What You Forgot About the Neurologic Exam, Part 2:

A systematically performed neurologic screening assessment need not be time-consuming, and it can yield crucial information. Let the patient's complaint, the history, and the results of the basic examination guide you to the salient findings that require more thorough investigation.

For example, a full mental status examination may not be warranted if the patient is awake, oriented, and able to converse, but it is required for patients with altered mental status or a history of a change in behavior. Similarly, when the patient has no sensory complaints, a determination of his or her ability to distinguish sharp from dull sensations bilaterally is sufficient, whereas a patient who complains of vague sensory deficits may need to be tested for extinction on simultaneous sensory stimulation, for astereognosis (inability to identify an object by palpation), or for sensory level.

A principal objective of the evaluation is to distinguish central from peripheral nervous system abnormality and upper from lower motor neuron involvement. Asymmetry-whether of strength, reflexes, or sensory function-is often a crucial localizing finding.

In part 1 of this article (CONSULTANT, December 2004, page 1773), we reviewed the essential points of the history taking and the evaluation of mental status and cranial nerves (CNs). Here, we discuss the remaining components of the neurologic screening examination: the assessments of motor function, reflexes, sensory status, and coordination and balance. Again, we use clinical case reports to exemplify basic concepts.

MOTOR FUNCTION

This part of the evaluation begins with the assessment of overall strength, focusing initially on the patient's ability to breathe. Then, it is especially important to look for asymmetric deficits of strength, which may indicate an acute CNS lesion.¹ Testing motor strength is difficult or impossible if the patient is uncooperative, and results may be significantly affected by pain.

In general, it is not necessary to test every muscle group individually; instead, test for the presence of "drift." The patient, with eyes closed, holds his arms out horizontally, palms up, for 30 seconds. If weakness is present, the hand and arm on the affected side will slowly drift or pronate. You can check lower extremity drift by having the patient lie supine with legs extended above the bed at a 30-degree angle. A weak leg tends to drift downward within 30 seconds.

Other motor tests for extremity weakness include hand grasp and foot plantar flexion and dorsiflexion. Grasp testing of the ulnar aspect of the hand is more reliable than that of the radial aspect. In cases of possible peripheral nerve or muscle injury, or of abnormal results of motor testing as described above, more formal testing of the extremity is in order.

CASE 1: INCREASING WEAKNESS IN AN HIV-POSITIVE MAN

The case. A 34-year-old man with AIDS and a CD4⁺ lymphocyte count of 10/µL complained of diffuse weakness. He reported that he had been weak for months but that over the past several days the weakness in his legs had increased, and he had begun to have difficulty in standing and walking without assistance. He denied fevers, cough, bowel or bladder dysfunction, and back pain.

The patient's history included episodes of pneumonia and oral thrush. He did not adhere to his prescribed antiviral and antifungal drug regimens.

On examination, he appeared cachectic but in no distress. Vital signs were stable. Head, ears, eyes, nose, and throat (HEENT), as well as heart, lungs, and abdomen, appeared normal. Rectal tone was good; stool was guaiac-negative.

The CNs were intact. Motor testing revealed no upper extremity drift; however, the lower extremities exhibited spasticity and showed bilateral drift after 5 seconds. Lower extremity strength was assessed as 3/5 in all the muscle groups. (A grading scale for motor strength is provided in Table 1.)

On sensory testing, the patient could distinguish sharp from dull sensations in the upper and lower extremities, but vibratory sense was absent in the lower extremities. Deep tendon reflexes were 2/2 (graded as described below, under "Reflexes") at the biceps, and patella reflexes were 4/2 bilaterally. Extensor plantar reflexes (Babinski reflex) also were present bilaterally.

The patient underwent MRI of the spinal cord to assess for a mass lesion. The MRI findings were normal, and a cerebrospinal fluid (CSF) analysis was performed. Tests for syphilis and mycobacterial, cryptococcal, herpesvirus, and cytomegalovirus infections were negative. A diagnosis of HIV-related 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 examinations in differentiating central from peripheral lesions. This patient had clear findings of upper motor neuron dysfunction, including spasticity, hyperreflexia, and Babinski reflex (Table 2).

Myelopathy is seen in up to 90% of patients with end-stage HIV disease.² Clinically, patients present with leg weakness, unsteadiness, gait impairment, and variable sensory impairment. Bowel and bladder dysfunction can occur.

On examination, patients have spasticity, weakness, hyperreflexia, and extensor plantar responses. Reflexes may be decreased, however, since these patients often have associated peripheral neuropathies. Sensory deficits involve primarily vibratory and position sense. Management focuses on eliminating reversible causes of myelopathy.^3,4

REFLEXES

Reflex testing in the screening examination includes the major deep tendon reflexes and the plantar reflex (Babinski reflex). The major deep tendon reflexes are the patellar (L3, 4), Achilles tendon (S1, 2), biceps (C5, 6), and triceps (C7, 8) reflexes. The response is graded from 0 (no reflex) to 4+ (hyperreflexia) (Table 3).

