The Neurologic Examination for the Emergency Physician

Case Presentation
This presentation addresses how Emergency Physicians should conduct a
neurologic examination.
The Neurologic Examination for the Emergency Physician

Introduction
The neurologic screening examination focuses primarily on identifying acute,
potentially life-threatening processes, and secondarily on identifying disorders that
require referral to, and management by, other specialists. In recent years there have
been a number of advances in the management of neurologic disorders placing
emphasis on the importance of the neurologic exam. For many of these processes,
interventions can be time sensitive and can significantly reduce morbidity and
mortality; examples include thrombolytics for stroke, anticonvulsants for
nonconvulsive and subtle generalized status epilepticus, and plasmapheresis for
Guillain-Barre. The neurologic evaluation can only be accomplished successfully if
placed in the context of the patients overall medical history and physical. The six
major components of the neurologic exam include: 1) mental status 2) cranial nerve
exam 3) motor exam 4) reflexes 5) sensory exam 6) evaluation of coordination and
balance.
A comprehensive neurologic screening exam can be accomplished within minutes if
performed in an organized and systematic fashion. Based on the patients chief
complaint or findings on the screening exam, components of the evaluation are then
elaborated upon. For example, a full mental status exam is not necessarily warranted
in the patient who is awake, oriented, and conversant, while it must be fully
investigated in patients with altered mental status or a history of a change in
behavior. Likewise, in a patient with no sensory complaints, a determination of the
ability to distinguish sharp from dull bilaterally is sufficient, while a patient
complaining of vague sensory deficits might need to be tested for extinction on
simultaneous sensory stimulation, or for astereognosis (inability to identify an object
by palpation), or for a sensory level.
This article does not provide a comprehensive review of the full neurologic
examination. Instead, the intent is to review the basic components of a screening exam
in order to provide a framework for clinicians to work from. Some concepts are
introduced but not fully developed with the expectation that it will prompt further
reading in an appropriate reference. Actual cases that we have been involved in either
for medical-legal review, or in our clinical practices are presented to stimulate thought
and emphasize central concepts.
History

