ESSENTIAL NEUROSURGERY FOR MEDICAL STUDENTS
The Neurological Examination
Matthew McCoyd, MD∗
Arash Salardini, MD‡
José Biller, MD∗
∗
Department of Neurology, Stritch
School of Medicine, Loyola University
Chicago, Chicago, Illinois; ‡ Department
of Neurology, Yale School of Medicine,
New Haven, Connecticut
Given constraints of this publication
modality (ie, a book rather than journal
articles), the citations and bibliography
are not to the level of detail of a journal
article. Readers are directed to the
suggested reading lists, which contain
references to subsequent references and
derivatives of the article content.
Correspondence:
Matthew McCoyd, MD,
Department of Neurology,
Loyala University Health System,
2160 S. First Ave,
Maywood, IL 60153.
Email: mmccoyd@lumc.edu
Received, February 22, 2019.
Accepted, March 19, 2019.
Published Online, May 17, 2019.
Copyright 
C 2019 by the
Congress of Neurological Surgeons
OPERATIVE NEUROSURGERY
T
he fundamentals of the neurological
examination are essential to any neuro-
scientist. The neurological examination,
combined with obtaining a thorough medical
history, allows the examiner to define and localize
any neurological disorder. No ancillary testing is
necessary to conclude the correct localization and
diagnosis—testing only helps confirm what the
examiner has concluded based on the history and
physical examination. Armed simply with the
examiner’s eyes and ears, and the basic tools of the
neurological examination, a modern neurosci-
entist is as well armed as any of the legends of the
neurosciences such as Charcot and Cushing—if
he or she knows what to listen and look for. The
following section focuses on some of the funda-
mental aspects of the neurological examination
that may aid in the proper localization of neuro-
logical disease.
The neurological examination is the last of
the great examinations in medicine. Unlike other
specialties, the skill of the examining neuro-
scientist is not easily replaced by technology.
If the examiner takes a proper history and
performs a proper examination, the lesion can
be adequately localized, and ancillary testing is
then used to confirm the examiner’s suspicion.
Ancillary testing (magnetic resonance imaging
[MRI], nerve conduction studies, electroen-
cephalography, etc.) is of little value in the
absence of the clinical context.
In assessing a patient, the examiner should be
able to answer the following questions:
1. Is there a primary neurological problem (or is
the primary pathology non-neurological)?
2. If there is a primary neurological disorder,
does it involve the central (CNS) or peri-
ABBREVIATIONS: APB, abductor pollicis brevis;
ADM, adductor digiti minimi; CNS, central nervous
system; ED, emergency department; EIP, extensor
indices proprius; EMG, electromyography; GBS,
Guillain-Barré syndrome; MRI, magnetic resonance
imaging; NCS, nerve conduction study; PNS,
peripheral nervous system; VPM, ventral posterior-
medial
WWW.CNS.ORG
pheral nervous system (PNS; as there are very
few disorders that affect both)?
3. If the disorder is primary to the CNS, does
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it involve the cortex, subcortical structures,
brainstem, cerebellum or spinal cord?
4. If the disorder is primary to the PNS, does it
involve the neuron (motor or sensory), nerve
(be it the root, plexus, individual nerve or
group of nerves), neuromuscular junction, or
muscle?
The neurological examination, with its certain
tell-tale signs, should help the examiner make
these determinations. A thorough neurological
examination does not take long, particularly
if performed efficiently—in a well-organized
examination each tool needs only be pulled
out once, used to completion, and put away
(Table 1). The neurological examination does
require an understanding of neuroanatomy, as
the examination is based on the fundamentals of
neuroanatomy. Neuroanatomic knowledge is the
currency of the neuroscientist, affording him or
her the ability to make the proper diagnosis,
even when challenging. Syndromic learning—
memorizing lists of symptoms and associating
them with a name—is pointless other than for
historic interest. It is more important to under-
stand the anatomic relationship between struc-
tures so one can easily localize a lesion that would
affect them.
The neurological examination also requires
the examiner to recognize that the neurological
examination is actually being performed. The
neurological examination begins as soon as the
examiner lays eyes on the patient. When one
first enters the encounter with the patient, what
does he or she look like? Is the patient awake
and alert, confused and disheveled, unable to be
even aroused? With your opening questions, is
the patient able to understand you and answer
back properly, suggesting he or she can hear you,
language centers are intact, and motor pathways
for speech are functioning? What does his or her
voice sound like? Is it normal, soft and breathy,
or dysarthric? As you move about the room, is
the patient able to follow your movements with
his or her eyes? Does the face appear symmetric,
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McCOYD ET AL

TABLE 1. The Neurological Examination

Initial survey of the patient: What does he or she look like and sound like? A great deal of the neurological examination can be
done just while interviewing the patient!
If possible, have the patient stand from a seated position, without the use of his/her arms, The ability to stand and walk tests numerous
and walk down a hall on his/her tiptoes, walk back on his/her heels, and tandem systems. While it may not localize to 1 specific
disorder, it helps identify a neurological disorder if
present.

