Ординатура / Офтальмология / Английские материалы / The Neurology of Eye Movements_Leigh, Zee_2006

endolymph at different rates and so creates a density gradient, making the cupula

gravity sensitive, the so-called buoyancy hypothesis.163'436*

The aminoglycoside antibiotics are notorious for causing irreversible failure of vestibular function without vertiginous warning or hearing loss.574 A number of other causes of acute vertigo are enumerated in Table 10-9, and some are discussed in the following section.

Recurrent Vertigo

MENIERE'S SYNDROME

Meniere's syndrome (endolymphatic hydrops) is a common cause of recurrent vertigo that is usually accompanied by prominent auditory symptoms. Attacks of vertigo, fluctuating hearing loss and tinnitus, and aural fullness are its hallmarks. A failure of resorption of endolymph is presumed to lead to an increase in endolymphatic pressure. Symptoms are probably caused both by direct compression of sensory structures within the cochlea and vestibular labyrinth and by leakage of potassiumrich endolymph onto the vestibular nerve thrpugh breaks in the membrane separating the endolymph and perilymph spaces. The vestibular nerve may first be excited and then depressed in a depolarization block.

A typical attack in Meniere's syndrome is heralded by a sensation of fullness in the ear, tinnitus, and impaired hearing. The vertigo that ensues is often severe and usually prostrates the patient. After several hours, or sometimes longer, the attack begins to abate. Sometimes the hearing symptoms subside when the vertigo begins

(Lermoyez syndrome).

Examination during the attacks commonly shows nystagmus that changes its direction during the attack. At the onset of the attack, an irritative nystagmus with horizontal slow phases directed away from the affected ear (ipsilateral-beating nystagmus) may occur. Slow phases toward the side of the lesion then appear soon after the onset of the attack (the "paretic" phase); finally another reversal of the di-

rection of the nystagmus, with slow phases away from the affected ear, can occur a few hours later (recovery nystagmus).919,1064 pos_

tural unsteadiness may persist for several days. Vertigo may be the predominant symptom in some patients with Meniere's syndrome. Commonly, however, audiometric testing shows a characteristic fluctuating low-frequency hearing loss with recruitment. Electrocochleography (ECOG) may show an increase in the ratio between the summating and the action potential, a pattern seen in Meniere's syndrome and with perilymphatic fistula. An MRI scan may show contrast enhancement of labyrinthine structures during attacks, but this finding must be distinguished from changes due to acute viral infec-

tions, autoimmune diseases, and other processes.481'905'1431

Some patients may suddenly fall without warning; these events, which may even occur early in the course of the disease, are referred to as Tumarkin's otolithic crisis'79 and should be differentiated from other forms of drop attack. Meniere's syndrome is a disease of adults, often beginning in the third or fourth decade; it rarely occurs in children.596 The natural history of Meniere's syndrome is one of progression but often with extended periods of remission.546 Although the cause of Meniere's syndrome is unknown, endolymphatic hydrops may follow other afflictions of the ear including head trauma and viral infections.806'1240 An autoimmune basis has been suggested for some patients with Meniere's syndrome;592'1304 patients with arteritis may present with a Meniere's-like syndrome.926 (See also the discussion of Cogan's syndrome, below.) The incidence of migraine is probably increased in patients with Meniere's syndrome.1130 The distinction between the two conditions may be difficult, since vestibular and audi-

tory symptoms and signs may occur with classic migraine.204'2393'1043'1433

OTOSCLEROSIS

Otosclerosis, a common cause of dominantly inherited deafness, may also cause attacks of recurrent vertigo that may mimic Meniere's syndrome.1060'1204'1369

