Benign paroxysmal positional vertigo was first described by Barany in 1921. It may occur after diverse labyrinthine damage from trauma, infection, or vascular occlusion, during prolonged systemic illness, or after exposure to toxins. No definite cause can be established in many patients. The attacks occur almost exclusively when the patient assumes certain positions, regardless of the speed of head or bodily movements involved. Assuming the supine position, turning over in bee or tilting the head backward while erect may evoke moderately severe vertigo and nausea, but rarely vomiting. The symptoms and associated nystagmus may be reproduced by a test procedure elaborated by Dix and Hallpike.
With the patient sitting on a table and facing the examiner, his. head is grasped firmly and then head and body are quickly guided to a position in which the patient is supine with his head tilted 30 degrees over the end of the table and 30 to 45 degrees to one side. A positive response may occur only when the affected ear is placed undermost. The response begins after a measurable delay, often up to five seconds. A period of intense distress then ensues and the patient often cries out and struggles to free himself. A chiefly rotatory nystagmus with or without a horizontal component is observed. The fast phase of the 12 o’clock portion of the globe rotates toward the undermost ear. The symptoms and nystagmus last only a few seconds and become progressively more difficult to elicit upon immediate retesting.
Pathologically, there is atrophy of the superior division of the vestibular nerve and its sense organs, the macula of the utricle, and cristae of the horizontal and superior semicircular canals. These .structures are all nourished by the anterior vestibular artery, which has been postulated but not proved to have been occluded in patients presenting with this syndrome. Any pathophysiologic theory must explain the latent period before symptom production, the brief but severe vertigo, and the fatigability of the phenomenon. Schuk- richt believes that crystalline calcium carbonate statoconia released from the damaged utricle fall slowly through the endolymph into the posterior canal ampulla and displace its cupula. However, the induced nystagmus often is inconsistent with an origin solely from posterior canal stimulation.
Benign Paroxysmal Positional Vertigo In Vestibular Disorder
Benign Paroxysmal positional vertigo is not always a benign end organ disorder. Positional vertigo or nystagmus of central origin has been described with cerebellar or temporal lobe tumors and after brainstem damage. Central positional nystagmus characteristically occurs in more than one position, has a rapid onset and does not fatigue with repeated testing. The nystagmus either beats away from the undermost ear (convergent type), toward the undermost ear (divergent type), or resembles the peripheral form (Dix and Hallpike). Caloric tests are normal in less than half of either the peripheral or central types of positional nystagmus.Vestibular nerve section should be considered for the peripheral variety when vertigo is very frequent, disabling, or refractory to antivertiginous drugs. Successful results have been reported in several cases.