What You Forgot About the Neurologic Exam, Part 2:Published on Psychiatric Times(http://www.psychiatrictimes.com)

What You Forgot About the Neurologic Exam, Part 2:January 01, 2005By Silvana Riggio, MD [1] and Andy Jagoda, MD [2]

ABSTRACT: Asymmetry-whether of strength, reflexes, or sensory function-is animportant localizing finding in the neurologic evaluation. Asymmetric deficits of strengthmay indicate an acute CNS lesion. Symmetric hyperreflexia or hyporeflexia alone is notdiagnostic; compare reflexes between sides of the body and between upper and lowerextremities. The extensor plantar response (Babinski reflex) suggests an upper motorneuron lesion. During the sensory examination, look for asymmetry and determinewhether both light touch and pinprick sensation are intact. Simultaneous stimulationwith 2 sharp objects on opposite sides of the body-done to detect extinction of responseon 1 side-can uncover subtle sensory deficits. Source:

A systematically performed neurologic screening assessment need not be time-consuming, and itcan yield crucial information. Let the patient's complaint, the history, and the results of the basicexamination 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 historyof a change in behavior. Similarly, when the patient has no sensory complaints, a determination ofhis or her ability to distinguish sharp from dull sensations bilaterally is sufficient, whereas a patientwho complains of vague sensory deficits may need to be tested for extinction on simultaneoussensory stimulation, for astereognosis (inability to identify an object by palpation), or for sensorylevel.A principal objective of the evaluation is to distinguish central from peripheral nervous systemabnormality 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 pointsof the history taking and the evaluation of mental status and cranial nerves (CNs). Here, we discussthe remaining components of the neurologic screening examination: the assessments of motorfunction, reflexes, sensory status, and coordination and balance. Again, we use clinical case reportsto exemplify basic concepts.MOTOR FUNCTIONThis part of the evaluation begins with the assessment of overall strength, focusing initially on thepatient's ability to breathe. Then, it is especially important to look for asymmetric deficits ofstrength, which may indicate an acute CNS lesion.1 Testing motor strength is difficult or impossible ifthe 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 presenceof "drift." The patient, with eyes closed, holds his arms out horizontally, palms up, for 30 seconds. Ifweakness is present, the hand and arm on the affected side will slowly drift or pronate. You cancheck lower extremity drift by having the patient lie supine with legs extended above the bed at a30-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 anddorsiflexion. Grasp testing of the ulnar aspect of the hand is more reliable than that of the radialaspect. In cases of possible peripheral nerve or muscle injury, or of abnormal results of motor testingas described above, more formal testing of the extremity is in order.CASE 1: INCREASING WEAKNESS IN AN HIV-POSITIVE MANThe case. A 34-year-old man with AIDS and a CD4+ lymphocyte count of 10/µL complained ofdiffuse weakness. He reported that he had been weak for months but that over the past several daysthe weakness in his legs had increased, and he had begun to have difficulty in standing and walkingwithout 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 hisprescribed antiviral and antifungal drug regimens.On examination, he appeared cachectic but in no distress. Vital signs were stable. Head, ears, eyes,

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What You Forgot About the Neurologic Exam, Part 2:Published on Psychiatric Times(http://www.psychiatrictimes.com)

nose, and throat (HEENT), as well as heart, lungs, and abdomen, appeared normal. Rectal tone wasgood; stool was guaiac-negative.The CNs were intact. Motor testing revealed no upper extremity drift; however, the lower extremitiesexhibited spasticity and showed bilateral drift after 5 seconds. Lower extremity strength wasassessed as 3/5 in all the muscle groups. (A grading scale for motor strength is provided in Table 1.)

