半规管的角加速度刺激会导致初级管传入神经元的放电速率增加,从而导致健康成年动物的眼球震颤。然而,半规管裂开后,患者的声音或振动也可能导致管传入神经元放电率增加,所以这些不寻常的刺激也会引起眼球震颤。Iversen和Rabbitt的最新数据和模型表明,声音或振动可能会通过锁定到刺激的各个周期的神经激活或由于流体泵送(“声流”)引起的激发速率的缓慢变化而增加激发速率,导致杯体偏转。这两种机制都将增加主要传入放电率,从而引发眼球震颤。豚鼠的主要传入数据表明,在某些情况下,这两种机制可能相互对立。这篇综述显示了这三种临床现象-颅骨振动引起的眼球震颤,增强前庭诱发的肌源性电位,和Tullio现象-有一个共同的联系:它们是由半规管传入神经元在半规管开裂后对声音和振动的新反应引起的。
Angular acceleration stimulation of a semicircular canal causes an increased firing rate in primary canal afferent neurons that result in nystagmus in healthy adult animals. However, increased firing rate in canal afferent neurons can also be caused by sound or vibration in patients after a semicircular canal dehiscence, and so these unusual stimuli will also cause nystagmus. The recent data and model by Iversen and Rabbitt show that sound or vibration may increase firing rate either by neural activation locked to the individual cycles of the stimulus or by slow changes in firing rate due to fluid pumping (\"acoustic streaming\"), which causes cupula deflection. Both mechanisms will act to increase the primary afferent firing rate and so trigger nystagmus. The primary afferent data in guinea pigs indicate that in some situations, these two mechanisms may oppose each other. This
review has shown how these three clinical phenomena-skull vibration-induced nystagmus, enhanced vestibular evoked myogenic potentials, and the Tullio phenomenon-have a common tie: they are caused by the new response of semicircular canal afferent neurons to sound and vibration after a semicircular canal dehiscence.