Some patients also suffer from positional vertigo. Diagnosis is relatively easy in patients with a conductive hearing loss, tinnitus, and a history of affected family

members. A CT scan of the petrous bone may help.1431

INFLAMMATORY DISORDERS CAUSING RECURRENT VERTIGO

Syphilis is a rare but important cause of recurrent vertigo.1489 Inflammation of the membranous labyrinth and osteitis of the surrounding bone occur with both congenital and acquired forms. The clinical picture is episodic vertigo with progressive loss of vestibular and auditory function. Other features of syphilis may be present, especially with the congenital form. The results of the serum fluorescent treponemal antibody absorption test (FTA) are positive, and cerebrospinal fluid abnormalities may be present. Lyme disease, another infectious process,

may cause a variety of vestibular syndromes,681'796'1177 though the ocular motor

manifestations are more common.65 Cogan's syndrome is characterized by

interstitial keratitis, hearing loss, and re-

current attacks of vertigo that mimic Meniere's syndrome.253'599'6083'902'1242'1436 It

is often associated with a systemic collagen vascular disease, and some patients develop aortic insufficiency; test results for syphilis are negative. Corticosteroid therapy usually produces improvement, and should be instituted promptly for hearing and vestibular loss. Susac's syndrome is characterized by a triad of microangiopathy of the brain and retina with eighth nerve involvement.66'1022'1344 Youngwomen are most commonly affected. Patients have an encephalopathy, branch retinal artery occlusions, and a Meniere's-like syndrome with spells of vertigo withlower-frequency hearing loss. Other forms of immune inner ear disease leading to progressive vestibular and hearing loss, with or without

associated systemic involvement, have been described.125'481'592'921'926'1398 Sarcoid

also has a predilection for the eighth cranial nerve; it may even cause BPPV, presumably by selectively involving the superior division of the vestibular nerve.592-1438

paroxysmal vertigo of childhood, which usu-

ally has its onset between the ages of 1 and 4 years.733'443'811'1062-1401 It is probably a

variant of migraine. The attacks are typically brief and consist of unsteadiness, pallor, nausea, and vomiting. Older children describe vertigo. Nystagmus or torticollis may be noted; younger children may only show torticollis. The attacks may come every week or month, or in clusters, between which the children feel well. Tests of labyrinthine function sometimes suggest a peripheral abnormality. The attacks usually cease in the course of a few months or years. Migraine and seizure disorders should be considered first in the differential diagnosis of vertigo in childhood, although there are other developmental and metabolic causes, including vertigo as a feature of acetazolamide-responsive, fa-

milial episodic vertigo and ataxia type 2

(EA-2).158'184'307'1062'1401

In adults, too, recurrent vertigo may be a manifestation of migraine.2393,314,472,1221

As a component of migraine attacks, frequently vertigo may overshadow the headache and often occurs independent of the headaches. Vertigo in migraine syndromes tends to occur in two time frames: lasting an hour or so, similar to a classic migraine aura, and lasting for days or sometimes weeks in a milder form, producing motion sensitivity and imbalance.314 Hearing loss may also be associated.1433 Headache and vertigo associated with other symptoms, such as dysarthria and ataxia, suggest a basilar-artery form of migraine. Such attacks are particularly common in adolescent girls131'589 but also occur in older patients of both sexes.

VASCULAR DISORDERS AND RECURRENT VERTIGO

In older individuals, transient attacks of

acute vertigo may be caused by vertebrobasilar insufficiency.37'68'441'451'526'541'1019'1028 Usu-

ally associated neurologic symptoms or signs point to a central disorder, but isolated attacks due to ischemia, especially of the cau-

dal cerebellum, are not uncommon;526'1019 they may be the harbinger of brain stem or cerebellar stroke. Isolated attacks of vertigo may also be due to ischemia of the labyrinth, commonly in the structures within the distribution of the anterior vestibular artery (the anterior and lateral semicircular canals and the utricle). Since the anterior vestibular artery is an end artery with poor collateral supply, isolated attacks of vertigo may occur without hearing loss or tinnitus in patients with hypoperfusion of the labyrinth due to vertebrobasilar insufficiency. Such attacks may occasionallybe associated with bilateral hearing loss.664

Hemorrhage into the vestibular organ is rare but can cause severe vertigo and deafness.1241 Acute vertigo is often a prominent symptom in brain stem and cerebellar infarction, which are discussed below.

