Neurologic Examination
Neurologic examination of the patient with cerebrovascular disease is similar to any other formal neurologic examination. However, certain combinations of neurologic signs may establish the location of the disease. A complete neurologic examination is necessary to determine current neurologic status, and serial assessments are often desirable to determine whether there is any improvement or worsening of the condition. Some elements of the neurologic examination relating to preliminary evaluation of the level of consciousness, mental status, speech, vision, and focal weakness of the limbs are completed when the history is taken and also during the general examination.
Other elements of the neurologic examination provide further details about whether the patient’s current illness is caused by cerebrovascular disease and, if so, the location and sometimes the type and the origin of the lesion(s). With the data from the history and the general and neurologic examinations, a logical differential diagnosis and evaluation strategy can be proposed. Further evaluation of laboratory study results usually helps to clarify the diagnosis and define an appropriate treatment plan.
NEUROVASCULAR EXAMINATION
Auscultation
Auscultation of the proximal great vessels (Fig. 5-1) arising from the aortic arch (over the supraclavicular fossa), the carotid arteries (particularly over the carotid bifurcation below the angle of the mandible), the orbits (while closing the eye being auscultated), and the cranial vault is performed to listen for bruits. With the patient lying or sitting, the bell of the stethoscope should be applied over the area being examined without using pressure, which may produce artificial noise. First, the cardiac sounds should be auscultated over the base of the heart, and then the stethoscope should be moved superiorly to distinguish transmitted cardiac sounds from sounds arising in brachiocephalic, subclavian, vertebral, or carotid arteries. Bruits that are heard proximally over the aortic arch vessels may be associated with transmitted cardiac murmurs, underlying large vessel stenosis or tortuosity, or no identifiable underlying abnormality.
A bruit is a reflection of turbulence in the underlying artery. Bruit loudness can be graded on a scale of 1 to 6 according to their intensity (1, barely audible with stethoscope; 6, audible without a stethoscope). The quality of a carotid bruit is often recorded, but overall is a poor predictor of the severity of the underlying stenosis. A carotid bruit without regard to its quality or duration is a relatively
poor predictor of stenosis of the internal carotid artery in asymptomatic patients. It is noted in approximately 40% of patients with stenosis of more than 90% of the diameter of the artery, but 10% of patients with stenosis of less than 50% of the artery’s diameter may have an audible bruit. In patients with symptoms of cerebral ischemia, however, a diffuse or localized bruit is 85% predictive of a moderate or high-grade stenosis. Soft, continuous cervical bruits that vary with changes in neck position or that can be obliterated by jugular compression are suggestive of a benign venous hum.
poor predictor of stenosis of the internal carotid artery in asymptomatic patients. It is noted in approximately 40% of patients with stenosis of more than 90% of the diameter of the artery, but 10% of patients with stenosis of less than 50% of the artery’s diameter may have an audible bruit. In patients with symptoms of cerebral ischemia, however, a diffuse or localized bruit is 85% predictive of a moderate or high-grade stenosis. Soft, continuous cervical bruits that vary with changes in neck position or that can be obliterated by jugular compression are suggestive of a benign venous hum.
 FIGURE 5-1. Sites for neurovascular auscultation. |
Most arterial bruits begin in systole, but systolic-diastolic bruits strongly suggest high-grade arterial stenosis (>90% cross-sectional area stenosis). While listening over the carotid arteries, the physician should distinguish diffuse bruits (relatively constant magnitude and pitch along the carotid arteries in the neck or mildly decreasing distal intensity) from localized carotid bruits, although either may or may not be associated with underlying carotid stenosis. Diffuse bruits, especially if bilateral, often reflect a transmitted heart murmur; an aortic arch lesion; or a condition of diffuse, increased flow and turbulence without an underlying structural lesion. It may be difficult or impossible to distinguish lesions of the internal carotid artery from stenoses of the common carotid or external carotid arteries or to distinguish lesions of the vertebral artery from those of the subclavian or brachiocephalic arteries on the basis of the location or sound characteristics of a bruit.