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Have the patient stand with feet close together, arms outstretched, and eyes closed Romberg sign: patient cannot perform. Also
indicates a likely neurological disorder but does not
localize to the CNS or PNS
If standing, have the patient sit down on the examination table (or sit up in the bed if
possible).
Observe the patient’s face and eyes for asymmetry.
With the lights off and an appropriate light source, test each eye independently for pupil Afferent pupillary defect can represent a retrobulbar
response to direct and indirect light. optic neuritis: asymmetric pupils are pathological
until proven otherwise.
Have the patient look towards the junction of the wall and ceiling to perform the Papilledema represents increased intracranial
funduscopic examination in each eye pressure from some etiology and urgent imaging is
warranted.
Have the patient track your finger in the horizontal and vertical planes
Examination sensation in the face, working from side-to-side and from the inner face to The sensory innervation of the face is an
the outer face “onion-skinned” pattern with the fibers from the
outer face resting as caudally as the cervical spine.
Have the patient smile, bite down, and raise his/her eyebrows Spontaneous smiling and volitional smiling have
different pathways
Examine the patient’s tongue at rest for evidence of atrophy and/or fasciculations. Observe Palatal tremor can occur with lesions involving the
the elevation of the palate. Guillain-Mollaret triangle, such as AVMs of the
brainstem.
Observe the patient’s muscle bulk Patients must be appropriately disrobed to examine
muscle bulk.
Check muscle tone in both passive and active range of motion
Check muscle strength: deltoid, biceps, triceps, flexor carpi radialis, and interossei; in doing If an abnormality is found, check other muscles
so the examiner has checked each and every nerve and nerve root. For the lower supplied by the same nerve and nerve root.
extremities: iliopsoas, quadriceps, hamstrings, tibialis anterior, gastrocnemius, extensor
digitorum brevis
Check reflexes: biceps, triceps, brachioradialis, patellae, ankle. Check side-to-side to A reflex hammer must be used and should be of
observe for differences sufficient weight swung at a sufficient velocity.
Check vibratory sensation, position sense, and pin sensation. Start at the toes and proceed A 128-Hz tuning fork should be used for vibratory
rostrally sensation
The motor examination of the upper extremity should be done first, then upper extremity
reflexes, then lower extremity reflexes, then sensation of the lower extremity working back
upwards to the upper extremity. In doing so, the examiner takes each tool out only once, uses it
to completion, and then returns it.

AVM, arteriovenous malformation; CNS, central nervous system; PNS, peripheral nervous system

and does it remain so when the patient smiles on command and
spontaneously? Can he or she hold her head up? Do the shoulders
appear symmetric or drooped? Are the arms at rest or is there the
presence of a rest tremor? Is the patient able to arise from a chair
in the room or from the hospital bed? All of this information, and
more, can be—and should be—gathered before one even begins
the traditional “formal” neurological examination.
Institutional Review Board approval was not necessary for this
study. Patient consent for the cases in each section was obtained
directly from the patients; in instances in which consent could not
be obtained, patient information has been anonymized.
CHAPTER 1: CRANIAL NERVES AND BRAINSTEM
Case Presentation
Before presenting the case, refer to Figure 1. Is this normal
or abnormal? Look at it again after reviewing the case and
discussion.
A 67-yr-old woman presented to the clinic with complaint of
the gradual development of difficulty in swallowing. Her voice
was noted to be slightly soft, and she and her husband attested
that they had noticed voice changes at about the same time and
pace as the swallowing problems. She did not have double vision