The patients chief complaint often serves to direct the examination, however, caution
must always be exercised in order to avoid introducing bias into the evaluation. The
subarachnoid hemorrhage patients presenting complaining of a migraine, or the
patient with Guillain-Barre complaining of the flu are examples in the risk
management literature. Consequently, a careful history is the key to successful
management. The history often provides important clues to the etiology of the patients
condition, and may direct diagnostic testing. For example, an alert patient with a
headache associated with neck pain that started after a car accident might direct the
examination and radiographic imaging to focus on carotid or vertebral artery dissection.
The history begins with a definition of the patients complaint since many neurologic
symptoms are nonspecific, e.g. it is important to distinguish vertigo from dizziness,
blindness from decreased family members or bystanders can be critical since they
are often able to place the patients complaint in perspective with other events. Key
components of the history include: Time of onset, mode of onset, progression,
associated factors which improve or exacerbate the symptoms, and a prior history of
similar problems. The acute onset of a neurologic complaint suggests a vascular
event and requires immediate attention. The patients past medical history,
occupation, medications, or illicit drug use must also be investigated in that they may
help in making the diagnosis or have bearing on therapeutic interventions.
Case #1:
A 46 year old woman presented to the emergency department (ED) complaining of a
severe migraine. She had a past history of monthly migraines without aura that she
described as being unilateral and throbbing, associated with nausea and vomiting. She
had taken 500 mg of naproxen without relief and presented 12 hours into the event.
She visited the ED 3 or 4 times a year for refractory migraines. She claimed that the
present migraine was similar in intensity to past events but different in location in that it
was bilateral and radiated into her occiput. A neurologic examination was deferred
because the patient was uncomfortable and the diagnosis appeared evident to the
treating physician. Prochloperazine, 10 mg IV, was given with resolution of the
headache. The patient was discharged home with instructions to follow-up with her
private physician. Eighteen hours later she was found unresponsive by her family and
brought to the ED by EMS. A diagnosis of subarachnoid bleed was made by
noncontrast head CT; the patient had a complicated hospital course and died eight
days later.
Commentary
This case emphasizes two fundamental concepts: 1) A change in clinical presentation
of an existing condition requires an evaluation as if the patient had a new complaint. In
this case, the patient clearly stated that her headache was different from past
headaches and therefore she needed to be approached with an open differential
diagnosis. The decision to treat with prochlorperazine was appropriate for managing a
migraine, however, prochlorperazine being a serotonin receptor modulator will
attenuate headache pain regardless of the underlying pathology. 2) Patients with a
neurologic complaint require a neurologic examination. In cases of headache, the
exam focuses on CN II, III, IV, and VI (see section on CNs). There is the possibility that
in this patients case, the exam would have revealed a dilated pupil since the most
common cause for subarachnoid hemorrhages is a ruptured cerebral aneurysm and a
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common site is at the posterior communicating artery which is located next to CN III;
compression of CN III results in parasympathetic dysfunction hence the dilated pupil.
Physical Exam Mental
Status
The neurologic examination begins by assessing the patients mental status. Often
times, subtle changes in mental status are not overtly obvious and careful
consideration must be given to concerns expressed by family. The mental status
evaluation begins with a basic determination using the A,V,P,U method: A, alert; V,
responsive to verbal stimuli or commands; P, responsive to painful stimuli only; U,
unresponsive. The Glasgow Coma Scale (GCS) score was developed as a prognostic
tool for traumatic brain injured patients. The score is a calculated value from the best
eye opening response (1-4), verbal response (1-5), and motor response (1-6) with a
score of 3 consistent with coma and a score of 15 consistent with minor or no trauma
related dysfunction. The GCS is not useful in patients with metabolic or toxic
conditions.
Having a systematic approach to the mental status is helpful in diagnosing acute
processes in patients with chronic disease, such as the demented patient with
delirium. The confusion assessment method or CAM score was developed to assist
in diagnosing delirium. This method assesses four components: presence of acute
onset, fluctuating course, inattention, and disorganized thinking or an altered level of
consciousness. The Mini-mental status method is reserved for patients with
suspected cognitive dysfunction. A full discussion is beyond the scope of this article,
however, in essence, the mini-mental status method evaluates five areas:
orientation, registration, attention, recall, and language.

Case #2
A 78 year old man was brought to the ED by his family who claimed that he was not
acting himself. The patient had a history of hypertension but otherwise in excellent
health until two days prior when he began just not being himself and expressing
paranoid ideations. According to the family, during the episode on the day of
admission, the patient had tried to leave the apartment claiming that someone was
trying to hurt him.
Medications included procardia and one baby aspirin a day. There was no past
psychiatric history. On exam, the blood pressure was 148/92, pulse 82, respirations 16,
skin warm and dry, and finger stick glucose was 110. The patient appeared comfortable
and cooperated with all questions. He was alert, oriented to person, place, and time but
his answers were slow and he appeared distracted (which according to the family was
very unlike him). The physical and neurologic exam were reported as normal and the
patient was admitted to the psychiatry service with a diagnosis of psychosis. Three
days after being on the psychiatry service the patient experienced a brief tonic-clonic
seizure after which he returned to the baseline established at admission. A neurology
consultation was obtained during which it was noted that the patient had subtle
intermittent tics on the left side of his mouth. A bedside EEG was obtained and a
diagnosis of nonconvulsive status epilepticus was made. The patient was given

