The Neurologic Examination for the Emergency Physician
The Neurologic Examination for the Emergency Physician
Andy Jagoda, MD, FACEP
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
patient’s 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 patient’s 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
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.
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Andy Jagoda, MD, FACEP
The patient’s 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 patient’s 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 patient’s complaint since many neurologic symptoms
are nonspecific, e.g. it is important to distinguish vertigo from dizziness, blindness from
decreased vision, or weakness from fatigue. Corroboration from family members or bystanders
can be critical since they are often able to place the patient’s 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 patient’s 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
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.
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
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Andy Jagoda, MD, FACEP
possibility that in this patient’s case, the exam would have revealed a dilated pupil since the most
common cause for subarachnoid hemorrhages is a ruptured cerebral aneurysm and a 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.
The neurologic examination begins by assessing the patient’s 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.
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
afterwhich 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
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Andy Jagoda, MD, FACEP
made. The patient was given lorazepam, 2 mg IV, with normalization of the EEG and complete
resolution of his abnormal behavior.
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
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
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. Horner’s syndrome or carotid artery dissection. Bilateral
pupillary constriction is seen with pontine hemorrhage or as the result of drugs (e.g. opiates,
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 peripheral VIIth nerve lesions, including Bell’s Palsy, may have a
complete facial weakness that includes the forehead. Of note, an isolated central VIIth lesion is
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Andy Jagoda, MD, FACEP
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 patient’s 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.
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 patient’s 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.
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 space-occupying lesion or ventricular enlargement on CT, and normal CSF
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
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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”.
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.
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 HIV-related myelopathy was made.
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
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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.
Reflex testing in the screening exam includes the major deep tendon reflexes and the planter
reflex (Babinski’s 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
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.
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 over-the-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 patient’s 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 polyneuropathy (Guillain-Barre Syndrome) was suspected and
confirmed with CSF analysis which revealed a protein of 140. The patient was admitted to the
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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.
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.
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
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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.
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
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 examiner’s 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.
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
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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 patient’s 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.
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 patient’s 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 patient’s 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.
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.
The Neurologic Examination for the Emergency Physician Page 12 of 13
Andy Jagoda, MD, FACEP
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
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 Page 13 of 13
Andy Jagoda, MD, FACEP
The Neurologic Examination for the Emergency Physician
1. Kasner S, Grota J. Emergency identification and treatment of acute ischemic stroke. Ann
Emerg Med 1997:30:642-653.
2. DeLorenzo R, Waterhouse E, Towne A, et al. Persistent nonconvulsive status epilepticus
after the control of convulsive status epilepticus. Epilepsia 1998;39:833-840.
3. Goldberg S: The Four-Minute Neurologic Exam. Miami, MedMaster, Inc., 1987.
4. Mayo Clinic and Mayo Foundation. Clinical Examinations in Neurology. Mosby Year
5. Brazis P, Masdeu J, Biller J. Localization in Clinical Neurology, 2nd Edition. Little,
Brown, and Company, Boston, 1990.
6. Duus P. Topical Diagnosis in Neurology. Thieme Medical Publishers, New York, 1989.
7. Lewis L, Miller D, Morley J, et al. Unrecognized delirium in ED geriatric patients. Am J
Emerg Med 1995; 13:142-145.
8. Ellis J, Lee S. Acute prolonged confusion in later life as an ictal state. Epilepsia
9. Guberman A, Cantu-Reyna G, Stuss D, et al, Nonconvulsive generalized status epilepticus:
clinical features, neuropsychological testing and long-term follow-up. Neurology
10. Lee S, Nonconvulsive status epilepticus: ictal confusion in later life. Arch Neurol
11. Haerer AF: Examination in cases of suspected hysteria and malingering. In DeJong RN:
The Neurologic Examination, ed 5. Philadelphia, JB Lippincott Company, 1992, p
12. Edwards F. Overcoming the diagnostic challenges of dizziness, vertigo, and syncope.
Emerg Med Report 1994;15:1-7.