Acute unilateral loss of vestibular function.

Sudden unilateral loss of vestibular function is the most severe condition that can occur in the vestibular system. The clinical syndrome is caused by the physiologic properties of the vestibulo-ocular reflex (VOR) arc. In the normal situation, the two peripheral vestibular end organs are connected to a functional unit in coplanar pairs of semicircular canals working in a push-pull mode. "Push-pull" mode means that, when one side is excited, the other side is inhibited, and vice versa due to two mechanisms. First, first-order vestibular afferents are bipolar cells. They have a tonic firing rate that is modulated up or down depending on the direction of rotation. Second, via inhibitory neural connections of second-order vestibular neurons between the vestibular nuclei (vestibular commissural system), the excited side inhibits further the contralateral side. The neural signals are encoded as the difference of the change in firing rate of the vestibular neurons modulating the tonic firing rate on both sides in opposite directions (one side up, the contralateral side down). When the head is not moving, the two peripheral vestibular end organs generate a resting firing rate, which is exactly equal on both sides. When the head is rotated, for example, to the right, the right-sided first-order vestibular afferents increase their discharge rate and the left-sided ones decrease their firing rate. This leads to increase in firing rate of also the type I second-order vestibular neurons in the vestibular nuclei, which synapse with inhibitory type II neurons on the contralateral side, further decreasing the firing rate in the second-order vestibular neurons in the contralateral vestibular nucleus. When the direction of head rotation is reversed, the behavior of the type I neurons on the two sides of the head is reversed. The same relation exists between the coplanar vertical canal afferents on the two sides of the head. When there is unilateral damage to the end organ or the vestibular nerve, the resting firing frequency is drastically reduced or even silenced on the lesioned side, thereby creating a tonic imbalance between the normal resting firing on the healthy side and the lesioned side. This tonic imbalance mimics a permanent rotation toward the healthy side (the side with the higher firing rate), resulting, via the VOR, in a slow-phase drift of the eyes toward the side of the lesion, interrupted by rapid quick-phase resetting eye movements toward the healthy side. This leads to the typical vestibular spontaneous horizontal-torsional nystagmus together with rotational vertigo and postural imbalance, with the tendency to fall toward the lesioned side. The tonic imbalance with the hallmark of spontaneous nystagmus usually recovers within days to weeks after the lesion due to the central restoration of tonic activity on the lesioned side. The dynamic changes, however, might be long-lasting when the peripheral sensors do not recover their function. This causes asymmetric VOR responses, with weaker responses when the head is rotated rapidly toward the lesioned side, leading to transient oscillopsia.