lorazepam, 2 mg IV, with normalization of the EEG and complete resolution of his
abnormal behavior.
Commentary
This case demonstrates the importance of carefully considering concerns expressed
by family, evaluating patients with altered behavior for medical causes before
prematurely diagnosing a psychiatric disorder, and including nonconvulsive status
epilepticus in cases of altered mental status.Nonconvulsive status epilepticus (NCS),
like convulsive status epilepticus, results from either a primary generalized process
(absence status), or a secondary generalized process (complex partial status). The
hallmark of NCS is altered mental status and therefore, unless it is suspected, the
diagnosis can be easily missed. Patients in NCS can appear totally functional and
perform complex tasks such as driving a car. Other changes can include speech
arrest, cognitive deficits, delusions, paranoia, hallucinations, or psychosis.
Disturbances in speech patterns are frequently seen ranging from verbal
perseveration to aphasia. Motor activity, including automatisms, is rarely the
predominant clinical finding in NCS, though when present may be helpful towards
making the diagnosis.

The literature has many reports of patients presenting with altered mental status who
were initially labeled as having a psychiatric problem, and only at a later time in their
evaluation was the correct diagnosis identified, either by EEG or by the onset of a
convulsive component. There appears to be a distinct subgroup of patients who
develop NCS in later life either due to metabolic abnormalities, drug withdrawal, or
idiopathically. When presented with a patient who is thought to be in NCS, EEG
confirmation is recommended before instituting pharmacologic interventions. NCS is
reportedly highly responsive to the benzodiazepines, either diazepam or lorazepam.

Cranial Nerve (CN) Exam

In general, CN II - VIII are of the most value in the neurologic screening exam;
testing the other cranial nerves is complaint based.
CN II: Testing the optic nerve involves visual acuity (central vision), gross visual
fields (peripheral vision), and the ophthalmoscopic exam. Visual acuity must be
checked individually in each eye. Changes in visual acuity are due to either
refractive error or optic nerve dysfunction; the former will correct with a pinhole test
while the later does not. Optic nerve function is tested using the swinging flashlight
test (discussed below under CN III). Peripheral vision is checked by a visual field
exam, testing each eye individually using the confrontation method. Blindness in
one eye suggests a lesion in front of the chiasm; bitemporal hemianopsia suggests
a lesion at the optic chiasm; a quadrant deficit suggests a lesion in the optic tracts;
bilateral blindness suggests cortical disease. The ophthalmoscopic exam evaluates
the optic disc, retinal arteries, and retinal veins. Pearls in diagnosing papilledema
include blurring of the lateral margin of the optic disc, loss of blood vessels as they
cross the edematous disc, distended veins, and loss of venous pulsations.
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CN III, IV, VI: CN III, innervates the extraocular muscles effecting primarily adduction
and vertical gaze. CN III function is tested in conjunction with CN IV, which aids in
internal depression via the superior oblique, and CN VI, which controls abduction via
the lateral rectus. Extraocular muscle function is tested by holding a pen vertically in
front of the patient.
Instructing the patient to follow while the pen is moved horizontally, the patient is asked
how many pens he sees (split images suggests diplopia). This is repeated in the
horizontal plane. Diplopia requires binocular vision and thus will resolve when one eye
is occluded (dislocated lens or retinal detachment can cause distorted images but not
split images). While checking the extraocular movements, the presence of nystagmus
is noted. Slight nystagmus on extreme lateral gaze may be normal. Marked nystagmus
on lateral gaze or any nystagmus on vertical gaze is abnormal, suggesting a peripheral
or central nervous system lesion. Vertical nystagmus is seen in brainstem lesions or
intoxication with phencyclidine. Pendular nystagmus (equal to and fro movements) is
generally a congenital condition.
The pupillary light reflex is mediated via the parasympathetic nerve fibers which run on
the outside of CN III. The pupillary response is tested by shining a light individually into
each eye. In the swinging flashlight test a light in shined from one eye to the other;
when the light is shined directly into a normal eye, both eyes constrict via the direct
light response and the consensual light response. A Marcus-Gunn pupil is a pupil that
constricts to the consensual response but dilates when light is shined directly into it
indicating an afferent nerve defect; this is seen in optic nerve disease, e.g. multiple
sclerosis.

