Since vertigo is known to be caused by vertebrobasilar arterial occlusive disease (ex. vertebrobasilar insufficiency; VBI), an electrophysiological study was performed to examine the effects of a unilateral vertebral artery (VA) occlusion on the neuronal activities of the medial vestibular nucleus (MVN) and vestibular ganglion (VG) in alpha-chloralose-anesthetized cats. Single neuronal activity in the MVN and VG was recorded extracellularly with a glass-insulated silver wire microelectrode. When the unilateral VA was occluded for 5 min. the spontaneous firing rate in the MVN was altered as follows. The type A pattern exhibited a transient increase, followed by a decrease. The type B pattern showed a gradual decrease, and no further changes after the onset of occlusion. Type A and B patterns were observed respectively in MVN ipsi- and contra-lateral to the VA occlusion. In contrast, the VG neuronal firing rate was not affected by the occlusion. These results seem to support the clinical suggestion that the vertigo in VBI is produced by a difference in the function between the bilateral vestibular nuclei. rather than by the peripheral vestibular nerve.
Vestibular neuronal function of cats following unilateral vertebral artery occlusion. Publishing Authors By Initials