EPILEPSY AND OTHER MISCELLANEOUS CAUSES OF VERTIGO

Other causes of recurrent vertigo are listed in Table 10-9. Seizures—tornado epilepsy—may cause vertiginous feelings, but patients with epilepsy more commonly experience vertigo as a side effect of anticonvulsant and other medications. A posterior fossa tumor rarely causes recurrent vertigo. Tumors of the eighth cranial nerve commonly are associated with progressive hearing loss rather than with vertigo,126 although nearly half of such patients experience vertigo at some time during the course.957 Vertigo is a prominent feature of the rare familial episodic vertigo and ataxia type 2 (EA-2), which usually responds to acetazolamide and is

related to a calcium channel abnormality

on chromosome I9.90'175'486'1411'1413'1517a

UNDIAGNOSED RECURRENT VERTIGO

Some patients report episodes of recur-

rent vertigo for which no cause can be found.1198 Long-term follow-up has shown

that about 30% develop into either Meniere's syndrome or benign paroxysmal positional vertigo, while the other

70% remain undiagnosed. Some of these patients almost certainly have vestibular migraine. Less commonly, patients may have attacks that affect first one and then the other ear; the bilateral vestibular loss causes oscillopsia with head movements and during walking.76'77'1243 Examination of the temporal bone of three patients who had suffered recurrent episodes of vertigo showed varying degrees of inflammation and destruction within the vestibular system, and mild involvement of the cochlear system.680

Some patients with chronic unsteadiness have the syndrome ofmal de debarquement.198'984 This is an exaggerated form of a normal response that many individuals have when they return to land after sea travel. Patients have a rocking and swaying sensation, usually with no abnormalities on examination or testing. The etiology is unclear: psychiatric disorders, migraine, fistulas, otolith disturbances, and vascular loops have been invoked. Fortunately, most patients will spontaneously recover or respond to antianxiety or antidepressant medications and physical therapy.

Recurrent attacks of disabling vertigo have been attributed to vascular loops or tortuous vessels that compress the eighth cranial nerve, analogous to the syndromes of hemifacial spasm and trigeminal neuralgia. Microvascular decompression has been reported to produce dramatic cures in a large percentage of these patients.975 Clinical features that suggest the diagnosis include short-lived episodes (seconds or minutes) of vertigo or imbalance, often related to a change in head posture; hyperacusis or tinnitus; and a salutary response to carbamazepine.171 Abnormalities of brain stem auditory evoked potentials and an exacerbation of symptoms or induction of nystagmus with hyperventilation (altering conduction on a compressed and demyelinated nerve) also point to the diagnosis. Unfortunately, reliable laboratory methods to identify such patients have not been established,124'975 especially since many asymptomatic normal individuals have loops of the anterior inferior cerebellar artery touching the eighth nerve complex in or near the internal auditory meatus. In

patients with unexplained vertigo or dysequilibrium, the diagnosis of microvascular compression of the vestibular nerve, or of a spontaneous oval or round window perilymphatic fistula, is often raised; exploratory surgery is often considered. There is no convincing evidence, however, that patients will benefit from such procedures unless they meet strict clinical criteria.1238 Vestibular migraine, Meniere's syndrome, epilepsy, multiple sclerosis, and even benign paroxysmal positional vertigo may have atypical presentations. Unusual conditions such as familial episodic vertigo and ataxia type 2 (EA-2) should be considered and treated medically before exploratory surgery for fistula or microvascular compression.

Posturally-Induced Vertigo

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)

Clinical Features of BPPV

Barany first described BPPV. It was further characterized by Dix and Hallpike.810 Classic BPPV usually arises from a posterior semicircular canal that has become gravity sensitive, but lateral-canal variants are becoming increasingly recognized. The syndrome is presumably caused by floating debris—otoconia—either within the long arm of the semicircular canal (canalolithiasis, probably the most common occurrence) or on the ampullary side of the cupula, either floating free or adherent to the cupula (cupulolithiasis). Typically, patients complain of brief episodes of vertigo precipitated by changes of head posture such as turning over in bed, looking up to a high shelf, or backing a car out of a garage. Patients can usually identify the offending head position, which they often carefully avoid. Many patients also complain of mild postural instability between attacks. Women are more commonly affected than men. The condition affects all age groups but is common in the elderly. Spontaneous remissions are the rule, but symptoms may trouble the patient intermittently for years. BPPV may follow head injury, viral neurolabyrinthitis,

or labyrinthine ischemia and occasionally occurs after assumption of unusual head postures (e.g., prolonged reclining in a dental chair or working underneath a car), prolonged bedrest, or exposure to continuous jarring, such as cycling over rough terrain or high-impact aerobics.1463 In over half of affected patients, no cause can be identified.74

The clinical examination may help confirm the diagnosis (Fig. 10-19A,B). Having reassured the patient (who is often apprehensive of being moved) and emphasized the importance of keeping the eyes open, the patient's head is turned 45° to one shoulder and the head and neck are quickly moved "en bloc" into a headhanging position (just over the edge of the examining table, about 120° from the upright). This is the Dix-Hallpike maneuver.