Pupillary size must be observed and documented. Asymmetric pupils of <1mm are of
no pathologic significance. A larger difference in pupil size suggests a CN III
compression; this can result from compression of the nerve by aneurysms, or, in
patients with an altered mental status, by cerebral herniation. Bilateral pupillary dilation
is seen with prolonged anoxia or due to drugs (anticholinergic, sympathomimetic
agents). Unilateral pupillary constriction in seen in sympathetic chain dysfunction, e. g.
Horners syndrome or carotid artery dissection. Bilateral pupillary constriction is seen
with pontine hemorrhage or as the result of drugs (e.g. opiates, organophosphates,
clonidine).
CN V: The trigeminal nerve has both sensory and motor function. A central nervous
system lesion affecting CN V usually involves all three branches, making individual
testing unnecessary. Sensory function is most reliably tested using double
simultaneous stimulation, see below in the section on sensory testing. CN V also
supplies the muscles of mastication which are tested by palpating the masseter
muscles while the teeth are clenched.
CN VII: The facial nerve innervates the motor function to the anterior scalp and face,
and sensory to the anterior two-thirds of the tongue, to the ear canal and behind the
ear. Weakness is often apparent as a facial droop or flattening of the nasolabial fold.
In more subtle cases, weakness becomes apparent by asking the patient to show his
teeth or whistle. Central lesions cause contra-lateral weakness of the face below the
eyes but with forehead sparing due to the crossing of central fibers; thus with central
lesions the eyebrows can be elevated and the eyes tightly closed. Patients with
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peripheral VIIth nerve lesions, including Bells Palsy, may have a complete facial
weakness that includes the forehead. Of note, an isolated central VIIth lesion is rare,
therefore absence of brow and forehead involvement does not necessarily indicate a
central lesion, especially if the patient is otherwise neurologically intact.
CN VIII: The acoustic nerve has a vestibular and a cochlear component. The
vestibular nerve supplies the semi-circular canals, the cochlear nerve supplies the
Organ of Corti (hearing). Decreased hearing is due to either a conductive defect (e.g.
wax in the ear canal) or a sensorineural defect. An easy screening test for hearing
defects is accomplished by asking the patient to hum; in conductive defects, the
affected ear hears the hum louder. In sensorineural defects it is the normal ear which
hears the louder hum.

When vestibular nerve defects are suspected, patients are assessed for nystagmus
and a Nylen-Barany maneuver is performed by rapidly taking the patient from a sitting
to supine position where the head lies 45 degrees below the horizontal. The test is
repeated with the patients head turned 30-45 degrees to the right and then to the left.
The test is considered positive with either the onset of nystagmus, reproduction of
vertigo, or both, and suggests a peripheral cause of vertigo. The nystagmus of
peripheral vertigo has a brief period of latency prior to onset, is suppressible by visual
fixation, is fatigable, and worsens with changes in position. Central vertigo has
nystagmus of immediate onset and is not suppressible, fatigable, or positional.
Case #3
A 38 year old man presented to the ED complaining of double vision when looking to
the left. The patient complained of a dull, persistent frontal headache that had been
present for two months. He denied fevers, nausea or vomiting, weakness, or fatigue.
He had no past medical history and was on no medications. On physical exam he
appeared comfortable and had stable vital signs. Pupils were equal and reactive to
light; the fundi were not visualized. There was no ptosis, CN III and IV were intact; on
left lateral gaze the left eye did not move past the midline. A noncontrast head CT was
obtained and was normal. A neuro-ophthalmology consultation was obtained to
evaluate the patients sixth cranial nerve palsy. The eyes were dilated and the findings
shown in Figure 4. A lumbar puncture was performed with an opening pressure of 260
mm of water and otherwise a normal CSF analysis. The diagnosis of idiopathic
intracranial hypertension (IIH) was made.

