2006 年 65 巻 3 号 p. 191-196
Galvanic nystagmus (GN) has been studied with regard to equilibrium. However, the nystagums-provoking mechanism has not been clarified. In this study, we considered Meniere's disease (MD) to be a unilateral vestibular disorder model, and analyzed GN recorded in MD by video-oculography.
The subjects were 10 patients with MD (38-60 years). The patients were divided into an acute group of 5 patients who had the last insult within 2 weeks and a chronic group of 5 patients who had the last insult more than 4 weeks before. Stimulation of the cathode using direct current at 1, 2, or 3 mA for 30 sec was alternately performed on the affected and healthy sides in the acute and healthy subjects as controls using the mean frequency of nystagums and slow phase velocity.
The mean frequency of nystagmus caused by stimulation at 2 MA on the affected side was significantly lower in the acute group (0.453±0.354 Hz) than in the control group (1.088±0.437 Hz) (P<0.05). The mean slow phase velocity was also lower in the acute group (1.494±1.223 deg/sec) than in the control group (5.053±5.236 deg/sec)(P<0.1). There were no significant differences in the mean frequency of nystagmus and slow phase velocity caused by stimulation between the healthy side in the acute group and the control group. The mean frequency of nystagmus and slow phase velocity caused by stimulation on the affected and healthy sides were not significantly different between the chronic and control groups.
The reduction of responses on the affected side in the acute MD stage suggested the involvement of the vestibule and semicircular canal as the stimulation receptors of GN examination. In the chronic stage, since the condition was considered to be the steady state without vertigo, the results were considered to be due to central and peripheral compensation.