The first part of the Epley canalith repositioning maneuver (Fig. 14-6) is similar to the diagnostic Hallpike maneuver, the only difference being that the patient is positioned without extending the head into the hanging position of the Dix-Hall-pike diagnostic maneuver, first with one ear down and the head turned, then the other ear, in order to establish the side responsible for symptoms. Next, with the patient in the position that causes symptoms, the head is turned in a series of three steps, each separated by about 20 s: first the head is turned 45 to 60 degrees toward the opposite ear; the patient is then turned onto his side and the head turned an additional 45 degrees, until the head is parallel to the ground; then the head is turned once more until it more nearly faces the floor. We have become aware that this last step, which is a necessary part of the maneuver, is sometimes omitted by neurologists. After about 20 s, the patient is returned to the upright position. It was formerly believed that the patient should be instructed to avoid the head-down position for 24 hours, but recent studies have demonstrated that this is probably not necessary. Often a single treatment sequence suffices to terminate a period of positional vertigo (approximately 80 percent respond), but a second sequence carried out immediately after the first probably gains another small group who derive benefit. Additional treatments carried out in the same session are said to add no further benefit. In recalcitrant cases, our otolaryngology colleagues have applied a large vibrator to the temporal bone while the Epley maneuver was being performed, after which the episodes ceased; presumably this mobilizes the crystals and aids in moving them out of the canal. An incompletely implemented Epley maneuver risks converting the usual posterior semicircular canal cupulolithiasis to one involving the lateral canal, which may be more difficult to treat.
Patients who fail to respond to the Epley maneuver may respond to variations of repositioning such as the Semont maneuver (the patient begins in a sitting position with the head turned 45 degrees to one side, then drops laterally to a side lying position on the opposite ear, followed by a brisk swing of the body to drop the opposite side lying position) or the similar Brandt-Daroff exercises (sitting, to side lying, to sitting, performed repeatedly).
Positional vertigo caused by lateral canalolithiasis causes a purely horizontal nystagmus rather than the torsional and vertical type described previously. In this case, another repositioning maneuver that involves rolling from one side to the other is used to liberate and reposition the otolithic debris.
It is important to reiterate that in some patients with positional vertigo, the disorder is neither benign nor paroxysmal. Jannetta and colleagues have described a group of patients in whom symptoms of vertigo and disequilibrium were almost constant (even in the upright position) and disabling and unresponsive to habituation and other medical therapy (disabling positional vertigo). They attributed this disorder to cross-compression of the root entry zone of the eighth cranial nerve by an adjacent blood vessel and have reported that decompression of the nerve provides lasting relief of symptoms.
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 independently, on the vestibular labyrinths. Prolonged exposure to these agents produces 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 bedbound patient tries to walk.