by the superior salivatory

nucleus in the pons and is responsible for tear and saliva production. It innervates all
salivary glands in the head with the exception of the largest gland, the parotid gland,
which is controlled by CN IX.
Finally, the sensory component of CN VII is controlled by the nucleus solitarius in the
medulla, and is responsible for taste from the anterior two-thirds of the tongue.
Take Home Messages
CN VII innervates the muscles of facial expression through the temporal,

zygomatic, buccal, mandibular and cervical branches.
An UMN type facial droop will spare the forehead; a LMN facial droop will
involve the entire face.
CN VII’s parasympathetic component innervates the lacrimal and salivary
glands (except the parotid gland) and its sensory component provides
taste to the anterior two-thirds of the tongue.
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Figure 3.13 The Functions of Cranial Nerve VIII and Cranial Nerve IX
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The Functions of Cranial Nerve VIII and Cranial Nerve IX 81
CN VIII should really be thought of as two separate nerves that travel together for a short
time. CN VIII has two nuclei: the vestibular nucleus, responsible for balance, and the
cochlear nucleus, responsible for hearing.
CN VIII emerges from the brainstem at the interface between the pons and medulla.
Along with CN VII it enters the base of the skull at the IAM and then immediately splits
into the vestibular nerve and the cochlear nerve.
The vestibular nerve innervates the semicircular canals near the inner ear. The semi-
circular canals work on a similar principle as the bubble level used in carpentry. The
bubble tells you the position of the object you place it on; if the object is not level, the
bubble is not in the center of the field. In addition, if you were to move that object,
the bubble would move, giving you information about the acceleration of the object.
The semicircular canals are filled with fluid and, utilizing the same principles, gives
proprioceptive information about the position and acceleration of the head.
The cochlear nerve innervates the cochlea. When a sound wave enters the ear it reverberates
the tympanic membrane, which transmits a signal to the cochlea. The cochlea transduces
this signal into a nerve impulse, which travels up the cochlear nerve into the brainstem.
CN IX has a motor, sensory and parasympathetic component.
CN IX enters the jugular foramen at the base of the skull. Upon reaching the inferior
ganglion, it bifurcates. The parasympathetic component travels through the base of the
skull as the lesser petrosal nerve and eventually passes through the foramen ovale to
innervate the parotid gland, which is its sole function. The parotid gland is the main
producer of saliva for the mouth. The parasympathetic nucleus is the inferior salivatory
nucleus located in the pons.
The sensory and motor components exit the jugular foramen together. The motor
component only innervates a single muscle, the Stylopharyngeus, which is involved in
talking and swallowing; it is controlled by the nucleus ambiguus in the medulla.
CN IX has a grab bag of sensory functions; it provides input to a small portion of the
ear, the back of the throat and the posterior one-third of the tongue. These functions are
controlled by the nucleus solitarius.
Take Home Messages
CN VIII innervates both the semicircular canal, which is involved in sensing

the position and motion of the head, and the cochlea, which is involved in
hearing.
CN IX has a motor, sensory and parasympathetic component.
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Figure 3.14 The Many, Many Functions of Cranial Nerve X
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The Many, Many Functions of Cranial Nerve X 83
CN X has a motor, sensory and parasympathetic component. CN X enters and exits the
base of skull through the jugular foramen.
The motor component of CN X is controlled by the nucleus ambiguus in the medulla.

It provides innervation to the pharyngeal muscles involved in swallowing, as well as
laryngeal muscles for voice production.
The sensory component of CN X is controlled by the nucleus solitarius in the medulla. It

provides innervation to the taste receptors near the back of the throat.
The parasympathetic component of CN X is controlled by the dorsal motor nucleus in

the medulla. It provides parasympathetic innervation to nearly all the internal organs
(Fig. 1.9). Indeed, the reason CN X is named the “vagus” nerve is after the term “vagabond,”
which is a person that wanders from place to place, just as the parasympathetic com-
ponent wanders from place to place in the body.
Take Home Messages
The motor component of CN X controls the pharyngeal and laryngeal

muscles.
The sensory component is responsible for taste sensation at the back of
the throat.
The parasympathetic component provides innervation to nearly all of the
internal organs.
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Figure 3.15 Motor Innervation to the Neck and the Tongue
LMN: lower motor neuron.
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Motor Innervation to the Neck and the Tongue 85
Like CN VIII, CN XI is more accurately described as two separate nerves, but for historical
reasons has been referred to as a single one. CN XI has a “spinal part,” coming off the
high cervical cord, and a “cranial part” coming from the medulla. The two merge very
briefly to form CN XI. Soon thereafter the cranial part diverges and joins with CN X. The
spinal part exits the base of the skull through the jugular foramen (along with CN IX and
CN X) and continues into the muscles of the neck. Because CN XI is really two nerves, it
has two sets of nuclei; the cranial component’s nucleus is the nucleus ambiguus in the
medulla, and the spinal component’s nucleus originates in the gray matter of C1 to C5 in
the spinal cord.
CN XI only has a motor component. It provides innervation to the trapezius muscle as

well as the sternocleidomastoid (SCM). Activation of the trapezius causes shrugging of
the shoulders. Activation of the SCM causes the head to turn to the contralateral side
(i.e., the left SCM causes the head to turn to the right).
CN XII’s only function is to provide motor innervation to the muscles of the tongue, and
is controlled by the hypoglossal nucleus in the medulla. It exits the base of the skull via
the hypoglossal canal. The tongue is designed such that the muscles on one side of the
tongue push it to the contralateral side as it extends out of the mouth. Straight protrusion
of the tongue is caused by equal activation of muscles on both sides. Thus if one side of
the tongue is weak, the tongue will deviate to that side, due to unopposed action of the
healthy side.
Note that, like the forehead component of CN VII, the hypoglossal nucleus receives
innervation from both motor cortices. Because of this, UMN lesions of the hypoglossal
nerve do not result in any clinically detectable weakness or symptoms. Only LMN type
lesions can cause tongue weakness.
Take Home Messages
CN XI provides motor innervation to the trapezius, which causes

shrugging of the shoulder, and the SCM, which turns the head to the
contralateral side.
CN XII provides motor innervation to the tongue. Weakness of one side of
the tongue, due to a LMN lesion, will cause the tongue to deviate toward
the weak side.
CN XII receives bilateral UMN innervation. Thus, a single UMN lesion
does not have any clinically detectable effect on the tongue.
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Figure 3.16 Exit of the Cranial Nerves through the Base of the Skull
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Exit of the Cranial Nerves through the Base of the Skull 87
As a summary, and also because this topic tends to pop up in examinations, we have
included Fig. 3.16, which shows all of the exit sites of the CN. On the left are the exits of
the base of the skull and on the right are the nerves that pass through them.
Take Home Message
Really, this is all important stuff.
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Figure 3.17 The Rule of 4
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The Rule of 4 89
The importance of understanding the cross sectional anatomy of the brainstem cannot
be overemphasized. While most students approach the topic with trepidation, a few
simple rules will allow you to quickly recreate the anatomy at any point in the brainstem.
The brainstem is structured such that the medial components are supplied by a different
artery than the lateral components. Thus, the goal is to localize to medial or lateral parts
of the midbrain, pons or medulla.
As long as we remember the number “4,” we are well on our way to doing this:
• 4 CN lie in the midbrain (CN I – CN IV).
• 4 CN lie in the pons (CN V – CN VIII).
• 4 CN lie in the medulla (CN IX – CN XII).
There are 4 important medial structures that begin with the letter “M”:
1. The Motor pathway (corticobulbar tract and corticospinal tract).
2. The Medial lemniscus (ML: the continuation of the dorsal columns).
3. The MLF.
4. The Motor nuclei that divide equally into the number 12 (i.e., CN III, CN IV, CN VI, and
CN XII). All other nuclei (motor or sensory) lie in the lateral brainstem.
There are 4 important lateral, or side, structures that being with the letter “S”:
1. The Spinothalamic pathway.
2. The Sympathetics.
3. The Spinocerebellar pathway.
4. The Sensory component of CN V.
Neither the spinocerebellar pathway nor the sympathetics decussate.
The above is known as the “Rule of 4” and was created by Peter Gates in Australia.
Take Home Messages
Remembering these few simple rules will allow you to localize quickly and
accurately.
Study the Rule of 4 closely and use it to explain the Crossed Signs we saw
in our Immediate Localization.
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Figure 3.18 The Vascular Territories of the Medulla
PICA: posterior inferior cerebellar artery.
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The Vascular Territories of the Medulla 91
Let’s apply the “Rule of 4” to the medulla and then work our way up the brainstem.
What structures are in the midline? Based on our rule, we would predict the motor
pathway (corticobulbar/corticospinal tract), ML, MLF and CN XII nucleus should be
present. Figure 3.18 reveals that we are correct! The motor pathway is located in the most
anterior portion. Posterior to it is the ML followed by the MLF and the CN XII nucleus.
The CN XII fascicles extend across the medulla to exit anteriorly.
What structures are in the side, or lateral, portion? Based on our rule, we would predict
the spinothalamic tract (ST), sympathetics, spinocerebellar pathway and the spinal
nucleus of CN V. Once again, we are correct! The spinocerebellar tract lies in the cerebellar
peduncle and close to this lies the spinal trigeminal nucleus of CN V. Just anterior to
this lies the ST. Throughout the entirety of the brainstem the sympathetics lie directly
adjacent to the ST. Just anterior to the ST lies the inferior olive, which works closely with
the cerebellum to ensure the smooth control of voluntary movement.
Based on the equal division of CN across the brainstem, the nuclei for CN IX, CN X and
CN XI should be present as well. They lie, as the “Rule of 4” predicts, in the lateral section.
The nuclei for CN VIII straddle the border between the medulla and the pons.
As we saw in Fig. 2.13, two arteries supply the medulla. The vertebral artery supplies the
medial portion and the posterior inferior cerebellar artery (PICA) supplies the lateral
portion. This pattern follows for the rest of the brainstem as well; the medial portion is
supplied by the main artery (vertebral artery for medulla, basilar artery for the pons,
and the posterior cerebral artery for the midbrain), and the lateral section is supplied by
the cerebellar arteries [PICA for medulla, anterior inferior cerebellar artery (AICA) for
pons, and superior cerebellar artery (SCA) for the midbrain].
Take Home Messages
The medial medulla contains the corticospinal tract, ML, MLF and CN XII
nuclei.
The lateral medulla contains the ST, sympathetics, spinocerebellar tract,
sensory nucleus of CN V, and the CN VIII, CN IX, CN X and CN XI nuclei.
The medial medulla is supplied by the vertebral artery. The lateral medulla
is supplied by the PICA artery.
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Figure 3.19 The Vascular Territories of the Pons
AICA: anterior inferior cerebellar artery; MLF: medial longitudinal fasciculus.
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The Vascular Territories of the Pons 93
Let’s begin with the medial section of the pons. From our rule, we would predict the
midline structures to include the motor pathway (corticobulbar and corticospinal
tracts), the ML, the MLF, and CN VI. Indeed, these are all present and in the same relative
position as they were in the medulla. Just like CN XII in the medulla, CN VI is at the
posterior end of the brainstem and its neurons extend across the pons to exit anteriorly.
Employing the “Rule of 4” we would predict that the side, or lateral structures, would
include the spinothalamic tract, sympathetics, spinocerebellar tract and the trigeminal
nucleus. Figure 3.19 shows that this is indeed the case. Again, the sympathetics lie
adjacent to the ST. Not far away lies the trigeminal nucleus. The spinocerebellar tract lies
near the posterior side of the pons.
Based on the equal division of CN across the brainstem, we would also predict the nuclei
of CN VII and CN VIII to be present. Note that CN VII actually wraps around the CN VI
nucleus. This is very important clinically; because of this, it is unlikely to have a LMN
facial droop due to a lesion in the pons without also having an ipsilateral CN VI palsy.
Finding dysfunction of one on clinical exam should prompt a diligent search for the other.
As we saw in Fig. 2.13 the small perforators of the basilar artery supply the medial pons.
The AICA supplies the lateral pons.
Take Home Messages
The medial pons contains the corticospinal tract, ML, MLF and CN VI
nuclei.
The lateral pons contains the ST, sympathetics, spinocerebellar tract,
trigeminal nucleus, and the CN VII and CN VIII nuclei.
CN VII wraps around CN VI as it exits the pons.
The medial pons is supplied by the basilar artery. The lateral pons is
supplied by the AICA artery.
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Figure 3.20 The Vascular Territories of the Midbrain
MLF: medial longitudinal fasciculus; SCA: superior cerebellar artery.
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The Vascular Territories of the Midbrain 95
Before we apply the “Rule of 4” we should discuss some of the unique structures found
in the midbrain. The red nucleus lies in the central part of the midbrain and works with
the cerebellum to coordinate voluntary movement. Lesions of the red nucleus result
in the same ataxia seen in cerebellar lesions. The substantia nigra secretes dopamine,
which is an important neurotransmitter involved in voluntary movement. Lesions of the
substantia nigra result in the tremor seen in Parkinson’s disease.
The “Rule of 4” begins to break down in the midbrain, because we are quickly transitioning
to cerebrum. However, it is still useful.
We would predict that CN III and CN IV nuclei would be in the medial section of midbrain.
Indeed, both the oculomotor nucleus and the Edinger–Westphal nucleus is present. The
CN IV nucleus is in the midline but lies slightly more inferior than the cut we have shown
in Fig. 3.20. We would also predict the MLF to be present in the posterior portion of the
midline, which it is. The mesencephalic nucleus of CN V is also midline.
Recall from Fig. 2.6 that at the level of the midbrain the sensory pathways begin to
fuse. The ML has joined the ST in the more lateral aspect of the midbrain. Again the
sympathetics are adjacent to the ST.
The corticospinal and corticobulbar tracts lie in the anterior portion of the midbrain and
extend from the midline all the way to the lateral aspect.
In addition, the vascular supply of the midbrain can no longer be thought of as “medial vs.
lateral.” Two different oblong territories exist; one supplied by the SCA and one supplied
by the PCA.
Take Home Messages
The midbrain contains the red nucleus and the substantia nigra, both of
which help coordinate voluntary movement.
The two vascular territories of the brain are supplied by the SCA and the
PCA.

Blumenfeld H. Neuroanatomy Through Clinical Cases. Sinauer Associates, Inc, Sunderland, 2002.
Lanning K, Foroozan R. Neuro-Ophthalmology Review Manual. Slack, Inc, Thorofare, NJ, 2013.
Gates P. Clinical Neurology: a Primer. Churchill Livingstone: Elsevier, Sydney, 2010.
Wilson-Pauwels , Stewart PA, Akesson EJ, Spacey SD. Cranial Nerves: Function and Dysfunction.
People’s Medical Publishing House, Shelton, CT, 2010.
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Chapter 4
The Spinal Cord
Immediate Localization
Only lesions of the spinal cord can produce the following pattern of long tract
symptoms:
1. Crossed sensory signs – the patient will have ipsilateral loss of
proprioception and vibration and contralateral loss of pinprick and
temperature.
2. Sensory level or sensory band – the patient will complain of a distinct
transverse level, below which they have impaired sensation of either the
spinothalamic tract (ST), dorsal columns (DC) or both. Certain lesions can
cause two sensory levels, resulting in a “band” or “zone” of sensory loss.
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98 Chapter 4 The Spinal Cord
Figure 4.1 The Spine
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The Spine 99
The spinal cord and the bones and ligaments that surround it are collectively referred to as
the spine. Before we delve into the spinal cord itself, we should review these surrounding
structures.
As you’ll recall from Chapter 1, the bones that protect the spinal cord are called vertebrae
and are named using a combination of letters and numbers. The spinal cord, based
on changes to its internal morphology, is divided into four distinct sections: cervical,
thoracic, lumbar and sacral. The vertebrae share this convention, and are also numbered
according to position, i.e., the fifth cervical vertebra is named C5. As shown in Fig. 4.1,
there are 7 cervical vertebrae (C1 – C7), 12 thoracic (T1 – T12), five lumbar (L1 – L5) and
five sacral (S1 – S5).
Examining the vertebrae themselves, we can see they are composed of a large vertebral
body, two lateral projections called the transverse processes and a posterior projection
called the spinous process. Between the vertebrae lie intervertebral discs; these discs
act as shock absorbers and also allow the vertebrae to pivot about them, giving the spine
mobility. The spine is held in place by a set of ligaments, the most prominent of which is
the interspinous ligament that links spinous processes to each other.
The spinal cord sits in the vertebral foramen (foramen is Latin for “opening”) between
the vertebral body and the transverse processes. The nerve roots leave the spinal cord via
the neural foramen, and continue into the body. The nerve roots are named according
to which vertebrae they exit from.
The spinal cord actually ends at the L1 vertebra; it does not span the entire length of the
spine. The end of the spinal cord is called the conus medullaris. Nerve roots after L1
need to travel to their vertebra in order to exit the spine. Collectively, these travelling
nerve roots are called the cauda equina (Latin for “horse’s tail”).
Take Home Messages
The nerve roots of the spinal cord leave the vertebrae via the neural
foramen.
There are 7 cervical vertebrae (C1 – C7), 12 thoracic vertebrae (T1 – T12),
five lumbar vertebrae (L1 – L5) and five sacral vertebrae (S1 – S5).
The end of the spinal cord is called the conus medullaris and is located at
L1.
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Figure 4.2 The Anatomy of the Spinal Cord
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The Anatomy of the Spinal Cord 101
Now that we have an understanding of the structure of the spine, we can examine
the spinal cord itself. The spinal cord is the main interface between the peripheral
nervous system (PNS) and central nervous system (CNS) (the other interface being
the brainstem, as we saw in Chapter 3) so lesions of the spinal cord can produce many
unique patterns of symptoms.
Let’s study Fig. 4.2 from the outside in. A spinal nerve approaches the spinal cord. This
nerve carries both sensory and motor neurons, but does so in a nonorganized fashion;
both types of neuron are scattered haphazardly across the cross section of the nerve.
However, as it approaches the spinal cord, the nerve begins to demonstrate somatotopic
properties, which we know from our earlier chapters is a defining feature of the CNS. Just
before the nerve enters the cord, it splits into a posterior root, which carries only sensory
neurons, and an anterior root, which carries only motor neurons.
Looking at the spinal cord itself, we see that it is composed of gray matter and white
matter. Like in the cerebrum, the white matter houses the long tracts (corticospinal tract,
ST and DC). The gray matter serves as a connection site, or synapse, between neurons.
Recall from Chapter 1 that each neuron has a cell body. A group of cell bodies in the CNS
is called a nucleus, and in the PNS it is called a ganglion. The cell bodies for the sensory
neurons that make up the spinal nerve actually lie outside the spinal cord in the dorsal
root ganglion (DRG). The nuclei for motor neurons that make up the spinal nerve lie in
the gray matter of the spinal cord, in a part called the anterior horn cell (AHC).
The gray matter is exquisitely somatotopically organized. Figure 4.2 shows that each type
of information, motor or sensory, somatic or autonomic, has its own specific synapse
location in the gray matter.
Take Home Messages
Sensory neurons travel in the posterior root. The cell bodies for sensory
neurons lie in the DRG.
Motor neurons travel in the anterior root. The nuclei for motor neurons lie
in the AHC.
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Figure 4.3 Regional Variations in Spinal Cord Anatomy
AHC: anterior horn cell.
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Regional Variations in Spinal Cord Anatomy 103
We mentioned earlier that the spinal cord was divided into different sections: cervical,
thoracic, lumbar and sacral, based on differences in cross sectional morphology. These
differences are highlighted in Fig. 4.3 and we will turn our attention to them now.
In order to understand these differences, we need to know the area of the body each section
of the spinal cord innervates. Essentially, the cervical cord supplies innervation to the
arms, the thoracic cord to the trunk, and lumbar cord to the legs. The sacral part of the cord
innervates the bowel, bladder and the genitals. These are generalizations and while, as we
will see in Chapter 5, a few exceptions do occur, these suit our purposes nicely for now.
As a muscle grows either in size or complexity the amount of physical neuroanatomical

space needed to innervate it grows as well. Thus, it is much more challenging for the
cervical cord to innervate the arms, than it is for the thoracic cord to innervate the small
muscles of the trunk. The cervical spine simply requires more physical space in order
to provide this innervation. The same is true in the lumbar cord, in order to innervate
the legs. This results not only in a proportionally larger AHC in the cervical and lumbar
sections, but also an overall enlargement in cord diameter for these sections.
Figure 4.3 shows the cross sections of the spinal cord at each level. If you study them
closely, you will notice that the amount of white matter decreases as you move down the
cord. This is again because of a need, or lack there of, for neuroanatomical space. Consider
the high cervical cord; at this level, motor neurons to each area of the body (arms, trunk,
legs, and sacrum) are present. Similarly, sensory neurons from each area are also present.
Thus, the cervical cord requires a lot of white matter in order to carry all of these neurons.
Now consider the lumbar cord; motor neurons to the arm and thorax have already left
the cord, so only motor neurons for the legs and sacrum are present. Similarly, ascending
sensory pathways contain only sensory neurons from the sacrum and legs; sensory
neurons from the trunk and arms have not yet joined the cord. Thus, relatively little white
matter is needed at this level. This again demonstrates the need for physical tissue to
transmit neural impulses.
Take Home Messages
The cervical and lumbar enlargements refer both to a larger cord

diameter and a larger AHC. This physical increase in tissue is needed in
order to innervate the large muscles of the arms and leg.
As one travels inferiorly down the cord the relative amount of white
matter decreases because less information is being transmitted.
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Figure 4.4 Sensory Tracts in the Spinal Cord
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Sensory Tracts in the Spinal Cord 105
Before we continue on, let’s pause a moment and review the path of the sensory tracts
in the spinal cord, as lesions to them produce the symptoms we mentioned in our
Immediate Localization.
Sensory neurons travel in the spinal nerve and eventually enter the posterior root.
Here they pass by the DRG and eventually enter the posterior horn of the gray matter.
If the sensory neurons carry vibration and proprioceptive information they leave the
posterior root and travel up the ipsilateral DC. Eventually they synapse with their second
order neurons at the level of the medulla and decussate. If the neurons carry pain or
temperature information they enter the posterior horn of the gray matter and synapse
with their second order neuron. They then immediately decussate and travel up the
contralateral ST into the brainstem and thalamus. Remember from Chapter 2 that at the
thalamus the two sensory pathways synapse with the same tertiary neuron, and continue
together to the contralateral sensory cortex.
Consider a complete lesion to the spinal cord at a certain level; this will produce an abrupt,
transverse, loss of function of the sensory tracts. This transverse loss of function is called
a sensory level; this cannot be caused by a lesion anywhere else in the nervous system.
A sensory level can involve the ST, or DC or both, depending on the extent of the lesion.
How do we explain sensory bands, and why do they only involve the ST? They are caused
by a small lesion in the central gray matter that interrupts the decussation of the neurons
as they enter the ST. The ST itself is undamaged, which means pain and temperature
sensation is intact above and below the level the lesion. Usually these lesions are several
spinal segments long, and produce the band shown in Fig. 4.4.
Now consider the case where one-half of the spinal cord is affected, perhaps from a tumor
pressing on it laterally. The DC would be affected, so our patient would have ipsilateral
loss of vibration and proprioception. The ST is also affected but because these neurons
decussate as they enter the spinal cord our patient would have loss of pain and temperature
on the contralateral side of the body. This is referred to as crossed sensory signs.
Take Home Messages
Sensory neurons for the ST are the only neurons to decussate in the spinal
cord.
The decussation of spinothalamic neurons and the lack of decussation of
DC neurons allow for the unique patterns of dysfunction seen in sensory
bands and crossed sensory signs.
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Figure 4.5 The Somatotopy of the Spinal Cord
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The Somatotopy of the Spinal Cord 107
As with the rest of the CNS, the long tracts of the spinal cord are somatotopically arranged.
This is displayed in Fig. 4.5.
Remember, as we established in Fig. 4.3, “cervical” refers to the cervical cord, providing

innervation to the arm, “thoracic” to the thoracic cord providing innervation to the
trunk, “lumbar” to the lumbar cord innervating the legs, and “sacral” to the sacral cord
innervating the bowel, bladder and genitals.
Let’s begin with the corticospinal tract. It is organized such that sacral neurons are lateral
and cervical neurons are medial, with lumbar and thoracic lying between them. As you
can see from Fig. 4.5, neurons exit the corticospinal tract medially; as we progress down
the cord, first the cervical neurons will exit, then the thoracic neurons, followed by the
lumbar neurons and finally the sacral neurons.
The ST is organized the same way as the corticospinal tract: cervical neurons are medial
and sacral neurons are lateral. However, the DC are opposite: sacral neurons are medial
and cervical neurons are lateral. Another way of seeing it is that the ST adds neurons
medially and the DC adds neurons laterally. For example, as we ascend the cord, neurons
from the lumbar section are added medially to the ST, and then thoracic neurons are
added medially to those. However, for the DC, lumbar neurons are added laterally, and
thoracic neurons are added laterally to those.
Knowledge of somatotopic properties is critical because it helps us to identify whether

the lesion lies inside or outside the spinal cord. For example, consider a tumor pressing
on the lateral part of the corticospinal tract. As the corticospinal tract is compressed, the
first neurons to be affected are the sacral ones, causing dysfunction of the bowel and the
bladder. As the tumor grows, it would then start to compress lumbar neurons, causing
leg weakness, and then the cervical neurons, causing arm weakness. Conversely, if the
tumor was pressing on the corticospinal tract from inside the spinal cord, one would
expect the opposite pattern; first the cervical neurons would be affected causing arm
weakness, and then the trunk, legs and finally the bowel, bladder and genitals.
Take Home Message
An easy way to remember the somatotopy of the tracts is that the tracts
with the word “spinal” in them organize their neurons such that Cervical is
Central and Sacral is Side. The DC have the opposite somatotopy.
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Figure 4.6 The Stretch Reflex
Redrawn with permission from Blumenfeld H. Neuroanatomy Through Clinical Cases. Sunderland: Sinauer
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The Stretch Reflex 109
When the layperson discusses someone’s reflexes, they are usually referencing that
person’s response time. Clinically, we examine for a specific reflex called the stretch reflex.
Each orthopedic joint in the body has muscles that actively move it and passively
stabilize it. The underlying principle of the stretch reflex is that if the body senses a joint
is being moved in an unstable fashion, it will restabilize it by activating certain muscles
and deactivating other muscles.
This is depicted in Fig. 4.6. If we strike the triceps tendon, receptors in the triceps will,
erroneously, believe the elbow joint is being rapidly and unstably moved because of the
stretch of the tendon induced by the hammer. This will automatically cause the triceps
to contract and try to shorten the stretched tendon; this also results in extension of the
forearm.
How exactly does this reflex arc occur? Proprioceptive information about the stretch
induced by the hammer is sensed by the muscle spindle and travels in a sensory neuron,
past the DRG and the gray matter of the cord. Here, it synapses with two neurons. One
neuron is excitatory, telling the agonist muscle, in this case the tricep, to contract. The
other is an interneuron, which is inhibitory, telling the antagonist muscle, in this case
the biceps, to relax. By having simultaneous contraction of the triceps and relaxation of
the biceps, the forearm extends rapidly, pulling the elbow back into stability. While this
reflex arc does not involve the upper motor neuron (UMN), the UMN does act to inhibit
or dampen the lower motor neuron (LMN), as we will see shortly.
Clinical grading of reflexes is important. Reflexes are graded on a five-point scale (0 to

4+). The scale is as follows:
• 0 Completely absent reflex;

• 1+ Decreased reflex;
• 2+ Normal reflex;
• 3+ Increased reflex;
• 4+ Increased reflex with induction of clonus (a rhythmic muscle contraction we will
discuss further in a moment).
When we say that a reflex is increased or decreased, we are judging both its speed and
amplitude.
Take Home Message
The stretch reflex causes the agonist muscle that is stretched to contract,
and the antagonist muscle to relax.
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Figure 4.7 Upper and Lower Motor Neuron Lesions
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Upper and Lower Motor Neuron Lesions 111
As we saw earlier, the motor pathway is composed of two neurons: an UMN and a LMN.
An UMN lesion will produce very different symptoms than a LMN lesion. Recognizing
these different clinical presentations is often the first step in localizing.
In order to understand these different presentations, we need to understand how the

UMN, LMN, and muscle interact. In general, as one progresses down the chain from
UMN, to LMN and to muscle, there is a dampening or inhibitory affect; the UMN dampens
the LMN which dampens the muscle. Without the dampening affect, downstream
components will fire both spontaneously and randomly.
As we just saw, the reflex arc acts at the level of the spinal cord. The UMN acts to dampen
the LMN in this pathway; thus, lesions of the UMN present with increased reflexes, as the
LMN is no longer dampened. However, since the LMN is part of the reflex arc, damage to
it will result in decreased reflexes.
From the point of view of the muscle, as long as it is still connected to its LMN, it is fully
innervated. It has no idea that the LMN innervating it is actually controlled by an UMN.
UMN lesions do not have any affect on the muscle, other than weakness. Lesions to the
LMN, on the other hand, will produce significant atrophy of the muscle, since the muscle
no longer has a functional connection to the nervous system.
When a LMN is damaged, it can begin to fire inappropriately and without stimulus. This
process is sometimes called aberrant firing. These random firings of the LMN cause
chaotic and irregular contractions of the muscle called fasciculations.
Resting tone is defined as the resistance of muscles to passive movement provided by an

external stimulus (usually an examiner). Tone is increased in an UMN lesion (i.e., it is
harder for the examiner to move affected muscles groups), and decreased (i.e., it is easy
for the examiner to move affected muscle groups) in a LMN lesion.
Take Home Messages
The motor system is designed such that each component, UMN, LMN or
muscle, dampens the component that follows it.
UMN lesions are associated with increased tone and increased reflexes.
LMN lesions are associated with decreased tone and reflexes as well as
fasciculations and atrophy.
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Figure 4.8 Features of an Upper Motor Neuron Lesion
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Features of an Upper Motor Neuron Lesion 113
UMN lesions produce several additional clinical findings that have no LMN counterpart.
The first is the presence of an up-going toe, also called the Babinski sign, after the
neurologist that first described it. In an UMN, if the foot is stroked along the lateral
border, as in Fig. 4.8, the first toe will extend upwards. Note: the reverse is not true. If,
when the foot is stroked, the toe moves downwards, all that can be concluded is that an
UMN lesion is not present, not that there is a LMN lesion (i.e., a down-going toe can be
a normal finding). The mechanism by which a toe moves up or down is complicated and
of little practical value.
The second clinical finding is the presence of clonus, which is a series of involuntary,
rhythmic, muscular contractions that are induced by movement. Usually this is elicited
by having the examiner quickly and forcefully hyperflex a joint, as depicted with the ankle
joint in Fig. 4.8. In this instance, the ankle would repeatedly oscillate back and forth; each
oscillation is termed a “beat” of clonus. More than three beats of clonus is indicative of an
UMN lesion. Occasionally, reflex testing can spontaneously induce clonus.
As we just saw, an UMN lesion is associated with increased tone. However, there are
actually two types of increased tone. Rigidity is a velocity independent increase in tone
throughout the entire range of motion that the muscle is put through. The amount of
resistance exerted by the muscle is totally independent of how quickly the examiner
moves it; the analogy is often made to moving a lead pipe. Spasticity, on the other hand,
is a velocity dependent increase in tone throughout only part of the range of motion.
As the examiner moves the muscle, there appears to be no or minimal increased tone,
however if he quickly then jerks the muscle, he feels a sharp increased resistance, often
coined a “spastic catch.” The analogy here is made to opening a Swiss army knife.
Take Home Messages
An up-going toe is indicative of an UMN lesion. A down-going toe is

present in both LMN lesions and normal physiology.
More than three beats of clonus is indicative of an UMN lesion.
Rigidity is a velocity independent increase in tone.
Spasticity is a velocity dependent increase in tone.
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Figure 4.9 The Arterial Supply to the Spinal Cord
PICA: posterior inferior cerebellar artery.
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The Arterial Supply to the Spinal Cord 115
The spinal cord is supplied by three main arteries: the anterior spinal artery, which
supplies the anterior two-thirds of the spinal cord, and two posterior spinal arteries,
which together supply the posterior one-third of the cord.
As you’ll recall from Chapter 2, the vertebral arteries are a branch of the subclavian artery
and travel up, through the vertebra into the head to supply the posterior circulation.
Just before the two vertebral arteries merge to form the basilar artery, they each give
off branches that quickly unify to form the anterior spinal artery. This artery travels
longitudinally down the length of the spinal cord.
Similarly, the posterior spinal artery is a branch of the very proximal posterior inferior
cerebellar artery (PICA). As we have seen in Chapter 2, there are considerable variations
in the posterior circulation between individuals, and in some the posterior spinal artery
is actually a branch of the vertebral artery.
Just as the cerebrum has collateral vasculature in the form of the Circle of Willis, the spinal
cord has collateral vasculature through the mighty aorta itself. Throughout the thorax,
the aorta gives off small segmental arteries, which branch into the anterior radicular
artery and the posterior radicular artery. The anterior radicular artery travels to and
merges with the anterior spinal artery, and the posterior radicular artery travels to and
merges with the posterior spinal artery.
In this way, the “circle of vasculature” for the spinal cord is completed.
Take Home Messages
The anterior spinal artery is derived from the two vertebral arteries and
supplies the anterior two-thirds of the spinal cord.
The posterior spinal artery is a branch of the PICA (or in some cases the
vertebral artery) and supplies the posterior one-third of the spinal cord.
The spinal cord vasculature has a rich collateral vasculature linking the
posterior cerebral circulation directly to the aorta.
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Figure 4.10 The Approach to Spinal Cord Damage
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The Approach to Spinal Cord Damage 117
We’ve covered a lot in this chapter. Let’s reinforce and consolidate our knowledge of the
anatomy of the spinal cord by working through a case.
Consider an extrinsic lesion compressing the cord at C5. This lesion will produce two distinct
sets of symptoms, one from CNS dysfunction (interruption of the long tracts) and one from
PNS dysfunction (interruption of the neurons in the anterior and/or posterior roots).
We’ll begin with the root dysfunction first. As our lesion presses on the cord, we will get
LMN signs in the muscles innervated by C5 due to compression of either the AHC or the
anterior root. Similarly, if the DRG or posterior root is compressed, we will get sensory
dysfunction in the area supplied by C5 (i.e., the C5 dermatome: see Chapter 5).
In this way, recognizing PNS signs (LMN weakness and dermatomal sensory loss)
localizes the spinal cord lesion longitudinally.
Now lets consider the long tract dysfunction. If our lesion at C5 grows sufficiently large,
it will move beyond the DRG/AHC and begin to compress the long tracts. This interrupts
the corticospinal tract and causes UMN weakness below the level of the lesion. The
affected muscle groups can be predicted based on our somatotopic knowledge of the
corticospinal tract. In our example, we would expect sacral signs first, then the legs, and
finally the arms to be affected. Similarly, there will be a complete sensory loss below the
level of the lesion due to interruption of the ST and DC. Again, the areas of the body that
will be affected first can be predicted based on the somatotopy of the sensory tracts.
In this way, recognizing CNS signs (UMN weakness and complete sensory loss) localizes
the spinal cord lesion in cross section; it tells us how much of the spinal cord is involved.
For quick reference, the chart in Fig. 4.10 gives an estimation of where the lesion is, based
on motor signs.
Take Home Messages
Signs of PNS damage (LMN weakness and dermatomal sensory loss)

occur at the level of the lesion, and localize the lesion longitudinally.
Signs of CNS damage (UMN weakness and complete sensory loss), occur
below the level of the lesion, and allow us to determine how much of the
cord is lesioned.