Orbital bruits, particularly continuous, machinery-like bruits, are encountered with occlusive lesions of the carotid siphon, ipsilateral internal carotid artery occlusion with increased ophthalmic collateral backflow in the external carotid system, carotid-cavernous fistulas, and other lesions that produce intracranial turbulent flow, such as arteriovenous malformations (AVMs). Cephalic bruits are commonly found in otherwise normal children but may also be found in 10% to 25% of patients with intracranial AVMs (usually associated with a rhythmic, localized head noise referred to as “pulsatile tinnitus”).
Palpation
Palpation of the carotid pulses in the neck is generally unreliable (minor differences in the pulses of the left and right carotid arteries are unlikely to be important) and may even be dangerous, particularly at the level of the carotid bifurcation or over carotid arteries with associated bruit. Material from atheromatous plaques may be dislodged and cause cerebral infarction distally in the carotid system. Direct pressure applied to the carotid sinus may also cause cardiac arrhythmias.
Palpation of the superficial temporal, facial, infraorbital, and occipital arteries provides an estimate of flow in the external carotid system (Fig. 5-2). This flow may be reduced in the cranial arteries or with an ipsilateral common carotid or external carotid artery occlusion. Increased external carotid flow may reflect an occlusive lesion of the internal carotid artery with increased compensatory collateral flow. In addition, palpation of the superficial temporal arteries may be helpful in the diagnosis of cranial arteritis, which is indicated by a decreased pulse, increased arterial tenderness or beading, and erythema of the overlying skin. Palpation of the radial arteries may provide information about the status of the subclavian arterial systems: A weaker pulse in one radial artery or one pulse that follows the other asynchronously (delayed) suggests proximal stenosis in the subclavian system on that side.
Ophthalmic Ocular Examination
Ophthalmic examination consists of a careful evaluation of the patient’s history (see Chapter 2, Visual Disturbances), a general ocular examination, and special ophthalmic examinations.
 FIGURE 5-2. Common sites for palpation of the external carotid artery system. |
General Ocular Examination
General examination includes inspection of external ocular structures (lids, conjunctivae, corneas, sclerae, and lacrimal apparatus), irides, pupils, and position of the eyes; determination of visual acuity; and confrontational visual field testing.
Inspection of the external ocular structures allows detection of various disturbances, such as pupillary abnormalities, ptosis, exophthalmos, foreign bodies, inflammation, dryness, corneal clouding, and iridic color abnormalities. Both upper eyelids normally cover 1 to 2 mm of the irides. Unilateral ptosis of 1 to 2 mm associated with miosis is usually caused by Horner’s syndrome. Ptosis may also be caused by a lesion of the third cranial nerve (accompanied by convergent strabismus and pupillary dilation) or by muscle (such as muscular dystrophy) or neuromuscular junction abnormalities (such as myasthenia gravis—often fluctuating, gradually worsening, unilateral or bilateral ptosis with fatigability and associated diplopia). Other varieties are congenital ptosis, ptosis associated with aging (usually with redundant eyelid[s]), and ptosis associated with other mechanical factors (lid swelling, tumor, or xanthelasma). Erythema or congestion of the lids, conjunctivae, or sclerae may be caused by infection, trauma, allergy, or acute glaucoma.
Unilateral subconjunctival hemorrhage is commonly caused by trauma or rupture of a small conjunctival vessel; bilateral and recurrent subconjunctival hemorrhages may be caused by blood dyscrasias. The corneal reflex is tested by touching the lateral edge of the cornea with a wisp of cotton. The normal response is a bilateral equal and prompt blink and may be diminished or lost as a result of abnormality in the afferent portion of the fifth cranial nerve, the efferent portion of the seventh cranial nerve, or damage to their reflex connections within the pons.
Both irides are normally the same color (a lack of melanin pigment within the iris may cause a unilateral blue iris resulting from Horner’s syndrome that occurs congenitally or during the first 2 years of life; differences in iris color may also be inherited without Horner’s syndrome). Holes on the iris usually indicate atrophy; capillaries on the surface (rubeosis) usually indicate anterior segment ischemia.
Extraocular Muscle Movements
Movement of the eyes is normally smooth, in the same direction, and at the same speed, except for convergence, when both eyes move mediad. Ocular movements are normally tested by having the patient direct their gaze to follow the examiner’s finger to the extreme right and left in the horizontal plane, upward and downward in the vertical plane, and within a few inches of the face in the midline to test convergence.
