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VISION AND EYE MOVEMENT DISORDERS
Diverse elements of the central and peripheral nervous systems combine to produce vision; thus, examination of the visual system yields information about many parts of the nervous system and is especially useful for localizing lesions. Most tests can be done easily without special equipment. Characteristic visual field defects distinguish lesions in the retina, optic nerve, chiasm, optic tract, geniculocalcarine radiations, and visual cortex (see Ch. 228). Disease in the brainstem, cranial nerves 2 through 8, or cerebellum may lead to specific disturbances in ocular motility and pupillary reactivity. The autonomic system may be affected; eg, ptosis and loss of pupillary dilation--eg, Horner's syndrome--can arise from dysfunction of the sympathetic pathways in the diencephalon, brainstem, spinal cord, spinal root, or peripheral nerve. Finally, funduscopy of the retina provides direct visualization of neural tissue in health and disease, by which analogous changes in the brain may be inferred (eg, necrotizing arteriolitis). Funduscopy offers clues concerning the progression or resolution of certain local, systemic, and neurologic diseases (eg, raised intracranial pressure from tumor). Cerebrovascular disease may declare itself by amaurosis fugax (ie, carotid stenosis), hypertensive retinal changes, or retinal arterial emboli (eg, cholesterol).
Visual acuity of each eye is checked individually with a standard wall chart or convenient hand-held chart. (Because from a neurologic standpoint the best possible vision must be ascertained, the patient uses his corrective glasses.) To minimize an uncorrectable refractive problem, the patient can read through a pinhole in a card. If the vision cannot be quantitated by these means, some statement of acuity is noted (eg, the ability to count fingers at a certain distance or to perceive light). The baseline is established, since sudden changes in acuity can occur in some disorders, particularly those involving the vascular system or compressive lesions of the optic nerve.
Assessment of visual fields is done by confrontation testing. The examiner slowly brings a small target (eg, a red match or a white cotton applicator) from the patient's visual periphery into each of the 4 visual quadrants. The patient's head should be tilted away from any obstructing facial feature (eg, heavy eyebrows, large nose). An asymmetry in the initial target detection or other suspected defect (compared to the examiner's visual fields) should prompt quantitative perimetry for a more careful mapping of the visual fields. Central and paracentral visual field defects can be detected with an Amsler chart (a finely squared grid viewed from a distance of 35 cm [12 in.]).
Extraocular eye movements are checked by having the patient fix on the physician's finger, which is moved to the extreme gaze horizontally, upward, and downward, and then diagonally to either side. The extent of all these movements is noted, and the patient is asked if he has diplopia (double vision), which may be present with minimal nerve or muscle involvement; the oculomotor defect often is unapparent by external observation. If diplopia is reported in one direction, the eyes are individually occluded, and the patient is asked whether the peripheral or the central image disappears.
The following 2 rules apply to ascertain the weak muscle or affected nerve: (1) The objects increase their separation when moving in the direction of the affected movement, and (2) the image seen with the defectively moving eye is always the most peripheral. For example, if moving the finger horizontally to the patient's left results in an increasing separation of the fingers, the conclusion is that either the left lateral rectus or the right medial rectus is involved. If, on occluding the left eye, the most peripheral image disappears, the fault is with the left lateral rectus. Also, the patient tends to turn or tilt his head in the direction of the faulty eye movement so that diplopia is minimized.
While checking eye movements, the presence or absence of nystagmus (involuntary rapid oscillation of the eyeballs in a horizontal, vertical, or rotary direction) is noted. Nystagmus on extreme lateral gaze that fatigues quickly usually is physiologic. Sustained nystagmus should be described in regard to (1) the direction of fast and slow component; (2) its character, eg, regular, irregular, rotatory; and (3) the degree of involvement of either eye.