Symmetric hyporeflexia may be nonpathologic or indicative of metabolic derangements or peripheral neuropathy. Symmetric hyperreflexia may also have a systemic cause, frequently resulting from hypocalcemia or hyperthyroidism. Unilateral hyperreflexia suggests an upper motor neuron process. Asymmetric reflexes are generally pathologic.

Several reflexes indicate upper motor neuron disease, the most commonly elicited being the plantar flexion/extension reflex. A normal response to stroking the plantar surface of the foot is plantar flexion of the toes; Babinski reflex is characterized by dorsiflexion of the big toe with fanning out of the smaller toes.

CASE 2: YOUNG WOMAN WITH PARESTHESIAS

The case. A 23-year-old woman presented to the emergency department (ED) complaining of weakness and "heavy" and "tingly" feelings in her legs. For the preceding 3 days, she had had a "cold," with low-grade fever, myalgias, and sinus congestion. She had no significant medical history; her medications included an oral contraceptive and over-the-counter cold remedies. The ED record documented that she was afebrile and "HEENT-normal." A neurologic examination was not recorded on the chart.

The patient was discharged with a diagnosis of "viral syndrome." Over the next 12 hours, the heavy feeling in her legs increased and she returned to the ED. The patient required assistance to walk. Her vital signs were stable.

There were no CN deficits. On sensory testing, she could distinguish sharp from dull sensations in all 4 extremities. On upper extremity motor testing, she had 5/5 strength; on lower extremity motor testing, ankle flexion/extension was 2/5, and knee flexion/extension, 3/5; hip flexion was 4/5. Deep tendon reflexes were 2/2 in the upper extremities and 0/2 bilaterally at the patella and gastrocnemius muscle.

Acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome) was suspected. That diagnosis was confirmed by CSF analysis, which revealed a total protein level of 140 mg/dL. The patient was admitted to the ICU.

Commentary. This case demonstrates the importance of performing a neurologic examination of all patients with a neurologic complaint. Guillain-Barré syndrome can be rapidly progressive, and for this patient, discharge from the hospital could have been disastrous.

Guillain-Barré syndrome results from immune-mediated inflammation of myelin. Patients who have this polyneuropathy typically present with distal paresthesias followed by symmetric ascending paresis. Bulbar weakness, respiratory muscle involvement, and autonomic instability can occur. Because this is a lower motor neuron process, deep tendon reflexes are decreased.

Even when the patient has sensory complaints, sensory testing usually reveals minimal or no deficits. The straight leg raising test may show positive results, because of nerve root irritation. CSF analysis demonstrates an elevated protein level and normal glucose level, and the mononuclear cell count usually is below 10/µL. Since it may take up to 72 hours for abnormalities in the CSF to develop, a repeated lumbar puncture may be necessary when the initial results are normal but Guillain-Barré syndrome is still suspected.⁵

Patients with Guillain-Barré syndrome are at risk for respiratory compromise and arrhythmias; therefore, all but those with very mild, stable manifestations need to be admitted to a monitored setting. The disease may progress over 4 to 6 weeks before resolving, and approximately 5% of patients are left with residual symptoms.

Plasmapheresis has been shown to reduce the duration and severity of the disease.⁵ Administration of corticosteroids is not recommended, but gamma;-globulin therapy may decrease the disease's duration.⁶

SENSORY STATUS

This part of the screening examination includes testing of pain and light touch. The spinothalamic tract in the anterior cord carries fibers for temperature and both pain and light touch, while the posterior column carries fibers for light touch. This accounts for the preservation of light touch sensation in patients with anterior cord syndromes.

Testing for proprioception, stereognosis, and vibration is generally reserved for patients with suspected neuropathies or for further evaluation of sensory complaints. Dermatomal testing is performed in patients with suspected radiculopathies, since central lesions do not cause 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 2 sharp objects are simultaneously applied on opposite sides of the body. If the patient reports sharpness on 1 side only, a CNS sensory deficit is present on the other side. If he initially feels sharpness on both sides, repeated testing is performed to detect extinction of response on one side.

CASE 3: NUMBNESS IN WOMAN WITH CHRONIC DISEASES

The case. A 64-year-old woman with hypertension and diabetes complained of numbness in her left arm, which began 48 hours earlier. She did not have headache, weakness, or difficulty with speech, vision, or gait. She had no history of stroke. Her medications included enalapril and metformin.