Blumenfeld H. Neuroanatomy Through Clinical Cases. Sunderland: Sinauer Associates, Inc,
Sunderland, 2002.
Lindsay, KW, Bone I, and Fuller G. Neurology and Neurosurgery Illustrated. Churchill Livingstone:
Elsevier, Edinburgh, 2010.
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Chapter 5
The Peripheral
Nervous System
Suggestive Localization
Unfortunately the peripheral nervous system (PNS) is so varied that it
does not have an Immediate Localization. However, as we have seen, the
central nervous system (CNS) tends to produce lesions that affect one-half
of the body, or at least the entirety of a limb. PNS lesions tend to produce
irregular patterns of loss in a single limb only. For example, the ulnar nerve
doesn’t even provide sensory innervation to the entire hand. Similarly, PNS
lesions tend to only affect some of the muscles of a limb; again, dysfunction
of the ulnar nerve produces weakness in only some muscles of the hand.
While exceptions are always possible, whenever you are faced with such an
incomplete pattern of symptoms, a PNS lesion should be the first thing that
springs to mind.
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120 Chapter 5 The Peripheral Nervous System
Figure 5.1 Lesion Types in the Peripheral Nervous System
Redrawn with permission from Blumenfeld H. Neuroanatomy Through Clinical Cases. Sunderland: Sinauer
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Lesion Types in the Peripheral Nervous System 121
As we see in Fig. 5.1, nerve roots exit the spinal cord and travel through a complex network,
called a plexus. As they travel through the plexus they merge to form peripheral nerves.
Figure 5.1 demonstrates the brachial plexus, which innervates the arm; the lumbosacral
plexus serves to innervate the legs. Nerves that innervate the trunk do not travel through
a plexus, they arise directly from the spinal cord.
Neuropathy is a nonspecific term used to describe a lesion located somewhere in the

PNS. A lesion affecting the nerve root itself results in a radiculopathy, whereas a lesion
to the plexus results in a plexopathy. If the nerve itself is lesioned it is called a:
• Mononeuropathy if one individual nerve is lesioned.

• Mononeuropathy multiplex if two or more unrelated nerves are lesioned, resulting
in multifocal disease (i.e., dysfunction of a nerve in an arm and nerve in a leg).
• Polyneuropathy if the disease process is generalized, resulting in a symmetric
involvement of nerves on both sides of the body (i.e., the nerves involved in the right
leg are the same as the nerves involved in the left leg).
People will often refer to a mononeuropathy as simply a neuropathy, but this is technically
incorrect.
Examining Fig. 5.1 note that, uniquely, the C8 nerve root has no corresponding vertebra.
This means that up to the C7 vertebra, nerve roots leave the cord above their corresponding
vertebra; after C7 they leave below it.
Take Home Messages
Nerve roots travel through a plexus in order to merge and become

peripheral nerves.
The brachial plexus innervates the arms, and the lumbosacral plexus
innervates the legs.
Neuropathies are named according to how many individual nerves have
lesions.
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Figure 5.2 The Brachial Plexus
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The Brachial Plexus 123
Let’s consider the brachial plexus in further detail. All innervation to the arm is composed
of the C5 – T1 nerve roots, which travel through the brachial plexus before becoming
individual peripheral nerves. It is important to be able to draw the brachial plexus, and
we will turn our attention to that in a moment.
The brachial plexus is divided into five parts, beginning with the roots C5 – T1. These five
roots merge into three trunks, named the upper, middle and lower trunk. Each trunk
then bifurcates into an anterior and posterior division. These six divisions merge to form
three cords, called lateral, posterior and medial. Finally, the cords form five branches,
which are the peripheral nerves. They are the axillary nerve, musculocutaneous nerve,
radial nerve, median nerve and ulnar nerve.
For our purposes, we only need to focus on these five large nerves in order to fully
understand the arm, rather than the myriad of small branches they give off.
Take Home Messages
The brachial plexus is composed of roots (5), trunks (3), divisions (6), cords
(3) and branches (5).
The major peripheral nerves of the arm are: the axillary nerve, radial
nerve, musculocutaneous nerve, radial nerve and ulnar nerve.
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Figure 5.3 How to Draw the Brachial Plexus
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How to Draw the Brachial Plexus 125
Though the brachial plexus seems daunting, it can be very easily remembered by drawing
three “Y”s, a “W” and an “X.”
Begin by drawing three “Y”s, two running in one direction, and one running in the
opposite direction, and label them C5 – T1 as in Fig. 5.3. Now join the top and bottom
lines together by adding a “W” to the far end, as shown. An “X” is then added between
the first two lines. Finally, join the last two lines together with a slash. Those are all the
important connections of the brachial plexus.
Label the ends of the figure as the individual peripheral nerves, as shown.
Examining the figure, we can see that the musculocutaneous nerve is made up of C5,
C6 and C7. The ulnar nerve is made up of C8 and T1. The median and radial nerves
have contributions from all the nerve roots, C5 – T1. From Fig. 5.3, it would appear that
the axillary nerve is also made up of all the nerve roots, C5 – T1. However, the nerve
roots destined for the axillary nerve simply do not mix with the other nerve roots in the
posterior cord and the axillary nerve is only composed of C5 and C6. It is one of the
peculiarities of neuroanatomy that, unfortunately, needs to be committed to memory.
Take Home Messages
The musculocutaneous nerve is composed of nerve roots C5, C6 and C7.

The median nerve is composed of nerve roots C5 – T1.
The ulnar nerve is composed of nerve roots C8 – T1.
The axillary nerve is composed of nerve roots C5 and C6.
The radial nerve is composed of nerve roots C5 – T1.
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Figure 5.4 Sensory Innervation and Common Reflexes
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Sensory Innervation and Common Reflexes 127
Before we move on to cover the individual nerves of the arm, it is worth a moment to
pause and consider some potentially confusing terminology.
As we mentioned, nerve roots mix together as they travel through the plexus, and merge
to form individual nerves (i.e., C5, C6 and C7 merge to form the musculocutaneous
nerve). Via the mixing in the plexus, a single nerve root can contribute to multiple
different nerves (i.e., C5 and C6 also form the axillary nerve and C7 contributes to the
median, ulnar and radial nerves). Thus, a single nerve root will have multiple sensory
and motor functions, by contributing to multiple different nerves.
The region of skin innervated by a single nerve root is called that nerve root’s dermatome.
Similarly, the muscles innervated by a single nerve root are called its myotome.
When mapping the sensory innervation of an area, such as the arm in Fig. 5.4, one can
speak in terms of a) dermatomal innervation provided by the nerve root, or in terms
of b) innervation provided by the peripheral nerve. Note that they are not the same.
For example, the sensory innervation of the musculocutaneous nerve (C5, C6 and C7)
should be contrasted to the sensory innervation provided individually by C5, C6 and
C7. Why is this the case? Though C5, C6 and C7 all contribute to the musculocutaneous
nerve, they also contribute to other nerves that provide sensory innervation (such as the
axillary nerve for C5 and C6, and the median, ulnar and radial nerve for C7).
It is therefore quite important to see if a patient’s sensory loss matches the pattern
produced by a lesion to a peripheral nerve, or to a lesion of a nerve root.
We will cover myotomes in a moment. As we saw in Fig. 4.6, reflexes are a test of both
sensory and motor function. The nerve roots examined when testing common reflexes
are shown in Fig. 5.4, and thankfully can be remembered easily by recalling the “1, 2,
Buckle My Shoe” rhyme.
1,2 Buckle my shoe (ankle reflex mediated by S1 and S2),
3,4 Kick the door (knee reflex mediated by L3 and L4),
5,6 Pick up sticks (biceps reflex mediated by C5 and C6),
7,8 Lay them straight (triceps reflex mediated by C7 and C8).
Take Home Messages
The area of skin innervated by a single nerve root is called its dermatome.
The muscles innervated by a single nerve root are called its myotome.
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Figure 5.5 Dominant Myotomes
Some individual figures adapted from Waxman SG. Clinical Neuroanatomy. Lange, New York, 2013.
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Dominant Myotomes 129
While each nerve root contributes to multiple muscles, via the mixing that occurs in the
plexus, anatomical studies show that usually one (or at most two) nerve root provides
the dominant innervation to a muscle. This can be very useful clinically when there is a
concern of an injury to the spinal cord and accompanying nerve roots. By assessing a few
quick muscle groups, the examiner can quickly glean which nerve roots are intact and
which ones are damaged.
Figure 5.5 shows the dominant myotome for each nerve root. Thankfully there is a
pattern! Nerve roots tend to linearly follow major muscle groups as one moves down the
body. Let’s review this now.
We begin with the head and see that C1 is responsible for neck flexion. C2 is responsible
for neck extension. C3 is responsible for lateral neck flexion to both the left and the right.
As we continue down the body, we see that C4 elevates or shrugs the shoulders. C5
innervates the abductors of the shoulder. Moving into the arm, we see that C6 innervates
two muscle groups: those responsible for elbow flexion and wrist extension. C7 also
innervates two muscle groups: those responsible for elbow extension and wrist flexion.
Note that the elbow and wrist are always opposite. If a nerve root contributes to elbow
flexion it provides wrist extension, and vice versa. C8 is responsible for finger flexion and
T1 is responsible for finger abduction.
As we move down into the legs, the nerve roots innervate the anterior muscles, and
then circle around the foot, and work their way back up the posterior muscles. L2 is
responsible for hip flexion and L3 for knee extension. Both L4 and L5 innervate the
muscle for ankle dorsiflexion and L5 alone innervates the muscle that extends the first
toe. S1 is responsible for ankle plantar flexion and hip extension. As we move up the
posterior part of the leg we see that S2 is responsible for knee flexion.
Take Home Message
One can remember the dominant myotomes by remembering that nerve

roots linearly follow the muscles groups as one works down the body and
then circle up the posterior part of the leg.
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Figure 5.6 The Axillary Nerve (C5, C6)
The Musculocutaneous Nerve (C5, C6, C7)
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The Axillary (C5, C6) and Musculocutaneous (C5, C6, C7) Nerves 131
The first nerve we will consider is the axillary nerve, which is made up of nerve roots
C5 and C6. The axillary nerve comes off the posterior cord and travels a short distance
before wrapping around and ultimately becoming anterior to the humerus. Clinically, it
is responsible for innervation of the deltoid, which abducts the shoulder beyond the first
20°. The first 20° involve the muscles in the rotator cuff.
The axillary nerve is also responsible for sensory innervation to the upper lateral arm.
Remember to compare this to the C5 and C6 dermatome.
The musculocutaneous nerve comes off the lateral cord and is composed of C5, C6 and C7.
This nerve travels anterior to the humerus and terminates in the upper arm, innervating
the biceps, which flexes the forearm. Before terminating, the musculocutaneous nerve
gives off a branch, the lateral cutaneous nerve of the forearm. This nerve’s only function
is to provide sensation to the lateral aspect of the forearm.
Take Home Messages
The axillary nerve innervates the deltoid, which is responsible for

abduction of the arm beyond the initial 20°.
The musculocutaneous nerve innervates the biceps, which flexes the
elbow.
The musculocutaneous nerve also has a branch, the lateral cutaneous
nerve of the forearm, which provides sensation to the lateral forearm.
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Figure 5.7 The Radial Nerve (C5-T1)
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The Radial Nerve (C5-T1) 133
The radial nerve is composed of nerve roots C5 – T1 and comes off the posterior cord. It
initially travels posterior to the humerus, and branches to innervate the triceps, before
wrapping around to become anterior to the elbow. At the elbow, it branches into a
motor and sensory component. The motor component, the deep branch, travels into
the posterior forearm. The sensory component, known as the superficial branch, travels
down to the dorsum of the hand.
An easy way to remember the motor function of the radial nerve is that it supplies all
the extensor muscles in the arm, whether it is the forearm, wrist, finger or thumb.
The powerful triceps extend the forearm. The extensor carpi (‘carpi’ is Latin for wrist)
extends the wrist. Extension of the fingers is provided by the extensor digitorum. Finally,
extension of the thumb is provided by the extensor pollicis (‘pollicis’ is Latin for thumb).
In addition, the radial nerve also innervates the plainly named supinator, which
supinates the forearm.
The radial nerve supplies sensation to the posterior area of the arm, forearm, and to the
posterior aspect of the first three digits of the hand.
Note some movements listed, such as extension of the wrist, are actually provided by two
muscles, one on the radial side (i.e., the extensor carpi radialis) and one on the ulnar side
(i.e., the extensor carpi ulnaris). In addition, some muscles have multiple heads, usually
a longer one, “longus,” and a shorter one, “brevis,” such as extensor pollicis longus, and
extensor pollicis brevis. While more accurate, it is not particularly clinically relevant at
this stage of training, and we mention it only so as not to cause confusion with what is
listed in other texts.
Take Home Messages
The radial nerve innervates the triceps and then divides into a solely
motor component, the deep branch, and a solely sensory component, the
superficial branch.
The radial nerve innervates all the extensors of the arm, as well as the
supinator of the forearm.
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Figure 5.8 The Ulnar Nerve (C8, T1)
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The Ulnar Nerve (C8, T1) 135
The ulnar nerve is composed of nerve roots C8 and T1 and comes off the medial cord. It
travels through the upper arm medial to the humerus, and doesn’t provide any function,
motor or sensory, until it reaches the forearm. It continues in the forearm and travels into
the hand through Guyon’s canal at the wrist. Guyon’s canal is an important area because
it can be involved in a compressive neuropathy.
The ulnar nerve is very important because it supplies nearly all the muscles of the hand,
with a few exceptions that we will discuss shortly. Clinically important muscles in the
hand include the adductor pollicis, which adducts the thumb, and the dorsal interossei,
which spread, or abduct the fingers. In addition, the ulnar nerve is also responsible for
flexion of the 4th and 5th digit via the flexor digitorum.
The ulnar nerve has one motor function outside of the hand, and that is to flex the wrist
via the flexor carpi.
The sensory area supplied by the ulnar nerve is confined to the one-half of the 4th digit
and the entire 5th digit, as shown in Fig. 5.8.
Take Home Messages
As the ulnar nerve enters the hand, it passes through Guyon’s canal,
which is often the site of a compressive neuropathy.
The ulnar nerve innervates nearly all the muscles of the hand.
The ulnar nerve supplies sensation to the entire 5th digit, but only to one
half of the 4th digit.
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Figure 5.9 The Median Nerve (C5-T1)
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The Median Nerve (C5-T1) 137
The median nerve is composed of nerve roots C5 – T1 and is formed by the union of
lateral and medial cord. The median nerve travels down into the forearm, where it
provides innervation to several muscles. It continues into the hand through the carpal
tunnel, which can often be the site of a compressive neuropathy.
The median nerve has a grab bag of motor functions, and some argue it is best
remembered as the exception of the radial and ulnar nerve. Its sole forearm function
is pronation of the forearm, which is carried out by the pronator teres. It is responsible
for three of the five movements of the thumb, including opposition by the opponens
pollicis, abduction by the abductor pollicis, and flexion by the flexor pollicis. Finally, it
also flexes the second and third digits via the flexor digitorum.
The median nerve provides sensation to the palmar aspect of first, second, and third
digits, and to one-half of the fourth digit.
Take Home Messages
As the median nerve enters the hand, it passes through the carpal tunnel,
which is often the site of a compressive neuropathy.
The median nerve provides motor input to the opponens pollicis,
abductor pollicis, flexor pollicis, and the second and third tendons of the
flexor digitorum. All other hand muscles are supplied by the ulnar nerve.
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Figure 5.10 How to Draw the Lumbosacral Plexus
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How to Draw the Lumbosacral Plexus 139
Unlike the brachial plexus, the lumbosacral plexus is not divided into distinct sub-
sections (i.e., “trunks,” “divisions,” and “cords”). However, it is still important to know
which nerve roots contribute to the major nerves of the leg. Whereas the brachial plexus
was easily remembered with the letters “Y,” “W” and “X,” the lumbosacral plexus will be
remembered with numbers “4,” “5” and “3.”
Draw 7 straight lines labeled L2 to S3. Starting at L4, place a total of 4 bifurcations: one on
each of L4, L5, S1 and S2 as shown in Fig. 5.10. Join these together to form the common
peroneal nerve. Proceed a little further downstream on L4 and now draw a total of 5
bifurcations, just as before, on L4 to S3; join these together to form the tibial nerve.
Initially, the common peroneal and tibial nerve travel together in the same nerve sheath.
As a result, early anatomists thought they represented one nerve and called it the sciatic
nerve. Unfortunately, this erroneous distinction continues to this day.
Now draw 3 bifurcations beginning with L2, and moving downwards, just as before. Join
these together to form the obturator nerve.
We are nearly finished. Join the first three lines (L2 – L4) together to form the femoral
nerve. Join the next set of three lines starting from L5 (L5 – S2) together to form the
inferior gluteal nerve. Finally, join the three lines L4, L5 and S1 together to form the
superior gluteal nerve.
There are many more branches of the lumbosacral plexus, but the above scheme covers
the major clinically relevant nerves.
Take Home Messages
The obturator nerve is composed of L2 – L4.

The femoral nerve is also composed of L2 – L4.
The superior gluteal nerve is composed of L4 – S1.
The inferior gluteal nerve is composed of L5 – S2.
The common peroneal nerve is composed of L4 – S2.
The tibial nerve is composed of L4 – S3.
The common peroneal nerve and tibial nerve initially travel in the same
nerve sheath and are collectively referred to as the sciatic nerve.
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Figure 5.11 The Nerves and Muscles of the Hip
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The Nerves and Muscles of the Hip 141
The nerves of the arm have many branches and typically supply many different muscles.
When we looked at them it made sense to examine the path and branches of each nerve
first, and then its associated sensory and motor functions.
This is in contrast to the leg, where each nerve typically only has one or two motor
functions. Thus, a more useful approach is to first examine the movements of each joint
and then the nerve that supplies the muscle responsible for that movement.
We will begin with the hip. The four cardinal movements of the hip are flexion, extension,
abduction and adduction.
Hip flexion is facilitated by the iliopsoas muscle, which lies in the posterior compartment
of the abdominal cavity. It attaches the spine to the anterior side of the femur. Since this
muscle is so close to the lumbar plexus, it is not served by an individual nerve, but is
innervated directly by nerve roots L1 – L3.
Hip extension is achieved by the powerful gluteus maximus, which attaches the sacrum
to the posterior side of the femur. It is innervated by the inferior gluteal nerve (L5, S1 and
S2). The inferior gluteal nerve does not have a sensory component.
Hip adduction is provided by the obturator nerve (L2, L3 and L4), which innervates
a group of muscles simply referred to as the adductors. They attach the pelvis to the
medial side of the femur. The obturator nerve is infamously associated with trauma
from overzealous use of forceps during childbirth. The obturator has a modest sensory
component, providing innervation to a small area of the medial thigh.
Hip abduction is achieved by the gluteus minimus and gluteus medius through the
superior gluteal nerve (L4, L5 and S1). They attach the iliac crest to the femur at the
greater trochanter. The superior gluteal nerve does not have a sensory component.
Take Home Messages
The iliopsoas is responsible for hip flexion and is innervated directly by

L1 – L3.
The gluteus maximus is responsible for hip extension and is innervated
by the inferior gluteal nerve.
The adductors are responsible for hip adduction and are innervated by
the obturator nerve.
The gluteus minimus and gluteus medius are responsible for hip
abduction and are innervated by the superior gluteal nerve.
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Figure 5.12 The Nerves and Muscles of the Knee
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The Nerves and Muscles of the Knee 143
The knee only has two possible movements: extension and flexion.
Knee extension is performed by the quadriceps which, as the name implies, is actually
made up of four different muscles (the rectus femoris, vastus lateralis, vastus medialis,
and vastus intermedius). Practically, however, they can be thought of as one group. The
quadriceps attach proximally to both the femur and pelvis, and distally to the tibia. The
quadriceps are innervated by the femoral nerve (L2, L3 and L4). Knee extension is so
critical to life, as it is the main muscle involved in standing, that innervating the quads is
the sole motor function of the massive femoral nerve.
The sensory distribution of the femoral nerve is huge, and covers more than half of the
leg, as shown in Fig. 5.12.
As we mentioned, the common peroneal nerve and tibial nerve initially travel
together in the thigh as the sciatic nerve (L4, L5, S1, S2, S3). The sciatic nerve provides
innervation to the hamstrings. Again, this is a composite muscle and is made up of the
semi-tendinous muscle, the semi-membranous muscle and the biceps femoris. The
hamstrings attach the posterior part of the pelvis to the bones of the lower leg, the tibia
and fibula. Contraction of the hamstring results in knee flexion.
The sciatic nerve’s sensory component is simply the summation of the sensory
component of the common peroneal and tibial nerves (which we will cover next), and is
shown in Fig. 5.12.
Take Home Messages
The quadriceps are responsible for knee extension and are innervated by
the femoral nerve.
The hamstrings are responsible for knee flexion and are innervated by the
sciatic nerve.
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Figure 5.13 The Nerves and Muscles of the Ankle: I
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The Nerves and Muscles of the Ankle: I 145
Like the hip joint, the ankle has four possible types of movement: foot dorsiflexion, in
which the angle between the foot and the leg is decreased, foot plantar flexion, in which
the angle between the foot and the leg is increased, foot inversion and foot eversion.
Routinely, the toes are not assessed, with one major exception: extension of the first toe.
The muscles responsible for all these movements are innervated by the divisions of the
sciatic nerve: the tibial nerve, responsible for foot plantar flexion and foot inversion,
and the common peroneal nerve, responsible for foot dorsiflexion, foot eversion and
extension of the first toe.
We will begin with the tibial nerve. The sciatic nerve branches into the tibial nerve and
common peroneal nerve just superior and posterior to the knee. The tibial nerve travels
posteriorly into the foot. On its way, it innervates the gastrocnemius and soleus, which
together attach the femur, tibia and fibula to the posterior aspect of the foot, and are
responsible for ankle plantar flexion.
Slightly more distally, the tibial nerve also innervates the tibialis posterior, which is
responsible for foot inversion.
The tibial nerve provides sensory innervation to the entire sole of the foot.
Take Home Messages
The gastrocnemius and soleus are innervated by the tibial nerve and are
responsible for ankle plantar flexion.
The tibialis posterior is also innervated by the tibial nerve and is
responsible for inversion of the foot.
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Figure 5.14 The Nerves and Muscles of the Ankle: II
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The Nerves and Muscles of the Ankle: II 147
As we mentioned, the common peroneal nerve begins superior and posterior to the
knee. It immediately wraps around and enters the anterior compartment of the leg. As
it does so, it divides into the superficial peroneal nerve and the deep peroneal nerve.
The deep peroneal nerve supplies the tibialis anterior. This powerful muscle is the
primary dorsiflexor of the foot. Thus, problems with the tibialis anterior result in an
infamous clinical presentation, the “foot drop.” The deep peroneal nerve also supplies
the extensor hallucis longus, which is responsible for extension of the first toe.
The superficial peroneal nerve supplies the peroneus muscle. This muscle attaches the
lateral part of the fibula to the 5th metatarsal and is responsible for foot eversion.
The sensory distribution of the common peroneal nerve is shown in Fig. 5.14 and includes
the lateral aspect of the calf, as well as the dorsal aspect of the foot.
With that, we’ve covered all the elements of the PNS, from the individual nerve roots,
to the plexuses, and finally the individual nerves themselves. For your reference we’ve
included Fig. 5.15 and Fig. 5.16 as a summary of everything we’ve discussed.
Take Home Messages
The powerful tibialis anterior is responsible for ankle dorsiflexion and is

innervated by the deep peroneal nerve.
The extensor hallucis longus is responsible for extension of the first toe,
and is also innervated by the deep peroneal nerve.
The peroneus muscle is responsible for foot eversion and is innervated by
the superficial peroneal nerve.
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Figure 5.15 Sensory Map of the Peripheral Nervous System
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Sensory Map of the Peripheral Nervous System 149
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Figure 5.16 Summary of the Peripheral Nervous System
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Summary of the Peripheral Nervous System 151

Waxman SG. Clinical Neuroanatomy. Lange, New York, 2013.
O’Brien MD. Aids to the Examination of the Peripheral Nervous System.Saunders,
Edinburgh, 2010.
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Chapter 6
Localization Primer
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154 Chapter 6 Localization Primer
Our algorithm for localization is shown in Fig. 6.1.
Figure 6.1 Localization Algorithm
CNS: central nervous system; LMN: lower motor neuron; PNS: peripheral nervous system; UMN: upper motor neuron.
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Localization Algorithm 155
We’ve reviewed the neuroanatomy of the cerebrum, brainstem and cranial nerves (CN),
spinal cord as well as the peripheral nervous system (PNS). Your road map of the nervous
system is complete, and you can start to practice localizing in the accompanying 25 cases.
But before you do, let’s discuss how to go about applying the neuroanatomy you’ve learned.
It’s easy to get overwhelmed with information when you are reading a neurology case,
and thus it can be confusing to know where to start in the process of localization. Should
you focus on the patient’s visual field defects, or his sensory complaints, or perhaps his
hemibody weakness? While there are multiple ways to approach any neurology problem,
some localization algorithms are much more straightforward than others, and the one
we present here can be applied to the vast majority of neurological cases you will see.
Our first step is to decide if the lesion is in the CNS (UMN) or the PNS (LMN). Then
we localize longitudinally; we decide if the lesion is at the level of the cortex, internal
capsule, brainstem, or spinal cord for the CNS, or at the nerve root, plexus, or nerve for
the PNS. Deciding on this produces our initial localization (i.e., cervical spinal cord).
Once we have decided on this, we can draw that level in cross section and then decide
what components are affected, which produces our final localization (i.e., the right half
of the spinal cord at C6).
The localization process always begins by answering the following question:

Is the patient’s weakness upper motor neuron (UMN), lower motor neuron
(LMN) or both?
Categorizing the patient’s weakness into either UMN or LMN is the easiest way to
determine if the lesion lies in the central nervous system (CNS) or the PNS, respectively.
Depending on the answer to this question, our algorithm branches into three paths:
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Path 1: the patient has UMN weakness.
Step 1: Does the pattern of long tract symptoms suggest a localization?
This is a very important question to answer, as the pattern of long tract signs can often
yield an Immediate Localization (such as the crossed signs of the brainstem or the
sensory level of the spinal cord). Even if an Immediate Localization isn’t revealed, a
much shorter list of localizations can often be produced from this information.
Step 2: What is the highest level of dysfunction?
Determine the highest neuroanatomical level possible. See if the case involves any of
the higher functions of the cortex (aphasia, apraxia, or agnosia), CN palsies (brainstem)
or sensory levels (spinal cord). For example, if the patient presents with right sided
weakness and also has aphasia then the neuroanatomical level is the cortex. However,
if the patient instead has right sided weakness and a CN III palsy, the neuroanatomical
level is the brainstem. Similarly right sided weakness and a sensory level would localize
to the spinal cord.
At this point we will have finished localizing longitudinally and have our initial local-
ization.
Step 3: What is affected?
Since we now know the initial localization, we can draw that level in cross section and
determine what components are affected. This will give us our final localization.
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Localization Algorithm 157
Path 2: the patient has LMN weakness.
If the patient has only LMN weakness then we know the lesion lies in the PNS. Localizing
in the PNS is very different than in the CNS, and is more of a “trial and error” comparison.
Possible localizations in the PNS include the nerve root (a radiculopathy), the plexus
(plexopathy), and the nerve (neuropathy).
Step 1: Do the symptoms correspond to a single myotome and dermatome?
Figure 5.5 is our table of dominant myotomes. These muscles serve as a screen to see if
the patient has a radiculopathy.
If only one of the muscles listed in Fig. 5.5 is affected, go to Fig. 5.15 and find the root’s
corresponding dermatome. If the patient’s sensory loss matches this dermatome then
you can safely conclude the patient has a radiculopathy.
If the patient has more than one of the muscles in Fig. 5.5 affected, or the sensory loss
doesn’t match the dermatome, proceed to Step 2.
Step 2: Do the symptoms correspond to a single nerve?
Now see if the affected muscles and sensory loss correspond to a single nerve. If they do,
then the next step is to figure out where the lesion is along the path of the nerve. To do so,
begin distally, and walk up the length of the nerve, until you come across a muscle that
has not been affected by the lesion.
If the symptoms do not match to a radiculopathy or neuropathy, then by process of

elimination, the lesion must lie in the plexus.
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Path 3: the patient has both UMN and LMN weakness.
This can only be produced by a lesion of the spinal cord. Based on whether both the
arms and the legs are affected, determine whether the lesion lies in the cervical, thoracic,
lumbar or sacral spinal cord.
Don’t worry if the above algorithm seems a little opaque; solutions are provided for all of
the cases so you’ll see how we employ it.
Note that the above algorithm assumes that a focal lesion exists. The nervous system,
especially the PNS, is vulnerable to a whole host of diffuse disease processes that can affect
the entire nervous system at once, resulting in a general, gradual loss of function. In this
case the idea is to localize to the component of the nervous system (i.e., peripheral nerves
vs. spinal cord) that is diseased, as this greatly narrows down the differential diagnosis.
No algorithm will work 100% of the time and exceptions always exist (don’t worry, we will
cover the most common ones in the Cases section). However, following the logic laid out
above will always give you a good idea of where the lesion is in the vast majority of cases.
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Case Primer 159
Case Primer
Before you sink your teeth into the cases, we need briefly to talk about how to do a typical
neurological screening exam. Depending on the clinical situation you’re faced with, a
much more in-depth exam may need to be performed.
The format below assumes you have a patient who is not confused and is cooperative (by
no means does this occur all the time, particularly in the early hours of the morning when
on call). The neurological exam is unique in medicine as it is quite dependent on patient
cooperation, and sometimes simple inspection is all that can be accomplished. However,
given an ideal patient, a screening examination tests the following components:
Language: The patient may be aphasic. In order to classify it, note the patient’s fluency
and whether they comprehend verbal commands. Finally, see if they can repeat a
sentence.
Cranial nerves: A formal exam usually begins by assessing visual acuity using a Snellen
eye chart, but in routine screening exam this is usually omitted. CN II is tested by
assessing for a visual field defect. CN III, IV and VI are assessed by seeing if the eyes can
move in all the directions of gaze. The other components of CN III are checked by seeing
if there is ptosis of the eyelid and whether the pupil reacts to light (note this also tests
CN II). CN V is checked by seeing if sensation is intact in the face. CN VII is assessed by
noting whether the patient has a facial droop. Determine if the facial droop involves the
forehead (LMN facial droop) or not (UMN facial droop). CN VIII is not routinely assessed
in a screening exam. CN IX and X are assessed together by seeing if the patient’s palate
raises symmetrically. CN XI is tested by seeing if they have full power in head turning
and shoulder shrug. Finally, CN XII is tested by seeing if, when the tongue is stuck out,
it is straight, implying normal power, or if it is deviated to one side, implying weakness.
Motor system: Before assessing power, inspect the limbs briefly and look for atrophy
and fasciculations. Then assess tone, remembering that increased tone is a sign of UMN
weakness. Then power can be assessed; the first part of Fig. 6.2 shows what muscle groups
are routinely checked in a typical screening exam. However, if the patient complains of
very specific weakness, such as hand or foot weakness, more muscle groups may need
to be tested.
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Figure 6.2 Muscle Testing in a Screening Neurological Exam
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Muscle Testing in a Screening Neurological Exam 161
Power is assessed using the Medical Research Council Grading of Muscle Power
Scale (MRC Scale), which is shown in the bottom half of Fig. 6.2. The MRC Scale does
an admirable job of trying to evaluate power in as objective a fashion as possible, but
ultimately is still subject to considerable bias. For example, when examining a 91-year-
old the “full resistance” applied by the examiner is often significantly less than that which
is applied when examining a 24-year-old, and may show considerable interexaminer
variability.
Importantly, for a muscle to be graded at a certain level of power, it must be able to move
against the resistance applied by the examiner across the entire range of motion of the
muscle. This is a common source of grading error. For example, if a patient can only move
their bicep the first 20° against gravity, then they cannot be scored as an MRC grade 3.
Many clinicians also employ unofficial subgrades, the most common of which is the
4 -, 4.0 and 4+ designation, which indicates that the examiner is applying mild, moderate
and significant, but still not full, resistance, respectively. Since this is so common we have
chosen to use this convention in our Cases (Chapter 7).
Finally, the reflexes are examined.
Sensory system: The spinothalamic tract (ST) (pain and temperature) and dorsal
columns (DC) (vibration and proprioception) should be checked in all four limbs. There
is no need to test both modalities carried in a single tract; typically pain is assessed for
the ST (using a pin, to see if the patient recognizes it is sharp), and vibration for the DC
(using a tuning fork).
Coordination and gait: Finger to nose and heel to shin testing is examined first. These
tests can be difficult to interpret if the patient is weak. Finally, if the patient is able, it is
often very instructive to watch their gait to look for any subtle abnormalities.
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Figure 6.3 Muscle Table
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Muscle Table 163
Figure 6.3 lists many of the muscles that can be assessed on neurological examination.
When recording the power of muscle groups, clinicians usually use a chart format. An
unfortunate lack of convention has developed wherein some clinicians will write down
the name of the muscle tested (i.e., biceps) and others will instead identify the muscle
based on its function (i.e., elbow flexor). Usually the function of the muscle is written
down because it can be shortened (i.e., elbow flexor becomes EF). However, notable
exceptions occur and it is ultimately arbitrary. You need to be familiar with all potential
names, so we have included this chart so you can always see what muscle groups we
reference in the cases.
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Localization Key
Figure 6.4
ACA: anterior cerebral artery; FEF: frontal eye fields; MCA: middle cerebral artery; TCM: transcortical motor;
UMN: upper motor neuron.
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Localization Key 165
Figure 6.5
PCA: posterior cerebral arteries; UMN: upper motor neuron.
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Figure 6.6
INO: internuclear ophthalmoplegia; LMN: lower motor neuron; UMN: upper motor neuron.
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Figure 6.7
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Figure 6.8
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Figure 6.9
AHC: anterior horn cell; LMN: lower motor neuron; UMN: upper motor neuron.
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Figure 6.10
AHC: anterior horn cell.
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Figure 6.11
AHC: anterior horn cell; LMN: lower motor neuron; UMN: upper motor neuron.
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Figure 6.12
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Figure 6.13

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Figure 6.14
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Figure 6.15
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Figure 6.16
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Part Two
The Cases
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Case 1: The 72-year-old woman who talked only gibberish 179
Case 1: The 72-year-old woman who talked only gibberish
You are asked by your friends on the Internal Medicine team to come down and see a
72-year-old woman who is in their clinic for routine follow-up of her diabetes. She lives
alone. When her daughter went to pick her up for her appointment, she found the patient
“talking gibberish,” but decided not to take her to the Emergency Department, since
they were “going to go see a doctor anyway.”
When you see the patient she is now agitated. She says very little and what she does say
is nonsensical. She cannot repeat, nor does she obey your instructions. This frustrates
your neurological examination. However, you persevere and assess her cranial nerves
(CN). She appears to have lost her right visual field in both eyes. Her eyes are driven to
the left and she cannot look to the right. She has a right sided facial droop that spares her
forehead. Her tongue and palate appear midline. Motor examination reveals increased
tone on the right side, with 3+ reflexes. Her toe is upgoing on the right. Formal power
testing is impossible, but you notice she is not moving her right side. She is also not
responsive to pain on the right side. Coordination is impossible to assess.
Where is the lesion? What is going on here?
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180 Case 1: Findings
Case 1: Findings
AF: arcuate fasciculus; MCA: middle cerebral artery.
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Case 1: Solution 181
Case 1: Solution
1. Does the patient have upper motor neuron (UMN) weakness, lower motor
neuron (LMN) weakness or both?
Our patient has increased reflexes, increased tone and an upgoing toe, all signs of an
UMN type weakness. Thus, we know that the lesion lies in the central nervous system
(CNS).
2. Does the pattern of long tract symptoms suggest a localization?
In this case, our patient has weakness of the right face, arm and leg. Her facial weakness
does not involve the forehead, thus this is an UMN type facial droop. Our sensory testing
is less than ideal, but we do know she has impairment to pinprick on the right, indicating
the spinothalamic tract (ST) is damaged. Unfortunately this pattern is nonspecific, and
possible localizations include the cortex, internal capsule and brainstem.
3. What is the highest level of dysfunction?
Reviewing our symptoms, we see that our patient has an UMN facial droop. We therefore
know that the lesion must be above the level of the pons, or our patient would have a LMN
facial droop from involvement of the facial nucleus. Our patient has lost the right sided
aspect of her visual field in both eyes; she has a right sided homonymous hemianopsia
(RHH). In addition, she appears to be globally aphasic, as her fluency, comprehension
and ability to repeat are all impaired; aphasia is one the symptoms that is an Immediate
Localization to the cortex. Thus, the cortex is our initial localization, and we now must
decide what parts of it are affected.
4. What is affected?
Our patient has right sided UMN type weakness and right sided spinothalamic loss.
Since these tracts decussate at the level of the medulla, the left motor cortex and sensory
cortex must be involved. Recall that the frontal eye fields (FEF) drive the eyes to the
contralateral side. Since our patient’s eyes are deviated to the left, this means that the
right FEF are unopposed; the left FEF have also been lesioned. The global aphasia means
that both Broca’s area and Wernicke’s area are affected. The RHH can only be produced
by a lesion of the visual pathways that is posterior to the optic chiasm (Fig. 3.5).
Putting it all together, we see that nearly all of the left parietal and temporal lobe is
involved, as well as some of the frontal lobe. Reviewing Fig. 2.14, we see that this area
corresponds to the vascular territory supplied by the middle cerebral artery (MCA).
Indeed, this patient was unfortunate enough to have suffered a complete occlusion of
her left MCA.
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182 Case 1: Clinical Pearl
Figure 7.1 Causes of Stroke
Mozaffarian D, et al. Heart disease and stroke statistics – 2015 update, Circulation 2015;131:e310.
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Case 1: Clinical Pearl 183
Clinical Pearl: Causes of Stroke
A stroke, also called a cerebral infarction, is caused by an interruption of blood flow to an area
of the brain and results in the permanent loss of brain tissue. While stroke is the fifth leading
cause of death in the USA, it is the number one cause of adult disability. Understandably, the
economic impact of this disability is tremendous; Americans spent over $34 billion on the
direct cost of treating stroke in 2013. This number, while impressive, ignores the enormous
costs associated with the loss of productivity of stroke victims; many are unable to return to
work or have to do so on a part time basis and must rely on social assistance.
The interruption of blood flow that causes a stroke can either be the result of the occlusion
of a blood vessel, causing ischemia or the result of a rupture of a blood vessel, causing
a hemorrhage. 80% of strokes are ischemic in origin, and 20% result from hemorrhage.
Hemorrhagic strokes are usually due to focal bleeding from rupture of the brain tissue
and associated blood vessels. The patient usually has a history of poorly controlled blood
pressure, leading to weakening of the arterial wall.
Ischemic strokes are usually caused by a blood clot that occludes the artery. If the blood
clot was generated near the site of the stroke it is called a thrombus. If the blood clot broke
off from another location and travelled to the site of the stroke it is called an embolus.
The difference between a thrombus and an embolus is somewhat arbitrary and is of little
practical significance.
There are several major etiologies of ischemic stroke. Carotid artery disease and cardio-
embolism each account for 25% of ischemic stroke cases. While carotid stenosis can serve as
a source for embolism in ischemic stroke, it should be noted that no neurological symptoms
are caused by the stenosis itself; “neurological angina” does not exist, unlike chest pain due
to stenosed cardiac arteries. Rarely, ischemic strokes can be caused by insufficient blood
pressure to perfuse the brain, which is usually associated with cardiac arrest.
The most common cause of cardiac embolism is from arrhythmias like atrial fibrillation;
fibrillation results in static blood which naturally clots, forming an embolus. This embolus
is then pumped by the heart into the arterial circulation. Other causes of embolus
formation include prosthetic valves, congestive heart failure, and myocardial infarction.
If the underlying problem is not correctable, the patient will need to take anticoagulation
medication.
Lacunar stroke, also called small vessel disease, refers to thrombus formation in the
small penetrating arteries of the cerebral vascular system, usually coming off the MCA or
basilar arteries. These will be covered later.
Note that, despite aggressive investigation, about 20% of strokes remain cryptogenic,
meaning no cause can be found.
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Case 2: The 79-year-old man who whose legs felt funny 185
Case 2: The 79-year-old man who whose legs felt funny
You are asked to see a 79-year-old man who has had a recent string of unfortunate luck.
He developed intense abdominal pain and was diagnosed with a ruptured abdominal
aortic aneurysm for which he was operated on emergently. He survived the operation
but had a difficult postoperative course and has spent the last week in the intensive care
unit (ICU) in a medically induced coma. When he awoke from the coma yesterday, he
was thankful to be alive but quickly realized he could not move his legs. When the ICU
team removed his catheters they noted he had both bowel and bladder incontinence.
He complains to the nurses that his legs feel “funny.”
When you examine him, you find his language to be normal. His pupils, visual fields,
and eye movements are also normal. He does not have a facial droop and his tongue is
not deviated. Motor examination of the arms is also normal. However, you find a spastic
tone in both legs. His reflexes are 3+ in the knee bilaterally, and 4+ in the ankle bilaterally
(which, by definition, induces subsequent clonus). His power examination is listed
below, but he is barely antigravity in the proximal part of both legs. Toes are upgoing
bilaterally. His vibration sense is intact everywhere. Pinprick is intact in the arms, but he
states the pin feels dull in both legs. You run the pin down his trunk and he states that all
of a sudden it feels dull around the umbilicus. However, you find that his vibration sense
is intact everywhere. Coordination was not tested given the weakness.
Power Examination
Right Left
Deltoid 5 5
Bicep 5 5
Tricep 5 5
WE 5 5
FE 5 5
HF 3 3
KE 3 3
KF 3 3
ADF 2 2
APF 2 2
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Case 2: Findings
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Case 2: Solution
1. Does the patient have UMN weakness, LMN weakness or both?
Our patient has increased reflexes, spastic tone and upgoing toes, which are all signs of
an UMN lesion. Thus, we know that the lesion lies in the CNS.
Our patient has bilateral UMN type leg weakness. This has two main localizations and
they lie at opposite ends of the CNS. The first is a lesion to the thoracic or lumbar spinal
cord. The second is a cortical lesion that involves the medial aspect of both motor
cortices; this would not cause face and arm weakness as the neurons to these areas lie on
the lateral part of the motor cortex (Fig. 2.1). In order to differentiate between the two, we
have to hope for a clue in the sensory exam.
In this case we are quite fortunate as the sensory examination reveals an Immediate
Localization; our patient has a sensory level. He complains of loss of pinprick below the
level of the umbilicus. A sensory level can only be produced by a spinal cord lesion (see
Chapter 4).
Our patient has a sensory level to pinprick at the umbilicus; consulting our dermatome
map (Fig. 5.15) shows this area is innervated by T10. Thus our initial localization is the
spinal cord at the level of T10.
Since we now know that we are in thoracic spinal cord, we can draw it in cross section.
Our patient has UMN weakness in both legs, so we know that both corticospinal tracts
are involved. He does not have any loss of vibration, so the dorsal columns (DC) are
spared. However, the loss of pinprick below the level of T10 corresponds to lesions in
both STs. Joining these areas together, we see that he has almost two-thirds of his cord
involved. Our final localization is the anterior two-thirds of the spinal cord at T10.
The pattern described is known as anterior cord syndrome as it is typically caused by an

anterior spinal artery stroke. In this case, prolonged clamping of the aorta during the
emergency surgery likely caused unavoidable ischemia to the spinal cord.
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Figure 7.2 Other Patterns of Intrinsic Spinal Cord Disease
DC: dorsal column; ST: spinothalamic tract; SACD: subacute combined degeneration; LMN: lower motor
neuron; UMN: upper motor neuron.
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Clinical Pearl: Other Patterns of Intrinsic Spinal Cord Disease
For reasons that are incompletely understood, the spinal cord is particularly vulnerable
to many different kinds of nutritional and infectious insults. We will cover a few of the
more common ones; they are shown in Fig. 7.2.
Tabes dorsalis
Tabes Dorsalis is a late complication of syphilis caused by infection with Treponema
pallidum. It typically presents anywhere from 3 to 30 years after the initial infection
and affects the dorsal root ganglion (DRG), posterior root and the DC. Patients initially
complain of painful paresthesias (tingling sensation) due to DRG dysfunction. Soon
thereafter they develop a sensory ataxia from the lack of proprioception, due to the
involvement of the DC. On examination, these patients have poor vibration sense, and
are areflexic due to interruption of the reflex arc from the DRG lesion. Tabes dorsalis has
become rare with the advent of modern antibiotics, however it has experienced a re-
emergence due to the human immunodeficiency virus (HIV) epidemic.
Subacute combined degeneration

Subacute combined degeneration (SACD) is caused by a deficiency of vitamin B12,
but both copper and zinc deficiencies produce a very similar clinical picture. Vitamin
B12 deficiency first affects the peripheral nerves, causing a painful neuropathy. As it
progresses it then affects the DC causing a sensory ataxia. Eventually, the corticospinal
tract becomes involved, resulting in an UMN type weakness. On examination, patients
have weakness and spasticity from the UMN type lesion. However, they are areflexic
because by the time the corticospinal tract is involved, the diffuse neuropathy is so
advanced that muscles can no longer respond to the reflex stimulus.
Poliomyelitis
While the poliovirus endemic of the first half of the 20th century is over, poliomyelitis
remains a common topic for examinations. Poliomyelitis causes an acute flaccid
paralysis, due to attack on the anterior horn cell (AHC) in the spinal cord. This causes
a typical LMN picture; atrophy and wasting of muscles, decreased tone, and significant
weakness. Due to the extreme weakness, patients lose their reflexes, as the muscles can
no longer respond to the reflex stimulus. Initial treatment was mainly supportive and led
to the development of the infamous “iron lung,” until a vaccine became available in the
1950s.
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Case 3: The 21-year-old man who was near death 191
Case 3: The 21-year-old man who was near death
You have decided to do some locum work to help pay down your medical school debt
and are stationed in a remote region of Northern Ontario in Canada. All of a sudden
a horde of twenty–somethings burst through the Emergency Department’s doors and
demand you immediately see their friend, as they are convinced he is near death.
You find a 21-year-old man who seems to be clutching his right arm in pain, but
is able to tell you his story. He got lost on a camping trip with his fellow overzealous
twenty–somethings, and climbed a tree to get his bearings (you don’t bother to ask how
much alcohol was involved, as the tiny Emergency Department room now reeks of it).
Unfortunately he fell out of the tree but he was able to briefly grab a branch with his right
hand, slowing his descent. He rejoined his friends several hours later and then realized
that he couldn’t move his right arm (which you suspect he discovered when he went to
grab another beer bottle). At this point, one of his friends noticed his pupils were not
equal and insisted he come to the Emergency Department.
Initial x-rays are negative for any fractures, so you wonder about a neurological problem.
His language is normal. He has full visual fields, but his right pupil is 2 mm wide and
his left pupil is 3 mm wide. You turn off the lights and the right stays 2 mm, and the left
becomes 4 mm. He has full extraocular eye movements. Sensation in the face is normal
and he does not have a facial droop. His palate and tongue are midline. You move onto
the arm and notice that the right shoulder is red and inflamed. In addition, the right
arm seems fixed in an odd posture with the wrist hyperflexed. Formal power testing
is recorded below. His bicep reflex is decreased, but all other reflexes are normal. His
tone was decreased in the right arm but normal elsewhere. He had downgoing toes. His
sensory examination shows a loss of pinprick over the entire lateral aspect of the right
arm. Coordination was not tested in the left arm, due to loss of strength, but was normal
everywhere else.
Power Examination Where is the lesion?

Right Left What is going on here?
Deltoid 3 5
Bicep 4- 5
Tricep 5 5
WE 3 5
WF 5 5
FE 5 5
DI 5 5
FF 5 5
EP 5 5
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Case 3: Findings
Some individual figures adapted from Waxman SG. Clinical

Neuroanatomy. Lange, New York, 2013.
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Case 3: Solution
Our patient complains of arm weakness in the context of decreased right arm tone and a
decreased biceps reflex. This strongly suggests a LMN type problem, and we can conclude
that our lesion lies in the peripheral nervous system (PNS).
Possible localizations include a radiculopathy, plexopathy and neuropathy.
2. Do the symptoms correspond to a single myotome and dermatome?
Checking our table of dominant myotomes (Fig. 5.5) we see that the deltoid is innervated
by C5. However, both the bicep and extensor carpi are innervated by C6. This implies that
dysfunction of a single nerve root can’t cause our patient’s presentation.
3. Does the pattern of symptoms correspond to a single nerve?
In this case the three muscles that are weak correspond to three different nerves; the deltoid
is innervated by the axillary nerve, the bicep is innervated by the musculocutaneous
nerve and the extensor carpi are innervated by the radial nerve.
We can safely conclude that our patient’s symptoms are not due to a neuropathy.
By process of elimination we conclude that our patient has a brachial plexus problem.
Our patient’s muscle weakness and sensory loss are explained by a lesion to both C5 and
C6. The only place where C5 and C6 run together without the involvement of C7, C8 and
T1 occurs in the Upper Trunk, which is our final localization.
This is also called an Erb–Duchenne Palsy, and is most commonly seen in newborns
due to a traumatic delivery affecting the plexus, but can happen whenever traction is
placed on the shoulder, as in our case. Paralysis of the deltoid, bicep and extensor carpi
cause the “Bellman’s tip” posturing of the arm (so called, as back in the 1870s when it
was initially described, it was a social faux pas for the bellman or waiter to be facing the
patron when receiving a tip).
Now don’t worry, we haven’t forgot about the pupils. Our patient has an anisocoria
(unequal pupil size) whose difference is greater in dark than in light. This dysfunction
is known as Horner’s syndrome, which we will cover more in detail soon. Horner’s
syndrome is caused by a lesion to the sympathetics, and is another clue that the lesion,
in this case, must lie in the brachial plexus.
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Figure 7.3 Autonomic Neurotransmitters
Ach: acetylcholine ; NE: norepinephrine.
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Clinical Pearl: Autonomic Neurotransmitters
As we mentioned in Chapter 1, neurons communicate with each other at a synapse

through various chemicals called neurotransmitters. Sadly, the nomenclature about
these neurotransmitters is both unwieldy and largely redundant, which often causes
confusion. We’ll turn our attention to them now.
There are two principal neurotransmitters employed by the nervous system; acetylcholine
(Ach) and norepinephrine (NE). If a neuron releases Ach it is said to be cholinergic. If it
releases NE it is said to be adrenergic.
Let’s consider the motor, parasympathetic and sympathetic branches of the nervous
system.
We’ll begin with the motor system as it’s the simplest. The LMN innervates a muscle.
To communicate with it, the LMN releases neurotransmitters into the neuromuscular
junction (NMJ). This neurotransmitter is Ach, and it causes the muscle to contract.
Recall that the autonomic system is composed of two neurons; the preganglionic neuron
and the postganglionic neuron. The parasympathethic system is exclusively cholinergic;
both the preganglionic neuron and the postganglionic neuron employ Ach.
The sympathetic system has evolved to be more complicated. The preganglionic neuron
uses Ach as its neurotransmitter. While the vast majority (about 98%) of the postganglionic
neurons of the sympathetic system uses NE as their neurotransmitter. However, some
postganglionic neurons that innervate sweat glands use Ach as their neurotransmitter.
Waiting for chemicals to diffuse across the NMJ is a slow process. The adrenal glands
produce NE which is needed immediately upon a dangerous “fight or flight” situation
occurring. Thus, for the adrenals, the sympathetic system only employs one single
neuron. That neuron releases Ach to the adrenals, which then release NE directly into
the bloodstream.
Neurotransmitter receptors are named according to what chemicals they respond

to. There are actually two Ach receptors; a nicotinic acetylcholine receptor and a
muscarinic acetylcholine receptor; while they both respond principally to Ach, they
also respond weakly to nicotine and muscarine, respectively. The motor system’s Ach
receptor is the nicotinic subtype. For the autonomic nervous system the preganglionic
neuron is always nicotinic. The postganglionic neuron in the parasympathethic system
is muscarinic. The postganglionic neuron that innervates the sweat glands is muscarinic.
Finally, the single neuron that innervates the adrenal gland is nicotinic.
Knowing which Ach receptors are nicotinic and which are muscarinic is important
because certain drugs preferentially affect one type of Ach receptor.
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Case 4: The 71-year-old man who slurred his words 197
Case 4: The 71-year-old man who slurred his words
You are about to sit down to a difficult conversation with a patient’s family when you are
paged over to the cardiac catheterization lab. There, a particularly pale and distressed
cardiology fellow tells you that the 71-year-old man he has just performed a coronary
angiogram on is now complaining of slurred speech.
When you talk to the patient, you confirm the cardiologist’s finding of dysarthria.
Despite struggling with pronunciation you find his speech to be coherent and said at an
essentially normal rate. He is able to understand everything you say to him and is able to
repeat. Examining his CN you find his pupils and eye movements are normal, and he has
full visual fields. He does not have a facial droop and facial sensation is normal. However,
when he sticks his tongue out, you find that it is deviated sharply to the left. Formal power
examination is recorded below, but he is weak on the right. His reflexes are 3+ on the
right, and he has an upgoing right toe. Tone is normal. Sensory examination to pinprick
was normal. However, he complains of right sided vibration loss in the arms and the legs.
Coordination testing was felt to be normal given the patient’s weakness.
Power Examination
Right Left
Deltoid 4 5
Bicep 4 5
Tricep 4- 5
WE 4- 5
FE 4- 5
HF 4- 5
KE 4- 5
KF 4- 5
ADF 4- 5
APF 4 5
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Case 4: Findings
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Case 4: Solution
Our patient has weakness, increased reflexes and an upgoing toe, all indicative of UMN
type problem; our lesion lies in the CNS. Likely, the lesion is so acute that he has not had
the chance to develop increased tone, which can take up to 48 hours.
Our patient’s weakness is caused by a corticospinal tract problem and his vibration
loss indicates a DC problem. Unfortunately, since both of these symptoms occur on his
right side, they are quite nonspecific. Possible localizations include the cortex, internal
capsule, brainstem and cervical spine.
A cervical spine lesion could not account for tongue deviation, so we know our lesion
has to be higher than that level. Our patient does not have any signs, such as aphasia, or
apraxia to suggest a cortical lesion. We must return to the tongue, which is innervated by
CN XII. Recall from Fig. 3.15 that the hypoglossal nucleus of CN XII is dually innervated.
Thus, only a LMN lesion of CN XII will produce clinical symptoms. The hypoglossal
nucleus lies in the medulla, which is our initial localization.
If you look carefully, you’ll realize our patient’s pattern of weakness is an Immediate
Localization of the brainstem. Our patient’s tongue deviates to the left, which means
that it is the left part of his tongue that is weak. However, he has right sided weakness
of the arm and leg. This is an example of crossed signs and can only be produced by a
brainstem lesion (see Chapter 3).
We can now draw the medulla in cross section and begin to fill in affected components.
Our patient has UMN weakness in the right arm and leg so the left corticospinal tract is
involved. Similarly, he has loss of vibration in the right arm and leg, so the left DC must
be affected as well. He has left sided tongue weakness, so the left hypoglossal nucleus is
lesioned.
Putting it all together, our final localization is the medial aspect of the left medulla; indeed,
the above is known as medial medullary syndrome. An embolus was likely dislodged
during the coronary angiogram and shot up into the vertebral artery, causing a stroke.
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Figure 7.4 Locked-in Syndrome
MLF: medial longitudinal fasciculus.
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Clinical Pearl: Locked-in Syndrome
Locked-in syndrome is a devastating condition in which patients are fully aware but have
nearly complete paralysis of the face, arms and legs. Patients lose all voluntary muscle
control with the sole exception of the ability to move their eyes vertically. This subtle
finding can easily be missed by inexperienced clinicians who erroneously conclude the
patient is in a coma.
Classically, locked-in syndrome is caused by bilateral lesions of the medial pons, which
is somewhat similar to the anatomy we have just described in the medial medullary
syndrome above. As an exercise, try to predict the structures that would be involved by
using the Rule of 4.
The following structures would be affected, as shown in Fig. 7.4:

1) Bilateral corticospinal tracts – leading to an UMN type paralysis of the arms and the
legs.
2) Bilateral corticobulbar tracts – leading to a LMN type paralysis of all the subsequent
CN in the medulla including:
• CN IX and CN X – resulting in the inability to swallow and talk.
• CN XI – resulting in the inability to shrug and move the head.
• CN XII – resulting in the inability to move the tongue.
3) Bilateral involvement of CN VII – resulting in LMN facial weakness.
4) Bilateral involvement of CN VI and the medial longitudinal fasciculus (MLF) – leading

to the inability to generate horizontal eye movements. Vertical eye movements, which
are initiated by muscles controlled by CN III in the midbrain, are unaffected.
5) Bilateral involvement of the DC – resulting in loss of proprioception and vibration.