Typically there is a latent period, usually of about 2 to 5 seconds but sometimes as long as 30 seconds, followed by a sensation of discomfort and apprehension that will sometimes cause the patient to cry out and attempt to sit up. This is associated with vertigo, nausea, and a burst of nystagmus (see VIDEO: "Nystagmus with benign paroxysmal positional vertigo"). In the typical variant due to involvement of the posterior semicircular canal, the slow phases are directed downward, with intorsion of the lower eye and extorsion of the higher eye. Hence, the nystagmus is mixed upbeat and torsional. The nystagmus usually appears slightly disconjugate, more torsional in the lower eye (on the side of the dependent ear) and more vertical in the upper eye. The nystagmus also appears to change with the direction of gaze: On looking to the dependent ear it seems more torsional, and on looking to the higher ear, more vertical. A small horizontal component, greater in the lower eye, with slow phases toward the dependent ear, may also be evident if eye movements are recorded. Three-dimensional search coil recordings have shown that the slow phases of BPPV rotate the eye in a plane that is parallel to the posterior semicircular canal.438 This pattern of nystagmus corresponds closely to the results of experimental stimulation of the posterior semicircular canal of the dependent ear

(Fig. 2-2).277 The nystagmus increases for up to 10 seconds but then begins to fatigue and is usually gone by 40 seconds. In other words, this testing induces positioning nystagmus rather than positional nystagmus. In a small proportion of patients with BPPV, a low-amplitude, secondary nystagmus (in the opposite direction) may occur after the primary nystagmus has resolved, but this reversal is usually most prominent when the patient sits up. Repeating this procedure several times will decrease the

Figure 10-19. Diagnosis (Dix-Hallpike maneuver, A-C) and treatment (Epley maneuver, D, E) of benign paroxysmal positional vertigo due to otolithic debris in the right posterior semicircular canal. For each head position, the corresponding orientation of the right labyrinth is shown, with the arrow pointing to the presumed location of the otolithic debris in the posterior semicircular canal. (A)The patient's head is turned to the right shoulder. (B) The patient is rapidly moved from sitting to head-hanging position, with the head 45° below the horizontal and rotated to the right, as shown in C. After a brief latency, vertigo is induced and nystagmus commences; the direction of the quick phases of nystagmusinduced by this maneuver are shown (more upbeat in leftgaze and more torsional in rightgaze) (see VIDEO: "Nystagmus with benign paroxysmal positional vertigo"). (D) The patient's head is held still for 15 sec after the nystagmus and vertigo subside. Then the patient's head is extended slightly,and head and body are slowly rotated to the patient's left, so that the head rotates through 180° from the orientation in C. The patient is held in this position for 15-30 sec to allow time for the otolithic debris to exit from the common crux of the vertical canals (arrow). (E) Finally, the patient slowly sits up, keeping the head turned to the left. The patient is encouraged to sustain a head-erect posture for the next 24 hours (sleeping propped up), ifpossible. (Reproduced from Herdman SJ. Vestibular Rehabilitation, second edition, Philadelphia: F.A. Davis; 1999, with permission).

Continued onfollowing page

symptoms and make the signs more difficult to elicit; this lessening of the response is of diagnostic value, because positional nystagmus with central lesions usually does not habituate with repeated testing.

If the classic pattern of nystagmus associated with BPPV is not elicited with the Dix-Hallpike maneuver to either side, the patient should then be brought to the supine position with the head centered on the body. The patient's head (and body, for comfort) should then be turned 90° to

one side (right ear down), back to neutral (head supine), and then 90° to the other (left ear down). This is the best maneuver with which to elicit a horizontal positional nystagmus, as occurs, for example, with the lateral canal variant of BPPV, which is discussed later in this section.