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FIGURE 1. Before reviewing the case, is the above figure normal or abnormal (and if you have reflexively answered “abnormal”—what is the abnormality?). Ancillary
testing, in the absence of a well performed history and physical examination, is not particularly helpful. Now review the case—is it normal or abnormal and why?
at any point, numbness in her face or body, weakness of arms
or legs, or difficulty in walking. While conducting the interview,
the physician was able to note that the face was symmetric,
the palpebral fissures were symmetric, eye movements appeared
normal (later confirmed during the “formal” neurological exami-
nation), but that the right shoulder was notably drooped. When
asked, the patient reported that she also had difficulty raising her
right arm over her head. Notable findings on the patient’s neuro-
logical examination included incomplete right palatal elevation,
atrophy of the right trapezius, and the inability to abduct the
right arm above 90◦ (essentially to the level of the shoulder).
The remainder of the examination was largely normal, including
sensation of the face, finger–nose–finger and heel–shin testing,
tongue movements, pin sensation and vibratory strength in the
arms and legs, normal strength and reflexes.
Questions
1. Where is the lesion?
a. CNS
b. PNS
2. Which nerve is responsible for shoulder abduction above 90◦ ?
a. Axillary nerve (deltoid)
b. Suprascapular nerve (supraspinatus)
c. Dorsal scapular nerve (rhomboid)
d. Spinal accessory nerve (trapezius)
3. Which nerve is responsible for palatal elevation?
a. Hypoglossal nerve
b. Glossopharyngeal nerve
c. Vagus nerve
OPERATIVE NEUROSURGERY
THE NEUROLOGICAL EXAMINATION
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d. Spinal accessory nerve
4. Through which foramen do the vagus nerve, glossopharyngeal
nerve, and spinal accessory nerve exit the skull?
a. Foramen magnum
b. Foramen rotundum
c. Jugular foramen
d. Foramen ovale
Case Discussion
While possibly a more challenging case for learners of all levels,
there are several “clinical pearls” in this case that highlight a few
fundamental aspects of the neurological examination. The first
clinical pearl is in the fact that so much localizing information
was available to the physician simply by ‘listening’ to the patient and
‘looking’ at the patient (which cannot be done while staring at a
computer screen with one’s back to the patient). The patient has
a severely drooped right shoulder—which would suggest atrophy
of the trapezius, innervated by the spinal accessory nerve; the
trapezius serves to rotate the scapula to allow the arm to be
elevated above a 90◦ plane. There is the suggestion of palatal
weakness characterized by difficulty in swallowing and softening
of voice, which are functions supplied by the glossopharyngeal
and vagus nerves. The face is symmetric, suggesting the facial
nerve and its muscles are normal.
The second clinical pearl is that an understanding of basic
neuroanatomic fundamentals helps localize the lesion, even if one
is not completely confident as to the exact localization. Can you
localize this lesion to the CNS or to the PNS? There is weakness
of the trapezius and palatal muscles, but no numbness of the
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McCOYD ET AL
face or body. Throughout virtually all of neuroanatomy, motor
pathways are anterior, and sensory pathways are posterior (even
the spinothalamic tract, though found in the anterior lateral spinal
cord, slowly moves to the dorsal aspect of the brainstem as it
ascends before entering the posterior aspect of the thalamus). In
the spinal cord, the motor nuclei reside in the anterior horn cell,
the sensory neurons are found in the dorsal root ganglion. In the
thalamus, nuclei involved in motor planning (the ventral anterior
and ventral lateral nuclei) are anterior to the nuclei involved in
routing sensory information (the ventral posterior medial, ventral
posterior lateral, and the pulvinar). In the cortex, the motor
strip is anterior to the somatosensory strip. In the brainstem,
cranial nerve nuclei with sensory functions begin posteriorly and
are displaced laterally during development, ultimately residing
lateral to the sulcus limitans; cranial nerve motor nuclei remain
in a more anterior location, medial to the sulcus limitans. The
glossopharyngeal nerve, vagus nerve, and spinal accessory motor
nuclei are all classified as special visceral efferent nuclei, residing
in an anterior lateral position in the brainstem, just medial to
the sulcus limitans. The spinal trigeminal tract, a general sensory
afferent nuclei carrying pain and temperature sensation from
the face caudally to the upper cervical spine (before crossing the
midline to ascend to the ventral posterior-medial [VPM] of the
thalamus), resides just lateral to the sulcus limitans. In the clinical
case provided, the patient reported normal sensation in the face
and body—pathways that are immediately next to the glossopha-
ryngeal, vagus, and spinal accessory nuclei in the brainstem,
making a brainstem lesion highly unlikely to be the source of
the patient’s symptoms. Armed with the basic understanding of
anatomy and the patient’s physical examination, the physician
should be able to localize the lesion external to the brainstem (and
the CNS) and place it in the PNS (remember, a cranial nerve
becomes a peripheral nerve as soon as it pierces the dura and is
myelinated by Schwann cells instead of oligodendrocytes).
The third clinical pearl is that one often finds what one goes
looking for. Refer to Figure 1. Is it normal or abnormal? The
astute physician, having listened to the patient, observed the
patient, and examined the patient with a good understanding of
neuroanatomy, would have deduced that the patient’s symptoms
are the result of a lesion either at or near the jugular foramen—
one of the few places all 3 nerves are in close proximity to
each other and too little else—impinging the spinal accessory
nerve, glossopharyngeal nerve, and vagus nerve. The physician’s
attention on the imaging is drawn to the base of the skull on the
right, where a large glomus tumor becomes readily apparent.
Answers
1. B. Cranial nerves are mistakenly assumed to be entirely part of
the CNS by some learners. The cranial nerves (except cranial
nerves I and II) are simply peripheral nerves that exit the
cranium, with their respective nuclei housed in the brainstem
(the notable exception being the spinal accessory nerve, which
originates mostly in the cervical spine, exits the spinal cord,
ascends through the foramen magnum, then turns and passes
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through the jugular foramen. The accessory nucleus in the
brainstem is arguably part of the nucleus ambiguus). Once
nerves pierce the dura and are myelinated by Schwann cells
instead of oligodendrocytes, they are part of the PNS.
2. D. Spinal Accessory. The axillary nerve innervates the deltoid
and the suprascapular nerve innervates the supraspinatus,
which are responsible for abducting the shoulder. However,
to abduct above 90◦ the lateral edge of the scapula has to be
rotated upwards—which is done by the trapezius, the upper
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portion of which is innervated by the spinal accessory (the
lower trapezius is supplied by the motor roots of C3 and C4).
3. C. The vagus nerve is responsible for elevation of the palate
(as well as the larynx).
4. C. Jugular foramen.
CHAPTER 2: CROSSED-BRAIN FINDINGS
Case Presentation
A 36-yr-old woman presents to the emergency department
(ED) for sudden onset dizziness. For several days prior to presen-
tation she had noticed transient numbness of her left face, lasting
from just a few moments to no more than a few minutes, and
occasionally numbness of her right arm of a similar duration.
She had reported to her personal trainer a nagging neck pain,
which they both attributed to her recent exercise routine. The
day of presentation she had sudden difficulty while eating—she
had been holding a bowl of cereal with her left hand but clumsily
lost control of the bowl, spilling it in her rental car, had some
difficulty with speech with her words seeming “garbled,” and felt
quite off balance.
The ED physician consulted the neurosurgical team to evaluate
the patient for a possible aneurysm after astutely noticing mild left
eyelid ptosis. On examination, the patient had mild ptosis of the
left eyelid, just reaching the top of the iris on the left. The left
pupil was also noted to be slightly smaller than the right pupil;
both pupils were reactive to direct and indirect light. The patient
also reported decreased sensation to light touch involving her left
face as well as her right arm and right leg, with intact propri-
oception and position sense. There was normal strength of the
face, arms, and legs, with noted dysmetria on finger–nose–finger
testing of the left arm.
1. Where is the lesion?
a. CNS
b. PNS
2. What is the etiology of the patient’s ptosis within the context
of the overall examination?
a. Compressive lesion of the oculomotor nerve (third cranial
nerve)