Note that the ST is spared, allowing the patient to feel pain and temperature.
Locked-in syndrome is a terrible clinical condition caused by an opportune lesion

that affects a very densely populated neuroanatomical area. These lesions are typically
caused by a stroke. Locked-in syndrome has a dismal prognosis with 65% of patients
dying within 1 year due to respiratory failure.
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Case 5: Your 20-year-old brother, who had too much to drink 203
Case 5: Your 20-year-old brother, who had too much to drink
After getting the results of his MCAT, your brother, confident his future is now assured,
imbibed a significant amount of alcohol. You find him the next morning passed out, with
his right arm draped over a chair. Being the merciful soul you are, you decide to wake him
up and make him breakfast. When he does finally rouse, in addition to having a massive
hangover, he is shocked to find that he cannot use his right hand to grab the cup of
coffee you have generously brewed him. Startled, he tried to look at his right palm, but
couldn’t turn his right forearm.
In between sips of tea, you examine him carefully. His language examination is normal,
though his pronunciation is still somewhat slurred, but you chalk this up to his party the
night before. He has full visual fields, and his pupils are equal and reactive to light. He has
full eye movements, with no facial droop and his tongue and palate are midline. His formal
power examination is shown below, but his legs are normal strength. His reflexes are normal
bilaterally and he has downgoing toes. You feel confident that his tone is decreased in the
right arm. His sensory examination is normal, with the exception that he could not feel
the pin in the lateral aspect of the dorsal arm from the elbow to the hand. You feel that the
problems he has with coordination and gait are largely due to the alcohol, and dismiss them.
Power Examination
Right Left
Deltoid 5 5
Bicep 5 5
Tricep 5 5
SUP 3 5
PRO 5 5
WE 3 5
WF 5 5
FE 3 5
DI 5 5
FF 5 5
EP 3 5
ADP 5 5
FP 5 5
OP 5 5
ABP 5 5
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Case 5: Findings
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Case 5: Solution
Our patient has weakness of his right arm. An UMN type lesion is certainly possible, but
it would have to be rather small to affect the arm only. In addition, he does not have any
of the stigmata of UMN type weakness; his reflexes and tone are normal and his toes are
downgoing. It is thus more likely that he has a LMN type problem. Since his symptoms
arose overnight they are too acute to cause some of the findings associated with LMN
problems, such as fasciculations and atrophy.
Potential localizations include a radiculopathy, plexopathy or neuropathy.
Let’s check our table of dominant myotomes (Fig. 5.5); the only muscle on this table that
our patient has affected is his extensor carpi, which are innervated by C6. However, the
biceps are also innervated by C6, and our patient has normal power here. Given this we
must conclude that C6 is unaffected, and our patient does not have any dysfunction of
the nerve roots.
Overall, our patient has weakness of the following muscles:
• Extensor pollicis;
• Extensor digitorum;
• Wrist extensors (extensor carpi);
• Supinator muscle.
Put another way, our patient has weakness of the extensors of the fingers, thumb, and
wrist. Remember, the radial nerve supplies all of the extensors of the arm, so that would
seem to be a logical nerve to start with. Checking Fig. 5.7 we see that the radial nerve
also supplies the supinator, which is weak in our patient. In addition, the radial nerve’s
sensory area corresponds very well to our patient’s complaints. The radial nerve is our
initial localization.
Let’s draw the path of the radial nerve to see where our lesion is located. Working from
distal to proximal, we see we are at least at the level of the elbow, given the fact that the
superficial branch is involved, as our patient has sensory complaints. Extensor carpi is
weak so we know the lesion must be at least a little higher than the elbow. The last muscle
innervated by the radial nerve is the triceps, which is of normal power. Our lesion must
be below this. Thus, our final localization is somewhere about two-thirds of the way up
the radial nerve, below the branch that innervates the triceps.
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206 Case 5: Solution
In this case the lesion is in a part of the humerus called the spiral groove, which is a
frequent cause of external compression of the radial nerve. The key feature is that the
triceps are normal (both power and reflex). This is in opposition to the more common
compression at the level of the axilla, which would involve all of the muscles supplied by
the radial nerve.
Both compression at the spiral groove and at the axilla are examples of what is often
referred to as a Saturday Night Palsy, so named because the patient usually consumes
too much alcohol (or other drugs), and passes out in an atypical position. If this position
is such that his arm drapes over a hard surface, such as a chair, then the radial nerve is
typically compressed causing a transient loss of function.
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Figure 7.5 Carpal Tunnel Syndrome
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Clinical Pearl: Carpal Tunnel Syndrome
The most frequent mononeuropathy seen in clinical practice is compression of the

median nerve as it passes through the carpal tunnel in the wrist.
The first sign of carpal tunnel syndrome (CTS) is intermittent numbness and tingling
in the first three digits and the lateral aspect of the fourth digit. Patients may notice that
this occurs most often when the hand is flexed at the wrist, such as after typing, or upon
waking (most people have their wrists flexed during sleep). Eventually the numbness can
progress to significant pain. About 65% of patients will have symptoms in both hands.
If left untreated, patients will soon experience muscle weakness of the flexor pollicis,
opponens pollicis, abductor pollicis and the second and third digits of the flexor
digitorum. Note that because the lesion is at the wrist, the pronator teres is unaffected.
As the median nerve is the main innervator of the thumb, patients with long-standing
CTS will get significant atrophy of the thenar eminence.
Long-term atrophy of median supplied muscles will result in the hand taking on a
deformed shape called the Preacher’s Hand, or the Hand of Benediction, as it is similar
to configuration of the hand of a priest when he blesses someone. In this case, when a
patient tries to make a fist, he’ll be able to flex the 4th and 5th digits only; the second and
third digits will be hyperextended due to unopposed action of the extensor digitorum.
The thumb will be both extended and adducted due to the unopposed action of the
adductor pollicis (ulnar nerve) and the extensor pollicis (radial nerve).
First line treatment of CTS involves splinting of the wrist to keep it in a neutral position and
avoid compressing the median nerve. Corticosteroid injections can also be performed.
For truly refractory cases, surgical decompression can be performed.
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Case 6: The 34-year-old woman who had nothing wrong with her 209
Case 6: The 34-year-old woman who had nothing wrong with her
You receive a phone call from the Emergency Department asking you to come down
immediately and see a 34-year-old woman. You arrive and find her husband frantically
pacing about the room. He grabs you quickly and tells you, “you have to help her, we
have a 10-day-old baby at home.” Her husband states she was fine and talking to him
when she, mid sentence, screamed in incredible pain, put her hand to the right side of
her head, and then collapsed on the ground. When he went to pick her up, he noticed
she had cut herself quite badly on the left side. However, when he went to grab a towel
to cover the bleeding, she asked him what he was doing, and fervently denied anything
was wrong.
When you examine her she initially does not interact with you at all, despite you raising
your voice loudly. Your benevolent attending suggests you try examining her from
the other side of the bed. You walk to her right side and she greets you with a “hello
doctor.” On formal language exam, she is somewhat slow to respond as she complains of
significant pain, but you find her fluency, repetition and comprehension to be normal.
She interrupts you several times to ask to go home because “nothing is wrong with
me.” You see that her eyes are driven strongly to the right side. Her pupils are equal and
reactive to light. She does not register anything on the left part of her visual field. You
notice a facial droop on the left, but she is able to move her eyebrows. Her palate and
tongue are midline. She has normal power on the right, but when you ask her to move the
left side she fails to do so. However, you have noticed the left side moves spontaneously,
albeit weakly, as the two of you are talking. Your attending interrupts and grabs her left
hand and holds it infront of her face and asks “whose hand is this?”, to which she replied
“yours.” She then looks puzzled and demands to know how your attending got a hold of
her wedding ring. Her tone and reflexes are increased on the left side. She has an upgoing
left toe. She denies feeling any sensory feeling on the left side, despite you inflicting
significant painful stimulus. Coordination is not tested given her profound weakness on
the left.
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Case 6: Findings
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Case 6: Solution
Our patient has increased tone, reflexes and an upgoing toe also on the left, indicative of
an UMN type weakness; our lesion lies in the CNS.
Our patient has weakness of the left face, arm and leg, so we know the right corticospinal
tract is involved. She also denies any feeling on the left side, so the right ST is affected as
well. This doesn’t give us much information to go on; potential localizations include the
cortex, internal capsule and brainstem.
Since our patient is able to lift her eyebrows, we know she has an UMN type facial
droop, and our lesion must be above the level of the pons. Our patient has some very
odd symptoms on her left side, which we will cover in a moment. Her eyes are driven
strongly to the right. Since the FEF drive the eyes to the contralateral side, this implies
that either the left side is hyperactive (commonly see in a seizure), or the right side is
hypoactive, due to some sort of destructive lesion. Our patient’s presentation is not in
keeping with a seizure; we can conclude that the right FEF are not working, and thus our
initial localization is the cortex.
Reviewing our patient’s symptoms we know that the right motor and sensory cortices
are affected, as is our patient’s right FEF. The patient’s many left sided symptoms are all
just manifestations of hemi-neglect, which is often seen in right sided cortical lesions.
She continually states that nothing is wrong with her, despite her inability to move her
left arm. In fact she was even unable to recognize her left arm when it was shown to her
(a classic finding for hemi-neglect, as is the wedding ring confusion). It is often difficult
to distinguish a left sided visual field cut from left sided neglect, but the fact that she did
not register your voice and presence is more indicative of hemi-neglect. Her inability
to voluntarily move her left arm with preserved spontaneous movement is indicative of
an apraxia (which is an Immediate Localization to the cortex). Both hemi-neglect and
apraxia have multiple potential localizations, but it is safe to say that at least parts of
the frontal and parietal lobes are involved. Putting it all together it seems that our final
localization is almost the entire right hemisphere.
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212 Case 6: Solutions
In this case, the patient had an instantaneous and severe headache, commonly called
a thunderclap headache, which is usually indicative of a subarachnoid hemorrhage.
Indeed, this patient had a right sided MCA aneurysm that ruptured causing the
subarachnoid hemorrhage. For reasons that are not completely understood aneurysms
have a higher rate of rupture in the immediate postpartum period than during pregnancy.
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Figure 7.6 Levels of Consciousness and the Glasgow Coma Scale
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Clinical Pearl: Levels of Consciousness and the Glasgow Coma Scale
An aneurysmal rupture that does not receive prompt treatment can quickly cause
a decreased level of consciousness (LOC). There is a lot of confusion around the
terminology of the different levels of consciousness, so let’s review them now.
The reticular activating system (RAS) is a circuit in the brain that is responsible for
arousal and regulating the sleep wake cycle. Structural damage to this system will
produce a decreased LOC. The chief components of the RAS include the hypothalamus,
thalamus and the reticular formation in the midbrain.
There are several distinct levels of consciousness that one should be familiar with. We’ll
begin with the most depressed state, coma, and work our way up from there.
A coma is a state in which the patient is completely unresponsive and unarousable, even to
painful stimuli. Primitive brain reflexes may or may not still be present. A vegetative state
is where the patient gains the “vegetative” function of sleep wake cycles and has periods
where his or her eyes are open. However, any “responses” they show are purely reflexive
and they have no awareness of their environment. It is a true case of “the lights are on but
no one is home.” A patient who is stuporous is one that requires painful stimuli in order stay
awake. The obtunded patient is more alert than this and only requires verbal stimuli to stay
awake. Drowsiness is a subjective term that usually corresponds to a patient who is fully
alert but responds slower than the examiner would like. Beyond this patients are fully alert.
The above descriptors can be somewhat cumbersome in emergency situations when

information needs to be communicated quickly; to remedy this the Glasgow Coma Scale
was designed, as shown in Fig. 7.6. It is scored from 3 to 15; the minimum score is not 0.
The maximum score is 4 for eye opening, 5 for verbal response and 6 for motor response.
It can remembered using the following mneumonic:
• We test movement of the EYES (4 letters = max score 4);

• We test how VOCAL someone is (5 letters = max score 5);
• We test how MOBILE someone is (6 letters = max score 6).
The scoring systems for eye opening and verbal response are fairly self-explanatory. The
motor scoring can be a source of confusion. A score of 6 means the patient obeys you
perfectly. A score of 5 means that when you apply a painful stimulus, the patient swats at
you. A score of 4 means that the patient will try to withdraw the limb where you are applying
pain. A score of 1 indicates that there is no response by the patient to painful stimuli.
The postures associated with a score of 3 or 2 are called decorticate and decerebrate,
respectively. They are shown in Fig. 7.6 and sometimes also called flexor response, and
extensor response, respectively, given the position of the arms.
They are both indicative of severe brain damage and carry a guarded prognosis.
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Case 7: The 26-year-old woman who collapsed 215
Case 7: The 26-year-old woman who collapsed
You and your senior resident have just finished seeing a patient in the Emergency
Department and are looking forward to getting some much needed rest, when a
paramedic stops you and asks you take a look at another patient they are just wheeling
in. The paramedics were called by a bystander who saw a young woman collapse while
waiting to cross the street. The paramedics are quite concerned because her right pupil
is large and unreactive to light.
Your senior resident lets you examine the patient as she watches. When you find the
patient, she is stuporous and, by definition, only responds to pain. This certainly limits
your neurological exam, but you can still glean a fair amount of information. In order to
look at the right pupil, you have to lift her right eyelid as it is quite ptotic compared to
the left side. Once you do, you confirm the paramedic’s finding of a large, dilated pupil.
However, you do find that it reacts to light, just not as much as the left pupil. Since your
senior resident is watching, you note the size of each pupil in dark and light conditions,
which is recorded below. The right eye appears pulled to the right side and appears lower
than the left one. It cannot adduct or move upward. She does not appear to have a facial
droop. You open her mouth and see that her tongue and palate are midline. On motor
exam, she has normal tone, her reflexes are 2+ throughout and she has downgoing toes.
She cannot participate in formal power testing, but she moves all four limbs to painful
stimulus, which tells you that if weakness is present, it is not severe. Sensory testing
beyond the perception of pain is not possible, nor is coordination testing.
Pupil Examination
Dark Conditions Light Conditions
Right: 6mm Right: 5mm
Left: 4mm Left: 2mm
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Case 7: Findings
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Case 7: Solution
This case highlights one of the very few areas of neuroanatomy that should be committed
to memory. Because of this, in addition to the fact that our patient has no long tract signs
whatsoever, we make a break from our traditional localizing algorithm (though it would
still work for this case; if you don’t believe me, give it a try).
Our patient presents with an anisocoria (pupillary asymmetry). As we saw in Fig. 3.6,
pupillary size is controlled by the balance of forces from the sympathetics, which act
to dilate the pupil, and the parasympathetics, which act to constrict the pupil. The
sympathetics are carried to the pupil by CN V1 and the parasympathetics are carried by
CN III.
A lesion to the parasympathetics will cause the constrictive force to the pupil to diminish;
the sympathetic dilatory force will be largely unchecked resulting in a large pupil that
barely constricts (if at all) to light. It seems that this matches the symptoms of our patient
in her right eye! What about the other symptoms of the right eye?
We see that our patient has severe ptosis of the right eyelid. The levator palpebrae
superioris is the main muscle responsible for eye opening (the other is Muller’s Muscle
which is innervated by the sympathetics, but it only plays a minor role) and is also
innervated by CN III. Our patient’s right eye appears “down and out.” The resting position
of the eye is determined by the net balance of the relative contributions of the muscles
that surround it. If the eye is being pulled down and out, then the lateral rectus (CN VI)
and the superior oblique (CN IV) muscles are unopposed. Checking Fig. 3.7 we see that
all the weak muscles are innervated by CN III.
It would appear that our lesion is somewhere along the path of CN III. The exact location
of the lesion can’t be determined but given the patient’s presentation it is likely near the
brainstem, as brainstem compression can cause changes in levels of consciousness. In
this case the patient had a rupture of an aneurysm of the PCOM artery, which caused
immediate compression of CN III and her subsequent presentation.
The triad of a mydriatic (dilated) pupil, ptosis of the eyelid and the eye
appearing “down and out,” represents a CN III palsy, and should be committed
to memory.
In this case, identifying the CN III palsy was quite obvious; however, as we’ll see shortly,
there can be partial CN III palsies that are not accompanied by the eyelid ptosis and eye
K25928_C007.indd 217 12/01/2017 12:18

position changes. The pupil may still react to light and only be subtly different than the
unaffected pupil. How do you approach the case then?
The key is to note the pupillary sizes in light and dark, and see under which conditions
the anisocoria is greatest. Let’s use our example above. In the dark the anisocoria
between the two pupils is 2 mm (6 mm − 4 mm). In the light, the anisocoria has grown
to 3 mm (5 mm − 2 mm). The anisocoria is greatest in the light; the light conditions
test the integrity of the parasympathetic system. Since the difference is greatest here, we
can conclude that there is a parasympathetic problem, and that the larger pupil (which
should be constricting, but isn’t) is the dysfunctional one.
Stated another way:
Anisocoria greater in light conditions than dark conditions represents a CN III

palsy, and the larger pupil is the abnormal one.
K25928_C007.indd 218 12/01/2017 12:18

Figure 7.7 Medical vs. Surgical CN III Palsies
ACOM: anterior communicating artery; MCA: middle cerebral artery; PCOM: posterior communicating
arteries.
Adapted from Kline LB and Foroozan R. Neuro-Ophthalmology Review Manual. Slack Inc, Thorofare, NJ,
2013.
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Clinical Pearl: Medical vs. Surgical CN III Palsies
As we have just seen, a complete CN III palsy consists of a dilated, unreactive or minimally
reactive pupil, severe ptosis of the eyelid, and an eye that is “down and out”, due to the
unopposed actions of the lateral rectus and superior oblique muscles. Such patients are
said to have a “complete” CN III palsy, since the entire triad is present. However, a partial
palsy is also possible. There are two types of partial palsies, as shown in Fig. 7.7; in order
to understand them we need to review the anatomy of CN III.
Somatotopically, the motor function (eye movement and eye opening) of CN III is located
in the central part of the nerve. The parasympathetic fibers line the outside of the nerve.
Patients with vascular risk factors, such as hypertension and poorly controlled diabetes,
often infarct the central part of CN III. In doing so, the parasympathetics are spared, as
they have a different vascular supply. These patients present with eyelid ptosis and an
eye that is “down and out,” but the pupils are of equal size. Clinically, this is often called a
medical CN III palsy, as the management is medical optimization of vascular risk factors
in order to prevent future infarcts.
This is in contrast to a surgical CN III palsy. In this case, an expanding mass (often feared
to be a ruptured posterior communicating arteries (PCOM) aneurysm, as in our case)
extrinsically compresses CN III. If patients present very soon after aneurysm rupture,
only the parasympathetic component of CN III is affected; patients will have an enlarged
pupil but full eye movements and no eyelid ptosis. As the pressure increases, they rest of
the nerve will be compressed, leading to the full triad of a “complete” CN III palsy.
Whenever a patient presents with an anisocoria, clinicians fear that the enlarged pupil
represents a CN III palsy that has occurred due to a ruptured PCOM aneurysm. This is
for good reason; it carries a mortality rate of 50% and of those that do survive, 30% are
so neurologically impaired they require nursing home care. About 5% of the general
population has an unruptured cerebral aneurysm; of these people, 20% will have
multiple aneurysms. The most common type are saccular aneurysms, also called berry
aneurysms. These aneurysms have a distinct neck, and typically occur at the branch
points of the cerebral circulation. Anterior communicating artery (ACOM) and PCOM
aneurysms are the most common type, at about 30% each. The next most common occur
at the branching of the MCA in the Sylvian fissure and represent about 20%.
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Case 8: The 61-year-old woman with the large pupil 221
Case 8: The 61-year-old woman with the large pupil
Several days ago you admitted a 61-year-old woman with a transient ischemic attack
(TIA), which caused some temporary right arm weakness. A computed tomography
(CT) angiogram showed 88% stenosis of the left internal carotid artery, so she underwent
left carotid endarterectomy. She seemed fine post operatively. While you are rounding,
you receive an urgent page from the medical student from the previous case... he states
that the patient’s right pupil is enlarged. He is worried that her brain is herniating and
wants to call neurosurgery and the ICU.
When you arrive, you find a now very worried but completely alert patient. Language
examination shows normal fluency, comprehension and repetition.
Examining the eyes, you see that indeed, her left pupil is 2 mm in diameter, and her right
pupil is 3 mm. Both react to light. When you shut off the light, her left pupil remains
2 mm, but her right becomes 4 mm. You question whether she has a mild ptosis of the left
eyelid. She does not have a visual field defect, and she has full eye movements. She does
not have a facial droop and her tongue and palate are midline. Her motor exam, including
tone, reflexes and power, are normal. Sensory examination is normal to pinprick and
vibration. Her coordination examination is normal.
After the previous case, the medical student read all about “partial” CN III palsies and is
quite happy he identified it early before the patient had a “complete” palsy. He picks up
the phone to page neurosurgery but you stop him. You reassure both the medical student
and, more importantly, the patient, that she is not dying, and that the problem will likely
get better in a few days without any need for treatment.
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Case 8: Findings
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Case 8: Solution
Since we don’t have any long tract signs, and this case seems eerily similar to the previous
one, we’ll again depart from our traditional localization algorithm.
Once again, the patient has an anisocoria; this means that there is a problem either
with the sympathetic innervation (pupillary dilation) or parasympathetic innervation
(pupillary constriction).
There is an important subtlety to note before we begin our analysis; in this case we do not
even know which pupil is abnormal. The medical student has assumed the worst and is
fearful that the one on the right is abnormal because it is enlarged. In fact, the left side is
more likely to be abnormal as there is a slight ptosis of the eyelid on that side. However,
many people will have a slight eyelid ptosis if you look hard enough, so this is hardly
reliable.
We mentioned in the last case that the pupils should be examined both in light conditions
and dark conditions. If the anisocoria is largest in light conditions, this represents a
failure on behalf of the parasympathetic system to constrict. It turns out that the corollary
is also true. If the anisocoria is largest in dark conditions, when the sympathetic system
should most be active, then there is a lesion to the sympathetic system and the smaller
pupil (which should be dilating, but isn’t) is the abnormal one.
Let’s examine our case. In the light, when the parasympathetics are active, the anisocoria
is 1 mm (3 mm − 2 mm). In the darkness when the sympathetics are active, the anisocoria
has increased to 2 mm (4 mm − 2 mm). The smaller pupil, the left one, is the abnormal
one.
Stating it another way:
Anisocoria greater in dark conditions than light conditions represents a

sympathetic problem, and the smaller pupil is the abnormal one.
A lesion to the sympathetic system also explains the mild ptosis; the sympathetic system
innervates Muller’s muscle, which is one of the muscles response for opening the eye.
Lesions of the sympathetic system result in a clinical triad called Horner’s

syndrome: miosis (small pupil), ptosis of the eyelid, and anhidrosis (lack of
sweating). The sympathetics do not decussate so this all occurs on the ipsilateral
side of the lesion.
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Ideally, one would like to localize the lesion further; the sympathetic pathway is quite
vast, as shown in Fig. 3.6, and the causative lesion could lie in the brainstem, spinal cord,
or periphery. However, this requires pharmacological testing, which we will turn our
attention to next.
In this case, the patient developed a Horner’s syndrome due to the local manipulation
of the sympathetic fibers that lay on the carotid artery during the endarterectomy
procedure, which is a known complication. It resolved several days later. The medical
student never confused a CN III palsy with a Horner’s syndrome again.
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Figure 7.8 Horner’s Syndrome
NE: norepinephrine.
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Clinical Pearl: Horner’s Syndrome
As we mentioned, the triad of eyelid ptosis, miosis (small pupil) and anhidrosis (lack
of sweating) is referred to as Horner’s syndrome and is caused by interruption of the
sympathetic system.
As you can see from Fig. 7.8, the sympathetic system is divided into three neurons. The 1st
order neuron begins in the hypothalamus and synapses in the gray matter of the spinal
cord at the C8/T1 level. The 2nd order neuron travels from there into the sympathetic
chain and synapses in the superior cervical ganglion. Finally, the 3rd order neuron
travels from the superior cervical ganglion, up the internal carotid artery and into the
end muscles.
Certain chemical tests can be used to both confirm a Horner’s syndrome, and also help
localize between 1st order, 2nd order and 3rd order lesions. In the era of MRI they have
fallen somewhat out of favor but are still used by many clinicians. The mechanisms
of these tests are complicated and beyond the scope of this text but the results can be
remembered easily enough.
The first step is to confirm that a Horner’s syndrome is present. To do this 10% cocaine eye
drops are instilled into both eyes. One can think of cocaine as an irritant to the eye; any
irritant will activate the sympathetic system. In the normal eye the sympathetic system
activates and the pupil dilates. In the abnormal eye the sympathetic system is lesioned,
so the pupil remains unchanged, confirming the Horner’s syndrome.
Hydroxyamphetamine drops (1%) can help us to localize where the lesion is along
the sympathetic pathway. Recall from Fig. 7.3 that the sympathetic system uses the
preganglionic neurotransmitter Ach (1st and 2nd order neuron), and the postganglionic
neurotransmitter NE (3rd order neuron). Hydroxyamphetamine acts as a replacement for
Ach and can be used to stimulate the 3rd order neuron.
Let’s consider two scenarios. In the first, there is a lesion to the 1st or 2nd order neuron. In
this case the 3rd order neuron can still respond to Ach, but it is not being secreted by the
2nd order neuron. Here, Hydroxyamphetamine will stimulate the functioning 3rd order
neuron to release NE and the pupil will dilate.
What if there is a lesion of the 3rd order neuron? The 1st and 2nd order neurons
appropriately secrete Ach, but the 3rd order neuron cannot respond to it. In this case
Hydroxyamphetamine will have no effect and the pupil remains constricted.
Since 1st and 2nd order neurons both employ Ach, there is no pharmacological way to
differentiate between the two.
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Case 9: The 39-year-old woman who didn’t feel her sunburn 227
Case 9: The 39-year-old woman who didn’t feel her sunburn
You’re quite puzzled by a 39-year-old woman whom you are seeing early one morning.
She previously enjoyed perfect health other than being the victim of an assault 15 years
prior. She states that about 8 months ago she began to feel numbness and tingling on
the 4th and 5th digits of her hands bilaterally. Her mother told her it was carpal tunnel
syndrome and she dismissed it. On a recent trip to the beach, she fell asleep and
inadvertently received an overzealous tan all over her body. Upon waking she was startled
to realize that she only felt the burn in her legs and abdomen; despite being sunburned
over her chest, she did not feel any pain in that area. She grew concerned and drove to
the Emergency Department, where she now sits across from you.
When you examine her, you find normal fluency, comprehension and repetition of
language. CN examination reveals equally sized pupils, full eye movements, full visual
fields, no facial droop, normal facial sensation and a tongue and palate that are midline.
Motor examination reveals normal reflexes and normal tone. Her power examination is
totally normal in the legs, but her arms show mild distal weakness, as recorded below.
Her toes are downgoing. Her vibration testing is normal, but her pinprick examination
is confusing. When you run the pin down her trunk, she feels it normally, but then states
it becomes dull just below shoulder level. It remains dull until just below the level of the
breasts, where it becomes sharp again. The pin is also dull over the entire medial aspect
of both arms as well as the 4th and 5th digits of the hand. Finger to nose and heel to shin
coordination testing is normal.
Power Examination
Right Left
Deltoid 5 5
Bicep 5 5
Tricep 5 5
WE 5 5
WF 5 5
FE 5 5
FF 4 4
DI 4 4
EP 4 4
FP 4 4
OP 4 4
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Case 9: Findings
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Case 9: Solution
Our patient has weakness in her hands and thumbs; unfortunately there are no other
signs such as reflexes or tone to help guide us, so we cannot classify the pattern.
Since the motor system does not help us, we must turn our attention to the sensory
symptoms. Thankfully these efforts do not go unrewarded, as the pattern of sensory loss
is one we examined in an Immediate Localization! Our patient complains of a sensory
band between the shoulders and just below the breasts; this can only be produced by a
spinal cord lesion (see Chapter 4). Thus our initial localization is the spinal cord.
The highest sensory symptom our patient experiences is the loss of pinprick just below
shoulder level. She also complains of loss of pinprick down the medial aspect of the arm.
Consulting our dermatome map (Fig. 5.15) we see that these areas correspond roughly
to the C8/T1 area. This is also consistent with the weakness she has in her hands and
thumbs, as these muscles are innervated by C8 and T1. We can refine our localization to
the C8/T1 level of the spinal cord.
Knowing that the lesion is at C8/T1, we can draw the cross section of the cord at that
level. Our patient has bilateral loss of pinprick, which implies the ST is involved. The
only lesion that can produce this lies at the very heart of the gray matter in the spinal
cord. As we reviewed in Fig. 4.4, sensory neurons enter the cord and decussate to the
contralateral ST. A lesion in the central grey matter would block this decussation and
produce symptoms at the dermatome. As the lesion grows, it extends longitudinally to
involve more and more dermatomes until a “band” of sensory loss occurs, as in this case.
Eventually it begins to grow axially and encompasses the AHC, causing bilateral LMN
type weakness. In this case that was the C8/ T1 AHC, which caused the hand weakness.
The pattern described here is known as central cord syndrome. It is most commonly
caused by a syringomyelia, which is a fluid filled cavity that forms many years after an
initial trauma; its pathogenesis is far from understood.
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Figure 7.9 Central Cord Syndrome
DC: dorsal column; LMN: lower motor neuron; ST: spinothalamic tract; UMN: upper motor neuron.
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Clinical Pearl: Central Cord Syndrome
Central cord syndrome is one of the most common types of spinal cord lesions seen
in clinical practice. As mentioned, it is usually due to the formation of a syringomyelia
which occurs in response to a long preceding trauma. The cervical spine is particularly
prone to syringomyelia formation, usually from an injury involving hyperextension of
the neck, such as the “whiplash” injury that occurs in motor vehicle accidents. Reviewing
the symptoms produced by an expanding central cord lesion is a great way to cement our
knowledge of spinal cord anatomy, so we will do that now.
Stage 1: Small lesion

Let’s consider a small lesion occurring at C5. The lesion is initially so small that the
only thing it does is interrupt the decussation of sensory neurons on the way to the
contralateral ST. This results in a bilateral loss of pinprick and temperature in the C5
dermatome distribution, as we have outlined in the figure.
Stage 2: Longitudinally growing lesion

Central cord lesions tend to expand longitudinally before growing axially. Some time
has elapsed and our lesion now extends down to T4. It still does not involve any of the
long tracts but it now interrupts the decussation of sensory neurons from multiple levels
(in this case C5–T4). There is now a band of sensory loss (sometimes called a suspended
sensory loss) to pinprick and temperature. Another way to think of it is that the patient has
two sensory levels, one at C5 and the other at T4, and there is a zone of loss in between.
The sensory loss depicted in Fig. 7.9 (Stage 2), involving the trunk and the arms, is
sometimes called a “cape” or “shawl” loss, as it traces the outline of someone wearing a
small cape or shawl.
Stage 3: Transversely growing lesion