Commentary

This case emphasizes the importance of the CN assessment in patients complaining

of headache or disturbances with vision; ophthalmoscopy is an important component
of the assessment. In this case, the finding of papilledema in a patient with a normal
CT lead to the correct diagnosis. IIH, once termed pseudotumor cerebri, is a
diagnosis made by documenting elevated intracranial pressure, normal neurologic
findings except for papilledema and an occasional CN VI palsy, absence of space6

occupying lesion or ventricular enlargement on CT, and normal CSF composition.

The differential of diplopia includes processes affecting the muscles (e.g. thyroid
disease or other myopathies), the neuromuscular junction (e.g. myasthenia gravis,
botulism), or cranial nerve function. The cranial nerve may be affected by extrinsic
compression (i.e. mass lesions) or by intrinsic pathologies (e.g. ischemia). An isolated
CN VI palsy is often caused by head trauma since this is the longest intracranial CN; it
is rarely caused by those processes affecting the neuromuscular junction or the
muscles since these generally have more diffuse involvement. Interestingly,
approximately 30% of patients with IIH have a CN IV palsy in which case it is thus
labeled a false lateralizing sign.
Motor exam
The motor screening exam focuses on detecting asymmetric strength deficits since
this may be an indication of an acute CNS lesion. Testing motor strength is difficult or
impossible in the uncooperative patient, and results may be significantly affected by
pain. In general, it is not necessary to test every muscle group individually but instead
to test for the presence of a "drift". The patient, with eyes closed, holds his arm out
horizontally, palms up, for 30 seconds. If weakness is present, the hand and arm on
the affected side will slowly drift or pronate. Lower extremity drift can be checked by
having the patient lie prone with knees bent 90 degrees and legs pointing vertically up.
A weak leg will tend to drift downwards within 30 seconds. Other motor tests for
extremity weakness include hand grasp, and foot plantar and dorsiflexion. Hand grasp
testing of the ulnar aspect of the hand is more reliable than the radial aspect. In the
case of possible peripheral nerve or muscle injury, or in the case of abnormal results
with motor testing as described above, more formal testing of the extremity is in order.
Case #4
A 34 year old male with AIDS and a CD4 count of 10 presented to the ED complaining
of diffuse weakness. The patient claimed that he has been weak for months but over
the past week he has had increased weakness in his lower extremities and has had
new onset of difficulty standing and walking without assistance. He denied fevers,
cough, bowel or bladder dysfunction, or back pain. Past history included two episodes
of pneumonia and oral thrush. He was noncompliant with antiviral and antifungal
medications. On exam the patient appeared cachectic but in no distress. Vital signs
were stable; HEENT, heart, lungs, abdomen were normal. On rectal exam there was
good tone, stool was guaiac negative. The cranial nerves were intact; on motor testing
there was no upper extremity drift, lower extremity testing revealed spasticity and there
was bilateral drift after 5 seconds; lower extremity strength was assessed to be 3/5 in
all the muscle groups; on sensory testing the patient could distinguish sharp from dull
in upper and lower extremities, vibratory sense was absent in the lower extremities;
deep tendon reflexes were 2/2 at the biceps, and patella reflexes were 4/2 bilaterally;
extensor plantar reflexes were present bilaterally. The patient had magnetic resonance
imaging (MRI) of the spinal cord to assess for the presence of a mass lesion; the MRI
was normal and a CSF analysis was performed . Tests for syphilis, mycobacterium,
cryptococcus, herpes, and cytomegalovirus were negative. A final diagnosis of HIVrelated myelopathy was made.

Commentary
This case demonstrates the potential difficulty in assessing a patient with chronic
disease who has an acute complaint; it also demonstrates the utility of the motor,
sensory, and reflex exam in differentiating central from peripheral lesions. This
patient had clear findings of upper motor neuron dysfunction including spasticity,
hyperreflexia, and positive Babinski reflexes.

