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From the Department of Neurology (Drs. Kim, Liu, and Baloh), Division of Surgery (Head and Neck) (Drs. Lopez, Ishiyama, and Baloh), and Department of Pathology (Dr. DiPatre), UCLA School of Medicine, Los Angeles, CA.
Address correspondence and reprint requests to Dr. Robert W. Baloh, Department of Neurology, UCLA School of Medicine, Box 951769, Los Angeles, CA 90095-1769; e-mail: rwbaloh{at}ucla.edu
OBJECTIVE: To study the pathophysiology of labyrinthine infarction.
BACKGROUND: The syndrome of sudden onset vertigo or hearing loss is commonly attributed to inner ear vascular disease, yet histologic studies of isolated labyrinthine infarction in humans have been rare and have not included a complete examination of the vertebrobasilar vascular system.
METHODS: Temporal bones, brainstem, cerebellum, and the supplying blood vessels were subjected to gross and microscopic postmortem examinations in a 92-year-old woman who had a sudden onset of vertigo and hearing loss in the right ear 7 years before death.
RESULTS: There were prominent atherosclerotic changes at the vertebrobasilar junction, but the internal auditory artery and its branches were patent on both sides. Histologic studies showed degenerative changes in the cochlea and vestibular labyrinth on the right. The posterior canal ampulla and saccular macule were relatively preserved showing partial areas of intact sensory epithelium with underlying nerve fibers. The right vestibulocochlear nerve showed a fibrotic scar and multiple patchy areas of degeneration. These findings are most consistent with a transient period of reduced perfusion of the internal auditory artery.
CONCLUSION: The partial sparing of the inferior vestibular labyrinth may indicate a decreased vulnerability to ischemia because of its better collateral blood supply.
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