b. Microvascular intrinsic lesion of the oculomotor nerve
(third cranial nerve)
c. Lesion of the descending sympathetic pathway in the
brainstem
d. Damage to intracranial sympathetic plexus on the internal
carotid artery
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3. Involvement of which structure is contributing to the left arm
dysmetria?
a. Right globose cerebellar nuclei
b. Right inferior cerebellar peduncle
c. Left superior cerebellar peduncle
d. Right corticospinal tract
Case Discussion
This case, hopefully, highlights how a well-prepared neurosci-
entist can quickly localize a neurological lesion armed with basic
information about the neurological examination and the funda-
mentals of neuroanatomy. While the emergency room physician
should be commended for noticing the patient’s ptosis, he or she
failed to recognize the type of ptosis within the context of the
overall neurological examination.
If there is perhaps 1 major clinical pearl to take from this case,
it is that “crossed-brain” findings localize to the brainstem until
proven otherwise. The patient reported numbness of the left face,
due to involvement of the ipsilateral spinal tract of the trigeminal
nerve (but not proprioceptive or vibratory dysfunction, which
enters the brainstem with the other trigeminal fibers, cross the
midline immediately, and ascend in the medial aspect of the
medial lemniscus to reach the VPM nucleus of the thalamus),
and numbness of the right body due to involvement of the
neighboring ascending spinothalamic tract, which crosses from
right-to-left shortly after entering the spinal cord. There are
a number of crossed-brain findings, involving cranial nerve
dysfunction on one side and some focal neurological deficit
on the contralateral side of the body, all of which immediately
localize to the brainstem.
A second clinical pearl is that ptosis is not pathognomonic for an
aneurysm or a herniation syndrome. Ptosis in-and-of-itself does not
have a strong localizing quality, as it may be due to dysfunction
of nerve, the neuromuscular junction, or muscle. The degree
of ptosis and the degree of pupil involvement are critical. The
pupil, in its neutral state, is usually 4 to 6 mm in diameter. It
is enlarged by sympathetic drive and constricted by parasympa-
thetic drive. Conversely, damage to the parasympathetic pathways
(leading to relative sympathetic overdrive) causes mydriasis and
damage to sympathetic pathways (causing relative parasympa-
thetic overdrive) causes miosis. Patients with ptosis due to oculo-
motor nerve dysfunction often have complete lid ptosis (as it
innervates the levator palpebrae, the main elevator of the lid)
and the eyeball may be “down and out” (due to the unopposed
action of the abducens-innervated lateral rectus and the trochlear-
innervated superior oblique). The oculomotor nerve carries
parasympathetic fibers on its outer periphery. Compressive lesions
will damage the parasympathetic fibers early, causing mydriasis.
Microvascular lesions tend to damage the inner core of the oculo-
motor nerve, sparing the parasympathetic fibers and having no
impact on pupil size. However, a word of caution—while true
in textbooks and on tests, a pupil-sparing incomplete third nerve
palsy should still be assumed to be compressive in nature.
OPERATIVE NEUROSURGERY WWW.CNS.ORG
THE NEUROLOGICAL EXAMINATION
Patients with ptosis due to damage to the sympathetic pathway
often have mild ptosis due to weakness of the superior tarsal
muscle (or Müller’s muscle), as well as miosis and possibly
decreased facial sweat response (“Horner’s syndrome”). However,
while the combination of ptosis and miosis localizes to a lesion
of the ipsilateral sympathetic pathway (one of the few pathways
that never crosses the midline), it does not localize well to
where in the pathway. The sympathetic pathway begins in the
posterior hypothalamus, descends through the midbrain, pons
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and lateral medulla where it courses in close proximity to the
spinal tract of the trigeminal nerve, then into the cervical spinal
cord before exiting around C8-T2 (the Ciliospinal center of
Budge and Waller), ascends to the superior cervical ganglion
before joining the carotid artery, dividing eventually between the
external carotid artery (fibers dedicated to the sweat response)
and the internal carotid artery (fibers for pupil dilation and lid
elevation). The fibers coursing along the internal carotid briefly
enter the cavernous sinus, then ride briefly along the trigeminal
nerve, and finally approach the pupil itself.
Taken in the context of the patient’s examination—with
findings including ipsilateral facial numbness, contralateral body
numbness—the ptosis localizes to a lesion of the sympathetic
pathway in the brainstem (and not an aneurysmal compression
of the oculomotor nerve as suspected by the ER physician).
What else is near these pathways in the lateral medulla? The
inferior cerebellar peduncle, the main input pathway from the
contralateral olivary complex to the lateral cerebellar hemisphere.
The left cerebellum exerts an effect on the left body—and
accounts for the patient’s ipsilateral ataxia.
Knowing what you know now, refer the MRI (Figure 2). There
is a small area of restricted diffusion in the lateral medulla. If one
does not know to look in that area, on a quick review of the
imaging (while on call at night, rushed to complete notes and
respond to pages), it could be easily missed. But it is the easily
noticed tell-tale sign, the confirmation of the examiner’s suspi-
cions, if one knows to look there. And it also alerts the neuro-
scientist to consider the significance of the patient’s neck pain—
likely a symptom of a recent vertebral artery dissection.
Answers
1. A. CNS
2. C. Lesion of the descending oculo-sympathetic pathway in the
brainstem
3. Right inferior cerebellar peduncle
CHAPTER 3: SPINAL CORD AND SENSORY
LEVELS
Case Presentation
A 24-yr-old woman presents for rapidly progressive ascending
numbness and gait instability. The patient woke up in the
morning and went through her normal morning routine without
any difficulty. She then noticed that her feet became numb, which
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McCOYD ET AL
FIGURE 2. Restricted diffusion A, with apparent diffusion coefficient (ADC) correlates B, involving the dorsolateral medulla causing a classic Wallenberg syndrome
due to a left vertebral artery dissection C. Brainstem lesions classically cause “cross-brain” findings due the level of decussation of cranial nerve fibers vs fibers from the
body.
progressed over the course of several hours to affect her legs, then
extending above her hips, at which time she noticed that her
walking was becoming increasingly off-balanced. The numbness
reached the mid-chest when she went to the emergency room for
evaluation. On examination, the patient was able to provide a
thorough history without any difficulty. Her cranial nerve exami-
nation was normal. Her motor examination, including muscle
bulk, tone, and strength, was normal. Her sensory examination
was notable for absent vibratory sensation involving the toes,
ankles, knees, pelvic rim, and to the level of the fifth cervical
rib. Vibratory sense was intact at the level of the clavicles and
throughout the arms. Pin sensation was intact throughout upper
and lower extremities. Muscle stretch reflexes were normal. Gait
was broad based with an ataxic appearance.
Questions
1. Which diagnostic study should be ordered first based on local-
ization of the lesion?
a. Electromyography/nerve conduction study (EMG/NCS)
to evaluate for an acute demyelinating neuropathy
b. Lumbar puncture to evaluate for elevated protein
suggestive of an inflammatory process
c. MRI of the brain
d. MRI of the thoracic spine
e. MRI of the lumbar spine
2. What is the most likely causative lesion?
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a. Immunologically mediated damage to the dorsal root
ganglion
b. Anterior spinal artery infarct damaging the anterior spinal
cord
c. Spinal cord syrinx
d. Inflammatory lesion of the dorsal columns
3. What is the somatotopic organization of the dorsal columns
a. Lower extremity fibers closest to the central gray matter
of the spinal cord, upper extremity fibers closer to the
periphery of the spinal cord
b. Lower extremity fibers closest to the periphery of the spinal
cord, upper extremity fibers closer to the central gray
matter of the spinal cord
c. Lower extremity fibers closest to the midline of the dorsal
columns, upper extremity fibers more lateral
d. Lower extremity fibers closest to the periphery of the dorsal
columns, upper extremity fibers more medial
4. The fasciculus gracilis is found closest to the midline of the
dorsal columns. What does the word “Gracilis” mean?
a. Wedge shaped
b. Thin, slender of calf-like
Case Discussion
The classic “buzzwords for the boards” of “ascending
numbness” makes many students quickly jump to the diagnosis
of Guillain-Barré syndrome (GBS), failing to review the case
appropriately. As mentioned in the introduction, when evaluating
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 THE NEUROLOGICAL EXAMINATION