HIV myelopathy is seen in up to 90% of patients with end-stage disease. Clinically

patients present with leg weakness, unsteadiness, gait impairment, and variable
sensory impairment. Bowel and bladder dysfunction can occur. On exam patients
have spasticity, weakness, hyperreflexia, extensor planter responses. Reflexes may
be decreased since these patients often have associated peripheral neuropathies.
Sensory deficits involve primarily vibratory and position sense. Management focuses
on eliminating reversible etiologies of myelopathy.
Reflexes
Reflex testing in the screening exam includes the major deep tendon reflexes and the
planter reflex (Babinskis Sign). The major deep tendon reflexes are the patellar reflex
(L3,4), Achilles reflex (S1,2), the biceps reflex (C5,6), and the triceps reflex (C7,8). The
response is graded from O (no reflex) to 4+ (hyperreflexia). Symmetrical hyporeflexia
may be normal, or indicative of metabolic derangements or of a peripheral neuropathy.
Symmetrical hyperreflexia may also be systemic in origin, frequently resulting from
hypocalcemia or hyperthyroidism. Unilateral hyperreflexia suggests an upper motor
neuron process. Asymmetrical reflexes are generally pathologic.
There are several reflexes which indicate upper motor neuron disease, the most
commonly elicited is the planter flexion/ extension reflex (Babinski reflex). A normal
response to stroking the planter surface of the foot is plantar flexion of the toes; a
positive Babinski reflex is characterized by dorsiflexion of the big toe with fanning out
of the smaller toes.
Case #5
A 23 year old woman presented to the ED complaining of weakness and of her legs
feeling heavy and tingly. For the preceding three days she complained of having
had a cold with low grade fevers, myalgias, and sinus congestion. She had no
significant past medical history; medications included birth control pills and overthe-counter cold remedies. The ED record documented that she was afebrile and
HEENT - normal. A neurologic exam was not documented on the chart. The
patient was discharged with a diagnosis of viral syndrome. Over the next 12
hours, the heaviness in the patients legs increased and she returned to the ED
requiring assistance for ambulation. On exam her vital signs were stable. There
were no CN deficits; on sensory testing she could distinguish sharp from dull on all
four extremities; on upper extremity motor testing she had 5/5 strength; on lower
extremity motor testing ankle flexion/extension was 2/5, knee flexion/extension was
3/5, hip flexion was 4/5; deep tendon reflexes were 2/2 in the upper extremities, 0/2
bilaterally at the patella and gastrocnemius. Acute inflammatory demyelinating
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polyneuropathy (Guillain-Barre Syndrome) was suspected and confirmed with CSF

analysis which revealed a protein of 140. The patient was admitted to the ICU.
Commentary
This case demonstrates the importance of performing a neurologic exam in all patients
with a neurologic complaint. Guillain-Barre can be rapidly progressive and discharging
this patient from the hospital placed her at risk for a negative outcome. Guillain-Barre
Syndrome is a polyneuropathy resulting from immune-mediated inflammation of the
myelin. Clinically, patients typically present with distal paresthesias followed by
symmetrical ascending paresis. Bulbar weakness, respiratory muscle involvement,
and autonomic instability can occur. Since this is a lower motor neuron process, deep
tendon reflexes are decreased. Despite sensory complaints, sensory testing usually
reveals minimal or no deficits. Patients may have a positive straight leg raising test
due to nerve root irritation. CSF analysis demonstrates an elevated protein, normal
glucose, and usually less than 10 mononuclear cells. It may take up to 72 hours for
abnormalities in the CSF to develop making a repeat spinal tap necessary when an
initial tap is normal yet the diagnosis is suspected.

