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Gravity Figure 15-5 Dix-Hallpike maneuver to elicit benign positional vertigo (originating in the right ear) The maneuver begins with the patient seated and the head turned to one side at 45 degrees (A), which aligns the right posterior semicircular canal with the sagittal plane of the head The patient is then helped to recline rapidly so that the head hangs over the edge of the table (B), still turned 45 degrees from the midline Within several seconds, this elicits vertigo and nystagmus that is right beating with a rotary (counterclockwise) component An important feature of this type of peripheral vertigo is a change in the direction of nystagmus when the patient sits up again with his head still rotated If no nystagmus is elicited, the maneuver is repeated after a pause of 30 s, with the head turned to the left Treatment with the canalith repositioning maneuver is shown in Fig 15-6
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Utriculus Superior canal Figure 15-6 Bedside maneuver for the treatment of a patient with benign paroxysma positional vertigo affecting the right ear The presumed position of the debris within the labyrinth during the maneuver is shown on each panel The maneuver is a fourstep procedure First, a Dix Hallpike test is performed with the patient s head rotated 45 degrees toward the (affected) right ear and the neck slightly extended with the chin pointed slightly upward This position results in the patient s head hanging to the right (Panel A) Once the vertigo and nystagmus provoked by this maneuver cease, the patient s head is rotated about the rostral caudal body axis until the left ear is down (Panel B) Then the head and body are further rotated until the head is almost face down (Panel C) The vertex of the head is kept tilted downward throughout the rotation The patient should be kept in the nal, facedown position for about 10 to 15 seconds With the head kept turned toward the left shoulder, the patient is brought into the seated position (Panel D) Once the patient is upright, the head is tilted so that the chin is pointed slightly downward
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PART 2
CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE
the eighth cranial nerve by an adjacent blood vessel and have reported that decompression of the nerve provides lasting relief of symptoms
Toxic and Idiopathic Bilateral Vestibulopathy
The common and serious ototoxic effects of the aminoglycoside antibiotics have already been mentioned both on the cochlear hair cells, with loss of hearing, and, often independently, on the vestibular labyrinth Prolonged exposure to these agents can produce a bilateral vestibulopathy without vertigo Instead, there tends to be a disequilibrium associated with oscillopsia The symptoms are especially troublesome when the patient moves Often the disequilibrium is not discovered until a bedfast patient tries to walk Less well appreciated is the occurrence of a slowly progressive vestibulopathy for which no cause can be discerned The latter disorder affects men and women alike, with onset in middle or late adult life The main abnormalities are unsteadiness of gait, which is worse in the dark or with eyes closed, and oscillopsia, which occurs with head movements and is particularly noticeable when walking Vertigo and hearing loss are notably absent, as are other neurologic abnormalities The bilateral vestibular loss can be documented with caloric and rotational testing Baloh and colleagues, in a report of 22 patients with bilateral idiopathic vestibulopathy of this type, found that a signi cant proportion (9 of 22 cases) had a prior history of prolonged episodes of vertigo consistent with the diagnosis of bilateral sequential vestibular neuronitis
Vestibular Neuronitis (Labyrinthitis)
This was the term applied originally by Dix and Hallpike to a distinctive disturbance of vestibular function, characterized clinically by a paroxysmal and usually a prolonged single attack of vertigo and by a conspicuous absence of tinnitus and deafness The entity is, however, more nebulous than most discussions indicate This disorder occurs mainly in young to middle-aged adults (children and older individuals may be affected), without preference for either sex The patient frequently gives a history of an antecedent upper respiratory infection of nonspeci c type, but it is not clear whether this is requisite for the diagnosis Usually the onset of vertigo is fairly abrupt, although some patients describe a prodromal period of several hours or days in which they felt topheavy or off balance Persistence of the symptoms for a day or more differentiates the process from Meniere disease The vertigo ` is severe as a rule and is associated with nausea, vomiting, and the need to remain immobile Nystagmus (quick component) and a sense of body motion are to the opposite side, whereas falling and past pointing are to the side of the lesion In some patients the caloric responses are abnormal bilaterally, and in some the vertigo may recur, affecting the same or the other ear Auditory function is normal Examination discloses vestibular paresis on one side, ie, an absent or diminished response to caloric stimulation of the horizontal semicircular canal If the patient will tolerate the small head movements, the previously described rapid-head-impulse test of Halmagyi and Cremer is one of the best means of demonstrating absent function of one lateral semicircular canal Although the symptoms can be quite disabling for a short period, vestibular neuronitis is a benign disorder The severe vertigo and associated symptoms subside in a matter of several days,
but lesser degrees of these symptoms, made worse by rapid movements of the head, may persist for several weeks or months The caloric responses are gradually restored to normal as well In some patients there has been a recurrence months or years later The portion of the vestibular pathway that is primarily affected in this disease is thought to be the superior part of the vestibular nerve trunk, which was observed to show degenerative changes by Schuknecht and Kitamura Earlier, Dix and Hallpike had reasoned that the lesion was located central to the labyrinth, since hearing is spared and vestibular function usually returns to normal They used the term vestibular neuronitis because of the uncertainty of more precise localization within the peripheral vestibular pathway The cause is uncertain, but most authorities have attributed it to a viral infection of the vestibular nerve, analogous to Bell s palsy, and from time to time, enhancement of the eighth nerve or the membranous labyrinth is seen after gadolinium administration on MRI For want of more speci c etiologic or pathologic data, many neurologists prefer the term vestibular neuropathy or neuritis or acute unilateral peripheral vestibulopathy It is likely that many of the conditions described under the terms epidemic vertigo, epidemic labyrinthitis, and acute labyrinthitis or neurolabyrinthitis refer to the same process These many names attest to the fact that the distinction between vestibular neuronitis and labyrinthitis has never been clari ed; some otolaryngologists use the term labyrinthitis for a vestibular neuronitis with mild or moderate hearing loss Certainly herpes zoster oticus causes this syndrome (as well as affecting the seventh nerve); this characterizes the Ramsay Hunt syndrome (pages 642 and 1183) During the acute stage, antihistamine drugs, phenergan, clonazepam, and scopolamine may be helpful in reducing the symptoms Vestibular exercises are recommended by Baloh in his review of the subject (2003) One study has demonstrated a more rapid recovery with the use of methylprednisolone, 100 mg orally, tapered over 3 weeks; valcyclovir did not have this effect (Strupp et al)
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