We report the clinical and oculographic features in 240 patients with benign positional vertigo (BPV). In each case, after a rapid position change from the sitting to head-hanging position, a stereotyped torsional paroxysmal positional nystagmus was visually observed and recorded with electronystagmography (ENG). The mean age of onset was 54 years, with a range of 11 to 84 years. In slightly more than one-half of the cases (122/240) a likely diagnosis was determined. The most common identifiable causes were head trauma (17%) and viral neurolabyrinthitis (15%). Females outnumbered males approximately two to one in the idiopathic group. Abnormalities on bithermal caloric testing were found in 47% of patients. Only two patients, both with well-documented neurologic disorders, had central signs on ENG. Our data are consistent with a peripheral, posterior semicircular canal origin of BPV.

A method for rapid, accurate measurement of saccade amplitude, duration, and velocity (average and maximum) was developed as a functional test of the extraocular motor system. Recordings were made with a direct-current electro-oculographic system, and data analysis was performed on a laboratory digital computer. Saccade amplitude and duration were found to be linearly correlated in 25 normal subjects, with a mean slope of 2.7 msec per degree over a large amplitude range. In the same subjects, saccade amplitude and velocity (maximum or average) had a nonlinear relationship that was best fit by an exponential equation. The two constants of this equation adequately characterized the relationship between saccade amplitude and velocity and permitted rapid statistical comparison between normal and abnormal subjects.

We report the clinical features and results of quantitative eye-movement testing in 13 patients with episodic positional vertigo and nonfatiguing direction-changing horizontal positional nystagmus (beating to the right with the head turned to the right and beating to the left with the head turned to the left). The benign history and lack of associated neurologic findings support a peripheral localization of the lesion. This syndrome probably represents a horizontal semicircular canal variant of benign positional vertigo. Free-floating debris in one horizontal canal may explain many of the clinical and oculographic findings.

Positional nystagmus that does not fatigue, persists as long as the position is held, and changes direction in different head positions has typically been attributed to central vestibular lesions. We recently studied three patients who presented with positional nystagmus having these features but almost certainly of benign peripheral origin. All three had an initial history typical of benign positional vertigo and, in two, the persistent direction-changing positional nystagmus occurred after the patient underwent a maneuver to remove debris from the posterior semicircular canal. The positional nystagmus profile and clinical course are consistent with the debris leaving the posterior semicircular canal and becoming attached to the cupula of the horizontal semicircular canal.

Although sway amplitude and velocity were consistently increased in patients with bilateral vestibular loss and patients with cerebellar atrophy, none of the posturography measurements reliably distinguished the 2 patient groups. The finding of increased frequency of sway in the anteroposterior direction in patients with cerebellar atrophy was of limited value since the tremor was visible at the bedside.