Intermittent vertigo represents one of the most disabling symptoms encountered in otologic practice. The recurrent nature of this disability implies a reversible alteration in vestibular nerve physiology caused by changes in the neuron or its environment. Three of the most common clinical syndromes manifesting as recurrent vertigo are benign paroxysmal positional vertigo (BPV), Ménière's disease (MD) and vestibular neuronitis (VN). The morphologic evidence presented in previous chapters supported by molecular [1, 2], immunologic [3-6] and clinical observations [7][8][9][10][11][12][13][14][15][16][17][18][19] indicates that these common, and some less common, recurrent vestibulopathies are manifestations of reactivation of latent viral vestibular ganglionitis.The agents responsible for the ganglionitis are neurotropic (NT) viruses, likely herpes simplex (HSV) or zoster virus. Other NT viruses that may be included in this group are cytomegalovirus, Epstein-Barr and pseudorabies virus. The ubiquity of HSV accounts for the high exposure rates recorded in the world population. Elevated serum antibody titers to HSV-1 have been recorded in 70% of 25-year-olds, while at the age of 60 years the rate is over 90% [20]. After the NT virus has entered a sensory nerve, it may acquire a latent state in its ganglion cells. Reactivation of the virus from latency is reflected in clinical signs and symptoms.Because the clinical syndromes with recurrent vertigo are varied, it is useful to construct a classification system based on vestibular ganglionitis [21]. We propose a new classification system based on three bodies of information: (1) a review of temporal bone (TB) specimens, (2) case reports and (3) a clinical series.