Table 1 – Grading scalefor motor strength

5 = Normalstrength

4 = Weakbut able to

resistexaminer3 = Moves

againstgravity butunable to

resistexaminer2 = Movesbut unable

to resistgravity

1 = Flickerbut no

movement0 = No

movement

On sensory testing, the patient could distinguish sharp from dull sensations in the upper and lowerextremities, 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 4/2bilaterally. 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 werenormal, and a cerebrospinal fluid (CSF) analysis was performed. Tests for syphilis and mycobacterial,cryptococcal, herpesvirus, and cytomegalovirus infections were negative. A diagnosis of HIV-relatedmyelopathy was made.Commentary. This case demonstrates the potential difficulty in assessing a patient with chronicdisease who has an acute complaint. It also demonstrates the utility of the motor, sensory, andreflex examinations in differentiating central from peripheral lesions. This patient had clear findingsof upper motor neuron dysfunction, including spasticity, hyperreflexia, and Babinski reflex (Table 2).

Table 2 —Distinguishing upper motor neuronfrom lower motor neuron involvement

Type DTRsMuscletone

Atrophy

Fasciculations

Babinskireflex

UpperIncreasIncreasNNP

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What You Forgot About the Neurologic Exam, Part 2:Published on Psychiatric Times(http://www.psychiatrictimes.com)

motorneuron

ededo*oresent

Lowermotorneuron

Decreased

Decreased

Yes

Yes

Absent

DTRs, deep tendon reflexes.*Not significant but can occur.

Myelopathy is seen in up to 90% of patients with end-stage HIV disease.2 Clinically, patients presentwith leg weakness, unsteadiness, gait impairment, and variable sensory impairment. Bowel andbladder 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 peripheralneuropathies. Sensory deficits involve primarily vibratory and position sense. Management focuseson eliminating reversible causes of myelopathy.3,4

REFLEXESReflex testing in the screening examination includes the major deep tendon reflexes and the plantarreflex (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).

Table 3 –Grading scalefor deep tendon reflexes

0 = Reflexabsent

1 = Reflexpresent butdiminished2 = Reflex

normal3 = Reflexincreasedbut not

pathologic4+ =Reflex

markedly hyperactive,

with orwithoutclonus

Symmetric hyporeflexia may be nonpathologic or indicative of metabolic derangements or peripheralneuropathy. Symmetric hyperreflexia may also have a systemic cause, frequently resulting fromhypocalcemia 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

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What You Forgot About the Neurologic Exam, Part 2:Published on Psychiatric Times(http://www.psychiatrictimes.com)

flexion/extension reflex. A normal response to stroking the plantar surface of the foot is plantarflexion of the toes; Babinski reflex is characterized by dorsiflexion of the big toe with fanning out ofthe smaller toes.CASE 2: YOUNG WOMAN WITH PARESTHESIASThe case. A 23-year-old woman presented to the emergency department (ED) complaining ofweakness 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 recorddocumented that she was afebrile and "HEENT-normal." A neurologic examination was not recordedon the chart.The patient was discharged with a diagnosis of "viral syndrome." Over the next 12 hours, the heavyfeeling in her legs increased and she returned to the ED. The patient required assistance to walk. Hervital signs were stable.There were no CN deficits. On sensory testing, she could distinguish sharp from dull sensations in all4 extremities. On upper extremity motor testing, she had 5/5 strength; on lower extremity motortesting, ankle flexion/extension was 2/5, and knee flexion/extension, 3/5; hip flexion was 4/5. Deeptendon reflexes were 2/2 in the upper extremities and 0/2 bilaterally at the patella andgastrocnemius muscle.Acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome) was suspected. Thatdiagnosis was confirmed by CSF analysis, which revealed a total protein level of 140 mg/dL. Thepatient was admitted to the ICU.Commentary. This case demonstrates the importance of performing a neurologic examination of allpatients with a neurologic complaint. Guillain-Barré syndrome can be rapidly progressive, and forthis patient, discharge from the hospital could have been disastrous.Guillain-Barré syndrome results from immune-mediated inflammation of myelin. Patients who havethis polyneuropathy typically present with distal paresthesias followed by symmetric ascendingparesis. 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 nodeficits. The straight leg raising test may show positive results, because of nerve root irritation. CSFanalysis demonstrates an elevated protein level and normal glucose level, and the mononuclear cellcount usually is below 10/µL. Since it may take up to 72 hours for abnormalities in the CSF todevelop, a repeated lumbar puncture may be necessary when the initial results are normal butGuillain-Barré syndrome is still suspected.5Patients 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 monitoredsetting. The disease may progress over 4 to 6 weeks before resolving, and approximately 5% ofpatients are left with residual symptoms.Plasmapheresis has been shown to reduce the duration and severity of the disease.5 Administrationof corticosteroids is not recommended, but gamma;-globulin therapy may decrease the disease'sduration.6SENSORY STATUSThis part of the screening examination includes testing of pain and light touch. The spinothalamictract in the anterior cord carries fibers for temperature and both pain and light touch, while theposterior column carries fibers for light touch. This accounts for the preservation of light touchsensation in patients with anterior cord syndromes.Testing for proprioception, stereognosis, and vibration is generally reserved for patients withsuspected neuropathies or for further evaluation of sensory complaints. Dermatomal testing isperformed in patients with suspected radiculopathies, since central lesions do not cause dermatomaldeficits.Evaluating sensation in patients with vague complaints is best done by testing for extinction ondouble simultaneous stimulation. In this test, the patient closes his eyes, and 2 sharp objects aresimultaneously 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 DISEASESThe case. A 64-year-old woman with hypertension and diabetes complained of numbness in her leftarm, 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.