Nystagmus associated with changes in head posture is sometimes attributed to extension, flexion, or lateral rotation of the head on the body, but with rare exceptions, the nystagmus actually appears because of a change in the position of the head with respect to gravity. To make this distinction, the trunk can be pitched forward and the head hyperextended at the neck, or the trunk pitched backward and the head flexed on the neck, in order to keep the attitude of the head with respect to gravity the same as in the normal upright posture. If the vertigo is due to flexion, extension, or rotation at the neck, this maneuver should provoke nystagmus.

The lateral-canal variant of BPPV, while less common than the posterior canal

variant, has become increasingly recognized.78'91'335'4393'1027'1320'1341 Lateral canal

BPPV may occur as a transient complication following positioning maneuvers used in testing for, or treating, posterior canal BPPV (and vice versa).614 Patients may have both lateral and posterior canal variants simultaneously or sequentially. Lateral canal BPPV produces symptoms in both the right-ear-down and left-ear- down positions. There may be geotropic nystagmus (beating toward the ground), in which case the nystagmus is usually more intense with the affected ear down, or there may be apogeotropic nystagmus (beating away from the ground), in which case the nystagmus may be more intense with the intact ear down. This difference between the intensity of nystagmus in geotropic and apogeotropic BBPV may represent Ewald's second law (ampulla movement in the excitatory direction elicits a brisker

nystagmus than the opposing ampulla movement in the inhibitory direction).

The nystagmus of lateral-canal BPPV may reverse its direction if the offending position of the head is maintained. When the head is brought to the supine position from a sustained lateral position, a nystagmus occurs as if the head were being brought from supine to the opposite lateral position (equivalent to the nystagmus reversal that appears with posterior canal BPPV when the patient sits upright). With lateral-canal BPPV, the initial horizontal nystagmus may last longer and be less susceptible to fatigue with repetitive testing than the vertical-torsional nystagmus of posterior-canal BPPV.The increased duration and the tendency for the nystagmus to increase in intensity as the offending head position is maintained may reflect the action of both the central velocity-storage mechanism (which perseverates peripheral labyrinthine signals, especially from the lateral semicircular canal) and the continuous application of the equivalent of a constant acceleration from gravity (especially when the offending particles are on the ampulla side), causing the nystagmus to grow. Canalolithiasis and cupulolithiasis may both play a role in lateral-canal BPPV. If the nystagmus is geotropic, the particles probably are in the posterior portion of the long arm of the lateral semicircularcanal, relatively far from the cupula. If it is apogeotropic, the particles could also be in the long arm but in its anterior aspect relatively close to the cupula, or on the opposite, ampullary side of the cupula. Patients may show geotropic nystagmus at some times and apogeotropic at other times. Presumably this is due to a difference in the relative distance of the offending particles from the cupula within the long arm of the lateral semicircular canal or due to movement of the particles from the long arm of the canal to the ampulla side with certain provocative head maneuvers.

Anterior-canal BPPV is the most unusual variant. The nystagmus should be downbeat with a torsional component but is difficult to recognize with certainty.

Bilateral BPPV occasionally occurs, but if the patient's head is not positioned

correctly during positional testing (not moved exactly in the plane of the posterior semicircular canal when testing the unaffected side), debris on the affected side can rest against the cupula and simulate an excitatory nystagmus from the unaffected ear.1320 Rarely, the nystagmus of BPPV may be purely vertical or purely torsional due to debris floating in both

tion, torsional if it floats in opposite directions). This circumstance is an exception to the rule that pure vertical or pure torsional nystagmus always indicates a central problem.

In some patients, no nystagmus will be elicited with postural testing; the diagnosis must then be made based on the history. It is helpful to reexamine the patient if symptoms persist, especially at a time when they exacerbate. Mastoid vibration may help provoke the typical nystagmus. If the nystagmus is not typical for BPPV, an effort to identify disease of the brain stem or cerebellum is appropriate, although in most cases, no morbid disease process will be found. Apart from the findings during positional testing, other tests of ocular motility may be normal. In a minority of patients, particularly those with a prior history of viral or ischemic neurolabyrinthitis, the head-thrust maneuver will show a unilateral deficit, or caloric responses are reduced in the affected ear.

