HIGH ACCELERATION IMPULSIVE ROTATIONS REVEAL SEVERE LONG-TERM DEFICITS OF THE HORIZONTAL VESTIBULOOCULAR REFLEX IN THE GUINEA-PIG

While there is agreement that unilateral vestibular deafferentation (U VD) invariably produces an immediate severe horizontal vestibule-ocula r reflex (HVOR) deficit, there is disagreement about whether or not th is deficit recovers and, if so, whether it recovers fully or only part ly. We suspected that this disagreement might mainly be due to experim ental factors, such as the species studied, the means chosen to carry out the UVD, or the nature of the test stimulus used. Our aim was to s ort out some of these factors. To do this, we studied the HVOR of aler t guinea pigs in response to low and high acceleration sinusoidal and high acceleration impulses after UVD by either labyrinthectomy or by v estibular neurectomy. The HVOR in response to high acceleration impuls ive yaw rotations was measured before, and at various times after, eit her unilateral labyrinthectomy or superior vestibular neurectomy Follo wing UVD, there was a severe impairment of the HVOR for ipsilesional r otations and a slight impairment for contralesional rotations, after e ither operation. This asymmetrical HVOR deficit in the guinea pig para llels the deficit observed in humans. Between the first measurement, w hich was made 1 week after UVD, and the last, which was made 3 months after UVD, there was no change in the HVOR. This lack of recovery was the same after labyrinthectomy as after vestibular neurectomy. The HVO R to low and high acceleration sinusoidal yaw rotations were measured after UVD, and the results were compared with those in response to imp ulsive rotations. For low acceleration sinusoidal rotations (250 degre es/s(2)), the gain was symmetrical, although reduced bilaterally. As t he peak head acceleration increased, the HVOR became increasingly asym metric. The HVOR asymmetry for sinusoidal rotations was significantly less than for impulsive rotations that had the same high peak head acc eleration (2500 degrees/s(2)). Our results show that the HVOR deficit after UVD is the same in guinea pigs as in humans; that it is the same after vestibular neurectomy as after labyrinthectomy; that it is last ing and severe in response to high acceleration rotations; and, that i t is more obvious in response to impulses than to sinusoids.