Reflex (“doll’s eyes”) ocular movements are occasionally tested to differentiate supranuclear from nuclear palsies; the patient fixes gaze on a central point straight ahead, and the examiner then moves the patient’s head from side to side and up and down. Gaze palsies may result from supratentorial and infratentorial lesions. Destructive cerebral lesions, such as cerebral infarcts, often cause conjugate ocular deviations toward the side of the lesion, with the head turned in the direction of deviation, whereas activating lesions, such as seizures, cause deviation of the eyes and head away from the lesion. Destructive cerebral lesions typically cause a contralateral hemiparesis in which the eyes look at the lesion and away from the hemiparesis. Lesions in the brainstem may also cause lateral gaze palsies. Destructive lesions may cause conjugate or dysconjugate ocular deviation, usually away from the side of the lesion. These brainstem lesions
are often accompanied by diplopia and may also produce a contralateral hemiparesis. A lateral gaze deviation with a lesion at a brainstem site has the eyes looking away from the lesion and at the hemiparesis. Supratentorial gaze palsies may occur with both frontal and occipital lobe lesions. In frontal lobe lesions, voluntary eye movement to command (without following the examiner’s finger) away from the side of the lesion is lost; in occipital lobe lesions, however, such eye movement to command is spared (Table 5-1).
are often accompanied by diplopia and may also produce a contralateral hemiparesis. A lateral gaze deviation with a lesion at a brainstem site has the eyes looking away from the lesion and at the hemiparesis. Supratentorial gaze palsies may occur with both frontal and occipital lobe lesions. In frontal lobe lesions, voluntary eye movement to command (without following the examiner’s finger) away from the side of the lesion is lost; in occipital lobe lesions, however, such eye movement to command is spared (Table 5-1).
TABLE 5-1 Localization of Eye Movement Disorders | |||||||||||||||||||||||||||||||
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Vertical gaze palsy that affects downgaze may be caused by infarcts in the territory of the paramedian thalamomesencephalic or posterior cerebral arteries. Ocular apraxia, inability to move the eyes voluntarily to command, with a full range of random eye movements, occurs with bilateral prefrontal motor cortex damage. In internuclear ophthalmoplegia, weakness of adduction on the side of a lesion of the medial longitudinal fasciculus occurs with monocular, horizontal nystagmus of the abducting eye. Typical causes include various disorders involving the brainstem, such as multiple sclerosis, infarction, trauma, encephalitis, and syringobulbia.
Tectal or pretectal lesions in the midbrain, caused by pineal region tumors, in-filtrating gliomas, infarction, hemorrhage, trauma, or multiple sclerosis, may produce Parinaud’s syndrome. This syndrome is characterized by loss of voluntary upward gaze; light-near reflex dissociation of the pupils (sluggish in response to light but brisk constriction to near gaze or accommodation); and, occasionally, retraction nystagmus, paralysis of convergence, ptosis, papilledema, or third cranial nerve palsy. Spasm of the near reflex (convergent strabismus, diplopia, miotic pupils, and spasm of accommodation) is usually caused by encephalitis, tabes dorsalis, meningitis, or functional disturbances. Skew deviation (a vertical misalignment of the eyes) usually signifies a structural brainstem lesion, with the higher eye ipsilateral to the side of the lesion. Impairment or paralysis of convergence (sudden onset of diplopia for near vision, with absence of any individual extraocular muscle palsy) may be caused by rostral midbrain lesions (such as infarction, multiple sclerosis, encephalitis, tabes dorsalis, tumors, Parkinson’s disease) or may be functional. Limitation of ocular movements may also result from paresis of the third, fourth, or sixth cranial nerve (see Oculomotor [III], Trochlear [IV], and Abducens [VI] Nerves, p. 54).
Nystagmus
Nystagmus is an involuntary, rapid to-and-fro eye movement that may be either pendular in type, with smooth movements, or jerk nystagmus, with a slow drift and quick corrective movement. When classifying nystagmus, one must consider the type of movement (horizontal, vertical, rotatory, or mixed), whether it is pendular or has quick and slow components, the direction of the fast component, whether the nystagmus direction changes with gaze direction, and whether the nystagmus is similar in both eyes. Nystagmus subtypes are classified in Table 5-2.