Now our lesion has been allowed to grow transversely. All aspects of the DC are affected,
causing proprioceptive and vibration loss below the level of the lesion. The AHC are
enveloped bilaterally, causing a LMN type weakness in the C5 muscles. The lesion
envelops most of the ST and corticospinal tracts on both sides. This causes a near complete
loss of these functions below the level of the lesion. However, re-familiarize yourself with
Fig. 4.5 and look at what is NOT involved; the sacral elements of the corticospinal and
STs. They lie the most lateral and so will be the last to be affected. This is referred to as
“sacral sparing” as the patient now has, what appears on first glance, to be a complete
loss of neurological function from the neck down but retains sensory and motor function
of the bowel and bladder.
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Case 10: The 49-year-old man who was told he had carpal tunnel syndrome 233
Case 10: The 49-year-old man who was told he had carpal tunnel
syndrome
You are asked to see a 49-year-old man with a bizarre sounding history. He tells you that
about 2 years ago he started to notice difficulty typing with his left hand. He started to
drop objects from it and was told he needed carpal tunnel surgery. He proceeded with
surgery but found that it didn’t help. He then found that the same thing began to happen
in his right hand. On the advice of a friend, he sought out a chiropractor who told him he
had a disc pressing on his cervical spine, but many rounds of chiropractic manipulation
failed to help. Around this time his wife began to notice that parts of his arms would
“twitch” excessively for a few moments, and then go back to normal.
When you examine him you find his language to be entirely normal. On CN examination
you find he has full eye movements, full visual fields, and pupils that are equal and
reactive to light. His facial sensation is normal and he does not have a facial droop. His
palate and tongue are midline, though his tongue seems to be unable to stay still. You
move onto his arms and find extensive atrophy, especially in his hands, worse on the left
than the right. You agree with his wife that his muscles seem to “twitch” in the upper part
of both arms. You examine his legs and find the same twitching is his right thigh and calf,
but none on his left leg. You wonder about some mild atrophy of his right quadriceps. His
power examination is shown below but he is quite weak other than the left leg, which is
normal. You expect to find decreased tone in his arms, but his tone is actually normal.
Furthermore he actually has increased reflexes in both arms. His tone is decreased in the
right leg but he has 2+ knee and ankle reflexes. His left leg has normal tone and 2+ reflexes.
He also has downgoing toes bilaterally. His sensory examination to pinprick and vibration
is completely normal. Coordination testing, given his weakness, is normal.
Power Examination
Right Left
Deltoid 4 4
Bicep 4 4-
Tricep 4 4-
WE 3 3
FE 4- 3
HF 4- 5
KE 4 5
KF 4 5
ADF 4- 5
APF 4 5
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Case 10: Findings
UMN: upper motor neuron; LMN: lower motor neuron.
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Case 10: Solution
This is a confusing case. The argument for both an UMN pattern and a LMN pattern can be
made. Our patient has atrophy of both arms, and the right leg, and has fasciculations of the
right side, all in keeping with a LMN pattern. However, he also has increased reflexes in the
arms and normal tone (preserved, or normal, tone or reflexes in the context of atrophied
muscle groups are considered to be signs of an UMN problem), suggesting an UMN pattern.
Our patient doesn’t have any sensory abnormalities to help us in our localization. When
you see a combined pattern of UMN and LMN weakness, only two possibilities exist:
• a focal lesion is affecting the brainstem or spinal cord in such a way that it produces
LMN weakness at the level of the lesion, due to interruption of the nerve roots, and UMN
weakness below the level of the lesion, due to interruption of the corticospinal tract.
• a diffuse disease process is targeting one aspect of the nervous system; in this case,
motor neurons in the AHC, causing the LMN findings and motor neurons in the
cortex, causing the UMN findings.
Before we say that there is a diffuse disease process affecting motor neurons, we must
make sure that a single focal lesion isn’t responsible for our patient’s symptoms. Since our
patient’s CN are normal, the only possible focal lesion would be in the cervical spine; this
could certainly cause both arm and leg symptoms. However, it is important to recognize
why this is NOT the case in this example.
A lesion to the cervical spine would produce LMN symptoms at the level of compression,
and UMN symptoms below the lesion. So we would expect our patient to have some
LMN symptoms in the arm (fasciculation of the upper arm and atrophy of the shoulders)
corresponding to the root involvement, and UMN symptoms below that (the increased
reflexes and preserved tone). So far so good.
But in the right leg the patient has fasciculations and atrophy, with downgoing toes.
These are signs of LMN disease. It is impossible for a lesion of the cervical spine to do
this; a cervical spine lesion can only cause UMN weakness of the legs (Fig. 4.10).
In this case a focal lesion is impossible. We are forced to conclude that this patient has
a disease process targeting the motor neurons. In this case that disease is amyotrophic
lateral sclerosis (ALS), which we now discuss.
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Figure 7.10 Amyotrophic Lateral Sclerosis
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Clinical Pearl: Amyotrophic Lateral Sclerosis
ALS, also known as Lou Gehrig’s disease after a famous case, is a devastating neurological
disorder that has little effective treatment despite tremendous investigation and study.
ALS exclusively targets motor neurons, so patients should only complain of weakness.
Any sort of sensory, coordination or autonomic findings on examination virtually
excludes the disorder.
ALS targets both the UMNs of the motor cortex and the LMNs of the CN nuclei in the
brainstem and the AHC in the spinal cord.
The El Escorial World Federation of Neurology criteria, drafted in 1994, are often
used to diagnose ALS. The criteria divide the body into four distinct regions, as shown
in Fig. 7.10. Each region corresponds to a different part of the neuraxis. It includes the
bulbar region, which corresponds to the brainstem, cervical spine, thoracic spine and
lumbosacral spine.
A definite diagnosis of ALS requires the combination of UMN and LMN findings present
in each of at least three regions. For example, the patient may have increased tone and
fasciculations in the leg (lumbosacral region), increased reflexes and atrophy of the
arm (cervical region), and an increased jaw jerk reflex and fasciculations of the tongue
(bulbar region). Under certain circumstances the patient can be diagnosed when they
only have UMN findings on clinical examination if they have additional evidence from
certain electrophysiological studies such as electromyogram (EMG).
On average, patients live about 3 years after being diagnosed. The mechanism of death
is usually aspiration pneumonia from bulbar weakness, or primary respiratory muscle
failure. Two interventions have been shown to prolong life; external ventilation devices,
such as bilevel positive airway pressure (BiPAP) machines, and the oral medication
Riluzole, a glutamate antagonist, which has been shown to increase survival by about
3 months.
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Case 11: The 68-year-old man with previous TIAs 239
Case 11: The 68-year-old man with previous TIAs
You are seeing a 68-year-old man with symptoms concerning for stroke. As the patient
is being offloaded from the ambulance, you talk to his daughter who says that her father
was seen for TIAs or “mini strokes” about 3 months ago, and was started on aspirin
and other medications. She states her father experienced two episodes of right sided
weakness with “garbled speech” and agitation. His daughter remembers to tell you, “he
had his neck arteries scanned.”
When you arrive you note that not only is he speaking nonsense but his speech is also
dysarthric. He says very little, and appears to have great difficultly saying any particular
word, which frustrates him greatly. When he does manage to get a word out, it appears
to be random. He cannot repeat a sentence. He does appear to understand what you’re
saying, which you find of great relief as you proceed with the rest of your neurological
exam. He has full visual fields and pupils that are equal and reactive to light. However,
his eyes are driven to the left and he cannot look to the right. You note a right sided facial
droop that spares the forehead. His tongue and palate are midline. Motor examination
shows increased tone on his right side, and he even has five beats of clonus at the right
ankle. Reflexes are 3+ in the right arm and leg. He has an upgoing toe on the right. Power
testing is shown below but he is weak on the right side. He also has impaired sense to
pinprick examination in the right arm and leg. Vibration could not reliably be assessed.
Coordination testing could not be carried out given his level of weakness.
Power Examination
Right Left
Deltoid 3 5
Bicep 4 5
Tricep 4- 5
WE 4- 5
FE 4- 5
HF 4+ 5
KE 4+ 5
KF 4 5
ADF 4+ 5
APF 4 5
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Case 11: Findings
B: Broca’s area; C: conception tract; MCA: middle cerebral artery; W: Wernicke’s area.
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Case 11: Solution
Our patient has all the stigmata of an UMN process; increased tone, increased reflexes,
an upgoing toe, and a pathological amount of clonus at the right ankle. We can safely say
that our lesion lies in the CNS.
Our patient has weakness and decreased sensation involving his right face, arm and leg.
This isn’t a lot of information to go on; possible localizations include the cortex, internal
capsule and brainstem.
Reviewing our symptoms, we see that our patient has an UMN facial droop, so we know
the lesion must lie above the level of the pons. However, his language examination reveals
an Immediate Localization; in addition to his dysarthria he is also aphasic. He has trouble
getting any words out (decreased fluency), and cannot repeat. However, understanding
is intact. This is a problem with the generation of language and corresponds to a
Broca’s aphasia. Aphasia can only be produced by a cortical lesion, which is our initial
localization.
Reviewing our patient’s symptoms, we see that he has weakness and sensory loss on the
right. The long tracts have decussated by the time they reach the cortex, so we know that
our patient’s right sided symptoms are produced by a lesion of the left cortex.
Broca’s aphasia is caused by a lesion in Broca’s area, which sits in the inferior part of the
frontal lobe.
Finally, our patient’s eyes are driven to the left. Remember that the FEF drive the eyes
to the contralateral side. Since his eyes are driven to the left, it means that nothing is
opposing the FEF on the right; the left FEF must be affected by the lesion.
Putting it all together, we see that almost the entire lateral aspect of the left frontal lobe
is involved. This territory is supplied by the superior branch of the MCA. Imaging later
revealed that this unfortunate fellow suffered a stroke in this location.
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Figure 7.11 Carotid Stenosis
Barnett HJ, et al. Beneficial effect of carotid endarterectomy in symptomatic patients with high grade carotid
stenosis. NEJM 1991;325:445– 453.
Brott TG, et al. Stenting vs endarterectomy for treatment of carotid artery stenosis. NEJM 2010;363:11– 23.
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Clinical Pearl: Carotid Stenosis
Plaque in the carotid arteries, as in this case, can often serve as a nidus for embolism in
the anterior circulation (anterior cerebral artery (ACA) and MCA territory), and is a
common cause of stroke or transient ischemic attack (TIA). A TIA, as the name implies,
occurs when an area of brain is deprived of blood, which causes neurological symptoms.
However, this blood supply is soon restored, leading to a resolution of symptoms and no
permanent neurological damage. All patients who present with an anterior circulation
TIA or stroke should undergo vessel imaging to see if there is significant plaque causing
a stenosis of the carotid artery.
This naturally leads to the question of how much stenosis of the carotid artery is
significant enough to warrant treatment? Further, should the treatment be aggressive
medical therapy or more surgical in nature?
These questions were answered in the landmark North American Symptomatic Carotid
Endarterectomy Trial (NASCET trial) in 1991. It demonstrated that for patients with a
stenosis occluding more than 70% of the diameter of the internal carotid arteries (ICA),
surgery was more effective then medical management; at 2 years, the rate of re-stroke
was 26% in the medical group and 9% in the surgical group. Still, this result has been
questioned in recent years, as medical treatment has advanced significantly over the last
25 years.
Note that the above was for symptomatic stenosis. It is only valid for patients who have
had an anterior circulation TIA or stroke believed to be caused by the carotid stenosis. It
cannot be generalized to asymptomatic patients.
Patients in the surgical arm underwent a carotid endarterectomy. This procedure was
first performed in 1954 and is shown in the bottom left of Fig. 7.11. The carotid artery is
clamped, and the brain is perfused via the collaterals in the Circle of Willis. The ICA is
then cut, and the plaque removed. Carotid stenting is a newer technique, which is less
invasive. In this procedure, a stent is fed up into the carotid artery and then deployed over
the plaque. Eventually, the body will cover the stent with a new layer of tissue, effectively
sealing up the plaque.
The Carotid Revascularization Endarterectomy Stenting Trial (CREST trial) compared

endarterectomy to stenting. It demonstrated that the two procedures are equally effective.
However, younger patients (< 70 years old) experienced fewer complications with stenting
and older patients (> 70 years old) had fewer complications with endarterectomy.
A trial comparing carotid stenting to medical management has yet to be performed.
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Case 12: The 55-year-old man with seizures 245
Case 12: The 55-year-old man with seizures
You are spending an afternoon catching up on some paperwork in the staff lounge when
you’re paged by an Emergency Doctor who says she needs you to come see a patient right
away. When you arrive, she tells you that a 55-year-old man came into the Emergency
Department with a 4-hour history of right sided weakness. She diagnosed him with a
left MCA stroke and was going to call you to come see him later that day, but she’s now
concerned that he’s having seizures and wants you to assess him immediately.
You find a quite obtunded patient whose responses to your questions are limited to a
short few words. Despite this, you feel that, while confused, he does not have any sort
of obvious language problem, and he does participate in your neurological exam. He
sounds dysarthric and his wife confirms that this is not his normal speech. He has full
visual fields and his pupils are equal and reactive to light. However, his eyes appear
driven to the right, and he cannot get them to cross midline in order to look left. Upon
close inspection you also notice a subtle droop of the entire face on the left hand side.
You ask the patient to raise his eyebrows, but he is unable to do so on the left side. The
tongue and palate are midline. On motor exam, you find increased tone in the right arm
and leg. He also has 3+ reflexes on the right. Formal power examination is shown below,
but he is weak on the right side. He has an upgoing toe on the right. Sensation is normal
to pinprick. Given his obtunded state, vibration testing isn’t possible. Coordination was
felt to be normal given the weakness.
Power Examination
Right Left
Deltoid 4+ 5
Bicep 4+ 5
Tricep 4 5
WE 4- 5
FE 4- 5
HF 4+ 5
KE 4+ 5
KF 4 5
ADF 4 5
APF 4 5
Where is the lesion? What is going on here? Why did the Emergency Doctor think the
patient was having seizures?
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Case 12: Findings
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Case 12: Solution
Our patient has increased reflexes, increased tone and an upgoing toe, all signs of an
UMN type weakness. Thus, we know that the lesion lies in the CNS.
In this case, our patient has right sided weakness of the arm and leg, and left sided weakness
of the face; this is an example of crossed signs, and is an Immediate Localization to the
brainstem (see Chapter 3).
Our patient has a facial droop affecting all of his face on the left side, including the
forehead. This is an example of a LMN type facial droop. A LMN facial droop can be
caused by a lesion to either the facial nerve itself (PNS) or to the facial nucleus and its
neurons, which are located in the pons (CNS). Since we know our lesion is in the CNS, we
can safely say it is the latter; our initial localization is the pons.
Since we know the location of our lesion, we can draw the pons in cross section.
Let’s fill in what we know. Our patient has UMN weakness of the right arm and leg, so the
left corticospinal tract is involved. In addition, he has left sided LMN facial weakness, so
the left facial nucleus must be affected.
Note how the facial neuron wraps around the abducens nucleus of CN VI. It would be
quite difficult to have a lesion to the facial nucleus and NOT involve CN VI. Let’s return
to our patient; he cannot initiate gaze to the left with either eye. Remember that the
abducens initiates horizontal gaze for both eyes (Fig. 3.9). So our patient also must have
left abducens nucleus involvement.
For this reason, a patient with a LMN type facial droop (CN VII) should always be
carefully assessed to see if they have an ipsilateral CN VI involvement (sometimes
referred to colloquially as “make sure seven doesn’t have six”).
This syndrome is called Millard Gubler syndrome, after the physicians that described
it. It can be associated with strokes of the basilar artery, which is likely what happened
here. We will now turn our attention to why the Emergency Doctor thought the patient
was seizing.
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Figure 7.12 Wrong Way Eyes
FEF: frontal eye fields; MLF: medial longitudinal fasciculus; PPRF: paramedian pontine reticular formation.
Top portion redrawn with permission from Greenberg D, et al. Clinical Neurology. McGraw–Hill Education,
New York, 2015.
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Clinical Pearl: Wrong Way Eyes
Voluntary eye movement is initiated by the FEF in the cortex. The FEF synapse with the
contralateral abducens nucleus, which is responsible for initiating horizontal gaze. In
doing so, the left FEF drive the eyes to the right and vice versa.
Lesions of the cortex, such as in the common MCA stroke, damage the FEF. Let’s consider
what would happen if the left FEF was damaged from an MCA stroke (Lesion 1 in Fig. 7.12).
The right FEF would be completely unopposed and since the FEF drive the eyes to the
contralateral side, the eyes would drift to the left. The left MCA stroke would also damage
the left motor cortex, causing right sided weakness of the face, arm and legs. Thus, the
eyes are deviated to the opposite side of the weakness; clinicians sometimes remember
this by the inelegant saying “the eyes look away from the paralyzed side in disgust.”
However, the patient in our case had a lesion of the pons (Lesion 2 in Fig. 7.12). Review
his symptoms; his eyes were deviated toward his weak arms and legs, or the “wrong way”
compared to the much, much more common cortical lesion caused by the MCA stroke.
This is because the abducens nucleus initiates gaze to the ipsilateral side for both eyes;
the right CN VI nucleus initiates gaze to the right side for both eyes, via the MLF. Thus,
a lesion to the right CN VI nucleus would result in eyes deviated to the left side. A right
lesion in the pons affecting the corticospinal tract would also result in left sided weakness
as the corticospinal tract decussates in the medulla. Thus, the patient looks toward the
weak side, or the “wrong way.”
A seizure hyperactivates an area of the cortex (Lesion 3 in Fig. 7.12). What if our patient
was having a focal seizure that started in the left hemisphere? Then his left FEF would
be hyperactive and overcome the normal right FEF, and his eyes would be driven to the
right. Once the seizure spreads to the left motor cortex, it would cause right sided face,
arm and leg seizure activity. If this activity is prolonged, the muscles will continue to
seize until they’re totally exhausted and can no longer contract at which point they’d
appear weak. However, the eyes would still be deviated to the right. Thus the eyes would
look toward the weak side, or the “wrong way.” It was because of these “wrong way” eyes,
that the Emergency Doctor erroneously concluded that the patient was having a seizure
post stroke.
In the absence of a clinical seizure, “wrong way” eyes is another way to immediately
localize a lesion to the pons.
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Case 13: The 61-year-old man with the encouraging wife 251
Case 13: The 61-year-old man with the encouraging wife
You are seeing a 61-year-old man who reluctantly came to the Emergency Department
for right sided weakness. When you talk to him, he, with some gentle “encouragement”
from his wife, tells you he fell this morning getting out of bed because his right leg
wouldn’t work. He then went to grab his glasses but he found his right hand to be clumsy
and he dropped them. His wife thinks his speech is slurred but he disagrees. When
examining his chart, you notice multiple entries by physicians about poor compliance to
medications for his diabetes and high blood pressure.
His language examination shows normal fluency, comprehension and repetition. You
agree with his wife that he is dysarthric. CN examination reveals full visual fields, pupils
that are equal and reactive to light and he has full eye movements. He has a facial droop
on the right but he is able to move both eyebrows. His tongue and palate are midline.
Motor examination shows increased tone and 3+ reflexes on the right, with upgoing toe
on that side. His formal power examination is shown below but he is weak on the right
side. Sensory examination was normal to pinprick and vibration. Coordination testing
was felt to be normal, given the weakness.
As you walk out of the room, you glance at the monitor and note his blood pressure is
189/79.
Power Examination
Right Left
Deltoid 4+ 5
Bicep 4 5
Tricep 4- 5
WE 4- 5
FE 4- 5
HF 4 5
KE 4 5
KF 4- 5
ADF 4- 5
APF 4- 5
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Case 13: Findings
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Case 13: Solution
Our patient has increased tone and reflexes as well as an upgoing toe, which are all signs
of an UMN type weakness. Thus, we know that the lesion lies in the CNS.
Our patient’s sensory examination is normal, but he has weakness of the right face, arm
and leg. This pattern is nonspecific and could be caused by a lesion in the cortex, internal
capsule or brainstem.
A facial droop that spares the forehead represents an UMN CN VII lesion. As we’ve seen
previously, this means that the lesion must be above the level of the facial nucleus in the
pons. Unfortunately this is the only refinement we can make to our localization.
In this case, there are not any further symptoms to guide our localization. However, the
paucity of symptoms itself can suggest a localization. In order to cause such extensive
right sided weakness, a cortical lesion would have to be very large, such as in an MCA
stroke. However, our patient does not have any of the other symptoms we would expect
with such a large cortical lesion, like visual field defects, aphasia, apraxia or neglect. This
makes a cortical localization unlikely.
Small lesions in very neuroanatomically dense areas can present with significant
symptoms. In this case the patient had a stroke of the posterior limb of the internal
capsule. As we saw in Fig. 2.4, motor neurons to the face, arm and leg pass through this
very small area; hence, small lesions here can have devastating large effects. These types
of infarcts are called lacunar strokes and are quite common.
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Figure 7.13 Lacunar Strokes
AICA: anterior inferior cerebellar artery; PCA: posterior cerebral arteries; PICA: posterior inferior cerebellar
artery; SCA: superior cerebellar artery.
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Clinical Pearl: Lacunar Strokes
Lacunar strokes (Lacunar is Latin for “tiny lake”) are small infarcts that occur in
neuroanatomically dense areas of the brain. Despite their small size, because of their
strategic location, they produce tremendous symptoms. The arteries involved are usually
the tiny perforating arteries of the MCA, collectively called the lenticulostriate arteries
or the perforating arteries of the basilar, called the basilar perforators.
Because the culprit is these tiny arteries, lacunar strokes are also referred to as small
vessel disease, in contrast to strokes from the much larger carotid and vertebral artery,
which are known as large vessel disease.
Lacunar strokes are often thought to be due to a pathologic processes called

lipohyalinosis. This typically happens in patients with poorly controlled blood pressure
and diabetes. As a person’s blood pressure increases, the friable walls of small vessels
must thicken, or hypertrophy, in order to withstand the pressure. Uncontrolled diabetes
accelerates this process. Eventually one of two processes occur. In the first, the continued
high blood pressure overcomes the ability of the vessels walls to hypertrophy and a small
hemorrhage occurs. In the second, the arterial walls hypertrophy so much that effective
blood flow to the brain is cut off, and the brain undergoes infarction.
Lacunar stroke patients often have a “honeymoon” period for the first 48 hours, where
their symptoms can vary significantly in severity, before the dysfunction becomes
permanent. The pathophysiology behind this is not understood.
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Case 14: The 39-year-old woman who couldn’t see out her left eye 257
Case 14: The 39-year-old woman who couldn’t see out her left eye
You are called into the Emergency Department in the early hours of the morning to see a
39-year-old woman. Her friends tell you she was out with them celebrating; 2 weeks prior
she had been in hospital for the removal of a breast tumor which turned out to be benign.
While partying, the patient’s friends were startled to see that her right pupil appeared
much larger than the left. They tried to convince her to go to the hospital, but it was no
use. Soon thereafter, she began to complain of seeing double, but chalked it up to the
copious amount of alcohol she was enjoying. Only when she lost vision in her left eye
did she finally agree to come to the hospital.
When you see her, she is agitated and yelling that, “the purple children in the corner
need to stop running around my bed!” You check her toxicology screen, which is negative
for drugs and try to reassure her, but you are only partially successful. Still, from what
you can piece together you feel that her language examination shows normal fluency,
repetition and comprehension. You agree with her inebriated friends; her right pupil is
quite large, and appears not to react to light. The eye also appears down and to the right
side; it does not adduct or move upward. She has a moderate ptosis of the right eyelid.
She has lost her left visual field in both eyes. She also has a left sided facial droop which
does not involve the forehead. Her tongue and palate are midline. Motor examination
shows normal tone, but 3+ reflexes on the left with an upgoing toe on the same side.
You find a mild weakness in her left arm and leg, as shown below. Vibration testing and
pinprick, though not the most reliable, appear normal.
You move onto coordination testing but as you do she slumps over, and will not rouse to
sternal rub. You call for an emergency intubation and watch as she is wheeled to the ICU.
Power Examination
Right Left
Deltoid 5 4+
Bicep 5 4+
Tricep 5 4
WE 5 4
FE 5 4
HF 5 4+
KE 5 4+
KF 5 4
Where is the lesion? ADF 5 4+
What is going on here? APF 5 4
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Case 14: Findings
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Case 14: Solution
Our patient has increased reflexes and an upgoing toe, both signs of an UMN type
weakness. Thus, we know that the lesion lies in the CNS.
Our patient does not have any sensory symptoms, so we can conclude the DC and ST
are not involved. She has UMN weakness of the left arms and legs, and as the forehead
is spared, a left UMN facial droop. As we’ve seen before, this potentially localizes to the
cortex, internal capsule and brainstem.
Our patient has lost her left visual field in both eyes; she has a left homonymous
hemianopsia (LHH). Note that she erroneously, as most patients do, misinterpreted this
as visual loss from her left eye. A homonymous hemianopsia can only be produced by a
lesion to the cortex, which is our initial localization.
Let’s return to our patient’s LHH. Since the optic neurons decussate at the chiasm, we
know that a left visual field defect is caused by a right cortical lesion. Further, because it
is a homonymous hemianopsia we know that the lesion must be posterior to the chiasm
(Fig. 3.5).
What about our patients other visual symptoms? Her right eye appears “down and out”
and she has ptosis of the right eyelid. Already you should be thinking of a right CN III palsy.
As we saw earlier, a CN III palsy causes dysfunction of parasympathetic innervation to
the pupil. If the parasympathetic system is lesioned, then the pupil receives unopposed
dilatation from the functioning sympathetic system, which is the case here. Thus, her right
CN III or its nucleus is involved. CN III lies in the midbrain. Reviewing our symptoms, we
see she has UMN weakness in her face, arm and leg on the left side. The corticospinal and
corticobulbar tracts at the level of the midbrain are likely involved.
But what about our patient’s hallucinations and personality change? How can she have
a midbrain lesion AND a cortical lesion? This case is an example of the top of the basilar
syndrome. Here, an embolus (in this case it was from a dissected vertebral artery, likely
due to intubation process from her breast surgery), traveled to the proximal or “top”
of the basilar, and lodged itself there. It then acts as a further source of emboli causing
infarctions of areas supplied by the posterior cerebral arteries (PCA) and superior
K25928_C007.indd 259 12/01/2017 12:19

cerebellar artery (SCA). Let’s review the timeline of our patient’s symptoms. She began
with pupil dysfunction and double vision; the first embolus did not travel far and infarcted
the right midbrain causing the CN III lesion and UMN weakness. She then developed
the LHH; the second embolus traveled a little farther into the PCA and caused a right
sided occipital lobe stroke. Then she developed agitation and hallucinations; the third
embolus infarcted her right thalamus, causing personality change and hallucinations.
She then became comatose; another embolus infarcted her other thalamus. Bilateral
thalamic infarctions result in a depressed level of consciousness, as we saw in Chapter 3.
Whenever you see anyone who develops new neurological dysfunction in a stepwise
fashion, as above, you should be concerned about top of the basilar syndrome. This is a
true medical emergency as it can have disastrous outcomes, as we saw in our unfortunate
case above.
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Figure 7.14 Brain Herniation Syndromes
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Clinical Pearl: Brain Herniation Syndromes
When faced with the case above many clinicians would have been concerned that some
sort of mass was causing a fatal herniation of brain tissue.
Herniation occurs when tissue from one anatomical compartment inappropriately

expands into another anatomical compartment. This can occur in the brain, often due to
some sort of expanding mass (such as a hemorrhage, tumor or abscess), which increases
the intracranial pressure (ICP).
There are several types of brain herniation:
1) Subfalcine: The medial cortex herniates underneath the falx cerebri, sometimes
tearing itself in the process and causing leg weakness. Most cases are asymptomatic but
warn of impending herniation at other sites. This is the most common type of herniation.
2) Central: The temporal lobes and basal ganglia herniate through the tentorium cerebelli.
Initially, compression of the hypothalamus causes a loss of sympathetic function,
resulting in small but reactive pupils. However, soon the midbrain is compressed causing
larger, unreactive pupils and decreased LOC. As herniation continues the basilar artery
is torn which is uniformly fatal.
3) Uncal: The medial temporal lobe, also called the uncus, herniates through the
tentorium cerebelli and begins to compress the midbrain causing an ipsilateral CN III
palsy. Soon thereafter, there will be decreased LOC. Importantly, paralysis can be on
either side of the body. If the ipsilateral midbrain is compressed first, then a contralateral
weakness occurs. If the midbrain is compressed such that it moves as a whole, it will
be compressed by the contralateral tentorium cerebelli (in an area called Kernohan’s
Notch), causing paralysis on the same side as the CN III palsy. Thus, it is more reliable to
localize based on the location of the CN III palsy, not the body weakness.
4) Upward: The cerebellum and brainstem herniate superiorly through the tentorium
cerebelli; this is caused by an expanding mass in the cerebellum. Compression of blood
vessels can cause cerebellar infarcts. As the mass expands it compresses the fourth ventricle,
causing an obstructive hydrocephalus, which rapidly worsens the already high ICP.
5) Tonsillar: The cerebellum and brainstem herniate through the foramen magnum.
Decreased LOC and paralysis accompany deformations to the brainstem. Autonomic
instabilities involving blood pressure, pulse and respiratory rate ensue, and death follows
shortly after. Colloquially, tonsillar herniation is known as ‘coning’.
Any herniation syndrome requires prompt neurosurgical intervention with either

resection of the offending mass lesion or by providing an alternate way for the brain to
release pressure. This is usually achieved with the placement of a temporary external drain.
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Case 15: The 46-year-old woman who kept tripping over her right foot 263
Case 15: The 46-year-old woman who kept tripping over her right foot
You have been asked by a family doctor friend of yours to see a 46-year-old female
migrant strawberry picker. Through her son, who translates for her, she states that over
the last 2 months, she has had difficulty walking. Her son volunteers that she seems to
trip over her right foot. She demonstrates this for you as she walks. You notice that she
seems to hyperflex her right hip in order to get her foot to clear the floor and when she
fails to do so you hear the foot loudly slap against the ground.
With the aid of her son, you find her language to be of normal fluency, repetition and
comprehension. Her pupils are equal and she has full eye movements and full visual
fields. She does not have a facial droop and her tongue and palate are midline. Her formal
power examination is recorded below, but she has normal power in her arms. She has
normal tone and reflexes everywhere. Her toes are downgoing. Her sensory examination
shows an almost complete loss of pinprick on the dorsal aspect of the foot and the lateral
part of the leg up to the knee. Coordination testing was normal, except in the affected leg,
due to weakness.
Power Examination
Right Left
HF 5 5
HE 5 5
KF 5 5
KE 5 5
ADF 2 5
APF 5 5
INV 5 5
EV 3 5
EHL 3 5
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Case 15: Findings
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Case 15: Solution
Our patient has isolated weakness of her right foot. This could be caused by an UMN
lesion but is unlikely as the lesion would have to be quite small to only involve the foot.
Our patient’s tone and reflexes are normal and her toes are downgoing, which are not in
keeping with an UMN type problem. It would appear that the foot weakness is more in
keeping with a LMN presentation and that the lesion lies in the PNS.
Possible localizations include a radiculopathy, plexopathy and neuropathy.
Consulting our table of dominant myotomes (Fig. 5.5) we see that ankle dorsiflexion
(ADF) is innervated by L4/L5, and the extensor hallucis longus (EHL) by L5. The foot
evertors are not included in our table as they have innervation from many different
spinal roots.
It seems that the common root among the affected muscles is L5. What does the L5
dermatome look like? Consulting the table of dermatomes (Fig. 5.15) it appears that the
L5 dermatome matches our patient’s sensory loss.
An L5 radiculopathy perfectly explains our patient’s symptoms… humor me though and

see if you can match the dysfunction to a single nerve.
Our patient has weakness of the ankle dorsiflexion, first toe extension, and foot eversion.
Recall from Chapter 5 that the muscles responsible for these functions are all innervated
by the common peroneal nerve. In addition, we see that the sensory innervation from
the common peroneal nerve matches our patient’s complaints.
We seem to be in quite a pickle; an L5 radiculopathy and a common peroneal neuropathy

both account for our patient’s presentation. Which is the correct one?
Differentiating between an L5 radiculopathy and a common peroneal neuropathy is a

classic neuroanatomy localization question. It is probably so popular both because of
its educational value in demonstrating the neuroanatomy of the foot, and because the
management of the two possibilities is so different. An L5 radiculopathy may require
urgent neurosurgical decompression; a peroneal neuropathy will likely improve
significantly with conservative management.
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How do we approach such a problem? Firstly, note that the sensory examination is useless
since the L5 dermatome and the common peroneal sensory area are virtually identical.
Whenever you are confronted by a radiculopathy vs. neuropathy problem (such as an L3
radiculopathy vs. femoral neuropathy, or C8 radiculopathy vs. ulnar neuropathy), the
key is to find a muscle that is supplied by the same nerve root but a different nerve. If that
muscle is weak then the lesion lies in the nerve root. However, if that muscle is normal
strength, the lesion lies in the nerve.
For this case the key muscle turns out to be tibilais posterior, which inverts the foot.
This muscle is supplied by L5, but is innervated by the tibial nerve, not the common
peroneal nerve. We see that our patient’s tibialis posterior strength is normal. Thus we
can conclude that our patient has a peroneal neuropathy.
The peroneal nerve is exquisitely sensitive to compression. It runs right beside the
head of the fibula. Whenever a person crosses their legs, they can cause the nerve to be
pressed against the fibula. People who do this excessively have been known to cause
transient palsies of their peroneal nerve. The same occurs whenever a person squats,
so professions that due this often (bricklayers, floorers, or certain fruit pickers), also can
cause significant damage to the nerve, giving it the nickname, the strawberry picker’s
palsy.
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Figure 7.15 Detailed Anatomy of the Lumbosacral Region
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Clinical Pearl: Detailed Anatomy of the Lumbosacral Region
In our previous case, our main consideration was a L5 radiculopathy or a common