Patients with Guillain-Barre are at risk of respiratory compromise and arrhythmias and
therefore all but the mildest, stable cases need to be admitted to a monitored setting.
The disease may progress over 4 to 6 weeks before resolving; approximately 5% of
patients are left with residual symptoms. Plasmapheresis has been shown to reduce
duration and severity of the disease. Steroids are not recommended, while gamma
globulin might decrease duration of the disease.

Sensory exam
The screening sensory exam consists of testing pain and light touch; the
spinothalamic tract in the anterior cord carries temperature and both pain and light
touch fibers, while the posterior column carries fibers for light touch thus explaining
preservation of light touch in patients with anterior cord syndromes. Testing for
proprioception, stereognosis and vibration is generally reserved for patients with
suspected neuropathies or further evaluation of sensory complaints. Dermatomal
testing is performed in patients with suspected radiculopathies since central
lesions do not present with dermatomal deficits.
Evaluating sensation in patients with vague complaints is best done by testing for
extinction on double simultaneous stimulation. In this test, the patient closes his eyes
and two sharp objects are simultaneously applied. If the patient reports sharpness on
one side only, a sensory deficit on the other side is present. If both sides are initially
reported as sharp, repeated testing is performed looking for extinction of response on
the affected side.
Case #6
A 64 year old woman with hypertension and diabetes presented complaining of

numbness in her left upper extremity for 48 hours. She denied headache, weakness,
difficulty with speech, vision, or gait. She had no past history of strokes. Medications
included enalapril and metformin. On exam she was alert, oriented to person, place,
and time, and had fluent speech. Blood pressure was 150/90, respirations 16, pulse
76; fingerstick glucose was 130 mg/dl. On exam the cranial nerves were intact
including no facial asymmetry and normal CN V testing; motor testing revealed no
drift; deep tendon reflexes were 2/2 and symmetrical; toes were downgoing. On
sensory testing the patient distinguished sharp from dull on the left upper extremity
but demonstrated extinction on simultaneous testing; on further testing she
demonstrated astereognosis when asked to identify a quarter placed in her left palm.
A noncontrast head CT was obtained and demonstrated a right parietal cortex infarct.
Commentary
This case demonstrates the importance of pursing the clinical evaluation in a patient
with a neurologic complaint. The patient had a sensory complaint that was not evident
on the initial exam; a more indepth evaluation uncovered the sensory deficit. Making
the final diagnosis of a cortical stroke was key to the proper management of this
patient. Patients who have had one stroke are at increased risk for another event and
thus reversible causes of thromboembolism must be searched for. These patients
require a careful evaluation that includes an electrocardiogram, echocardiogram,
carotid artery imaging, and a complete hematologic assessment.
Coordination and Balance
Coordination is a function of the cerebellum combined with input from vision,
proprioception, and vestibular sense. Cerebellar function can be easily evaluated by
asking the patient to close his eyes and rapidly alternate touching the finger from one
hand between a finger on the other hand and his nose. A variation of this test involves
the patient rapidly alternating touching his finger from his nose to the examiners finger
though in this case the patient must open his eyes and therefore visual problems may
interfere with performance. Heel-to-shin testing is another frequently used test of
cerebellar function. Difficulty in performing rapid alternating movements may also
demonstrate cerebellar pathology.

Balance requires an integration of cerebellar, visual, vestibular, and proprioception

input. It is evaluated by the Romberg test and tandem gait (heel-to-toe). In the
Romberg test, the patient is asked to stand with his feet together (proprioceceptive
input), without support; first with eyes open (visual input) and then with eyes closed.
Closing the eyes eliminates vision, but with proprioception and vestibular sense intact,
the patient will not sway. If there is a proprioceptive deficit, the patient will keep his
balance with the eyes open and lose his balance when the eyes are closed. When this
occurs, the Romberg test is positive. If the patient sways with the eyes open or closed,
this is suggestive of a cerebellar lesion which is not compensated by sensory input
from the other systems.
Case #7