Pupils
The pupils should be inspected for (1) size, (2) shape (they should be approximately equal in size and round), (3) reaction to light (bright light directed into the pupil of one eye normally causes equal and quick constriction of both pupils; the contralateral response is called the consensual response), and (4) accommodation/convergence (the pupils normally constrict equally under the stimuli of accommodation and convergence). Pupillary constriction on near gaze is tested by asking the patient to look first at a distant object and then at a close object.
The pupils may be markedly constricted from the effect of narcotics, parasympathomimetic drugs, central nervous system (CNS) syphilis, or pontine disorders such as pontine hemorrhage, in which the reaction to light is difficult to observe but should be present. Argyll Robertson pupils caused by CNS syphilis are commonly irregular, eccentric, and small (<3 mm in diameter). They react promptly on convergence and accommodation for near objects but do not contract to light and dilate poorly with mydriatics. This type of light-near dissociation of pupillary response, with greater response to convergence than to light, may also occur in patients with tumors of the midbrain, diabetes mellitus, encephalitis, multiple sclerosis, CNS degenerative disease, meningitis, and chronic alcoholism. The pupils may be relatively fixed and equally dilated as a result of diffuse
cerebral swelling or sympathomimetic or anticholinergic drugs (epinephrine, ephedrine, amphetamine, cocaine, atropine, homatropine, scopolamine, pilocarpine, and acetylcholine).
cerebral swelling or sympathomimetic or anticholinergic drugs (epinephrine, ephedrine, amphetamine, cocaine, atropine, homatropine, scopolamine, pilocarpine, and acetylcholine).
TABLE 5-2 Classification of Nystagmus | ||||||||||||||||||||||||||
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Adie’s pupil is typically a unilaterally dilated pupil that has slow reaction to light and that may respond to accommodation. This is a benign condition that usually affects young women and may be related to dysfunction of the ciliary
ganglion or postganglionic neuron. The pupil characteristically promptly constricts with administration of low-dose pilocarpine. When the pupil is completely unreactive to both light and accommodation, with depressed or absent deep tendon reflexes, the condition is called Holmes-Adie syndrome.
ganglion or postganglionic neuron. The pupil characteristically promptly constricts with administration of low-dose pilocarpine. When the pupil is completely unreactive to both light and accommodation, with depressed or absent deep tendon reflexes, the condition is called Holmes-Adie syndrome.
Nonreactive pupils 3 to 5 mm in diameter may accompany a midbrain lesion. A unilaterally dilated, fixed, and unreactive pupil may be a sign of third cranial nerve compression caused by temporal lobe herniation. Unequal pupils (anisocoria) may be a normal finding, especially when associated with a normal reaction to light. However, if one or both pupils do not react well to light, then a pathologic process is strongly suggested. For example, pathologic anisocoria may result from third cranial nerve involvement at the level of the midbrain (infarction, basilar aneurysm, demyelination, and tumor), interpeduncular cistern (aneurysm of the posterior communicating or basilar artery, transtentorial herniation, basal meningitis, oculomotor nerve trunk infarction), cavernous sinus (intracavernous aneurysm, cavernous sinus thrombosis, pituitary adenoma, meningioma, metastasis, and nasopharyngeal carcinoma), or orbit or orbital fissure (tumor, periostitis, and sphenocavernous lesion).
Horner’s syndrome, with unilateral miosis, ptosis, lower eyelid elevation, and loss of sweating on the same side of the face, may result from an ipsilateral lesion that causes sympathetic nervous system damage at various levels: hypothalamus (tumor and vascular lesion), brainstem (tumor, vascular lesion, and syringobulbia), middle fossa (tumor and granuloma), carotid artery in the neck (dissection, occlusion, aneurysm, and trauma), cervical sympathetic chain (enlarged cervical lymph node, goiter, aneurysm of the subclavian artery, carcinoma of the lung apex, apical tuberculosis, or mediastinal tumor), anterior C-8, T-1, T-2, or T-3 roots (neurofibroma, lower brachial plexus palsy, and Pancoast tumor), or other cervical lesions (vertebral fractures, tabes dorsalis, syringomyelia, and tumor).