On examination, she was alert; was oriented to person, place, and time; and had fluent speech. Her blood pressure was 150/90 mm Hg; respiratory rate, 16 breaths per minute; pulse, 76 beats per minute. Her blood glucose level, measured with a finger-stick test, was 130 mg/dL.

Figure 1

CNs were intact, with no facial asymmetry and normal CN V function. Motor testing revealed no drift. Deep tendon reflexes were 2/2 and symmetric; Babinski reflex was negative. On sensory testing, the patient distinguished sharp from dull on the left upper extremity but exhibited 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 scan revealed a right parietal cortex infarct (Figure).

Commentary. This case demonstrates the importance of pursuing the clinical evaluation of a patient with a neurologic complaint. The patient had a sensory deficit that was not evident during the initial examination; a more in-depth evaluation uncovered it.

Making the final diagnosis of a cortical stroke was the key to proper management of this patient. Because patients who have had one stroke are at increased risk for another, it is necessary to search for reversible causes of thromboembolism. These patients require a careful evaluation that includes an ECG, an echocardiogram, carotid artery imaging, and a complete hematologic assessment.⁷

COORDINATION AND BALANCE

Coordination is a function of the cerebellum that involves integrated visual, proprioceptive, and vestibular input. You can easily evaluate cerebellar function by asking the patient to close his eyes and, with the finger of one hand, touch a finger of the other hand and his nose in rapid alternation. In a variation of this test, the patient alternately touches his nose and the examiner's finger with his eyes open; in this case, visual problems may interfere with performance. Heel-to-shin testing-in which the patient runs the heel of one foot up and down the shin of the opposite leg-is frequently used to assess cerebellar function. Difficulty in performing rapid alternating movements of the hands may also demonstrate cerebellar abnormality.

Balance requires an integration of cerebellar, visual, vestibular, and proprioceptive input. It is evaluated with the Romberg test and the tandem gait (heel-to-toe) test. In the Romberg test, the patient is asked to stand with his feet together (proprioceptive 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 test result is positive. Swaying with the eyes open or closed suggests a cerebellar lesion that is not compensated by sensory input from the other systems.

CASE 4: MAN WITH VERTIGO

The case. A 64-year-old man with vertigo was brought to the ED by ambulance. He reported that he had had several similar episodes over the past year, which his physician had diagnosed as benign positional vertigo and had treated with meclizine. On this occasion, the "room spinning" had started approximately 6 hours before the patient came to the ED. It was accompanied by severe nausea and vomiting. The patient had taken 25 mg of meclizine without improvement.

He was taking atenolol and hydrochlorothiazide for hypertension. On the basis of the reported history of benign positional vertigo, he was symptomatically treated with promethazine, 25 mg IV. Three hours later, his symptoms persisted; a physical examination was then performed.

His blood pressure was 190/100 mm Hg; heart rate, 64 beats per minute; and respiratory rate, 18 breaths per minute. The patient continued to complain of vertigo, but he was alert and oriented to person, place, and time. He was cooperative and able to answer questions clearly. CNs II, III, IV, and VI were intact, but pronounced vertical nystagmus was present and was not suppressed with fixation.

The patient displayed no facial asymmetry, his hearing was decreased on the left side, his speech was clear, and he was able to handle secretions and swallow normally. There was no weakness in his extremities, but limb ataxia was noted on the left side. Finger-to-nose testing revealed gross dysmetria (missing the target with pass pointing) on the left side. MRI of the brain revealed a left ventral cerebellar infarct.

Commentary. In this case, management relied on a previous diagnosis and the correct diagnosis was delayed. A neurologic examination was performed only when the initial treatment failed to relieve the patient's symptoms. Its findings clearly pointed toward a central cause of the patient's vertigo.

Vertical nystagmus strongly suggests central abnormality, as do the associated findings here of decreased hearing, ataxia, and dysmetria.⁸ Peripheral causes of vertigo include lesions of the semicircular canals, utricle, or saccule.

Vertigo induced by cupulolithiasis (called benign positional vertigo) usually is not present at rest but is induced by movement. (In vestibular neuronitis and acute labyrinthitis, vertigo can be present at rest.) In benign positional vertigo, nystagmus has a delayed onset after change in position, is fatigable with repeated provocation, and can be suppressed with fixation.^9,10 Benign positional vertigo is not associated with cerebellar or CN deficits.

The vertigo associated with central lesions is often present at rest, although it may be worsened by changes in position. It tends to be less severe but more persistent than vertigo caused by a peripheral cause, and it is not fatigable; it is usually associated with cerebellar or brain stem deficits.⁸

In this case, the workup ultimately included arteriography, which demonstrated stenosis of the left vertebral artery. The prior episodes of vertigo were most likely caused by transient ischemic attacks that resulted from thromboembolism in the posterior circulation.

References:

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