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A 64 year old man was brought to the ED by ambulance with a chief complaint of
vertigo. According to the patient, he had several similar episodes over the past year
which his physician had diagnosed as benign positional vertigo and treated with
meclizine. On this presentation, the patient claimed that the room spinning had started
approximately 6 hours prior to presentation while he was watching television. It was
associated with severe nausea and vomiting. He had taken 25 mg of meclizine without
improvement. Past medical history was positive for hypertension; medications included
atenolol and hydochlorothiazide. Based on the past history of benign positional vertigo,
the patient was symptomatically treated with phenergan, 25 mg IV. Three hours later,
his symptoms persisted and a physical exam was performed.
On physical exam, the patients blood pressure was 190/100 mm Hg; heart rate, 64
beats per minute; respiratory rate, 18 breaths per minute. The patient was lying still on
the stretcher with his eyes closed complaining that the room was spinning. He was
alert, orientated to person, place, and time. He was cooperative and able to articulate
clear answers to all questions. Cranial nerves II, III, IV and VI were intact though it was
noted that he had pronounced vertical nystagmus that was not suppressed with
fixation. There was no facial asymmetry, hearing was decreased on the left, speech
was clear, and he was able to handle secretions and swallow normally. There was no
extremity weakness though limb ataxia was noted on the left. On finger-to-nose
testing, gross dysmetria (missing the target with pass pointing) was also present on
the left. A magnetic resonance image of the brain revealed a left ventral cerebellar
infarct.

Commentary
Correctly diagnosing this case was delayed as a result of initiating management based
on the label given by another care provider prior to performing a neurologic exam.
Findings on the exam clearly pointed towards a central cause of the patients vertigo
instead of a peripheral cause. Vertical nystagmus is strongly suggestive of central
pathology and supported in this case by the findings of decreased hearing, ataxia, and
dysmetria. Peripheral vertigo results from lesions of the semicircular canals, utricle, or
the saccule. When peripheral vertigo is induced by cupulotithiasis it is referred to as
benign positional vertigo in which case the vertigo is usually not present at rest but
induced by movement (in vestibular neuronitis and acute labyrinthitis vertigo can be
present at rest). In benign positional vertigo, onset of nystagmus is delayed after
change in position, it fatigues with repeat provocation, and can be suppressed with
fixation. It is not associated with cerebellar or cranial nerve deficits. The vertigo
associated with central lesions is often present at rest, though may be worsened by
changes in position. It tends to be less severe but more persistent than peripherally
induced vertigo, it does not fatigue, and it is usually associated with cerebellar or
brainstem deficits. In this patients case, the work-up ultimately included an arteriogram
which demonstrated stenosis of the left vertebral artery. The prior episodes of vertigo
were most likely due to transient ischemic attacks from thromboemboli in the posterior
circulation.

Conclusions

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1. The neurologic screening examination when performed in a systematic manner

provides the clinician with the necessary data to make management decisions. It
focuses on differentiating central from peripheral nervous system pathology; upper
from lower motor neuron involvement.

2. Family and friends can often provide the historical key to the evaluation. Subtle,
but significant, changes in mental status may not be initially evident to the clinician.
3. Cranial nerves II, III, IV, and IV are critical components of the screening exam
and must be carefully assessed in all patients with neurologic complaints.
4. Motor testing for facial asymmetry and extremity drift provides an excellent screen
for a central nervous system motor lesion.
5. Central lesions (upper motor neuron) result in hyperreflexia, increased muscle tone,
but no atrophy or fasciculations; peripheral lesions (lower motor neuron) result in
hyporeflexia, decreased muscle tone, atrophy, and fasciculations.
6. Simultaneous sensory extinction testing is used to uncover subtle central nervous
system sensory deficits.
7. Balance requires the integration of cerebellar, visual, vestibular, and proprioceptive
functions; each must be considered individually in patients suspected of having a
balance or coordination problem.

The Neurologic Examination for the Emergency

Physician
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