Visual Acuity
Visual acuity is usually tested for each eye separately at a near point (˜14 cm) with a handheld card (patients who wear glasses for reading should wear them during the test). To overcome hypermetropia or myopia refractory errors without glasses, the patient may look at the card through a pinhole to restrict vision to the central beam of light, which is undisturbed by abnormal ocular distances or transparent media. Once refractory defects have been excluded, acute impairment of visual acuity in one eye usually suggests a vascular lesion such as acute occlusion of the ophthalmic or central retinal artery, a lesion that affects the macular region of the retina (e.g., a hemorrhage in the macular area), or ischemic optic neuropathy. Gradual impairment of vision may be caused by optic atrophy that results from compression, toxins, ischemia, neuritis, retinitis pigmentosa, macular degeneration, choroiditis, diabetic retinopathy, or retinoblastoma (Table 5-3). Unilateral lesions of the optic tract, lateral geniculate body, optic radiation, or striate cortex usually do not impair optic acuity, but bilateral occipital cortex lesions can cause complete blindness.
Visual Fields
Visual fields are assessed clinically to detect areas of partial or complete loss of vision by confrontation testing. The examiner covers one of the patient’s eyes at a time. The examiner then holds up one or two fingers in the six primary visual quadrants, and the patient identifies whether the examiner is holding up one or two fingers while looking straight ahead at the examiner’s nose. Alternatively, the examiner may move his or her finger or, for a more precise determination, move a red 5-mm pin from the extreme periphery toward the center. The patient reports
when he or she first sees the object while looking straight ahead at the examiner’s nose. Repeated testing from multiple directions provides a record of affected or spared visual fields.
when he or she first sees the object while looking straight ahead at the examiner’s nose. Repeated testing from multiple directions provides a record of affected or spared visual fields.
TABLE 5-3 Causes of Unilateral Visual Loss | |||||||||||||||||||||||||||
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For detection of visual neglect (in which the patient ignores one half of the visual field), both eyes are uncovered, and the patient looks at the examiner’s nose. The examiner then asks the patient to identify which finger(s) is wiggling while wiggling fingers in one of the primary peripheral quadrants, either unilaterally or bilaterally. Patients with visual neglect often ignore fingers to one side when the examiner is wiggling fingers simultaneously on each side. In addition, the patient with left visual neglect, when drawing a clock face, will write all of the numbers on the right-hand side of the clock or, when trying to mark the center of a line, will place the mark far to the right of the real midpoint of the line.
Monocular visual field defects are usually caused by retinal or optic nerve lesions; binocular defects usually reflect a lesion localized at or behind the optic chiasm. The precise determination of visual field defects has an important role in the localization of vascular lesions. Some of the most common variants of visual-spatial disorders are depicted in Figure 2-1. Central scotoma may result from retrobulbar neuritis (sometimes as the first sign of multiple sclerosis) or optic nerve compression (anterior communicating artery aneurysm, meningioma, granuloma, or hyperostosis of the optic canal from Paget’s disease). Cecocentral scotoma is characteristic of toxic (alcohol, tobacco) amblyopia. An arcuate scotoma often reflects underlying glaucoma, and a junctional scotoma indicates the presence of an optic nerve lesion immediately anterior to the optic chiasm.
Bitemporal hemianopia with involvement of the upper quadrants first indicates compression of the optic chiasm from below by lesions such as a pituitary adenoma, nasopharyngeal carcinoma, or sphenoid sinus mucocele; involvement of the lower quadrants first indicates compression of the optic chiasm from above, such as a craniopharyngioma or third ventricular tumor. Homonymous hemianopia may have sudden onset, typically of vascular cause, or gradual onset, caused by neoplastic, infectious, or inflammatory conditions. Lesions may involve the contralateral geniculate body (homonymous defect in the upper and lower quadrants with sparing of a horizontal sector), optic radiations, or occipital lobe. Inferior quadrantanopia is more often caused by lesions of the optic radiations deep in the parietal lobe or cuneus of the occipital lobe; superior quadrantanopia arises from lesions involving the temporal loop of the optic radiations or inferior bank of the calcarine fissure.
Bilateral homonymous hemianopia results in complete visual loss (cortical blindness) with or without sparing of a small central visual field (macular sparing) and the pupillary response. In Anton’s syndrome, the patient denies the visual defect and confabulates about what is being seen because of bilateral visual association cortex damage that results from occlusion of either the basilar or both posterior cerebral arteries.
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