Opticokinetic nystagmus is the eyeball movement induced by looking at a rapidly repeated pattern (eg, at passing telegraph poles from the windows of a moving train). The eyes normally show pursuit (slow component of nystagmus) toward movement, but are regularly interrupted by saccades in the opposite direction (fast component of nystagmus). A parietal lesion (with or without hemianopia) can disrupt efferent pathways from the visual cortex to lower conjugate gaze centers and abolish opticokinetic nystagmus, tested by passing a striped cloth (or a standard tape measure) across the visual field toward the side of the lesion. Opticokinetic nystagmus is preserved in hysterical blindness.
The pupils are inspected for size (eg, pinpoint with opioids, pilocarpine, or pontine hemorrhage), equality (eg, enlarged from 3rd cranial nerve compression in transtentorial herniation), and regularity (eg, irregular in the Argyll Robertson pupil). The pupils should constrict promptly and equally to accommodation and to direct and indirect light (ie, consensual light reflex). If the light reflex is diminished in one eye, a swinging flashlight test may discriminate between an afferent (eg, retina or optic nerve) lesion and an efferent (eg, 3rd cranial nerve or pupillary muscle) lesion. A deafferented pupil will constrict consensually but not to direct light, paradoxically enlarging when the light is quickly brought from the unaffected side (Marcus Gunn pupil). An efferent lesion will prevent both direct and consensual constriction while the unaffected eye maintains both a direct and consensual light reflex.
In the Adie syndrome, an abnormally tonic pupil is dilated in comparison with the normal pupil, and both direct and consensual light reflex responses are absent or markedly diminished. On fixed-gaze accommodation, the pupil constricts and may become smaller than the normal one and takes much longer to dilate afterwards. Deep tendon reflexes are absent, but there are no other neurologic findings. Most patients are women between the ages of 20 and 40 and onset is usually sudden. Vision may be slightly blurred; otherwise there are no symptoms. The condition is permanent, but nonprogressive; etiology is un-known.
Ptosis, if present, should be quantitated by noting the width of the palpebral fissures. In Horner's syndrome, variable ptosis, miosis, and loss of sweating develop on the same side of the face following injury to ipsilateral sympathetic fibers in either the central or peripheral nervous system. Central lesions (eg, brainstem ischemia, syringomyelia) disrupt sympathetic pathways between the hypothalamus and the upper thoracic cord (C-8 to T-3) where the sympathetic fibers emerge. Peripheral lesions (eg, Pancoast's tumor, cervical adenopathy, neck and skull trauma) damage the cervical sympathetic chain, the superior cervical ganglion, or the sympathetic plexus adhering to the common internal and external carotid arteries. In congenital Horner's syndrome, the iris fails to become pigmented and remains blue-gray.
Exophthalmos can be detected by looking down on the head to inspect the eyes from above. Checking the corneal response and noting ability to blink the eyes provides information about the 5th and 7th nerves. The first sign of 7th-nerve involvement often is a decrease in blinking on the affected side.
The oculovestibular reflex tests brainstem integrity in patients with depressed consciousness. Rapid turning of the head results in a lag of eye movement, as if gaze were fixed ("doll's eye" response), followed by a slow drift back to central fixation. A more vigorous test (ice-water calorics) involves instillation of ice water (50 mL) into the ear canal (after otoscopic exclusion of tympanic injury) that should elicit conjugate eye deviation to the same side. Both maneuvers test the integrity of neural pathways (from the labyrinth to the brainstem nuclei) that control eye movements. The induction of fine nystagmus contralateral to the deviation indicates that the patient is awake.
Funduscopic examination includes observations of the optic nerve, blood vessels, and appearance of the retina to detect papilledema, optic atrophy, vascular disease, retinitis, or other disorders. Papilledema usually implies an increase in intracranial pressure and shows up as blurring and disappearance of the disk margins, elevation of the nerve head, absence of retinal vessel pulsation, and, occasionally, hemorrhages and exudates. Surveying the retinal vessels in cases of stroke is important, as small emboli often can be seen.
MOTOR WEAKNESS
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