Yamanaka T, Yamamoto T, Miyahara H, Matsunaga T
Department of Otolaryngology, Nara Medical University, Kashihara, Japan.
Acta Otolaryngol Suppl. 1998;533:26-9.
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.
由于已知眩晕是由椎基底动脉闭塞性疾病(如椎基底动脉供血不足;VBI)引起的,因此进行了一项电生理研究,以检查单侧椎动脉(VA)闭塞对α-氯醛糖麻醉猫的内侧前庭核(MVN)和前庭神经节(VG)神经元活动的影响。用玻璃绝缘银丝微电极在细胞外记录MVN和VG中的单个神经元活动。当单侧VA闭塞5分钟时,MVN中的自发放电率变化如下。A型模式表现出短暂增加,随后下降。B型模式显示逐渐下降,闭塞开始后无进一步变化。在VA闭塞同侧和对侧的MVN中分别观察到A型和B型模式。相比之下,VG神经元放电率不受闭塞影响。这些结果似乎支持了临床提示,即VBI中的眩晕是由双侧前庭核之间的功能差异产生的,而不是由外周前庭神经产生的。