peroneal neuropathy. The neuroanatomy of the cauda equina can be challenging due to
its varied presentations, so we should take a moment to review it here.
The most common cause of an L5 radiculopathy is a disc herniation. Recall from Chapter
4 that the spinal cord sits between bones called vertebrae, and that between the vertebra
are discs that act as shock absorbers. The spinal cord terminates at the conus medullaris
at L1. Nerve roots beyond L1 travel together as the cauda equina and eventually leave the
vertebral column via the neural foramen.
Disc herniation can occur in two ways; posterolateral herniation and central herniation.
In order to understand the symptoms produced, two facts must be remembered:
1. The further down the cord, the more central and posterior the nerve roots lie in the
vertebral coloumn; i.e., the L2 roots lie more anteriolaterally than the S5 roots which lie
very central and posterior.
2. Nerve roots exit very high in their foramen.
Let’s consider a posterolateral herniation at the L5/S1 disc space. The L5 nerve root exits
very high in its foramen, and thus is unlikely to be damaged by the herniation. However,
the S1 root is quite vulnerable. Thus, posterolateral herniation tends to damage the root
below them.
Now consider a central herniation, again at the L5/S1 interspace. The central herniation
damages the roots that are most central; in our example this is the S2 root. Then as the
herniation worsens, the earlier nerve roots become involved in the reverse order, finally
ending with the L5 nerve roots. Thus, a central herniation often damages the most distal
nerve roots first, but if it is extensive enough it can involve all the nerve roots up to the
level of the herniation.
These two very different clinical presentations can be understood easily by remembering
the two rules above.
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Case 16: The 42-year-old kickboxing woman 269
Case 16: The 42-year-old kickboxing woman
You’re seeing a distressed 42-year-old woman who presents 3 days after taking up
kickboxing. She came to the Emergency Department because of intractable nausea.
She states that she’s been very dizzy and “off balance” recently, resulting in a fall. She
wonders if she has the flu. The Emergency Doctor treats her nausea, but also notices her
pupils are unequal and so pages you to come see her immediately.
When you see her she repeats her history for you and you notice she has mild dysarthria;
however, her formal language examination shows normal fluency, repetition and
comprehension. When you examine her, you notice that she has a subtle ptosis of her
right eyelid. In bright light her pupils measure 2 mm on the right and 3 mm on the
left. This difference increases in the dark; her right pupil increases to 3 mm but the left
increases to 5 mm. She has full visual fields and eye movements. She does not have a
facial droop. However, when you ask her to open her mouth, her palate does not raise
as much on the right side. Motor examination, including tone, reflexes and power were
all normal. She has downgoing toes. Pinprick testing revealed, curiously, that she has
decreased pinprick sensation on the right side of her face and on the left side of her body.
You repeat this several times to make sure. Vibration testing with tuning fork is normal.
Coordination testing revealed she is ataxic on her right side.
Distressed, she asks you to place a cold compress on her forehead. As you walk away she
mentions to you it doesn’t feel cold on the right side.
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Case 16: Findings
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Case 16: Solution
Unfortunately there are no motor symptoms in this case to guide us. Hopefully we’ll have
more luck with her sensory exam.
Our patient does not have any impairment of vibration, so we can conclude her DC are
normal. Thankfully, her pinprick examination reveals an Immediate Localization! Our
patient complains of pinprick loss on the right side of the face, but the left side of the
body; this is an example of crossed signs, and can only be produced by a brainstem
lesion (see Chapter 3). Thus, our initial localization is the brainstem.
We need to see which CN are affected to help us localize to the midbrain, pons or medulla.
Since her eye movements are not affected (CN III, CN IV and CN VI) we can conclude
that her midbrain and pons are both normal. Looking through the rest of her symptoms,
we see that her palate rose asymmetrically; both CN IX and CN X innervate the palate.
We can thus refine our initial localization to be the medulla.
Let’s work through our patient’s complaints. Our patient has an anisocoria that is greater
in the dark than in light, which means she has Horner’s syndrome, and that the smaller
pupil (right) is the abnormal one. Since the sympathetics do not decussate this tells us that
the right sympathetic pathway is involved. Her dysarthria is likely caused by her palate
rising asymmetrically. These functions are innervated by CN IX and X and controlled by
a single nucleus, the nucleus ambiguus. Thus, the right nucleus ambiguus is involved.
She is ataxic on the right side; the spinocerebellar tract doesn’t decussate so we know
the right spinocerebellar tract is affected. She is dizzy and off balance, likely caused
by dysfunction of the right vestibular nucleus of CN VIII. The decreased pinprick and
temperature sensation in the right face means the right CN V nucleus must be affected.
The decreased pinprick on the left side of her body must be due to a lesion of the right ST.
It would seem that the entire lateral aspect of the right medulla is affected; indeed this
is a case of lateral medullary syndrome or Wallenberg syndrome (named after the
physician whom first described it). In this case it was caused by a traumatic dissection of
the vertebral artery, likely due to the kickboxing, which then embolized causing a stroke.
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Figure 7.16 Vertebral Artery Dissection
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Clinical Pearl: Vertebral Artery Dissection
Artery dissection is an important mechanism of stroke. The walls of arteries are

composed of three layers: the adventitia (outermost layer), media (middle layer) and
intima (innermost layer). Kickboxing, chiropractic manipulation, intubation, even
sneezing and coughing are all types of trauma that have been known to “kink” arteries
and cause microtears of their walls. The tear slowly expands and ‘dissects’ the artery wall
layers apart until there is a true lumen, where normal blood flows, and a false lumen,
where blood gets stuck and subsequently clots. Eventually a piece of clot can break off
and travel up to the brain and interrupt blood flow, resulting in a stroke.
For mechanical reasons, the vertebral arteries seem more likely to dissect than the
carotid arteries. Typical treatment is with an anticoagulant or antiplatelet for 3–6 months
until the false lumen has resolved on repeat imaging.
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Case 17: The 31-year-old woman who saw double 275
Case 17: The 31-year-old woman who saw double
You’re asked to see a 31-year-old woman who comes to the Emergency Department with
new type of headache. She states that she used to be headache free, but over the last
18 months she has had headaches nearly every day for which she was seeing her family
doctor. She described these headaches as a dull ache, lasting all day, and about 6/10 in
intensity. Today, however, she was typing at her keyboard when she developed a 9/10 in
intensity headache that came on so quickly it was “like someone hit me over the head
with a baseball bat.” She stumbled across the room and decided to call an ambulance
because she was seeing double everywhere.
When you examine her, you feel a sinking feeling in your stomach as you see that
her blood pressure is 86/42 and dropping. You regain your composure enough to
examine her formally. Her language examination shows normal fluency, repetition and
comprehension. You immediately notice that her pupils are unequal; her left pupil is
2 mm and her right is 4 mm. The right pupil barely constricts to light and has a partial
ptosis of the eyelid. Curiously, you find that she has lost her right visual field in her right
eye, but she has also lost her left visual field in her left eye. She complains of diplopia in
all directions of gaze; her left eye appears to move well, but the right eye barely moves
at all. Pinprick examination of the face was normal on the left side. On the right side she
reports the pin feels dull in the forehead and cheek, but the area just above the chin is
normal. She does not have a facial droop, and her tongue and palate are midline. Formal
motor examination shows normal tone, 2+ reflexes and normal power in the arms and
legs. Sensory examination of the body is normal. Coordination testing is also normal.
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Case 17: Findings
CN: cranial nerve.
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Case 17: Solution
In this case, we have no motor symptoms to help guide us.
We are not having much luck with this case; our patient’s sensory examination of the
arms and legs were normal. We can only go on the fact that all of her symptoms are
confined to the head, so our lesion must lie above the cervical spine.
Let’s go through our patient’s complaints. Our patient’s right pupil is large and barely
constricts. She also has a ptosis of the right eyelid; both of these support a right sided CN
III palsy. She has diplopia in all directions of gaze, and the right eye barely moves, which
suggests that CN III, CN IV and CN VI must be involved. Finally, she states that the pin
is dull on the right forehead (CN V1) and right cheek (CN V2). Putting this together, you
could argue for a large lesion that involves the midbrain (CN III and CN IV), and the pons
(CN V1, CN V2 and CN VI).
However, that would be a lesion of considerable size; remember the Rule of 4. CN III, CN
IV and CN VI are all medial structures and CN V is a lateral structure. For such a large
lesion to not involve ANY of the long tracts would be very unlikely.
Can anything else help us? Well our patient has a visual field defect, which can only be
produced by a cortical lesion. She has lost right sided vision in her right eye and left sided
vision of her left eye. Another way of saying this is that she has lost the temporal aspect of
her vision in both eyes; she has a bitemporal hemianopsia.
This can only be caused by a lesion of the optic chiasm, as it is there that the temporal
fields decussate (Fig. 3.5). The optic chiasm is our initial localization.
How can we reconcile an optic chiasm lesion with dysfunction of the right CN III, CN IV,
CN VI, and CN V1 and CN V2? Recall Fig. 3.11. All of these CN pass through the cavernous
sinus, which lies directly below the optic chiasm.
In this case the woman had a pituitary gland tumor, which caused her dull headaches
over the last 18 months. The tumor then ruptured on the right side, causing bleeding into
the cavernous sinus. The bleeding caused compression of the optic chiasm and CN. This
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is a life threatening condition because the pituitary itself is soon compressed, causing a
defect in hormone secretion, including those hormones that support blood pressure, as
evidenced by our patient’s very low readings.
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Figure 7.17 Relative Afferent Pupillary Defect
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Clinical Pearl: Relative Afferent Pupillary Defect
A relative afferent pupillary defect (RAPD) is a related condition to the case just
presented and often serves as a frequent source of frustration for students. A RAPD, also
known as a Marcus Gunn pupil (after the ophthalmologist who first described it), occurs
whenever there is an incomplete lesion to one optic nerve. This incomplete lesion still
allows the neuron to send signals to the midbrain, however the strength of the signal is
reduced compared to the unaffected side.
The best way to understand what happens here is to work through an example. Let’s say
that the right optic nerve suffers an insult and only has one half of the working neurons
compared to the left side. Stated another way, what if the right eye could only detect one
half of the light that the left eye does?
Let’s work through this example. You decide to shine light into the right eye (“Case A” in
Fig. 7.17). Some light gets through, and the pupillary constriction pathway is completely
intact, so the right and left pupil constrict equally due to the dual innervation of the pupils.
You then decide to shine light into the left eye (“Case B”). This eye detects double the light
than in “Case A.” The pupils both constrict equally, but as there is more stimulating light,
they constrict to a smaller size than in “Case A.”
Note that there is never an anisocoria of the pupils! In both cases the pupils constricted
equally.
We now understand why it is called a relative afferent pupillary defect. It’s relative because
both eyes detect light, but one detects relatively less than the other. It’s afferent because
it has to do with signal input; the lesion occurs to the afferent pathway (the optic nerve).
Wait a moment, since both pupils constrict, how are you going to detect an RAPD on
examination? If you had shone light in the right eye, noticed the weak constriction, and
then waited 5 minutes to shine light in the left eye, to notice the stronger constriction,
you may have missed the difference in size between the two responses. The solution is
to do the swinging light test. In this case you swing the light quickly between the pupils.
Initially you shine light into the right eye (“Case A”), note the weak constriction of the
pupils, and then shine light into the left eye (“Case B”) and note the strong constriction of
the pupils. You then swing the light back to the right eye (“Case C”). As you do the pupils
will appear to paradoxically dilate; they are still constricted compared to their baseline
state, but less so than when you shone light into the left eye.
This paradoxical dilation is the key feature on examination to confirm a RAPD.
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Case 18: The 32-year-old man with the large ego 281
Case 18: The 32-year-old man with the large ego
A 32-year-old man presented to the Emergency Department with a 3-day history of leg
pain, left worse than right. He reports that he hurt himself at the gym when someone
said to him “do you even squat bro?”; after attempting to disprove his opponent by
overloading the bar, he immediately felt his feet go numb. Disturbed by the experience,
he went home, hoping that his ego was the only thing that was damaged. However,
12 hours later he began to notice a sharp pain in the buttocks bilaterally. He says that
this pain gradually spread over the entirety of both legs. He also states he hasn’t had a
bowel movement since the event at the gym. However, he only decided to seek medical
attention when, after 24 hours of not urinating, he spontaneously passed urine and did
not notice it until his wife pointed out his pants were wet. He begs you for medication,
stating the pain is excruciating.
From conversing with him about his history you determine he has normal fluency and
comprehension. His ability to repeat a sentence is also intact. He has full visual fields and
eye movements, and his pupils are equal and reactive to light. He does not have a facial
droop and his palate and tongue are midline. Motor and sensory examination in the arms
is normal. When you examine his legs, you do not find any atrophy or fasciculations, but
they do have decreased tone. His reflexes are completely absent at both the ankle and
knee and his toes are downgoing. He is quite weak in the legs, as shown below. Sensory
examination shows decreased vibration at the ankles and knees. Pinprick testing showed
lack of sensation along the anterior part of the leg to just above the knee. He had decreased
sensation over the penis, scrotum and sacral area. Coordination testing was normal in
the arms, and not tested in the legs, given the weakness.
Power Examination
Right Left
HF 5 5
HE 2 2
KE 4- 3
KF 2 2
ADF 3 3
APF 2 2
EHL 3 3
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Case 18: Findings
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Case 18: Solution
Our patient has decreased tone in both legs, as well as absent ankle and knee reflexes,
pointing to a LMN type problem. Note that downgoing toes are a normal finding, and
should not be used to conclude that the patient has LMN type weakness. However, the
constellation of findings above points to a lesion in the PNS.
Possible localizations include a radiculopathy, plexopathy or neuropathy.
Let’s review our table of dominant myotomes (Fig. 5.5). In this case only the hip flexors
(L2) are of normal power. The knee extensors (KE) (L3), knee flexors (KF) (S2), ADF
(L4/L5), ankle plantar flexion (APF) (S1), EHL (L5), and hip extensors (HE) (S1) seem
to all be affected. Certainly, this doesn’t correspond to a single myotome.
Our patient has weakness of nearly every muscle group, so a lesion in a single nerve is
impossible. Indeed, the femoral nerve (KE), sciatic nerve (KF), common peroneal nerve
[ADF, extensor hallucis (EH)], tibial nerve (APF), and inferior gluteal nerve (HE) are all
involved.
It would seem that to produce this pattern of loss, all of the above nerves would need to
be affected, on both sides!
Where do we go from here? According to our localization algorithm, if we have concluded

that the dysfunction isn’t due to a lesion or a single nerve root or single peripheral nerve,
we have to either conclude a) the lesion is in the plexus or b) there isn’t a focal lesion,
and a generalized disease process is causing dysfunction of multiple parts of the nervous
system.
The argument that this is due to a lumbosacral plexus lesion is made difficult because
both legs are affected, implying that you would need two (large, in this case) lesions
to affect both plexuses. Before we conclude that there is a diffuse disease at work,
recall Fig. 7.15; all the roots of the lumbosacral area travel in very close proximity. A
central herniation of a disc could affect all the roots from the level of the herniation
down.
We now need to figure out the level of this herniation. The ankle (S1, S2) and knee (L3,
L4) reflexes are both absent, so we know that the lesion is at least at the L3 level. Going
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back to the table of dominant myotomes (Fig. 5.5) the hip flexors, which are full power,
are innervated by L2. We can thus conclude that our lesion is at L3.
The above is called a cauda equina syndrome, because it doesn’t only involve the nerve
roots as they travel in the cauda equina, before they join the lumbosacral plexus. In this
case the patient’s overzealous squat caused a disc to rupture and herniate centrally,
causing impingement of nerve roots.
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Figure 7.18 Lumbar Puncture
CSF: cerebrospinal fluid; GBS: Guillain Barré syndrome.
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Clinical Pearl: Lumbar Puncture
If the mass responsible for the compression in the above case had been anything other
than a ruptured disc, our patient would have likely undergone a lumbar puncture. A
lumbar puncture is a useful diagnostic test, and can also be a therapeutic intervention.
The goal of a lumbar puncture is, in most cases, to obtain cerebrospinal fluid (CSF)
for analysis; CSF is most often used to confirm an infectious meningitis (see bottom
half of Fig. 7.18) but can also be used to diagnosis Guillain Barré syndrome (GBS),
subarachnoid hemorrhage, multiple sclerosis, and malignancies. Therapeutically, it can
be used to instill chemotherapy, as well as decrease elevated ICP by removing CSF.
In a lumbar puncture, a needle is inserted in the L3–L4 interspace, as shown in the top
half of Fig. 7.18. As we saw in the case above, the spinal cord ends at L1, so the needle is
being inserted into the space occupied by the cauda equina. Damage to the spinal cord
itself is not possible, and a lumbar puncture is viewed as a very safe procedure.
As the needle is inserted it passes through several layers, the first of which is the skin
and then the subcutaneous tissue. Next, it will pass through the ligaments that hold the
vertebrae together. Finally, it pierces the dura mater and arachnoid mater to enter the
subarachnoid space, where CSF is located.
The ability to quickly interpret lab values obtained from a lumbar puncture is important.
Typical CSF measures include protein concentration, glucose concentration and the
concentration of white blood cells (usually just referred to as “cells”). A normal lumbar
puncture should be clear in colour, with very little protein, and a maximum of 5 white
blood cells, as the CSF is normally sterile. In a bacterial infection, the protein is very
elevated, which indicates that the blood brain barrier has been broken. The glucose is
decreased because it is being consumed by bacteria, and the cell count is high with a
differential indicating neutrophil predominance. A viral infection is more subtle in
presentation; the protein is not as high, the glucose is normal, and there are typically less
cells, though they are more lymphocytic in nature. GBS will have a markedly elevated
protein, but NO increase in cells, as there is no infection, and the glucose will be normal.
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Case 19: The 59-year-old woman who was like stone 287
Case 19: The 59-year-old woman who was like stone
You walk into the Emergency Department to see your next consult and find a despondent
husband who brought in his 59-year-old wife. He states that over the last 18 months she
has become “like stone;” she has become very withdrawn and moves very slowly, or not
at all. Over this time, she refused to see a physician. He brought her to the Emergency
Department because over the last week she developed severe urinary incontinence,
though this didn’t seem to particularly bother her.
When you examine her, you agree that she has very little spontaneous verbal output, and
seems to just sit there; however, her ability to repeat and comprehend are intact. You find
her CN to be normal; pupils are equal and reactive, she has full eye movements and visual
fields, she does not have a facial droop and her tongue and palate are midline. Motor
testing is normal in the arms. However, her legs demonstrate increased tone, 3+ reflexes
and bilateral upgoing toes. She is quite weak in the legs; her formal power examination
is recorded below. Her pinprick and vibration testing is normal. You decide to challenge
her with some more strenuous sensory tests. You use your pen to trace out a number on
both her legs, but she is quite unable to tell you what that number is; she cannot even
identify that it was a number. However, when you repeat this on her hands, she (slowly)
gets the correct answer. When you ask her to rub her ankle down her shin as part of the
coordination examination, she just looks at you blankly. Similarly, when you ask her to
walk she just looks at you confused. You demonstrate walking, but she struggles to lift her
feet. She continues to look at you confused.
Power Examination
Right Left
HF 4- 4-
HE 4- 4-
KE 4- 4-
KF 4- 4-
ADF 3 3
APF 4- 4-
EHL 4 4
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Case 19: Findings
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Case 19: Solution
Our patient has weakness accompanied by increased reflexes, increased tone and
upgoing toes; these are all signs of an UMN problem. Thus, we know that the lesion lies
in the CNS.
In this case, our patient has UMN weakness of both legs, suggesting both corticospinal
tracts are involved. As we saw in Case 2, bilateral UMN leg weakness localizes to either
the thoracic/lumbar cord or to the medial aspect of both motor cortices. In this case,
our patient had normal pinprick and vibration testing. We must hope that her other
symptoms help us to differentiate between these two localizations.
While her primary sensory testing was normal, her further sensory testing reveals an
Immediate Localization to the cortex! She cannot discern the number traced on her leg;
this is an example of agraphesthesia. Similarly, the confused look the patient gives when
you ask her to perform any task with the leg, such as walking or the heel to shin testing,
is an example of apraxia. Our patient has intact proprioception and sufficient power to
walk, but cannot figure out how to execute this complex motor task. Agraphesthesia and
apraxia are examples of higher functions that can only be produced by a cortical lesion.
Thus, our localization must involve the medial aspect of both motor cortices.
Now that we know that both cortices are involved we can draw them in cross section. Our
patient also complains of incontinence, which we would expect since bowel and bladder
function is also controlled by the medial aspect of the motor cortex. In general, both
cortices need to be involved before incontinence occurs. The localization of the apraxia
and agraphesthesia is nonspecific, but may involve the frontal lobe.
In summary, we see that the medial side of both motor cortices is affected, and our
patient has evidence of marked frontal lobe dysfunction. While this might seem a
bizarre combination of symptoms, it is actually quite common and can be produced by
bilateral ACA strokes, or a disease known as normal pressure hydrocephalus, which we
will explore shortly. In this case, however, the patient had a parasagittal meningioma, a
benign tumor, compressing all of the above structures. Removal of the tumor improved
the weakness and incontinence greatly, but cognitive function only partially recovered.
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Figure 7.19 Hydrocephalus and Monro–Kellie Doctrine
Redrawn with permission from Waxman SG. Clinical Neuroanatomy. Lange, New York, 2013.
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Clinical Pearl: Hydrocephalus and Monro–Kellie Doctrine
Certain tumors can obstruct the drainage of CSF and result in hydrocephalus (Greek
for, literally, “waterhead”), which is defined as an abnormally high amount of CSF.
Hydrocephalus can be classified into two types; unfortunately two equally common
naming conventions exist, so one must be familiar with both.
• Obstructive (also called noncommunicating) hydrocephalus. An extrinsic mass

(usually a tumor, or clotted blood) blocks the flow of CSF, usually at the level of the
cerebral aqueduct or the 4th ventricle. The choroid plexus continues to produce
CSF however, and hydrocephalus results. As the blockage occurs in the inferior part
of the ventricular system, the lateral ventricles swell in size significantly, which can
be seen on imaging. It is called noncommunicating hydrocephalus as the two CSF
compartments, head and spine, are cut off from each other by the compression. The
majority of cases of hydrocephalus are of the obstructive type.
• Nonobstructive (also called communicating) hydrocephalus. This results either
from an overproduction of CSF by the choroid plexus (due to rare choroid plexus
tumors), or blockage of the resoprtion of CSF by the arachnoid granulations. The
arachnoid granulations can be prone to scarring which renders them ineffective,
usually after an infection such as meningitis, or after a subarachnoid hemorrhage.
On imaging, all the ventricles will be dilated, not just the lateral ones.
Hydrocephalus ties in closely with the concept of ICP and the Monro–Kellie Doctrine
(MK Doctrine). The MK Doctrine simply says that because the skull is a fixed volume, the
volume (V) of the all contents of the skull must be a constant, specifically:
VSkull = VBrain + VCSF + VArterial + VVenous
Stated in words, the total volume of the skull is equal to the volume of the brain plus the
volume of the CSF, arterial blood supply and venous blood supply.
What if there is an expanding mass, such as a tumor? Then the MK Doctrine states that:
VSkull = VBrain + VCSF + VArterial + VVenous +Vmass
The brain will attempt to compensate for the increasing volume of the mass.
Unfortunately, the brain can’t change its size, so VBrain is fixed. The first compensatory
measure will be to decrease the output of CSF, thus decreasing VCSF. The brain will then
increase venous drainage, decreasing VVenous. Finally, under truly dire circumstances the
brain will decrease VArterial, but this greatly increases the risk of significant ischemia and
stroke. When this fails, the relatively weak cortical veins will begin to be crushed under
the enormous pressure, which blocks venous drainage, leading to massive spikes in ICP.
Herniation of brain tissue through the foramen magnum, and death, is the final result.
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But what if the volume of the skull wasn’t fixed? Surgically, this can be achieved by placing
an emergency drain, or by removing part of the skull. Usually a drain is the preferred
method. This lowers the ICP by draining the CSF, and decreasing VCSF. This life saving
measure can often be carried out in a manner of minutes at the bedside.
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Case 20: The 19-year-old woman with a single complaint 293
Case 20: The 19-year-old woman with a single complaint
The next patient in your busy clinic is a 19-year-old woman referred to you by her
ophthalmologist. She states that over the last 3 weeks she has had double vision. When
you ask her if there is any pattern she mentions that she thinks it’s whenever she looks
to the right.
As you converse with her you find her fluency, repetition and understanding of language
to be normal. You examine her eyes closely; you cannot find any visual field defects,
pupillary abnormalities or any eyelid ptosis. Her eyes seem to be in perfect alignment with
each other as she looks forward. She does not have any diplopia on upgaze, downgaze or
leftward gaze, and her eyes move conjugately through these directions. However, when
she looks to the right, her right eye abducts but her left eye does not move. She does not
have a facial droop and her tongue and palate are midline. Motor examination reveals
normal tone, 2+ reflexes and no weakness. Sensory testing to pinprick and vibration is
normal. Coordination is normal in both the arms and the legs.
It would seem that the inability of the left eye to adduct whenever she looks to the right is
her sole abnormality on exam.
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Case 20: Findings
PRRF: paramedian pontine reticular formation.

Redrawn with permission from Greenberg D, et al. Clinical Neurology. McGraw–Hill Education, New York,
2015.
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Case 20: Solution
As our patient has absolutely no long tract signs whatsoever, we’ll make a brief departure
from our localizing algorithm. Indeed our entire neurological examination is normal
except for failure of the left eye to adduct. That’s it.
Since this is an eye movement problem, lets return to the pathway for eye movements
we outlined in Fig. 3.9, which is reproduced on the previous page. We’ll examine several
potential localizations in turn and we will hopefully find our answer.
1. FEF lesion: As we know the FEF drive both eyes to the contralateral side. A lesion of
the left FEF would mean that both eyes are strongly driven to the left side and unable
to cross midline. Clearly this doesn’t account for our presentation.
2. CN III lesion: The medial rectus muscle controls eye adduction, so our patient could
have a palsy of the left CN III. However, this would also cause problems with the
superior rectus, inferior rectus and inferior oblique muscles resulting in the classic
“down and out” eye. Let’s soldier on.
3. CN VI lesion: If we had a lesion to the right CN VI, the right eye would fail to abduct,
but the left eye would still adduct. This is the inverse of the problem we are faced
with.
4. Abducens Nucleus lesion: Remember that the abducens nucleus of CN VI initiates

horizontal gaze for both eyes. The right abducens nucleus initiates rightward gaze
for both eyes via the MLF. Thus, a lesion here would mean that both eyes would not
move when attempting to look right.
5. MLF lesion: The left MLF connects the right abducens nucleus to the left CN III
nucleus. A lesion here would not interfere with the abducens nucleus; the right
abducens nucleus fires, and the right eye abducts. However, the signal to the left CN
III nucleus is blocked, and the left eye fails to adduct. Eureka, we have found it!
A lesion to the MLF results in an internuclear ophthalmoplegia, or INO, which is named

because the lesion lies in between two nuclei. A lesion to any nucleus i.e., (CN VI or CN
III) is termed a nuclear lesion. Similarly, a lesion to the FEF or anywhere along the path
connecting the FEF to the brainstem is called a supranuclear lesion.
An INO in the absence of any other neurological symptoms is a classical finding for
multiple sclerosis (MS), and should be the first thing that springs to mind in an otherwise
healthy young woman.
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Figure 7.20 Multiple Sclerosis
MS: multiple sclerosis.
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Clinical Pearl: Multiple Sclerosis
MS is an autoimmune disease of the CNS. The immune system inappropriately attacks

the myelin of neurons (Fig. 1.2) in a process called demyelination. This results in greatly
slowed conduction of action potentials because they can no longer jump from Node of
Ranvier to Node of Ranvier. However, because the axon is undamaged the neuron still
lives, and oligodendrocytes can remyelinate the neuron, restoring at least part of its
function.
A key feature of MS is that it’s “multiple;” the patient suffers multiple attacks over time,
and in multiple locations, producing different symptoms. In order to be diagnosed with
MS the lesions need to satisfy McDonald Criteria and demonstrate dissemination in
time and dissemination in space. This can either be fulfilled by evidence of clinical
attacks or on MRI scan, or a combination of both.
There are three typical locations that MS affects. The first is the optic nerve, leading to
optic neuritis, in which the patient loses vision and has significant pain on moving the
eye. The second is the spinal cord, which usually results in total dysfunction of the cord
at the level which is attacked. The last is the brainstem, which can cause a variety of
symptoms such as dysarthria, dysphagia, diplopia (as seen in this case, due to an INO),
and weakness.
MS can follow certain patterns over time. The most common type of MS is Relapsing
Remitting MS, in which the patient experiences an attack of demyelination with
subsequent symptoms, which then remit once the oligodendrocytes repair the damage.
The patient returns to baseline until another attack, or relapse, occurs. However, long into
the course of the disease, oligodendrocytes begin to fatigue and can no longer fully repair
the demyelination. Clinically, the patient no longer returns to baseline between attacks
and they begin to accumulate disability. Eventually they may switch to a secondarily
progressive course in which they don’t suffer attacks at all and simply accumulate
disability with time.
Some patients have an atypical and rare version of MS in which they do not experience
relapses at all; they immediately begin to accumulate disability. These patients have
primary progressive multiple sclerosis.
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Case 21: The 62-year-old woman who kept burning her right hand 299
Case 21: The 62-year-old woman who kept burning her right hand
It has been a long night, and you are about to go home, when you are paged to the
Emergency Department to see a 62-year-old woman with a remote history of breast
cancer. When you arrive, the Emergency Doctor apologizes for the consult, and tells you
he thinks the patient is hysterical because her symptoms are “all left sided, except lack
of pain, which is right sided.” When you question her, you find an odd constellation of
complaints. She tells you she has had weakness in her left arm for the last 3 months,
but her right hand feels “strange,” and she has burnt it several times without noticing.
She’s had difficulty walking for the last 2 weeks. She finally came to the Emergency
Department because she’s recently noticed that she has to void urine up to 10 times
per day and she finds that when she gets the urge to void it is so strong that on several
embarrassing occasions she has not made it to the bathroom in time.
When you examine her, you find her language to have normal fluency, repetition and
comprehension. On CN examination you see that she has full visual fields and eye
movements, but her left pupil is 3 mm and her right pupil is 4 mm, which you find
unsettling. You shut off the light and find the left increases to 4 mm, and the right increases
to 6 mm. She does not have a facial droop and her tongue and palate are midline. She
is weak on her left side, and her formal power examination is recorded below. She has
spasticity in her left leg, but you wonder if her left arm has decreased tone. Her left bicep
reflex is 1+, but her tricep, knee and ankle are all 3+ on the left side, and she has an upgoing
left toe. She can not feel any vibration on the left side of her body below the level of the
shoulder, but the right side is entirely normal. However, on pinprick testing the opposite
was true, just as the Emergency Doctor reported; she cannot feel the pin on the right side
below the level of the shoulder, but the left side is entirely normal. Coordination testing
was deferred as she was quite weak.
Power Examination
Right Left
Deltoid 5 3
Bicep 5 3
Tricep 5 4
WE 5 4
FE 5 4
HF 5 4-
Where is the lesion? KE 5 4-
What is going on here?
KF 5 4-
ADF 5 4-
APF 5 4-
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Case 21: Findings
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Case 21: Solution
Our patient has increased tone in the left leg, increased reflexes at the left ankle, knee and
triceps and a left upgoing toe, which are all strongly indicative of an UMN type lesion.
However, her left arm has decreased tone and her left biceps reflex is decreased, which
are signs of a LMN type lesion. Thus, our patient has LMN type weakness at the bicep and
UMN type symptoms for the muscles below this level.
The combination of LMN type symptoms in one area of the body and UMN type
symptoms below that area can only be produced by a spinal cord lesion. In addition, her
sensory examination also suggests an Immediate Localization. Our patient has pinprick
loss on the right, but vibration loss on the left. This is an example of crossed sensory
signs, and can only be produced by a lesion to the spinal cord, which is our initial
localization.
Our patient complains of complete sensory loss below the level of the mid shoulder; this
is a sensory level and is another Immediate Localization to the spinal cord. Consulting
the dermatome map (Fig. 5.15) we see that this area is roughly innervated by C5 or C6.
Our patient has LMN weakness (decreased tone and 1+ reflexes) in the bicep, which after
checking our table of dominant myotomes (Fig. 5.5), we see is also innervated by C6. We
can refine our localization to be the spinal cord at C6.
Since we now know we’re in the cervical spinal cord, we can draw it in cross section.
Let’s start with motor symptoms. We have LMN signs in the left bicep, so we know
that the left AHC cell is involved. Below C6, we have UMN type weakness on the left
so the left corticospinal tract must be involved. The patient complains of vibration
loss below C6, so the left DC are involved. The patient also complains of loss of
pinprick on the right. Since the ST decussates immediately, that means the left ST is
involved.
Adding it all up, we see virtually the entire left side of the spinal cord is affected; our overall
localization is the left hemicord at C6. The total loss of one side of the cord is known as
Brown–Sequard syndrome. In this case, a metastasis from our patient’s previous breast
cancer was compressing the cord on the left side.
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You think we’ve forgotten about the pupils don’t you? We see that the anisocoria is greater
in dark than in light, so we have a Horner’s syndrome and the smaller pupil (left) is the
affected one. Remember the sympathetics travel into the spinal cord until about C8/T1,
as shown in Fig. 3.6. The sympathetics to the left pupil were affected by our lesion.
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Figure 7.21 Classification of Spinal Cord Lesions
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Clinical Pearl: Classification of Spinal Cord Lesions
Whether the causative lesion of spinal cord dysfunction is located inside or outside of
the spinal cord itself is of great clinical importance. For example, we know that multiple
sclerosis is a disease that targets the spinal cord tissue itself, and needs to be treated
medically. However, a slipped disc, or metastatic cancer, such as in our case, is a
lesion that actually lies outside the spinal cord; they cause dysfunction by extrinsically
compressing the cord and require surgical treatment.
Overall, spinal cord lesions can arise from three different areas:
1. Intramedullary lesions (‘medulla’ is Latin for ‘middle’)

