This disorder of labyrinthine function is more frequent than Ménière disease and—while it does not have the same implications in the long term, an acute attack can be quite disabling. It is characterized by paroxysmal vertigo and nystagmus that occur only with the assumption of certain positions of the head, particularly lying down or rolling over in bed, bending over and straightening up, or tilting the head backward. It is common for the patient to report that the paroxysm of vertigo began in the middle of the night or early morning, presumably while shifting position during sleep and rapidly making one ear dependent, on rolling over to get out of bed, or to turn off an alarm. Brandt and colleagues (1994) prefers the descriptive adjective positioning vertigo to positional vertigo, insofar as the symptoms are induced not by a particular head position but only by rapid changes in head position. This disorder was first described by Bárány (1921) but Dix and Hallpike emphasized its benign nature and were responsible for its further characterization, particularly the discrete positional movements that provoke it. Individual episodes last for less than a minute, but these may recur periodically for several days or for many months—rarely for years. As a rule, examination discloses no abnormalities of hearing or other identifiable lesions in the ear or elsewhere. A thorough summary of the condition has been given by Furman and Cass.
The diagnosis of this disorder is settled at the bedside by moving the patient from the sitting position to recumbency, with the head tilted 30 to 40 degrees over the end of the table and 30 to 45 degrees to one side, as originally described by Dix and Hallpike (Fig. 14-5). This need not be done abruptly but should occur in one smooth motion over a few seconds or less. After a latency of a few seconds, this maneuver provokes a paroxysm of vertigo; the patient may become frightened and grasp the examiner or the table or struggle to sit up. The dysfunctional ear is the one that is downward when vertigo is elicited. We cannot refute the contention made by von Brevern and colleagues that the right labyrinth is more often responsible. The vertigo is accompanied by oscillopsia and nystagmus with the rapid components away from the affected (dependent) ear. The nystagmus is predominantly torsional with an additional vertical component in the eye opposite the affected ear according to Baloh and colleagues. The induced vertigo and nystagmus last no more than 30 to 40 s and usually less than 15 s. Changing from a recumbent to a sitting position reverses the direction of vertigo and nystagmus (position-changing nystagmus), and this is perhaps the most certain sign that the disorder originates in the labyrinth. With repetition of the maneuver, vertigo and nystagmus become less apparent, and after three or four trials, they can no longer be elicited (referred to as “fatigue”); they can be reproduced in their original severity only after a protracted period of rest. The head-hanging maneuver does not always evoke vertigo and nystagmus in patients whose histories are otherwise consistent with the diagnosis of benign paroxysmal vertigo; therefore, Froehling and coworkers do not insist on it for diagnosis if the history is compatible but without the sign, we are uncertain how to confirm the diagnosis. It may still be appropriate to prescribe the corrective exercises as a trial.
Such attacks of vertigo may come and go for years, particularly in the elderly, and require no treatment. At the other end of the scale is the rare patient with positional vertigo of such persistence and severity as to require surgical intervention.