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What You Forgot About the Neurologic Exam, Part 2:Published on Psychiatric Times(http://www.psychiatrictimes.com)

On examination, she was alert; was oriented to person, place, and time; and had fluent speech. Herblood pressure was 150/90 mm Hg; respiratory rate, 16 breaths per minute; pulse, 76 beats perminute. 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, thepatient distinguished sharp from dull on the left upper extremity but exhibited extinction onsimultaneous testing. On further testing, she demonstrated astereognosis when asked to identify aquarter 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 apatient with a neurologic complaint. The patient had a sensory deficit that was not evident duringthe 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 searchfor reversible causes of thromboembolism. These patients require a careful evaluation that includesan ECG, an echocardiogram, carotid artery imaging, and a complete hematologic assessment.7COORDINATION AND BALANCECoordination is a function of the cerebellum that involves integrated visual, proprioceptive, andvestibular input. You can easily evaluate cerebellar function by asking the patient to close his eyesand, with the finger of one hand, touch a finger of the other hand and his nose in rapid alternation. Ina variation of this test, the patient alternately touches his nose and the examiner's finger with hiseyes open; in this case, visual problems may interfere with performance. Heel-to-shin testing-inwhich the patient runs the heel of one foot up and down the shin of the opposite leg-is frequentlyused to assess cerebellar function. Difficulty in performing rapid alternating movements of the handsmay also demonstrate cerebellar abnormality.Balance requires an integration of cerebellar, visual, vestibular, and proprioceptive input. It isevaluated with the Romberg test and the tandem gait (heel-to-toe) test. In the Romberg test, thepatient is asked to stand with his feet together (proprioceptive input) without support, first with eyesopen (visual input) and then with eyes closed. Closing the eyes eliminates vision, but withproprioception and vestibular sense intact, the patient will not sway. If there is a proprioceptivedeficit, the patient will keep his balance with the eyes open and lose his balance when the eyes areclosed. When this occurs, the test result is positive. Swaying with the eyes open or closed suggests acerebellar lesion that is not compensated by sensory input from the other systems.CASE 4: MAN WITH VERTIGOThe case. A 64-year-old man with vertigo was brought to the ED by ambulance. He reported that hehad had several similar episodes over the past year, which his physician had diagnosed as benignpositional vertigo and had treated with meclizine. On this occasion, the "room spinning" had startedapproximately 6 hours before the patient came to the ED. It was accompanied by severe nausea andvomiting. The patient had taken 25 mg of meclizine without improvement.He was taking atenolol and hydrochlorothiazide for hypertension. On the basis of the reportedhistory 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, 18breaths per minute. The patient continued to complain of vertigo, but he was alert and oriented toperson, place, and time. He was cooperative and able to answer questions clearly. CNs II, III, IV, andVI were intact, but pronounced vertical nystagmus was present and was not suppressed withfixation.The patient displayed no facial asymmetry, his hearing was decreased on the left side, his speechwas clear, and he was able to handle secretions and swallow normally. There was no weakness in hisextremities, but limb ataxia was noted on the left side. Finger-to-nose testing revealed grossdysmetria (missing the target with pass pointing) on the left side. MRI of the brain revealed a leftventral cerebellar infarct.