a patient, consider the following: Is there a primary neurological

problem? In this case, yes. Does the problem involve the CNS
or PNS? It is here that the localizing features on the neurological
examination are so helpful.
There are very few processes that affect both the CNS and
PNS, and there are extremely helpful localizing features of both.
Processes that affect the CNS can affect mental status (which
PNS lesions cannot directly); cause upper motor neuron findings
(which PNS lesions cannot), including increased muscle tone,

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often mild weakness, mild muscle atrophy, and increased reflexes
with pathological responses; and cause a sensory level, which would
be highly unusual with a PNS lesion.
Though one may consider GBS in the differential of a patient
with rapidly ascending neurological symptoms, it is essential
to establish if there is a sensory level. GBS is a PNS disorder
and rarely affects sensation in the torso. Spinal cord lesions,
however, due to dermatomal distribution, classically affect the
spinal cord and cause a sensory level. Any patient with a sensory
level should be assumed to have a spinal cord process until proven
otherwise. If a patient is noted to have absent sensation at the
feet, the examiner should continue the examination from distal
to proximal until a “normal” response is found—moving to the
ankles, then knees, the pelvis, the ribs, the clavicle—even to the
top of the head (the highest possible sensory level due to a lesion
at C2).
The patient has impaired vibratory sensation—indicating
a lesion of either the large fiber peripheral nerves (which
is not suspected due to the sensory level) or the dorsal
columns of the spinal cord. Within the dorsal columns, the
fibers carrying information from the feet are somatotoptically
organized near the midline, with both feet sitting next to each
other. A spinal cord MRI (Figure 3) revealed a characteristic
lesion.
Answers
1. D. (MRI of the thoracic spine). The patient has a sensory level
to about mid-chest, highly suggestive of a spinal cord lesion.
2. D. (Lesion of the dorsal columns). The only modality affected
is vibratory sense—strength (corticospinal tract) and pin
sensation (spinothalamic tract) are in the anterior aspect of
the spinal cord.
3. C. There is a somatotopic organization with the fibers
bringing sensation from the feet being pushed to the midline
(in the fasciculus gracilis) and the fibers of the upper extremity
more laterally (fasciculus cuneatus).
4. B. This can be useful to remember—the fasciculus gracilis
carries vibratory and position sensation from the lower extrem-
ities to brainstem (nucleus gracilis), eventually crossing the
midline on the way to the posterior thalamus. If one looks at
the back of the brainstem in a coronal view, there are 2 thin,
slender calf-like projections running right along the midline
of the dorsal brainstem—the fasciculus gracilis.
FIGURE 3. T2 hyperintensity in the dorsal columns. The patient presented
with rapidly ascending numbness starting in both feet. The layering of fibers
in the dorsal columns puts the feet immediately next to each other—one of the
few places in neuroanatomy a single lesion can cause bilateral symptoms.
CHAPTER 4: THE DECUSSATION OF THE
SPINOTHALAMIC TRACT
Case Presentation
An 18-yr-old man presented for left arm numbness. He
reported the insidious onset of a nonspecific headache. He
then noticed that he had a difficult time feeling objects (pens,
pencils, buttons) with his left hand, though he could not recall
a specific day or instance when the symptoms developed. When
he presented to clinic, his examination was notable for decreased
pin sensation involving the left hand, left arm, left upper chest
crossing the midline to involve the right shoulder. Pin sensation
was normal in the lower abdomen and legs. The remainder of the
neurological examination was normal, including motor strength
as well as vibratory and position sense.
Questions
1. What diagnostic study should be first ordered to evaluate his
symptoms?
a. EMG/NCS to evaluate for a left brachial plexopathy or
lower cervical radiculopathy
b. EMG/NCS to evaluate for a left lower cervical radicu-
lopathy
c. MRI of the brain
d. MRI of the cervical spine

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2. What is the most likely causative lesion?

a. Immunologically mediated damage to brachial plexus
(Parsonage-Turner syndrome)
b. Spinal dural arteriovenous fistula
c. Spinal cord syrinx
d. Inflammatory lesion of the left hemi-cord
3. Where do the spinothalamic fibers cross the midline?
a. Shortly after entering the spinal cord
b. Medullary pyramids

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c. Rostral medulla via internal arcuate fibers
d. Trapezoid body of the pons

Case Discussion
The distribution of specific symptoms is a road map for the VIDEO 1. AD: Syringomyelia in patient with prior surgery for Chiari 1 malfor-
neuroscientist. The patient has sensory dysfunction—but only mation.
involving 1 specific modality. The patient report decreased pin
sensation which is primarily mediated by small fiber peripheral
nerves which enter the spinal cord through the dorsal root, cross
the midline of the spinal cord in an anterior-lateral direction to to alert the neurologist as to an abnormal finding, there was only
form the spinothalamic tract, and then ascend up the ventral- interest at that size of the lesion, not its presence. Please see Video
lateral funiculus to the brainstem. The dorsal columns sitting 1 for a similar clinical case.
closely by near the dorsal root, and the corticospinal tract also
Answers
residing in the lateral funiculus of the spinal cord, are unaffected.
The distribution of symptoms is typical of a suspended sensory level, 1. D. MRI of the cervical spine
affecting the arms and upper torso but sparing the lower torso and 2. C. Spinal cord syrinx
legs. The only localization of the lesion is in the central cervical 3. A. Shortly after entering the spinal cord
spinal cord.
Armed with this knowledge, no esoteric diagnostic evaluation CHAPTER 5: HEMI-CORD SYNDROME
is necessary. The patient needs a cervical spine MRI to exclude
an intrinsic or extrinsic force exerting some pressure on the spinal Case Presentation
cord creating a syrinx (Figure 4). The patient’s history of headache A 43-yr-old woman presented for slowly progressive stiffness in
raises suspicion for a Chiari malformation. When radiology called her right leg. She vaguely recalls the onset of symptoms from at

FIGURE 4. Patient with a rather large syrinx due to a Chiari malformation. The patient presented with numbness to pin sensation of the
arm and upper chest, crossing the midline. While a lesion was suspected, the size of the lesion was surprising.