Pathophysiology of BPPV

A combination of careful clinical observation, clinicopathologic correlation, and physiologic experimentation has led to a

better understanding of the pathogenesis of

BPPV.129'173'422'810'849'1319'1320 Recent elec-

tron microscopic studies have confirmed that the debris consists of otoconia.1471 Originally, it was thought that degenerated utricular otoliths became detached and came to rest on the dependent cupula of the posterior semicircular canal, a state called cupulolithiasis.1^'1 More recent evidence suggests that the more usual cause may be free-floating debris on the other side of the cupula in the long arm of the

posterior semicircular canal, which is referred to as canalolithiasis.955'1065 The debris may coalesce and act as a plug so that under the pull of gravity, the moving debris (either with a plunger-like action or simply owing to hydrodynamic drag) causes the cupula to move, inducing nystagmus even when the head is still.173'422 In other words, the semicircular canal becomes a gravity detector. When the posterior semicircular canal is moved into an earth-vertical position, the net result is to produce false excitatory signals from the affected posterior semicircular canal. These signals primarily cause the ipsilateral superior oblique and contralateral inferior rectus muscles to rotate the eyes in a slow phase of nystagmus. The evidence for involvement of the posterior semicircular canal in BPPV is strengthened by the report that surgical section of the posterior ampullary nerve, which supplies the posterior semicircular canal, or plugging

of the posterior semicircular canal, cures the condition.497'1063 In a minority of pa-

tients, otolithic debris may preferentially affect the lateral or rarely the anterior semicircular canal. Exercises or maneuvers aimed at dispersing the otolithic debris from the cupula may promote recovery (see Treatment of Vertigo), although many patients will eventually improve spontaneously.

In patients in whom BPPV follows acute, peripheral vestibulopathy (viral or ischemic in origin), there may be selective damage to the structures innervated by the superior division of the vestibular nerve and perfused by the anterior vestibular artery: the anterior and lateral semicircular canals, and the utricle.436 Using click-induced EMG potentials in the sternocleidomastoid (a sacculocollic reflex),281'282 Murofushi and co-workers found that this reflex was intact in all patients who developed BPPV after vestibular neurolabyrinthitis, implying sparing of the inferior division of the vestibular nerve.983 Taps on the head with a reflex hammer can also be used to stimulate the sacculocollic reflex and probe the function of the saccule and the inferior division of the vestibular nerve.581

OTHER CAUSES OF POSITIONAL VERTIGO

Posturally induced vertigo due to central disorders may be relatively mild, and the nystagmus is usually more impressive than the subjective disturbance (Table 10-9). When the patient is placed in a headhanging position, usually the nystagmus persists for as long as the head position is maintained; rarely, the findings are similar to BPPV. Multiple sclerosis may cause positionally induced nystagmus, sometimes with accompanying vertigo;480'729 such symptoms may be the first manifestation of the disease. Occasionally, a cerebellar tumor,403 infarction, or hematoma731 may produce postural vertigo or vomiting. If nystagmus typical of BPPV is present with the patient's head turned to the right and to the left (bilateral BPPV), then head injury or brain stem ischemia is more likely to be implicated,875 but one must watch for improper positioning of the head during positional testing maneuvers before diagnosing bilateral BPPV.1319 Isolated vertigo due to neck movements that lead to kinking of the vertebral artery happens rarely;1176 associated neurologic symptoms are usually present.

Some normal subjects may show positional nystagmus—nystagmus that persists following a horizontal change in head po-

sition (e.g., with the subject supine, head turned to the right or left).524'917 It usually

beats in the same direction as the head is turned. In some patients, the nystagmus changes direction with lateral head turn, either always beating toward the earth (geotropic) or always beating away from the earth (apogeotropic). Such nystagmus most often reflects a lateral canal BPPV syndrome, as discussed above. Alcohol intoxication can produce a horizontal positional nystagmus by making the cupula relatively lighter (during intoxication) or heavier (during sobering up) than the surrounding endolymph, by virtue of differential absorption. During intoxication the nystagmus is geotropic; as the subject sobers up it is apogeotropic.4363'952

When due to central causes,93 positional nystagmus is relatively unchanging in slow-phase velocity and is almost always

