Vertigo and Nystagmus: The Role of the Velocity Storage Integrator in Skull Vibration Induced Nystagmus (SVIN)

This paper reviews the vestibular neural mechanisms that generate vertigo and nystagmus. Angular acceleration activates a group of neurons in the brainstem that cause the person to have the sensation of turning. But long after the end of the acceleration, these neurons continue to fire; they perseverate, causing afternystagmus, and I contend that this gives the false sensation that the person is continuing to turn when they are actually stationary. That false sensation, that illusion, is called vertigo, and the neural basis for it is the continued firing of this cluster of neurons in the brainstem which signal turning—firing long after the turn has stopped. Any other process that generates activity of this group of neurons—disease, dysfunction, other sensory input—will also result in that false sensation of turning—vertigo. The group of neurons is called the velocity storage integrator (VSI). The operation of this VSI network is directly linked to neural systems controlling nausea and postural stability, and it is a key part of a neural circuit generating the subjective sensation of vertigo. The VSI receives input from vestibular, optokinetic, and proprioceptive systems, and it projects to many neural systems to generate nystagmus, sensation, nausea, and postural responses.