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least several months prior to presentation, possibly over a year. She
has also noticed that her walking seems mildly, but progressively,
affected and the temperature of the shower water feels different on
her legs. On examination, she was noted to have normal muscle
bulk of the legs with mildly increased tone of the right leg and
mild weakness. She had decreased vibratory sense of the right leg
involving the toes, knee, and pelvic rim; the left leg was normal.
She had decreased pinprick sensation primarily of the left foot; the
right foot and leg were normal. Her right lower extremity reflexes
were increased with sustained clonus and extensor responses of the
right foot (Babinski sign); the left leg and upper extremity reflexes
were normal.
Questions
1. What diagnostic study should be ordered to confirm the
diagnosis?
a. MRI of the lumbar spine
b. MRI of the cervical and thoracic spine
c. MRI of the brain
d. EMG/NCS
2. Lesion of what pathway is responsible for hyper-reflexia?
a. Ipsilateral spinothalamic tract
b. Ipsilateral dorsal column
c. Ipsilateral corticospinal tract
d. Ipsilateral ventral spinocerebellar tract
3. Where is the causative lesion and what has been affected?
a. Central lesion/central cord syndrome affecting central
decussating fibers
b. Anterior horn cell lesion affecting the ventral root
c. Hemi-cord lesion affecting the spinothalamic, corti-
cospinal, and dorsal columns
d. Vascular lesion (anterior spinal artery) affecting the
anterior 2/3rs of the spinal cord containing the corti-
cospinal tracts and spinothalamic tracts
Case Discussion
As in an earlier case discussed, the patient seems to have cross-
bodied symptoms, with sensory symptoms involving both legs
and weakness in 1 leg. A few key findings help with localization.
TABLE 2. Upper and Lower Motor Neuron Findings
Lower motor neuron (LMN)
Muscle bulk Severely atrophied
Muscle tone Decreased/flaccid
Strength Severe weakness
Muscle stretch reflexes Hyporeflexia/areflexia
Clinical significance LMN signs usually occur with PNS pathology but can
occur with CNS pathology (usually spinal cord)
CNS, central nervous system; PNS, peripheral nervous system
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THE NEUROLOGICAL EXAMINATION
First, in answering if the lesion involves the CNS or PNS, few
findings help more than the presence of upper motor neuron
findings (Table 2), including pathological hyper-reflexia. Patho-
logical hyper-reflexia only occurs with lesions of the CNS, and
indicate some form of damage to the corticospinal tract. Hypore-
flexia is less helpful—it can occur due to a lesion of the PNS or
the CNS as the reflex arc passes through the dorsal root ganglion,
across the spinal gray to the anterior horn cell, exits via the ventral
root and then along a peripheral nerve to the relevant muscle. As
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the patient is hyper-reflexic, the lesion must be affecting the CNS.
The patient’s symptoms could occur due to a lesion of the right
corticospinal tract, the medullary pyramids, or the left cortical
motor pathways.
Secondly, there is dissociation of sensory abnormalities—
decreased vibratory sense involving the right leg (and evidence
of a sensory level to the pelvis, further evidence suggestive of a
CNS lesion), and decreased pin sensation of the left foot. There
is involvement of dorsal column and spinothalamic tract. As the
dorsal columns decussate in the medulla after ascending, and the
spinothalamic tract decussates shortly after entering the spinal
cord, the patient must have a lesion affecting the right dorsal
column and the right spinothalamic tract.
Putting it all together, the clinician can localize the patient’s
symptoms to the right spinal cord, or a hemi-cord syndrome
(referred to as Brown-Séquard Syndrome). Based on the clinical
examination alone, it would not be apparent if the lesion was
intramedullary or extramedullary. In theory, the lesion should
involve the thoracic spinal cord to account for the lower sensory
level. However, due to the layering of fibers in the spinal cord
(spinothalamic fibers layering outside-in with the feet closest to
the periphery of the cord), it is not uncommon for lesions to
appear higher than anticipated.
A contrast-enhanced MRI of the cervical and thoracic cord was
ordered, confirming a mass lesion in the spinal canal compressing
the spinal cord (Figure 5).
Answers
1. MRI of the cervical and thoracic spine. While the symptoms
localize the lesion to the thoracic spine (roughly T10),
Upper motor neuron (UMN)
Mild atrophy (if long standing)
Increased
Mild weakness
Hyper-reflexia with pathological responses
(Babinski, sustained clonus, Hoffmann)
UMN signs only occur with CNS pathology
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FIGURE 5. Sagittal and axial T2 imaging. The patient presented with decreased vibration sense of the right leg and decreased pin sensation
of the left leg, with mild weakness of the right leg. Though the sensory level would suggest a lower thoracic lesion (numbness to the lower
abdomen), the lesion was in the lower cervical spine/upper thoracic spine, likely due to the somatotopic layering of fibers. The relative lack of
symptoms for the large size of the lesion (which takes up almost the entirety of the spinal canal) was likely due to its slow development and the
gradual compression of the spinal cord.