Table 10-10. Some Commonly Used Vestibular Sedatives

Comments

Peak effects 8 h after ingestion; less sedative

Mildly sedative

More sedative, more antiemetic

Sedative and antiemetic

Less sedative, more antiemetic, suitable only to prevent motion sickness; can cause confusion, mydriasis, "dependency"

Powerful antiemetic; sedative

Antiemetic, developed for patients receiving cancer chemotherapy; may be effective controlling vertigo

and nausea due to CNS disease1141

Precautions

Asthma, glaucoma, prostate enlargement

Asthma, glaucoma, prostate enlargement

Asthma, glaucoma, prostate enlargement, epilepsy

Liver disease; in combination with CNS depressants or metoclopramide

Asthma, glaucoma, prostate enlargement

Can cause hypotension and extrapyramidal side effects; precautions: in liver and kidney disease

Headache; constipation

associated with other neurologic symptoms or signs. The cause of horizontal positional nystagmus in central disorders may relate to abnormalities of the linear (translational) VOR (discussed in Chap. 2). Pure vertical positional nystagmus— which is usually downbeating with respect to the head—frequently signals a disturbance in the cerebellum or at the craniocervical junction.

Characteristics of horizontal positional nystagmus that suggest a central disturbance and usually demand imaging include (1) a sustained, large-amplitude nystagmus that is present during visual fixation; (2) nystagmus that occurs in more than one head position; and (3)nystagmus that has an associated vertical (and especially downbeat) component. Even with these caveats, most patients with positional vertigo and positional or positioning nystagmus who have no other neurologic symptoms or signs will not have a central disturbance as the cause of their vestibular symptoms.

Treatment of Vertigo

General measures available for the treat-

ment of vertigo have been reviewed elsewhere;472'1126 here we summarize some ba-

sic principles. In acute vertigo due to a peripheral vestibular lesion such as a viral or ischemic neurolabyrinthitis, functional recovery is the rule in the ensuing weeks. Drugs that have a sedative effect (Table 10-10) should be used sparingly for treatment of vertigo, with the exception of Meniere's syndrome; in this case, the pathophysiology of the attack and the recovery relate to mechanical changes in the labyrinth, not central compensation, so a brief period of moderate sedation need not have any deleterious effects related to retarded central compensation. Patients should be encouraged to get up and increase their activities as soon as possible, since there is evidence that failure to do so will limit the recovery. Much current research is aimed at finding medications that promote vestibular compensation.1301 A course of specific vestibular exercises may be indicated.613'1277 Those patients

who develop enduring vestibular symptoms may have an underlying central nervous system disorder, typically involving the cerebellum,487'1194 and imaging studies are indicated.

Treatment of recurrent vertigo depends, however, upon the nature of the underlying disorder. For example, vertigo due to migraine can usually be successfully treated, whereas vertigo due to Meniere's syndrome is often difficult to manage, although a low-salt diet and diuretics help some patients.196 Intratympanic gentamicin has been shown to be an effective alternative to surgical ablation for in-

tractable vestibular symptoms in Meniere's syndrome.25'120'1055

scribed.129'174'422'614'847'849'920'1025'1027'1256'1258'

HIS Tne Epley maneuver is summarized in Figure 10-19. Drugs are not indicated in this condition except to relieve symptoms during the treatment maneuvers. Some authors advocate use of a mastoid vibrator during the repositioning maneuver to free otolithic debris that is adherent to the wall of the semicircular canal.422 A small percentage of patients do not improve with exercises. As previously mentioned, surgical section of the nerve to the posterior semicircular canal has been effective,497 but occlusion of the posterior semicircular

canal is currently the preferred intervention.1063 We have never had to refer a pa-

tient with BPPV for surgical intervention.

OSCILLOPSIA

Oscillopsia is an illusion of movement of the seen world. It is usually caused by excessive motion of images of stationary objects upon the retina (Table 10-11). Excessive retinal slip not only causes oscillopsia but also impairs vision. On the one hand, the relationship between retinal image velocity and visual acuity is a direct one: For higher spatial frequencies, image motion

in excess of about 5°/sec impairs vision.235'375 On the other hand, the rela-

tionship between retinal image velocity