Extract:
1. Lesions in the most rostral part of the vestibular ganglion (type I GC) are responsible for episodes of rotatory vertigo. A strong VOR disturbance (nystagmus) signals this form of vertigo.
2. If the ganglion cell lesion is located immediately caudal to this rostral pole of the superior division type II GC are affected. Unsteadiness, especially on head movement, will be experienced because these type II GC project to commissural pathways.
3. Degeneration of ganglion cells in ventral parts of both the superior (utricle) and inferior (saccule) divisions of the vestibular ganglion, causes loss of function in the vestibulospinal tract to neck, trunk and limb muscles. Frequently these are described by patients as “drop” attacks. Ataxia may be a lingering form of this form of dysequilibrium.
4. The most common form of vertigo encountered in practice is position induced. Short duration episodes of a rotatory vertigo which is fatiquable have been described since Barany [41]. Both Barany [41] and Citron and Hallpike [42] felt this was an otolith disorder but the nystagmus response observed in this syndrome prevented acceptance of an otolith cause. Hallpike's description of utricular degeneration [42] in the TB of BPPV was not enough to neutralize the predominant support of a canal etiology. Although the clinical response is a rotatory form of vertigo, the uninhibited response is caused by loss of the inhibitory role of the otolith organs.
5. Lesions in the saccular portion of the vestibular ganglion (inferior vestibular) may secondarily interrupt the efferent pathways to the cochlear and vestibular sense organs. Clinically, the loss of this control may be perceived as tinnitus and mot’on sickness