Sudden deafness with vertigo usually suggests the diagnosis of an inner ear disorder, eg, Meniere disease, acute labyrinthitis, autoimmune inner ear disease, or perilymphatic fistula. Previous reports of sudden, bilateral deafness caused by vertebrobasilar occlusive disease have been rare. In 1943, Adams15 was the first to completely describe the syndrome associated with AICA occlusion. In his patient, tinnitus was an early symptom, appearing soon after vertigo, and the patient had acute bilateral, asymmetrical hearing loss, suggesting bilateral ischemia. Adams alluded to the difficulty of assigning a time of onset to the symptom of hearing loss, noting that "deafness . . . may not at all attract the attention of an unobservant patient." Details of the timing of hearing loss in patients with stroke have seldom been reported, suggesting that the issue of transient ischemic attacks consisting of hearing loss could have been frequently overlooked. In 1990, Amarenco et al17 described a series of 20 patients with AICA distribution strokes: 5 of the 20 patients had hearing loss as part of the stroke syndrome. However, none had hearing loss at stroke onset, although 2 had tinnitus at onset. All patients with hearing loss had vertigo or unsteadiness at stroke onset. In 1998, Roquer et al18 described 15 patients with AICA strokes. All 15 patients had vertigo or ataxia, and 6 of the 15 had hearing loss. However, the timing of hearing loss in relation to vertigo and ataxia was not reported. Stephan et al11 described a patient with sudden, bilateral deafness caused by basilar artery occlusion who later developed progressive quadriplegia with mental status abnormalities. Huang et al12 described 7 patients with bilateral, sudden deafness in vertebrobasilar occlusive disease. All but 1 of the 7 patients had bilateral hearing impairment as the initial symptom. However, 3 of the 7 patients also had quadriparesis (n = 1), hemianesthesia (n = 1), or dysarthria (n = 1) at onset, and 4 had vertigo at onset. The report did not include audiometric data, limiting localization. Five of the patients in this series had poor outcomes, including the locked-in syndrome and severe ataxia with abasia. One patient had permanent bilateral deafness and diplopia, and only 1 patient made a good recovery. Presumably, these 2 previous reports reflect severe ischemic damage to multiple structures in the posterior fossa. Therefore, the clinical course in our patient may have been remarkable in that there were few residual deficits.