These are lesions of the spinal cord tissue itself (either the gray or white matter, or
both), such as the multiple sclerosis lesions mentioned above. Other examples include
primary tumors of the CNS, and lesions caused by nutritional deficiencies.
2. Extradural lesions
These lesions lie outside the dura mater of the meninges and hence lie completely
outside the CNS. They cause dysfunction by compressing the cord. Examples include
the slipped disc mentioned above, other trauma, and metastatic tumors.
3. Intradural extramedullary lesions

These are lesions that arise from the meninges themselves. They are intradural because
they are part of the CNS, but lie outside the cord, and so are extramedullary. They also
cause symptoms by compressing the cord. The majority of these lesions are due to
tumors of the meninges.
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Case 22: The 21-year-old man transferred from a remote hospital 305
Case 22: The 21-year-old man transferred from a remote hospital
Your next patient is a 21-year-old man arriving to you from a small hospital up north
via helicopter airlift. The patient was brought to the smaller hospital’s Emergency
Department by his girlfriend after he fell several times in the last 24 hours. Flipping
through the transfer notes, you see he was seen twice in the last 2 weeks. Originally he
was brought in with dehydration after severe diarrhea and needed IV fluids. He was
then seen 5 days later with a complaint of painful tingling in his feet up to his mid shin.
He had blood-work drawn, which was normal and was then sent home. Now, he states
that the painful tingling is present up to the hip level, and is also in the fingertips of
both hands. He is unsure as to why he is falling and why he has transferred hospitals.
As you converse with him you find his fluency, repetition and understanding of language
to be normal. His CN are normal; he has full visual fields and eye movements, pupils that
are equal and reactive, no facial droop and his tongue and palate are midline. His motor
examination in the arms is normal. However, in his legs he has remarkably decreased
tone. Despite several attempts, you cannot elicit reflexes at either the knee or the ankle.
Power examination in the arms are normal; however, he has significant weakness of both
legs. His toes are downgoing bilaterally. Sensory examination shows a complete loss to
vibration in the legs and in the hands in the upper extremity. He can feel vibration in
his elbows on both sides. He also shows a severe loss of proprioception in the legs. His
pinprick examination shows some mild loss in the same areas. He is quite unsteady on
his feet and he needs to be held up by his girlfriend in order to walk.
Power Examination
Right Left
HF 4+ 4+
HE 4 4
KE 4 4
KF 4- 4-
ADF 4- 4-
APF 4- 4-
EHL 3 3
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Case 22: Findings
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Case 22: Solution
Our patient complains of bilateral leg weakness in the context of decreased tone and
reflexes that cannot be elicited. This strongly points to a LMN problem and we can
conclude our lesion lies in the PNS.
Possible localizations include a radiculopathy, plexopathy or neuropathy.
Our patient has weakness of every muscle group of his legs; the HF (L2), KE (L3), KF (S2),
ADF (L4/L5), APF (S1), EHL (L5), KF (S2), and HE (S1) seem to all be affected.
He also has a complete loss of vibration and pinprick not only in the lower legs, but also
in his hands! Clearly this massive amount of dysfunction cannot be due to a lesion of a
single nerve root.
Unfortunately we run into the same problem here; our patient’s pattern of weakness would
involve the femoral nerve, inferior gluteal nerve, sciatic nerve, common peroneal nerve and
the tibial nerve. This does not even take into account his sensory complaints in the hand.
If our patient’s symptoms were confined to a single leg, we could argue that perhaps
there was a lesion affecting the entire lumbosacral plexus. However, even this is quite
unlikely as a lesion would have to be of quite impressive size to do so; in addition our
patient also has symptoms in his hands. This makes a lumbosacral lesion impossible.
What are we left with? The symptoms in this case cannot be caused by a focal lesion.
A nonfocal disease process (such as diabetes, thyroid dysfunction and other genetic
conditions) can attack the nerves as a whole resulting in multiple diffuse lesions. In this
case, our patient’s symptoms are best classified as a length dependent polyneuropathy,
in which the longest nerves are affected first. Dysfunction begins in the most distal
muscles and sensory areas. As the disease progresses, it moves up the body and affects
all the nerves it comes across. Once the disease reaches just above the knees, the nerves
of the arm will begin to be affected.
What could the etiology of this length dependent polyneuropathy be? There are several
clues in the case, the most important of which is the loss of vibration/proprioception and
the complete absence of reflexes. In fact, this represents a prototypical case of Guillain-
Barré syndrome (GBS), which we’ll turn our attention to now.
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Figure 7.22 Guillain–Barré Syndrome
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Clinical Pearl: Guillain–Barré Syndrome
GBS, named after the French physicians who first described it in 1916, is more accurately
known as acute inflammatory demyelinating polyneuropathy (AIDP).
Classically, GBS occurs after an exposure to a trigger, such as a recent infection, or in

rare cases, a vaccination. The most common cause is Campylobacter jejuni infection; this
bacteria is often present in rivers and other bodies of water in a forest.
The infection is believed to trigger an autoimmune attack in which the immune

system mistakes the myelin sheaths of the PNS for the offending agent; demyelination
subsequently occurs. For reasons that are not completely understood, the longest nerves
are typically affected first. The patient’s symptoms typically begin in their feet and then
slowly ascend up the body. Symptoms are symmetric and bilateral.
Motor, sensory and autonomic nerves can all be involved. Compromise of the autonomic
nerves can lead to dangerous levels of dysfunction; by the time that the level of the thorax
is involved, patients can have wild fluctuations in heart rate and blood pressure. Most
concerning is involvement of the nerves leading to weakness of the diaphragm and
eventual respiratory failure.
Due to involvement of both sensory and motor systems, patients quickly lose their
reflexes completely. This so called areflexic paralysis is a highly specific sign of GBS.
Another highly specific finding is albuminocytologic dissociation found on lumbar
puncture. CSF analysis shows the protein is highly elevated indicating breakdown of the
blood brain barrier, but there is no increase in the amount of cells present, indicating
lack of an infection.
The speed of the attack in GBS can be extremely varied. Some patients decline and
need ICU admission within a matter of hours, whereas some will only suffer modest
involvement and recover within several weeks. In addition, there are no predictors as
to how far GBS will ascend up the body before beginning to remit. The natural history of
GBS is such that it spontaneously remits, and does not recur, though there are exceptions.
Medical treatment is largely supportive. Typically, remyelination occurs and the patient
recovers neurological function. Despite the advances in intensive care, GBS carries a 5%
mortality rate, and 20% of patients will have permanent neurological deficits.
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Case 23: The 17-year-old quarterback who passed out 311
Case 23: The 17-year-old quarterback who passed out
You are enjoying a beautiful Sunday afternoon in September watching your brother
compete in a high school football game. Much to your dismay, your brother’s team’s star
quarterback takes a brutal tackle, and appears knocked out. You slowly get up from the
stands, and walk down onto the field, but, to your surprise, he gets up and appears fine.
You breathe a sigh of relief and sit back down as you have a score to settle with a delicious
smelling hotdog.
Several hours later, you begin your shift in the Emergency Department. You go to see
your first patient and recognize the quarterback from before. His football team mates tell
you he was not very lively during the after party and only had one beer. They found him
passed out in the bathroom, and they were unable to awaken him, so they brought him
to the hospital.
When you examine him, he keeps dozing off unless you yell his name in his ear. He is
very slow to respond and when he does talk you find him to be very confused. Given his
somnolence you defer from formally evaluating his language, but he does, with prompting,
obey your commands. His right pupil is large and does not constrict as much to light as
the left pupil. When you shut off the lights, the left pupil dilates, but the right remains the
same size. However, both eyes appear midline and he has full eye movements. He has
mild ptosis of the eyelid on the right side. He has a mild facial droop on the right side, but
he can move his eyebrows. The rest of the CN can’t reliably be assessed.
A full motor examination is impossible. When you look at him, you see that he has
assumed a rather odd posture. His right arm is extended at the elbow, but flexed at the
wrist. His right leg is extended at the knee, and the foot is plantar flexed and internally
rotated. He has tremendously increased tone on the right, so much so that you can barely
move the limbs. The left side is normal. He has 3+ reflexes in the arm, and his knee and
ankle reflexes elicit clonus. His right toe is strongly upgoing. Once again, the left side is
normal. The only part of the sensory examination that can be performed is reaction to
pain; he does not seem to wince when you poke him in the right arm or leg. When you
rub on his sternum he tries to swat you away with this left arm, but not his right.
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Case 23: Findings
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Case 23: Solution
Our patient has tremendously increased tone and increased reflexes on the right (the
knee and ankle being graded at 4+ due to the clonus). He also has a right upgoing toe.
These are all signs of UMN pathology, so we can conclude that the lesion lies in the
CNS.
Rubbing on someone’s sternum inflicts significant pain. We can conclude that our patient
is weak on the right since he only used his left arm to try to get us to stop.
He also doesn’t feel pain in the right arm or leg. Unfortunately this doesn’t help us too
much, and the lesion could be in cortex, internal capsule, brainstem or cervical spine.
Our patient has an anisocoria; the right pupil is larger than the left one. The right does
not constrict well to light, so we suspect a parasympathetic problem. This is confirmed
by noting the anisocoria is greater in light than dark. This means that there is a
parasympathetic problem, and that the larger pupil (right) is the abnormal one. This is
supported by our finding of mild ptosis on the right. The parasympathetics are carried
by CN III; either the CN III nuclei in the midbrain or CN III itself is affected by the lesion.
The lesion involves either the right CN III or its nucleus in the midbrain. Since our patient
also has weakness and numbness, we can safely say our lesion must be in the midbrain.
Our patient has UMN symptoms in the right arm and leg. Since the corticospinal tract
decussates at the level of the medulla, this means that the left corticospinal tract is
affected.
But wait a moment, this would imply two separate lesions! Examining the cross section of
the midbrain we see that the right CN III and the left corticospinal tract are very far apart
from each other. How are our patient’s symptoms possible?
In order to answer the question, you will have to be told that the quarterback suffered a
large bleed on the right side of the brain, when he was initially hit. This began to expand,
and eventually put local pressure on the right side of the midbrain. This local pressure
caused the right sided CN III findings. However, the pressure then became so high that
the entire midbrain shifted to the left side of the skull and it began to press against the
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dura at the level of the tentorum cerebelli. The compression of the left midbrain caused
dysfunction of the left corticospinal tract.
The indentation of the contralateral midbrain by the tentorum cerebelli is also known as
compression due to Kernohan’s Notch, after the physician who first described it. It is one
of the few false localizing signs in neurology. As you can see, if you had localized based on
the more obvious pattern of weakness, and not examined the eyes (but you would never
do that would you?), you would have concluded the lesion was on the left. This was of
more clinical importance 50 years ago before the advent of computed tomography (CT)
scanners; during this time physicians had to use the bedside examination to determine
which side of the head to drill in order to relieve the increased ICP.
However, it remains true that in cases of decreased LOC, localization should be decided
based on eye findings, rather than the pattern of weakness!
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Figure 7.23 Cerebral Bleeds
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Clinical Pearl: Cerebral Bleeds
The brain is susceptible to four different types of hemorrhages. They are named according
to where the collection of blood, called a hematoma, forms.
1. Epidural Hematoma: This hemorrhage is typically caused by a skull fracture that

tears the middle meningeal artery (MMA), and is what happened to our unfortunate
quarterback in the previous case. The MMA runs between the skull bone and the dura
mater, so blood accumulates in the epidural space. Typically the initial trauma that
ruptures the MMA also transiently stuns the brain resulting in a brief loss of consciousness.
The brain recovers and consciousness is regained, but blood begins to slowly pool
in the epidural space. Eventually the hematoma grows so large it begins to cause the
brain to herniate, resulting in another, permanent (if untreated) loss of consciousness.
Importantly, there is a “lucid interval” between the episodes of loss of consciousness, as
we saw with our football player. On imaging, the hematoma often appears “lens shaped”
as it is confined by the cerebral sutures. If it is detected before herniation occurs it is
highly treatable with a favorable prognosis.
2. Subdural Hematoma: This hemorrhage is caused by rupture of the bridging veins,

which run between the subarachnoid space and the dural sinuses. Blood accumulates
in the subdural space between the dura mater and the arachnoid mater. It usually
occurs in the elderly as a result of falls. There is no lucid interval and a decreased level of
consciousness can occur soon after the initial trauma. On imaging the hematoma takes
on a more crescent appearance as it is not confined by the cerebral sutures. Prognosis is
highly dependent on how early it is treated.
3. Subarachnoid hemorrhage: This hemorrhage typically occurs as the result of

aneurysmal rupture of an artery in the Circle of Willis. Since these arteries lie in the
subarachnoid space, blood quickly accumulates there and mixes with CSF; this allows for
diagnosis by lumbar puncture. Patients typically present with a “thunderclap headache,”
which comes on fulminantly. On imaging blood is found within the various sulci and
fissures of the brain. The prognosis is poor even with prompt treatment.
4. Intracerebral hemorrhage: This hemorrhage is caused by a rupture of a small artery

deep within the brain tissue itself. The hematoma occurs in whatever part of the brain
the rupture occurred. It is common in the elderly and in those with uncontrolled
hypertension. Its symptoms depend on its location but it is usually associated with a
headache. These bleeds have a highly variable prognosis, dependent on their size and
location.
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Case 24: The 51-year-old man with tingly fingers 317
Case 24: The 51-year-old man with tingly fingers
You are asked to see a 51-year-old truck driver. He states that about a year ago he began
to notice numbness and tingling in the 4th and 5th digits of his left hand. He thought little
of it, but over the last several months he has noticed that he keeps dropping things out
of his left hand. He thinks it is worst right after a long day of driving. He decided to seek
medical help when he could no longer hold onto his cell phone reliably.
His language examination shows normal fluency, repetition and comprehension. He

has pupils that are equal and full visual fields and eye movements. He does not have a
facial droop and his tongue and palate are midline. You examine his left hand and find
significant atrophy in nearly the entire hand, but it is especially pronounced near the 4th
and 5th digits. His formal power examination is recorded below but he has full strength in
his legs. His reflexes are normal and his toes are downgoing. His sensory examination is
normal in the legs, however, in the arms, he has a profound loss to pinprick in the 5th digit
of the left hand. Digits 1, 2, and 3 have normal sensation, and he could feel the pin on the
lateral aspect of the 4th digit, but not the medial. His coordination examination is normal.
Power Examination
Right Left
Deltoid 5 5
Bicep 5 5
Tricep 5 5
WE 5 5
WF 5 4-
FE 5 5
FF* 5 4
DI 5 4-
EP 5 5
FP 5 5
ADP 5 4-
ABP 5 5
OP 5 5
*4th and 5th digits only; 2nd and 3rd digits normal power.
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Case 24: Findings
Some individual figures adapted from Waxman SG.

Clinical Neuroanatomy. Lange, New York, 2013.
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Case 24: Solution
Our patient presents with isolated hand weakness. An UMN type problem is certainly
possible, but it would have to be a very small lesion in order to only affect the hand;
a LMN type problem is much more likely. In addition, the patient has normal reflexes
and downgoing toes which are not in keeping with an UMN type lesion. Finally, we have
found significant atrophy of the affected hand, which is characteristic of a LMN type
weakness; we can thus conclude that our lesion lies in the PNS.
Potential localizations include a radiculopathy, plexopathy, or neuropathy.
Checking our table of dominant myotomes (Fig. 5.5) we see that the dorsal interossei
are innervated by T1 and the flexor digitorum is innervated by C8. Furthermore, it is
only our patients’ 4th and 5th flexor digitorum that are weak, which cannot be caused by
a radiculopathy.
Checking our table of dermatomes (Fig. 5.15) you might be tempted to say that our
patient’s sensory loss corresponds to the C8 dermatome. But if you look closely, you’ll
see that the C8 dermatome involves both the 4th and 5th digits in their entirety. Our patient
has intact sensation of the medial side of the 4th digit but not on the lateral.
We can thus safely conclude our patient’s symptoms are not caused by a radiculopathy.
In Chapter 5 we mentioned that the ulnar nerve supplies the majority of the hand
muscles, with a few notable exceptions, so let’s consider whether our patient has an
ulnar neuropathy.
We’ll begin with the sensory exam; as you can see the ulnar nerve “splits” the 4th digit,
which is what our patient complains of. Splitting of sensation across the 4th digit is
completely unique to an ulnar neuropathy. In addition, the ulnar nerve innervates
the flexor digitorum of the 4th and 5th digit only! This again is characteristic of an ulnar
neuropathy. We can safely conclude that is what we are dealing with.
Let’s draw out the path for the ulnar nerve and see where exactly our lesion is located. It
is easiest to begin distally; we know that the hand muscles are involved so we are at least
at the level of the wrist/Guyon’s canal. Moving up, we see that wrist flexion, provided by
flexor carpi, is also affected, so we are at least at the level of the elbow. The ulnar nerve
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does not have any branches in between the elbow and axilla, so that is as far as we can
tell clinically.
This case is an example of an ulnar neuropathy at the elbow, which is the second most
common peripheral neuropathy after carpal tunnel syndrome. In this neuropathy, the
ulnar nerve gets compressed by the distal humerus in an area of the cubital tunnel. This
happens whenever people rest their forearms on objects, such as, in this case, the driver’s
window of a truck.
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Figure 7.24 Nerve Injuries
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Clinical Pearl: Nerve Injuries
There are several types of injury that can occur to peripheral nerves, but before we can
consider them we need to review the internal architecture of a peripheral nerve.
A nerve is a bundle of axons. There are several important layers of connective tissue in a
nerve. Each individual axon is covered in a layer of protective connective tissue called an
endoneurium. Axons travel together and are surrounded by a layer of protective tissue
called the perineurium. The perineurium and the axons that it contains is referred to as
a fascicle.
The outermost layer of tissue of the nerve is the epineurium. Between the fascicles is
adipose tissue and arteries, called the vasa nervorum, as well as veins. Infarction of the
vasa nervorum can lead to death of that part of the nerve.
In 1943, HJ Seddon came up with a classification of peripheral nerve injury still used
today. He separated nerve injuries into three types:
1. Neurapraxia – in this case, there has been an attack of focal demyelination, but the axon
of the nerve remains completely intact. The nerve does not conduct action potentials
because of the myelin disruption. However, the Schwann cells will soon replace the
myelin and the nerve is fully restored within hours to days.
2. Axonotmesis – in this case the axon itself has been disrupted, BUT the endoneural
sheaths remain intact. The nerve undergoes a process called Wallerian degeneration.
Distal to the injury, the axon and its components are degraded by macrophages. The axon
will regrow, and the intact endoneural sheath serves to guide it to the correct location in
the muscle. The axon grows at a rate of about 1.5 mm per day. Thus the nerve may take
months or even years to recover. Recovery will likely not be full.
3. Neurotmesis – in this case there is a disruption of the connective tissue. Less severe
injuries have a disruption of the axon and the endoneurium, but more significant injuries
will include the perineurium and even the epineurium, leading to a total transection of
the nerve. Wallerian degeneration occurs, but because there is no endoneurium to guide
it, growth of the axon is chaotic and occurs in all directions leading to the formation of
a useless neuroma. Nearly all cases require surgical intervention in order to reconnect
connective tissue. If successful, then the axon will regrow at the 1.5 mm/day as above.
If the axon cannot recover, the muscle that it innervates can be re-innervated by a
neighbouring axon in a process called sprouting.
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Case 25: The 59-year-old man who couldn’t read 323
Case 25: The 59-year-old man who couldn’t read
Your friend, a psychiatrist, has asked you to see a patient that was initially referred to her.
The patient is a 59-year-old right handed man who has the odd complaint of not being
able to read. He previously worked as an accountant and tells you that he just woke up
this way one day.
You text your soon to be ex–friend and ask her why on earth she referred the patient to
you. However, before you dismiss the patient’s complaint you decide to dutifully do a
neurological exam. His language examination is normal; he speaks fluently, understands
complex instructions and can repeat. You hand him a book, and ask him to read. He tries,
but he says he’s unsure if there are even words on the page. You give him a pen, and ask
him to write something, assuming that he will return to you some nonsensical scribbles.
You’re taken a back when he hands you back the sheet with “I am in the Doctor’s office,
because I cannot read.” You ask him to write several more sentences, and they all return
in perfect order. You shuffle the papers, and hand him a random sentence he wrote,
asking him to read it. He states he cannot.
You continue your examination; you are quite surprised to find that he has lost the
right aspect of his visual field in each eye. His pupils are equal and he has full eye
movements. He does not have a facial droop and his tongue and palate are midline. His
motor examination including tone, reflexes, and power is completely normal. He has
downgoing toes bilaterally. Sensory examination to pinprick and vibration is normal.
Coordination testing is also normal.
Where is the lesion? What is going on here? How expensive a dinner will you buy your
psychiatrist friend in apology?
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Case 25: Findings
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Case 25: Solution
In this case, we’ll make a quick departure from our regular localizing algorithm as there
are no long tract findings to guide us.
We should begin with our patient’s visual field complaints. He has lost the right side of
his visual field in both eyes. This is consistent with a RHH. Recalling the visual pathway,
Fig. 3.5, we know that this is only possible for lesions that are posterior to the optic chiasm.
Since our patient has a RHH, we suspect that there is a lesion of the left occipital lobe.
Remember, aphasia is a disorder of language, not just of speech, even though speech
problems are the most common presentation. Thus, our patient is aphasic. In this case
the patient cannot read, which is called alexia, but can write perfectly. In other words, he
has alexia without agraphia (agraphia is the inability to write).
Perhaps if we consider what brain processes are involved in reading we will be able to
further classify our patient’s lesion. Firstly, he has a RHH; he is completely dependent on
his left visual field for all visual information. Thus, all visual information, including words
on the page of a book, is being received by the right occipital lobe. Language is controlled
by the dominant hemisphere. Since our patient is right handed, this means that the
visual information needs to be transmitted to Wernicke’s area in the left hemisphere, for
interpretation. This is facilitated by the splenium of the corpus callosum.
We know that our patient must have a lesion to the left occipital lobe in order to cause
the RHH. A particularly large lesion would extend into the corpus callosum, cutting off
this decussation of visual information to Wernicke’s area. This means that the patient
can see the words, but not be able to send them to Wernicke’s area for interpretation into
language. This would explain the alexia. Wernicke’s area itself, however, is intact, which
is why he does not have any problems with understanding speech. In addition, Broca’s
area is also intact, meaning the production of language, speech or written, is normal; he
does not have agraphia. It seems that we can explain our patient’s symptoms with a large
lesion to the left occipital cortex, extending into the corpus callosum!
Alexia without agraphia is an example of a disconnection syndrome, where the

symptoms are caused by a lesion in the white matter. This causes a critical interruption
in the transmission of information from one part of the brain to another. While quite rare
in real practice, it is particularly known for coming up in exams.
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Figure 7.25 White Matter Tracts of the Brain
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Clinical Pearl: White Matter Tracts of the Brain
White matter tracts pervade the brain. The white matter just below the level of the cortex
is called the centrum semiovale. Just inferior to the centrum semiovale lays the corona
radiata. White matter can be divided into three different types of tract:
1. Projection tracts: these tracts connect the cortex to various other parts of the CNS,
including the basal ganglia, cerebellum and spinal cord. We have already met many
examples of these including the long tracts, optic radiations, auditory radiations and
thalamocortical fibers.
2. Association tracts: these tracts connect parts of the same hemisphere to each other;
an example is the arcuate fasciculus that connects Wernicke’s area to Broca’s area.
U-fibers connect adjacent areas of cortex. The uncinate fasciculus connects the inferior
frontal lobe to the temporal lobe. The inferior longitudinal fasciculus connects the
occipital lobe to the temporal lobe and allows for the recognition of objects. The superior
longitudinal fasciculus connects the frontal lobe to the parietal and occipital lobes. The
cingulum is part of the cingulate gyrus and helps connect the basal ganglia.
3. Commissural tracts: these tracts connect the individual hemispheres to each other. The
corpus callosum is by far the largest and most important tract in this category. The much
smaller anterior commissure connects the two temporal lobes to each other and the
posterior commissure connects the pretectal nuclei of the midbrain. The hippocampal
commissure connects the hippocampi and plays an important role in the circuits of the
brain responsible for memory.
Knowledge of the white matter tracts is very important because they are often hijacked
in patients with epilepsy and used to spread seizure discharges from one area of the
brain to another. For example, a corpus callosotomy is a procedure in which the corpus
callosum is surgically transected; in patients with certain types of epilepsy this procedure
can reduce seizure frequency by upwards of 90%.
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329
Index
Note: page numbers in italics refer to figures and tables.
1st, 2nd and 3rd order neurons 12, 13 ankle

common peroneal nerve 146–7
abducens nerve (CN VI) 56, 57, 69, 71 tibial nerve 144–5
exit from the brainstem 58 ankle reflex, innervation 126, 127
exit through the base of the skull 86 anosognosia 41
pathway through the cavernous sinus 76, anterior cerebral artery (ACA) 16, 17, 46,
77 47
abducens nucleus 68, 73 ACA stroke 164
abductor pollicis 136, 137 territory 50, 51
aberrant firing 111 anterior choroidal artery 46, 47
acetylcholine (Ach) 194–5 territory 50, 51
action potentials 7 anterior circulation 16, 17, 46–7
acute inflammatory demyelinating anterior commissure 327
polyneuropathy see Guillain–Barré anterior communicating artery (ACOM) 16,
syndrome 17, 46, 47
adductor pollicis 134, 135 aneurysms 219, 220
adrenal glands 195 anterior cord lesions 171
adrenergic neurons 194–5 case study 185–7
agnosia 23, 40, 41 anterior horn cells (AHCs) 10, 11, 33, 100,
agraphesthesia 40, 41 101
case study 287–9 lesions in poliomyelitis 188, 189
alexia, case study 323–5 anterior inferior cerebellar artery (AICA) 16,
amyotrophic lateral sclerosis (ALS) 236–7 17, 48, 49
case study 233–5 territory 91, 92, 93
aneurysms anterior limb, internal capsule 30, 31
common sites 219 anterior nerve roots 10, 11
MCA 209–12 anterior radicular arteries 114, 115
PCOM 215–18 anterior root, spinal nerves 100, 101
anhidrosis, Horner’s syndrome 223 anterior spinal artery 48, 49, 114, 115
anisocoria anterior spinal artery stroke 187
CN III palsy 215–18 aphasia 23, 37, 38–9
medical vs. surgical 219–20 case studies
epidural hematoma 311–14 MCA stroke 179–81
Horner’s syndrome 192, 193, 221–4, superior branch of the MCA stroke
225–6, 299–302 239–41
lateral medullary syndrome 269–71
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330 Index
apraxia 23, 43 territory 92, 93

case studies top of the basilar syndrome 257–60
parasagittal meningioma 287–9 basilar perforators 48, 49, 254, 255
subarachnoid hemorrhage 209–12 “Bellman’s tip” pose 192, 193
arachnoid granulations 18, 19 berry (saccular) aneurysms 220
arachnoid mater 18, 19 see also aneurysms
arcuate fasciculus (AF) 36, 37 bicep reflex, innervation 126, 127
areflexic paralysis 309 biceps 131
arterial supply bitemporal hemianopsia 64, 65
central nervous system 16, 17 pituitary gland tumor 275–8
anterior circulation 46–7 bleeds see cerebral bleeds; subarachnoid
medulla 90–1 hemorrhage
midbrain 94–5 brachial plexus 10, 11, 121, 122–3
pons 92–3 how to draw it 124–5
posterior circulation 48–9 lower trunk (Klumpke’s) palsy 173
vascular territories of the brain 50–1 upper trunk (Erb–Duchenne) palsy 173
spinal cord 114–15 case study 191–3
artery dissection 259, 272–3 brain herniation syndromes 261–2
association cortex 40, 41 brainstem 8, 9
association tracts 327 arterial supply 91
astereognosis 40, 41 exit of cranial nerves 58–9
ataxia 45 peduncles 58, 59
heel to shin test 44 “Rule of 4” 88–9
lateral medullary syndrome 269–71 brainstem lesions
atrial fibrillation 183 crossed signs 55
atrophy 111 in multiple sclerosis 296, 297
auditory agnosia 41 bridging veins, rupture of 316
auditory association cortex 40 Broca’s aphasia 38, 39
auditory cortex 40 case study 239–41
autonomic nervous system 4, 5 Broca’s area 24, 25, 36, 37
cranial nerves 56, 57 Brown–Sequard syndrome 171
overview 20, 21 case study 299–302
pupillary size control 66–7 buccal branch, CN VII 78, 79
see also parasympathetic nervous system; buccofacial apraxia 43
sympathetic nervous system
autonomic neurotransmitters 194–5 callosomarginal artery 46, 47
axillary nerve 125, 130, 131 Campylobacter jejuni, Guillain–Barré
formation in the brachial plexus 122 syndrome 308, 309
sensory distribution 148, 149 “cape” sensory loss 230, 231
axonotmesis 321, 322 cardiac embolism 183
axons 6, 7 carotid endarterectomy 242, 243
carotid stenosis 242–3
Babinski sign (up-going toe) 112, 113 carotid stenting 242, 243
basal ganglia 26, 27 carpal tunnel 136
arterial supply 50–1 carpal tunnel syndrome 207–8
basilar artery 16, 17, 46, 48, 49, 114 cauda equina 98, 99, 267–8
aneurysms 219 cauda equina syndrome 170
stroke 245–7 case study 281–4
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Index 331
caudate 26, 27 cingulum 326, 327

arterial supply 50 Circle of Willis 16, 17, 19
cavernous sinus 47, 52, 53, 76–7 clonus 112, 113
bleeding into 277–8 cocaine eye drops, diagnosis of Horner’s
central cord syndrome 172 syndrome 225, 226
case study 227–9, 230–1 cochlear nerve 80, 81
central disc herniation 267, 268 cochlear nucleus 80, 81
central herniation 261, 262 collateral vasculature
central nervous system (CNS) 4, 5 Circle of Willis 16, 17, 19
arterial supply 16, 17 of the spinal cord 115
anterior circulation 46–7 coma 214
medulla 90–1 Glasgow Coma Scale 213
midbrain 94–5 see also loss of consciousness
pons 92–3 commissural tracts 327
posterior circulation 48–9 common carotid artery 16, 17
vascular territories of the brain 50–1 common peroneal nerve 142, 143, 145,
long tracts 12, 13 146–7
overview 8, 9 formation in the lumbosacral plexus 138,
somatotopy 14, 15 139
central sulcus 9 sensory distribution 148, 149
centrum semiovale 327 common peroneal neuropathy 176
cerebellar peduncle 58, 59 case study 263–6
cerebellum 8, 9, 44–5 communicating arteries 16, 17
arterial supply 48–9 see also anterior communicating artery;
cerebral aqueduct 18 posterior communicating artery
cerebral bleeds 315–16 conception tract, language circuit 37
epidural hematoma, case study 311–14 conduction aphasia 38, 39
see also subarachnoid hemorrhage confluence of sinuses 52, 53
cerebral infarction see stroke ‘coning’ (tonsillar herniation) 262
cerebral peduncle 58, 59 conjugate eye movement 73
cerebrospinal fluid (CSF) 18, 19 conscious sensation 5
analysis of 285–6 consciousness 29
Guillain–Barré syndrome 309 levels of 213–14
hydrocephalus 290–2 see also loss of consciousness
cerebrum 8, 9 constructional apraxia 43
cervical branch, CN VII 78, 79 conus medullaris 98, 99
cervical cord 102, 103 coordination, screening examination 161
cervical cord lesions 116, 117 corpus callosum 24, 26, 27, 327
high transection 168 arterial supply 50, 51
low transection 169 cortex
cervical nerves 10, 11 arterial supply 50–1
cervical vertebrae 98, 99 cerebral 9
chief sensory nucleus 75 specialized areas 24, 25
cholinergic neurons 194–5 corticobulbar tract 31, 32–3
chorda tympani 78 see also motor pathways
choroid plexus 18, 19 corticospinal tract 12, 13, 32–3
ciliary ganglion 60, 66, 67 crossed signs 55
cingulate gyrus 24, 25, 26 in the internal capsule 31
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332 Index
lesions 117 decerebrate posturing 213, 214