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What You Forgot About the Neurologic Exam, Part 2:Published on Psychiatric Times(http://www.psychiatrictimes.com)

Commentary. In this case, management relied on a previous diagnosis and the correct diagnosiswas delayed. A neurologic examination was performed only when the initial treatment failed torelieve the patient's symptoms. Its findings clearly pointed toward a central cause of the patient'svertigo.Vertical nystagmus strongly suggests central abnormality, as do the associated findings here ofdecreased hearing, ataxia, and dysmetria.8 Peripheral causes of vertigo include lesions of thesemicircular canals, utricle, or saccule.Vertigo induced by cupulolithiasis (called benign positional vertigo) usually is not present at rest butis induced by movement. (In vestibular neuronitis and acute labyrinthitis, vertigo can be present atrest.) In benign positional vertigo, nystagmus has a delayed onset after change in position, isfatigable with repeated provocation, and can be suppressed with fixation.9,10 Benign positionalvertigo is not associated with cerebellar or CN deficits.The vertigo associated with central lesions is often present at rest, although it may be worsened bychanges in position. It tends to be less severe but more persistent than vertigo caused by aperipheral cause, and it is not fatigable; it is usually associated with cerebellar or brain stemdeficits.8In this case, the workup ultimately included arteriography, which demonstrated stenosis of the leftvertebral artery. The prior episodes of vertigo were most likely caused by transient ischemic attacksthat resulted from thromboembolism in the posterior circulation. References: REFERENCES:1. Kothari R, Hall K, Brott T, Broderick J. Early stroke recognition: developing an out-of-hospital NIHStroke Scale. Acad Emerg Med. 1997;4:986-990.2. Petito CK, Navia BA, Cho ES, et al. Vacuolar myelopathy pathologically resembling subacutecombined degeneration in patients with the acquired immunodeficiency syndrome. N Engl J Med.1985;312:874-879.3. Tucker T, Dix RD, Katzen C, et al. Cytomegalovirus and herpes simplex virus ascending myelitis ina patient with acquired immune deficiency syndrome. Ann Neurol. 1985;18:74-79.4. Woolsey RM, Chambers TJ, Chung HD, McGarry JD. Mycobacterial meningomyelitis associated withhuman immunodeficiency virus infection. Arch Neurol. 1988;45:691-693.5. Ropper AH. The Guillain-Barré syndrome. N Engl J Med. 1992;326:1130-1136.6. van der Meche FG, Schmitz PI. A randomized trial comparing intravenous immune globulin andplasma exchange in Guillain-Barré syndrome. Dutch Guillain-Barré Study Group. N Engl J Med.1992;326:1123-1129.7. National Stroke Association Consensus Panel. Stroke: the first hours. Stroke Clin Updates. 1997;(special issue):1-15.8. Edwards F. Overcoming the diagnostic challenges of dizziness, vertigo, and syncope. Emerg MedRep. 1994;15:1-7.9. Kroenke K, Lucas CA, Rosenberg ML, et al. Causes of persistent dizziness. A prospective study of100 patients in ambulatory care. Ann Intern Med. 1992;117:898-904.10. Brandt T, Steddin S, Daroff RB. Therapy for benign paroxysmal positioning vertigo, revisited.Neurology. 1994;44:796-800.

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