compressive spinal cord lesions are often higher than antici-
pated due to the somatotopic layering of fibers.
2. Lesions of the corticospinal tract cause hyper-reflexia. Hyper-
reflexia can only occur with CNS lesions affecting pyramidal
motor pathways.
3. The patient has a hemi-cord syndrome, with damage to the
corticospinal tract and dorsal columns affecting the ipsilateral
side and damage to the spinothalamic fibers affecting the
contralateral side (due to its decussation in the spinal
cord).
CHAPTER 6: THE BRACHIAL PLEXUS
Case Presentation
A 23-yr-old man presented following a motorcycle accident.
He had crashed his motorcycle on an open road at a high
rate of speed (>60 miles/h or >90 km/h). Not surprisingly,
he reported neck, shoulder, and arm pain. Following extensive
rehabilitation, he was seen in a peripheral nerve injury clinic
for sustained hand weakness. On examination, he had severely
reduced muscle bulk of the left hand, involving the thenar and
hypothenar eminence as well as the interossei, with weakness of all
finger movements, including the abductor pollicis brevis (APB),
adductor digiti minimi (ADM), and extensor indices proprius
(EIP). There was comparatively normal muscle tone and strength
of shoulder abduction and forearm flexion. Sensory examination
was notable for reduced sensation to light touch, pin sensation,
and vibratory sensation involving the medial aspect of the hand
(digits 4 and 5) and medial forearm. The left triceps reflex was
reduced compared to the right triceps reflex.
Questions
1. A lesion of what structure or structures is causing the patients
symptoms:
a. Ulnar neuropathy above the elbow
b. Medial cord plexopathy
c. Lower trunk plexopathy
d. C8 radiculopathy
2. What EMG/NCS findings would be most concerning for
poor prognostic outcome/recovery?
a. Conduction block at the spiral groove
b. Slowed conduction velocity in the forearm
c. Spontaneous activity on the needle examination
d. Inability to recruit motor units on the needle examination
Case Discussion
It is the authors’ opinion (or at least the opinion of 1
author) that while general neuroanatomy frightens most non-
neurologists, the anatomy of the PNS frightens most neurologists
(particularly the brachial plexus). If the neurological examination
is one of the last truly meaningful physical examinations in all of
medicine, it is the examination of the PNS that will forever be our
final bastion. There is no imaging modality or diagnostic study
that is more sensitive than the examination of the PNS combined
with a solid knowledge of the PNS.
The patient has a brachial plexus injury, but can you localize
which part of the brachial plexus? One of the challenges of the
brachial plexus, for most learners, is that is a 3-dimensional
structure is drawn (and learned) as a 1-dimensional structure.
Consider drawing—and remembering—the brachial plexus as
a single preclavicular structure (the roots and trunks; most

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FIGURE 6. Remembering the brachial plexus. 1. Draw the roots. 2. Four of the roots join (C5-C6, C8-T1); C7, “the middle finger” (in so many ways) runs alone (the
C7 dermatome is the middle finger) and the trunks are created, creatively named the upper, middle and lower trunks. 3. Next, and here is where most people lose it,
the divisions. But it can be easy: each of the 3 trunks has an anterior division and each of the trunks has a posterior division. 4. At this point, stop drawing the brachial
plexus as a single structure. After the division, no fibers that travel through an anterior division ever join a posterior division cord or branch; no fibers traveling through
a posterior division ever join an anterior division cord or branch. Try drawing the remainder of the brachial plexus as 2 separate structures—which is exactly what
they are from this point forward. 5. The fibers that traverse the posterior divisions all join to become the posterior cord and its branches; it is a “STAR” (subscapular
nerve, thoracodorsal nerve, axillary nerve, and radial nerve). 6. The fibers that traverse the anterior division, and become the lateral and medial cords, are slightly
more complicated, but not all that much if you remember that the medial cord is only a giver—it never receives any contribution from anything beyond the original
contributions from C8 and TI (true to the end—the ulnar nerve is derived almost only from C8-T1 roots) (there is some literature suggesting that some individuals
have some C7 contribution to the ulnar). 7. And because anatomy should always (mostly) inherently make sense, answer this: if a patient has a lateral cord plexopathy,
where would one expect sensory dysfunction? The lateral forearm and hand (the sensory fibers are from C5-C6). What about a medial cord plexopathy? The medial
forearm and hand (the sensory fibers are from C8-T1). 8. Finally, put the remaining branches in: the median nerve runs right down the middle, forming an “M” (the
median and radial nerves are 2 of the most complicated nerves in the body, each receiving some contribution from each nerve root [C5-T1]); the musculocutaneous is
fairly simple—almost exclusively C5-C6; the ulnar is the easiest—it is a straight shot from C8-T1.

preclavicular lesions present with symptoms affecting myotomes)
and 2 postclavicular structures (the cords and branches; most
postclavicular lesions present with symptoms affecting individual
nerves). Each of the 3 trunks of the brachial plexus divides into an
anterior division (becoming the medial and lateral cord), and each
trunk divides into a posterior division (becoming the posterior
division). After dividing, the fibers that travel through the anterior
divisions never join with fibers traveling through the posterior
division—the brachial plexus effectively acts as 2 distinct struc-
tures (Figure 6).
The above patient has a lower trunk plexopathy. How can
one tell? In evaluating a patient with a peripheral nerve injury,

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TABLE 3. Myotomes

Nerve Root: Nerve (Cord) C5/C6 C6/C7 C7/C8 C8/T1

Axillary (Posterior) Deltoid

Radial (Posterior) Brachioradialis Extensor carpi Triceps Extensor indicis
radialis longus proprius
Musculocutaneous (Lateral) Biceps
Median (Medial and Lateral) Flexor carpi Abductor pollicis
radialis brevis

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Ulnar (Medial) First Dorsal
Interossei

