Vestibular Vertigo

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Acute loss of vestibular function is also called vestibular neuritis, acute vestibular neuropathy, or an acute vestibular crisis. It can be produced by a variety of pathogenetic mechanisms, the most common of which is a viral infection. The patient suddenly experiences acute rotatory vertigo with nausea, vomiting, and falling to the side of the diseased vestibular organ. Every movement of the head makes the vertigo worse; therefore the patient, noting this, lies perfectly still. Examination reveals horizontally beating, spontaneous nystagmus in the direction opposite the side of the lesion, with a rotatory component. The nystagmus is more intense when the patient lies on the affected side; it can be diminished by visual fixation. The affected vestibular organ is less responsive than normal to caloric stimulation. Vertigo usually resolves fully within a few days, rarely within a few hours. Often a so-called "trigger labyrinth" remains as a residual phenomenon, i. e., vertigo on acceleration or rapid movements of the head. The condition may relapse.

Positional and positioning vertigo. These types of vertigo arise only with certain positions or positioning movements of the head and manifest themselves as brief attacks of vertigo that diminish in intensity if they are provoked in rapid succession. These conditions have a number of different causes.

Benign paroxysmal positioning vertigo is the most common type of positioning vertigo. It is provoked by changes in the position of the head, usually involving lying down rapidly, bending forward, turning in bed, or rapidly sitting up. It manifests itself as very brief (15-30 seconds) and very severe attacks of rotatory vertigo and nausea.

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With respect to the pathogenesis of this condition, it is thought that small pieces of the otolith membranes of the saccule and utricle can break off and float freely in the endolymph—usually in the posterior semicircular canal, less commonly in the horizontal one. When the head is moved, these free particles move together with the endolymph and slide over the hair cells of the cupula, even after the movement is completed. The abnormally prolonged activation of the hair cells induces acute rotatory vertigo. The condition is also termed cupulolithiasis or canalolithiasis.

The Hallpike positioning maneuver can be used as a diagnostic test (Fig. 11.22). The patient is rapidly taken from an upright sitting position into the supine position with the head held down 30° below the level of the examining table and turned 60° to the right or left. Within a few seconds, the examiner should be able to observe rotatory nystagmus, which then disappears after 5-30 seconds. This is easiest to see if the patient is wearing Frenzel goggles. If the head is turned to the right, the nystagmus is counterclockwise; if to the left, clockwise.

Certain positioning maneuvers, e.g., those of Epley and Semont, have been shown to be useful as treatment for this condition. These maneuvers work by flushing the floating otoliths out of the affected semicircular canal.

Central positional vertigo is a rarer type of positionally dependent vertigo appearing with certain tilted positions of the head. The nystagmus usually beats to the uppermost ear and does not habituate on repeated provocation. The vertigo is generally not very severe.

Meniere disease is a common cause of acute vestibular vertigo. It is caused by endolymphatic hydrops and manifests itself clinically in episodes of acute rotatory vertigo, a tendency to fall to the affected side, and horizontal, directional, spontaneous nystagmus, accompanied by nausea, vomiting, and tinnitus. Slowly progressive hearing loss is worse after each attack.

Bilateral vestibular deficits. While unilateral dysfunction of the vestibular apparatus can either recover or be compensated for by the intact opposite side within a matter of weeks, bilateral dysfunction deprives the regulatory system for balance of all incoming vestibular information. Consequently, the patient's gait becomes very unsteady in the dark (i.e., when visual input, too, is inoperative), or when the patient must walk on an uneven or soft surface (i. e., when the incoming proprioceptive information is difficult to interpret). Subjectively, the patient suffers from oscillopsia (apparent movement of the external world), particularly when walking, because the vestibulo-ocular reflex (p. 186) is inoperative and visual fixation is, therefore, unstable.

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