somatotopy 106, 107 decorticate posturing 213, 214
see also motor pathways decussation sites
corticothalamic fibers 31 corticospinal tract 33
cranial nerves 4, 5 dorsal columns 35
CN I (olfactory nerve) 86 long tracts 12, 13
CN II (optic nerve) 56, 57, 62, 63 optic chiasm 62, 63
CN III (oculomotor nerve) 49 spinothalamic tract 35
CN III palsy deep peroneal nerve 146, 147
case study 215–18 deltoid muscle 130, 131
medical vs. surgical 219–20 demyelination 297
CN IV (trochlear nerve) 69, 71, 76, 77 dendrites 6, 7
CN V (trigeminal nerve) 74–5, 76, 77 dermatomes 126, 127, 148, 149
CN VI (abducens nerve) 69, 71, 76, 77 diabetes, lipohyalinosis 254
CN VII (facial nerve) 78–9 diplopia
CN VIII (vestibulocochlear nerve) 80–1 multiple sclerosis 293–5
CN IX (glossopharyngeal nerve) 80–1 pituitary gland tumor 275–7
CN X (vagus nerve) 82–3 top of the basilar syndrome 257–60
CN XI (spinal accessory nerve) 84, 85 disconnection syndromes, case study 323–5
CN XII (hypoglossal nerve 84, 85 discs see intervertebral discs
exit from the brainstem 58–9 dissection, arterial 259, 271, 272–3
exit through the base of the skull 86–7 divisions of the nervous system 4, 5
extraocular muscle innervation 68–9 dominant myotomes 128–9
eye movements 70–1 dorsal columns (DC) 12, 13, 29, 34–5, 104,
conjugate gaze 72–3 105
facial sensation 74–5 crossed signs 55
motor innervation to the neck and the lesions 117
tongue 84–5 tabes dorsalis 188, 189
muscles of mastication 74, 75 screening examination 161
overview 56–7 somatotopy 106, 107
parasympathetic component 20, 21, dorsal interossei 134, 135
60–1 dorsal motor nucleus 60, 61, 82, 83
CN IX 80 location in the medulla 90
CN VII 78 dorsal root ganglion (DRG) 10, 11, 13, 100,
CN X 82, 83 101
pathway through the cavernous sinus lesions in tabes dorsalis 188, 189
76–7 “down and out” eye 215–18
screening examination 159 drowsiness 214
CREST (Carotid Revascularization dura mater 18, 19
Endarterectomy Stenting Trial) 243 dysarthria 37
cribriform plate 86 case study 197–9
crossed signs 55 dysconjugate gaze 73
basilar artery stroke 245–7
lateral medullary syndrome 269–71 Edinger–Westphal nucleus 60, 61, 66, 67, 94,
medial medullary syndrome 197–9 95
sensory 97, 104, 105 El Escorial criteria, amyotrophic lateral
cryptogenic stroke 183 sclerosis 236, 237
CSF see cerebrospinal fluid elbow, ulnar neuropathy 317–20
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Index 333
endarterectomy 242, 243 foramen magnum 86

endoneurium 321, 322 foramen ovale 86
epidural hematoma 315, 316 foramen rotundum 86
case study 311–14 fourth ventricle 18
epidural space 18, 19 frontal eye field (FEF) 24, 25, 73
epineurium 321, 322 lesions 181, 241, 248–9
Erb–Duchenne palsy 173 frontal lobe 8, 9
case study 191–3 arterial supply 50
extradural spinal cord lesions 303, 304
extensor carpi 132, 133 gait
extensor digitorum 132, 133 screening examination 161
extensor hallucis longus 146, 147 wide based 45
extensor pollicis 132, 133 ganglia 20, 21
external carotid artery 16, 17 definition of term 7
extraocular muscles 68–9 gastrocnemius 144, 145
eye movements 70–1 geniculate ganglion 78, 79
conjugate gaze 72–3 geniculate nuclei 28
“down and out” eye 215–18 genu
internuclear ophthalmoplegia 293–5 corpus callosum 26
“wrong way” eyes 248–9 internal capsule 30, 31
case study 245–7 geographic apraxia 43
Glasgow Coma Scale 213–14
facial droop 78, 79 global aphasia 38, 39
LMN 245–7 globus pallidus 26, 27
UMN glossopharyngeal nerve (CN IX) 56, 57,
lacunar stroke 251–3 80–1
MCA stroke 179–81 exit from the brainstem 58
subarachnoid hemorrhage 209–12 exit through the base of the skull 86
superior branch of the MCA stroke parasympathetic component 60, 61
239–41 gluteus maximus 140, 141
top of the basilar syndrome 257–60 gluteus minimus and medius muscles 140,
facial nerve (CN VII) 56, 57, 78–9 141
exit from the brainstem 58 gray matter
exit through the base of the skull 86 cerebral 9
parasympathetic component 60, 61 spinal cord 100, 101
facial nucleus 78, 92, 93 Great vein of Galen 52, 53
facial sensation 74–5 greater petrosal nerve 78
false localizing signs 314 Guillain–Barré syndrome 308–9
falx cerebri 18 case study 305–7
fasciculations 111 CSF analysis 285, 286
femoral nerve 142, 143 Guyon’s canal 134, 135
formation in the lumbosacral plexus 138, gyri 8, 9
139
sensory distribution 148, 149 hallucinations, top of the basilar syndrome
flexor carpi 134, 135 257–60
flexor digitorum 134, 135, 136, 137 hamstrings 142, 143
flexor pollicis 136, 137 Hand of Benediction (Preacher’s Hand) 207,
fluency of speech 39 208
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334 Index
headache, subarachnoid hemorrhage 209, inferior longitudinal fasciculus 326, 327

212, 316 inferior oblique muscle 68, 69
hearing 81 inferior olive 90, 91
heel to shin test 44, 45 inferior rectus muscle 68, 69
hemianopsia 64, 65 inferior sagittal sinus 52, 53
hemi-neglect 43 inferior salivatory nucleus 60, 61, 80, 81
case study 209–12 inferior vagal ganglion 82
hemispheres, cerebral 9 insula 26, 27
hemorrhage see cerebral bleeds; intercostal nerves, sensory distribution 148,
subarachnoid hemorrhage 149
hemorrhagic stroke 182, 183 internal acoustic meatus 78, 79, 86
herniation internal capsule 26, 27, 30–1
brain 261–2 arterial supply 50, 51
epidural hematoma 316 lesions
intervertebral discs 267–8 associated features 165
cauda equina syndrome 281–4 lacunar stroke 251–3, 254–5
higher functions 23 somatotopy 14
hip, nerves and muscles of 140–1 internal carotid artery (ICA) 16, 17, 46, 47
hippocampal commissure 327 pathway through the cavernous sinus 76,
homonymous hemianopsia 64, 65, 323–5 77
case studies internal cerebral veins 52
MCA stroke 179–81 internal jugular vein 52, 53
top of the basilar syndrome 257–60 internal medullary lamina 28, 29
homonymous quadrantanopsia 64, 65 internuclear ophthalmoplegia (INO) 295
homunculi 14, 15, 24 interspinous ligament 98, 99
horizontal gaze center (CN VI nucleus) 73 intervertebral discs 98, 99
Horner’s syndrome 225–6 herniation 267–8
case studies 221–4 cauda equina syndrome 281–4
brachial plexus lesion 191–3 intracerebral hemorrhage 315, 316
Brown–Sequard syndrome 299–302 intracranial pressure (ICP), Monro–Kellie
lateral medullary syndrome 269–71 (MK) Doctrine 291–2
hydrocephalus 290–2 intradural extramedullary spinal cord
hydroxyamphetamine, diagnosis of Horner’s lesions 303, 304
syndrome 225, 226 intralaminar nuclei, thalamus 29
hypertension, lipohyalinosis 254 intramedullary spinal cord lesions 303,
hypoglossal canal 86 304
hypoglossal nerve (CN XII) 56, 57, 84, 85 ischemic stroke 182, 183
exit from the brainstem 58
exit through the base of the skull 86 jugular foramen 86
hypoglossal nucleus 84, 85
location in the medulla 90 Kernohan’s notch 261, 262, 314
Klumpke’s palsy 173
ideomotor apraxia 43 knee, nerves and muscles of 142–3
iliopsoas muscle 140, 141 knee reflex, innervation 126, 127
inferior ganglion 80, 81
inferior gluteal nerve 140, 141 L5 radiculopathy 268
formation in the lumbosacral plexus 138, differentiation from peroneal neuropathy
139 265–6
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Index 335
lacunar stroke 183, 254–5 lumbar nerves 10, 11

case study 251–3 lumbar puncture 285–6
language in Guillain–Barré syndrome 309
screening examination 159 lumbar vertebrae 98, 99
see also alexia; aphasia lumbosacral anatomy 267–8
language areas 25 lumbosacral plexus 10, 11, 121
language circuit 36–7 how to draw it 138–9
and aphasias 38–9
lateral cutaneous nerve of the forearm 130, mandibular branch, CN V 74, 75
131, 148, 149 mandibular branch, CN VII 78, 79
lateral cutaneous nerve of the thigh 148, 149 Marcus Gunn pupil (RAPD) 279–80
lateral geniculate nucleus (LGN) 28, 62, 63 masseter muscle 75
lateral medullary syndrome 168 mastication 57, 74, 75
case study 269–71 maxillary branch of CN V 74, 75
lateral pons, lesions of 167 McDonald’s Criteria, multiple sclerosis 296,
lateral rectus muscle 68, 69 297
lateral ventricle 18 Meckel’s cave 75
lenticulostriate arteries 46, 47, 255 medial cutaneous nerve of the arm 148, 149
lesser petrosal nerve 80 medial geniculate nucleus (MGN) 28
levator palpebrae superioris 217 medial lemniscus (ML) 12, 13, 35, 293–5
level of consciousness (LOC) 213–14 location in the medulla 90
line bisection task 42, 43 location in the midbrain 94, 95
lipohyalinosis 254, 255 location in the pons 92, 93
localization, false signs 314 medial longitudinal fasciculus (MLF) 72–3
localization algorithm 154–8 lesions 293–5
locked-in syndrome 200–1 location in the medulla 90, 91
long tract lesions 117 location in the midbrain 94
crossed signs 55 location in the pons 92, 93
long tracts 12, 13 medial medullary syndrome 167
somatotopy 106–7 case study 197–9
see also corticospinal tract; dorsal medial pons, lesions 166
columns; medial lemniscus; medial rectus muscle 68, 69
spinothalamic tract median nerve 125, 136–7
loss of consciousness formation in the brachial plexus 122
brain herniation syndromes 261-2 sensory distribution 148, 149
epidural hematoma 311–14, 316 median nerve lesions 174
Glasgow Coma Scale 213–14 carpal tunnel syndrome 207–8
PCOM aneurysm rupture 215–17 medical CN III palsy 219, 220
top of the basilar syndrome 257–60 medulla 8, 9
Lou Gehrig’s disease see amyotrophic lateral exit of cranial nerves 58, 59
sclerosis lateral medullary syndrome 168, 269–71
lower motor neuron lesions 110–11 location of structures 90, 91
localization algorithm 154, 157–8 long tracts 12
see also facial droop medial medullary syndrome 167, 197–9
lower motor neurons (LMNs) 12, 13, 32, 33 vascular territories 90–1
lumbar cord 102, 103 meningeal dura mater 18, 19
lumbar cord lesions 116 meninges 18, 19
transection 170 meningioma, case study 287–9
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336 Index
meningitis, CSF analysis 285, 286 multiple sclerosis 296–7

mesencephalic trigeminal nucleus 75 case study 293–5
midbrain 8, 9 muscarinic acetylcholine receptors 195
exit of cranial nerves 58, 59 muscle table 162–3
long tracts 12 musculocutaneous nerve 125, 126, 127, 130,
vascular territories 94–5 131
midbrain syndrome 166 formation in the brachial plexus 122
middle cerebral artery (MCA) 16, 17, 46, 47 myelin 6, 7
aneurysms 219, 220 myotomes 127, 128–9
case study 209–12
MCA stroke 164 NASCET (North American Symptomatic
Case study 179–81 Carotid Endarterectomy Trial) 243
superior branch 239–41 neck, motor innervation 84, 85
territory 50, 51 neglect 43
middle meningeal artery (MMA) 316 case study 209–12
Millard Gubler syndrome, case study 245–7 nerve injuries 321–2
monocular vision loss 64, 65 nerve roots 121
mononeuropathy 120, 121 neural foramen 98, 99
common peroneal nerve 176, 263–6 neurapraxia 321, 322
median nerve 174 neuromas 322
carpal tunnel syndrome 207–8 neurons, anatomy of 6–7
radial nerve 174, 203–6 neuropathy 121
sciatic nerve 176 neurotmesis 321, 322
tibial nerve 175 neurotransmitters, autonomic 194–5
ulnar nerve 175, 317–20 nicotinic acetylcholine receptors 195
mononeuropathy multiplex 121 Nodes of Ranvier 6, 7
Monro–Kellie (MK) Doctrine 291–2 nondominant hemisphere lesions 43
motor cortex 8, 24, 25 nonobstructive (communicating)
arterial supply 50, 51 hydrocephalus 290, 291
somatotopy 14 nonspecific nuclei, thalamus 29
motor homunculus 24, 25 norepinephrine (NE) 194–5
motor pathways 12, 13, 32–3 nuclear lesions 295
crossed signs 55 nuclei for cranial nerves 57, 60–1
lesions 117 nuclei of the thalamus 28–9
amyotrophic lateral sclerosis 233–5, ‘nucleus’, use of the term 7
236–7 nucleus ambiguus 80, 81, 82, 83, 85
internal capsule stroke 251–3 location in the medulla 90
location in the medulla 90, 91 nucleus solitarius 57, 78, 79, 80, 81,
location in the midbrain 94, 95 82, 83
location in the pons 92, 93
somatotopy 106, 107 obstructive (noncommunicating)
motor system hydrocephalus 290, 291
muscle table 162–3 obtunded patients 214
neurotransmitters 194–5 case study 245–7
screening examination 159 obturator nerve 140, 141
muscle power assessment 160–1 formation in the lumbosacral plexus 138,
MRC Grading of Muscle Power Scale 160–1 139
Muller’s muscle 217 sensory distribution 148, 149
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Index 337
occipital lobe 8, 9, 62, 63 perineurium 321, 322

arterial supply 48, 49, 50, 51 periosteal dura mater 18, 19
oculomotor nerve (CN III) 56, 57, 69, 71 peripheral nerves 11
CN III palsy peripheral nervous system (PNS) 4, 5, 119
case study 215–18 dominant myotomes 128–9
medical vs. surgical 219–20 lesion types 120–1
exit from the brainstem 58 overview 10, 11
exit through the base of the skull 86 reflexes 126, 127
parasympathetic component 60, 61 sensory distribution 126–7, 148–9
pathway through the cavernous sinus 76, summary 150
77 peroneal neuropathy 176
pupillary size control 67 case study 263–6
oculomotor nucleus 68, 94, 95 peroneus muscle 146, 147
olfaction 57 pia mater 18, 19
olfactory nerve (CN I) 86 pituitary gland, relationship to the
oligodendrocytes 7 cavernous sinus 76, 77
ophthalmic artery 46, 47 pituitary gland tumor, case study 275–8
ophthalmic branch of CN V 74, 75 plexopathy 120, 121
opponens pollicis 136, 137 poliomyelitis 188, 189
optic canal 86 polyneuropathy 121
optic chiasm 62, 63 length dependent 307
relationship to the cavernous sinus 77 see also Guillain–Barré syndrome
optic nerve (CN II) 56, 57, 62, 63 pons 8, 9
exit from the brainstem 58–9 exit of cranial nerves 58, 59
exit through the base of the skull 86 lacunar stroke 254
optic neuritis 296, 297 lateral lesions 167
optic radiations 62, 63 long tracts 12
optic tract 62, 63 medial lesions 166, 245–7
otic ganglion 60, 80 “wrong way” eyes 248–9
vascular territories 92–3
pain sensation 13 postcentral gyrus 24, 25
see also spinothalamic tract posterior cerebral artery (PCA) 16, 17, 46,
paramedian pontine reticular formation 48, 49
(PPRF) 72, 73 PCA stroke 165
parasagittal meningioma, case study territory 50, 51, 94
287–9 posterior circulation 16, 17, 48–9
parasympathetic nervous system 4, 5 posterior commissure 327
cranial nerves 56, 57, 60–1 posterior communicating artery (PCOM) 16,
CN IX (glossopharyngeal nerve) 80 17, 46, 49
CN VII (facial nerve) 78, 79 aneurysms 219, 220
CN X (vagus nerve) 82, 83 case study 215–18
neurotransmitters 194–5 posterior cord lesions 172
overview 20, 21 posterior cutaneous nerve of the thigh 149
pupillary size control 66–7 posterior horn 104, 105
parietal lobe 8, 9 posterior inferior cerebellar artery (PICA)
arterial supply 50 16, 17, 48, 49, 114, 115
Parkinson’s disease 27, 95 territory 90, 91
pericallosal artery 46, 47 posterior limb, internal capsule 30, 31
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338 Index
posterior nerve roots 10, 11 radiculopathy 120, 121

posterior radicular arteries 114, 115 L5 268
posterior root, spinal nerves 100, 101 differentiation from peroneal
posterior spinal arteries 114, 115 neuropathy 265–6
posterolateral disc herniation 267, 268 Ranvier, Nodes of see Nodes of Ranvier
postganglionic neurons 21 recurrent laryngeal nerve 82
power assessment 160–1 red nucleus 94, 95
Preacher’s Hand (Hand of Benediction) 207, reflex arcs 108–9
208 effect of lower motor neuron lesions 111
precentral gyrus 24, 25 effect of upper motor neuron lesions 111,
preganglionic neurons 21 112
premotor cortex 24, 25 innervation 126, 127
pretectal nucleus 67 relapsing remitting MS 297
primary auditory area 24, 25 relative afferent pupillary defect (RAPD)
primary motor cortex 9 279–80
primary progressive MS 297 resting tone 111
primary sensory cortex 9 reticular activating system (RAS)? 214
projection tracts 327 retina 62, 63
pronator teres 136, 137 rigidity 112, 113
proprioception 13 “Rule of 4” 88–9
see also dorsal columns
prosopagnosia 41 saccular (berry) aneurysms 220
pterygoid muscles 75 see also aneurysms
pterygopalatine ganglion 60, 78 sacral cord 102, 103
ptosis sacral cord lesions 116
CN III palsy 215–17, 215–18, 219–20 sacral nerves 10, 11
epidural hematoma 311–14 sacral sparing, central cord syndrome 230,
Horner’s syndrome 222, 223, 225–6 231
pituitary gland tumor 275–8 sacral vertebrae 98, 99
top of the basilar syndrome 257–60 Saturday Night Palsy 203–6
pulvinar nucleus 28 Schwann cells 6, 7
pupillary light reflex 67 sciatic nerve 142, 143
pupillary size control 66–7 formation in the lumbosacral plexus 138,
relative afferent pupillary defect (RAPD) 139
279–80 sciatic nerve lesions 176
see also anisocoria screening examination
pure word deafness 41 coordination and gait 161
putamen 26, 27 cranial nerves 159
arterial supply 50 language 159
motor system 159
quadrantanopsia 64, 65 muscle power assessment 160–1
quadriceps 142, 143 muscle table 162–3
sensory system 161
radial nerve 125, 132–3 segmental arteries 114, 115
formation in the brachial plexus 122 seizures 249
sensory distribution 148, 149 semicircular canals 80, 81
radial nerve lesions 174 sensation, conscious and unconscious 5
case study 203–6 sensory association cortex 24, 25, 40
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Index 339
sensory bands 97, 104, 105 spinal cord 4, 8, 9, 99, 100–1

central cord syndrome 230–1 areas of body innervated by 102, 103
case study 227–9 arterial supply 114–15
sensory cortex 8, 24, 25 cross sections 102, 103
arterial supply 50, 51 long tracts 12
sensory homunculus 24, 25 sensory 104–5
sensory innervation 126, 127, 148 somatotopy 14, 106–7
axillary nerve 130, 131 stretch reflex 108–9
facial nerve (CN VII) 78–9 upper and lower motor neuron lesions
femoral nerve 142 110–11
glossopharyngeal nerve (CN VIII) 80–1 spinal cord disease 188–9
median nerve 136, 137 spinal cord lesions 116–17
musculocutaneous nerve 130, 131 anterior 171
obturator nerve 140, 141 case study 185–7
radial nerve 132, 133 Brown–Sequard syndrome 171
sciatic nerve 142 case study 299–302
tibial nerve 144 cauda equina 170
trigeminal nerve (CN V) 74–5 central cord syndrome 172, 230–1
ulnar nerve 134, 135 case study 227–9
vagus nerve (CN X) 82–3 cervical spine
sensory levels 97, 105 high transection 168
case study 185–7 low transection 169
sensory system, screening examination 161 classification of 303–4
sensory tracts 34–5 lumbar transection 170
spinal cord 104–5 posterior cord 172
see also dorsal columns; spinothalamic tract thoracic transection 169
“shawl” sensory loss 230, 231 spinal nerves 4, 5, 10, 11, 100, 101
sinuses, venous 18, 19, 52–3 spinal nucleus, location in the medulla 90
cavernous sinus 76–7 spinal trigeminal nucleus 75
sleep–wake cycle 29, 214 spine 98–9
small vessel disease see lacunar stroke spinocerebellar tract
soleus muscle 144, 145 location in the medulla 90, 91
solitary nucleus 90 location in the pons 92, 93
somatic nervous system 4, 5 spinothalamic tract (ST) 12, 13, 29, 34–5,
somatotopy 14, 15, 24 104, 105
cerebellum 44, 45 crossed signs 55
internal capsule 31 lesions 117
motor pathways 32–3 location in the medulla 90, 91
sensory pathways 34–5 location in the midbrain 94, 95
spinal cord 101, 106–7 location in the pons 92, 93
spinal nerves 101 screening examination 161
spasticity 112, 113 somatotopy 106, 107
specific nuclei, thalamus 29 spinous processes 98, 99
speech see aphasia; language areas; spiral groove, humerus 206
language circuit splenium, corpus callosum 26
spinal accessory nerve (CN XI) 56, 57, 84, 85 sprouting 322
exit from the brainstem 58 stenting 242, 243
exit through the base of the skull 86 sternocleidomastoid (SCM) muscle 84, 85
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340 Index
straight sinus 52, 53 superior longitudinal fasciculus 326, 327

strawberry picker’s palsy see common superior oblique muscle 68, 69
peroneal neuropathy superior orbital fissure 86
stretch reflexes 108–9 superior rectus muscle 68, 69
effect of lower motor neuron lesions 111 superior sagittal sinus 52, 53
effect of upper motor neuron lesions 111, superior salivatory nucleus 60, 61, 78, 79
112 supinator muscle 132, 133
grading of 109 supplementary motor area 24, 25
innervation 126, 127 supraclavicular nerves, sensory distribution
stroke 148
anterior spinal artery 187 supranuclear lesions 295
basilar artery 245–7 surgical CN III palsy 219, 220
causes of 182–3 swinging light test 279, 280
artery dissection 272–3 Sylvian fissure 8, 9
lacunar 254–5 sympathetic chain 20
case study 251–3 sympathetic nervous system 4, 5
lateral medullary syndrome 269–71 Horner’s syndrome 225–6
medial medullary syndrome 197–9 case study 221–4
middle cerebral artery occlusion 179–81 neurotransmitters 194–5
superior branch of the MCA overview 20, 21
case study 239–41 pupillary size control 66–7
top of the basilar syndrome sympathetics
case study 257–60 location in the medulla 90, 91, 92
stroke localization location in the midbrain 94, 95
ACA 164 location in the pons 92, 93
MCA 164 syringomyelia 229, 231
PCA 165
stupor 214 tabes dorsalis 188, 189
stylopharygeus muscle 80, 81 tactile agnosia 41
subacute combined degeneration (SACD), temperature sensation 13
spinal cord 188, 189 see also spinothalamic tract
subarachnoid hemorrhage 315, 316 temporal branch, CN VII 78, 79
case study 209–12 temporal lobe 8, 9
subarachnoid space 18, 19 arterial supply 48, 49, 50, 51
subdural hematoma 315, 316 temporalis muscle 75
subdural space 18, 19 tentorium cerebelli 18, 261
subfalcine herniation 261, 262 thalamocortical fibers 31
submandibular ganglion 60, 78 thalamus 26, 27
substantia nigra 26, 27, 94, 95 arterial supply 50
arterial supply 50 lacunar stroke 254
sulci 8, 9 lateral geniculate nucleus 62, 63
superficial peroneal nerve 146, 147 long tracts 13
superior cerebellar artery (SCA) 16, 17, 48, nuclei of 28–9
49 third ventricle 18
territory 91, 94 thoracic cord 102, 103
superior gluteal nerve 140, 141 thoracic cord lesions 116
formation in the lumbosacral plexus 138, transection 169
139 thoracic nerves 10, 11
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Index 341
thoracic vertebrae 98, 99 ulnar nerve lesions 175

thunderclap headache 209, 212, 316 case study 317–20
tibial nerve 142, 143, 144–5 uncal herniation 261, 262
formation in the lumbosacral plexus 138, uncinate fasciculus 326, 327
139 unconscious sensation 5
sensory distribution 148, 149 unconsciousness, Glasgow Coma Scale
tibial nerve lesions 175 213–14
tibialis anterior 146, 147 up-going toe (Babinski sign) 112, 113
tibialis posterior 144, 145, 266 upper motor neuron lesions 110–11
tone 111 clinical features 112–13
effect of upper motor neuron lesions 112, localization algorithm 154–6, 158
113 see also facial droop
tongue upper motor neurons (UMNs) 12, 13,
deviation of 197–9 32, 33
motor innervation 84, 85 upward herniation 261, 262
tonsillar herniation 261, 262 urinary incontinence, case study 287–9
top of the basilar syndrome 257–60
transcortical motor (TCM) aphasia 38, 39 vagus nerve (CN X) 56, 57, 82–3
transcortical sensory (TCS) aphasia 38, 39 exit from the brainstem 58
transient ischemic attacks (TIAs) 243 exit through the base of the skull 86
case histories 221, 239 parasympathetic component 60, 61
transverse myelitis 296 vasa nervorum 322
transverse processes 98, 99 vascular territories of the brain 50–1
transverse sinus 52, 53 medulla 90–1
trapezius muscle 84, 85 midbrain 94–5
tremor, heel to shin test 44, 45 pons 92–3
tricep reflex, innervation 126, 127 vegetative state 214
triceps 132, 133 venous drainage of the head 52–3
trigeminal ganglion 74, 75 venous sinuses 18, 19
trigeminal motor nucleus 74, 75 ventral anterior (VA) nucleus 28
trigeminal nerve (CN V) 56, 57, 74–5 ventral lateral nucleus (VLN) 28
exit from the brainstem 58 ventral posterior lateral (VPL) nucleus 28,
exit through the base of the skull 86 29, 35
pathway through the cavernous sinus 76, ventral posteromedial (VPM) nucleus 28,
77 29, 35
trigeminal nucleus 92, 93 ventricles 18, 19
trigeminal sensory nuclei 75 hydrocephalus 290–2
trochlear nerve (CN IV) 56, 69, 71 vermis 44, 45
exit from the brainstem 57, 58 vertebrae 98, 99
exit through the base of the skull 86 vertebral artery 16, 17, 46, 48, 49, 114, 115
pathway through the cavernous sinus 76, 77 territory 90, 91
trochlear nucleus 68 vertebral artery dissection 259, 271,
truncal ataxia 45 272–3
vertebral foramen 99
U-fibers 326, 327 vestibular nerve 80, 81
ulnar nerve 125, 134–5 vestibular nucleus 80, 81
formation in the brachial plexus 122 location in the medulla 90
sensory distribution 148, 149 location in the pons 92
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342 Index
vestibulocochlear nerve (CN VIII) 56, 57, Wallenberg syndrome (lateral medullary
80–1 syndrome) 269–71
exit from the brainstem 58 Wallerian degeneration 322
exit through the base of the skull 86 Wernicke’s aphasia 38, 39
vibration sensation 13 Wernicke’s area 24, 25, 36
see also dorsal columns “whiplash” injury 231
visual agnosia 41 white matter
visual association cortex 40 cerebral 9
visual cortex 24 tracts of the brain 326–7
visual field defects 64–5 in the spinal cord 100, 101
bitemporal hemianopsia 275–8 wide based gait 45
homonymous hemianopsia 323–5 Willis, Circle of see Circle of Willis
visual fields 62, 63 “wrong way” eyes 245–7, 248–9
visual pathway 62–3
vitamin B12 deficiency 189 zygomatic branch, CN VII 78, 79
voluntary-automatic dissociation 43
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Case Closed Neuroanatomy

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Case Closed Neuroanatomy

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CASE CLOSED!

K25928_C000.indd 1 10/01/2017 10:48

WARREN BERGER BSc BESc MD

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© 2017 by Taylor & Francis Group, LLC

No claim to original U.S. Government works

Printed on acid-free paper

International Standard Book Number-13: 978-1-4987-2852-2 (Paperback)

Visit the Taylor & Francis Web site at

and the CRC Press Web site at

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2 The Cortex and Associated Structures 23

3 The Cranial Nerves and the Brainstem 55

4 The Spinal Cord 97

5 The Peripheral Nervous System 119

6 Localization Primer 153

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In Chapters 1–5 we present the core fundamentals of neuroanatomy as we work through

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LOC level of consciousness RAS reticular activating system

ML medial lemniscus, also medial – SACD subacute combined

MLF medial longitudinal fasciculus SCA superior cerebellar artery

MMA middle meningeal artery SCM sternocleidomastoid

MRC Medical Research Council SO superior oblique muscle

MRI magnetic resonance imaging SR superior rectus muscle

MS multiple sclerosis ST spinothalamic tract

NE norepinephrine SUP supinator

NMJ neuromuscular junction TCM transcortical motor (aphasia)

OP opponens (short for opponens TCS transcortical sensory (aphasia)

PRO pronator (short for pronator WF wrist flexor

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Figure 1.1 Divisions of the Nervous System

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Let’s begin by examining the divisions of the nervous system.

Take Home Messages

The CNS is made up of the brain and spinal cord.

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Figure 1.2 Anatomy of a Neuron

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Before we continue, it is useful to go over the anatomy of a neuron. A neuron is a single

Take Home Messages

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Figure 1.3 Overview of the Central Nervous System

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Take Home Messages

The brain is made up of the cerebrum, brainstem and cerebellum.

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Figure 1.4 Overview of the Peripheral Nervous System

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Take Home Messages

31 paired spinal nerves exit the spinal cord: 8 cervical, 12 thoracic,

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Figure 1.5 Long Tracts of the Central Nervous System

LMN: lower motor neuron; UMN: upper motor neuron.

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Take Home Messages

Motor information is transmitted by the UMN (motor cortex to AHC) and

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Figure 1.6 Somatotopy of the Central Nervous System

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