Peripheral and Central Vestibular Disorders

Pathophysiology

The vestibulo-ocular reflex (VOR) is one of the most basic reflexes. It can even be observed in fish. After a short latency, the VOR generates eye rotations in the same plane as the head rotation that elicits them [6]. To do this, the oculomotor system uses information provided by the three pairs of orthogonally oriented semicircular canals. The right and left sides work together in a tradeoff manner (i.e. when one labyrinth increases the neuronal activity, the other decreases it) [6]. Disorders of the vestibular periphery cause nystagmus in a direction that is determined by the pattern of labyrinthine semicircular canals involved [6]. The complete, unilateral loss of one labyrinth causes a mixed hor- izontal-torsional nystagmus that is suppressed by visual fixation. Another consequence of peripheral vestibular lesions is a change in the size (gain) of the overall dynamic VOR response, i.e. the gain of the VOR for head movements toward the affected ear becomes smaller, and the subject has to refixate the object after the head movement by a saccade. The head-impulse test uses this feature clinically. As a result, patients may complain of oscillopsia during rapid head movements.

Central vestibular disorders are caused by lesions of pathways or areas involved in the adjustment of the VOR (e.g. the cerebellar connections to the vestibular nuclei) [2, 6]. These lesions result in upbeat, downbeat, torsional nystagmus or central positional vertigo.

Vestibular Neuritis

Clinical Aspects

The presenting sign of vestibular neuritis is an acute onset of severe rotatory vertigo that lasts for hours to days [7]. Hearing loss is normally not a sign of vestibular neuritis [7]. The horizontal contraversive beating spontaneous nystagmus has a torsional component and causes postural instability with a tendency to fall to the ipsiversive side.

Etiology

Recent findings support the view that an inflammation of parts of the vestibular nerve is the cause of vestibular neuritis and acute labyrinthitis. Most studies have shown the presence of latent herpes simplex virus type 1 in human vestibular ganglia [8, 9]. The imaging of 2 patients with vestibular neuritis using 3-tesla MRI and high-dose contrast medium revealed isolated enhancement of