TABLE 4. Classic Plexopathies

Name Lesion Muscles involved Common cause Fun fact

Erb’s palsy Upper trunk plexopathy Deltoid Stretching of the head What is the fifth letter of the alphabet?
Biceps away from the shoulder E. What nerve root is involved in an
Brachioradialis (obstetric, trauma) Erb’s palsy? The fifth.
“Waiter’s tip”
Klumpke’s Lower trunk plexopathy Intrinsic hand muscles Stretching of the arm up How many letters are in “Klumpke’s”?
and away from the torso Eight (count the “s”). What nerve root is
(trauma, surgical involved in Klumpke’s palsy? The
positioning) eighth.
“Klumpke’s monkey”
Parsonage-Turner Multiple Long thoracic Immune mediated Usually associated with severe pain
Suprascapular followed by weakness
Axillary
Musculocutaneous
Anterior interosseous
Phrenic

myotomes (the group of muscles supplied by a single nerve root)

are extremely helpful (Table 3). The patient has weakness of the TABLE 5. Nerve Roots and Dermatomes
ADM (ulnar nerve, medial cord, anterior division, lower trunk,
Nerve Root/Dermatome
C8/T1 nerve root); APB (median nerve, medial cord, anterior
division, lower trunk, C8/T1 nerve root); EIP (radial nerve, C5 Lateral shoulder
posterior cord, lower trunk, C8/T1 nerve root). Anytime there is C6 Lateral forearm, digits 1 “Six shooter”
involvement of a terminal branch of the posterior cord (primarily and 2
the axillary and radial nerve) and a terminal branch of the medial C7 Middle finger “Seven to Heaven”
C8 Digits 5 and 5, medial “Tea time’s at 8”
or lateral cord (musculocutaneous, median and ulnar nerves, all forearm
of which pass through the anterior divisions only) the lesion must T1 Medial forearm/hand
be at the trunk or root level. The classic brachial plexopathies are
presented in Table 4.
Dermatomes are less helpful (due to dermatomal overlap), but (“pinkie finger”), as our British colleagues may do when having
basic concepts can help, particularly as it relates to innervation tea, the C8 dermatome is represented and can be recalled as “Tea
of the hand (Table 5). C6 supplies the thumb and second digit. time at 8.”
If one puts the thumb up and the second digit pointed straight The median nerve innervated motor and sensory functions of
forward (as an American child might to form a “6 shooter” gun), the hand highlight the interplay of myotomes and dermatomes
the fingers represent the C6 dermatome. C7 supplies the middle and help explain the patient’s symptoms. The median nerve is
digit. If one extends the middle finger alone, which one should perhaps the most complex nerve in the body, receiving inputs
be cautious doing in public, the middle fingers represent the C7 from all roots (C5-T1) that contribute to the brachial plexus.
dermatome (“Seven to heaven”). If the fifth digit alone is extended The median nerve supplies sensation to the lateral hand (digits

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FIGURE 7. T2 imaging of the cervical spine showing evidence of a pseudomeningocele (arrow) due to root avulsion of the lower cervical spine.
FIGURE 8. Review the image before reviewing the case. Is the above image
normal or abnormal?
1-4, with the median nerve covering the lateral half of the fourth
digit). The median nerve sensory fibers for the thumb and second
digit originate from C5-C6 nerve roots (“Six shooter”). The
median motor fibers for the thumb and second digit originate
from the C8-T1 nerve roots. The patient has weakness of median-
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THE NEUROLOGICAL EXAMINATION
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FIGURE 9. Positive emission tomography scan of the same patient showing a
focal uptake in the right upper lung (pancoast tumor; pathology was consistent
with a squamous cell carcinoma), causing the clinical symptoms of a lower
trunk plexopathy with associated ptosis.
innervated hand muscles, but no sensory dysfunction in the
same fingers. One can immediately deduce that there is either
a problem isolated to the motor fibers (but the patient has
numbness in the medial hand), or the problem is affecting C8-
T1 fibers.
As part of his evaluation, the patient underwent imaging of
his cervical spine (Figure 7), which revealed a pseudomeningocele
consistent with a complete nerve root avulsion.
Answers
1. A. Lower trunk plexopathy
2. D. The inability to recruit motor units is a negative prognostic
finding, indicating there has been no reinnervation of the
muscle. Patients are unlikely to have spontaneous recovery.
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McCOYD ET AL
VIDEO 2. Elderly woman with right Horner syndrome associated with Pancoast
tumor.
CHAPTER 7: ARM PAIN AND HORNER’S
SYNDROME
Case Presentation
Knowing what you know now from the last several cases, refer
Figure 8 before reviewing the case. Is it normal or abnormal?
A 59-yr-old patient presented with a complaint of several years
of arm pain and weakness. Her examination was notable for
weakness of the intrinsic muscles of the right hand, including
finger extensors, with numbness of the medial hand and forearm.
The examiner also made note of mild right lid ptosis and miosis.
Questions
1. Is the imaging study normal or abnormal and does it account
for the patient’s symptoms?
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Case Discussion
Imaging alone in the absence of the history and a physical
examination is seldom helpful. The patient has evidence of a right
lower trunk plexopathy (as in the previous case) and mild right
lid ptosis. Ptosis tends to occur more frequently in patients with
malignant plexopathies. As discussed earlier, the localization of
ptosis is broad, but for this patient both findings can localize to
the lower trunk/proximal roots of the cervical spine. Imaging was
ordered because of the examination findings (an examination was
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not done just because of the imaging) and revealed a Pancoast
tumor (Figures 8 and 9). Please see Video 2 for a similar clinical
case.
The number and combination of neurological findings and
cases that can occur will take a career to experience. Diagnostic
studies will come and go (pneumoencephalograms were once all
the rage). The fundamentals of the neurological examination are
eternal.
Disclosures
The authors have no personal, financial, or institutional interest in any of the
drugs, materials, or devices described in this article.
SUGGESTED READING
1. Aids to the Examination of the Peripheral Nervous System. 5th ed. Philadelphia, PA:
Saunders Elsevier; 2010.
2. Biller J, Gruener G, Brazis B. DeMyer’s The Neurologic Examination: A Programmed
Text. 7th ed. New York, NY: McGraw-Hill Education; 2017.
3. Brazis P, Masdeu J, Biller J. Localization in Clinical Neurology. 7th ed. Philadelphia,
PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2017.
4. Campbell W. Dejong’s The Neurologic Examination. 7th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2013.
5. Russell S. Examination of Peripheral Nerve Injuries: An Anatomical Approach.
2nd ed. New York, NY: Thieme; 2015.
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