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Neurology 2001;56:472-480
© 2001 American Academy of Neurology


Articles

The functional anatomy of gaze-evoked tinnitus and sustained lateral gaze

A.H. Lockwood, MD;, D.S. Wack, MA;, R.F. Burkard, PhD;, M.L. Coad, BA;, S.A. Reyes, BS;, S.A. Arnold, PhD; and R.J. Salvi, PhD

From the Centers for Positron Emission Tomography (Dr. Lockwood, D. Wack, and M. Coad), Hearing and Deafness, Hearing Research Laboratory (Drs. Lockwood, Burkard, Arnold, Salvi, and S. Reyes), and School of Medicine and Biomedical Sciences (S. Reyes), and Departments of Neurology (Drs. Lockwood and Salvi), Nuclear Medicine (Dr. Lockwood, D. Wack, and M. Coad), Communicative Disorders and Sciences (Drs. Lockwood, Burkard, and Salvi), and Surgery (Otolaryngology) (Drs. Burkard and Salvi), and Veterans Administration Western New York Health Care System (Dr. Lockwood and D. Wack), State University of New York, University at Buffalo, and Buffalo State College (Dr. Arnold), NY.

Address correspondence and reprint requests to Dr. A.H. Lockwood, Center for PET (115P), VA Western NY Healthcare System, 3495 Bailey Avenue, Buffalo, NY 14215; e-mail: alan{at}petnet.buffalo.edu

OBJECTIVE: To identify neural sites associated with gaze-evoked tinnitus (GET), an unusual condition that may follow cerebellar–pontine angle surgery.

METHODS: The authors examined eight patients with GET and used PET to map the neural sites activated by lateral gaze in them and seven age- and sex-matched control subjects.

RESULTS: In patients with GET, tinnitus loudness and pitch increased with lateral gaze and, to a lesser extent, up and down gaze. Evidence for neural activity related to GET was seen in the auditory lateral pontine tegmentum or auditory cortex. GET-associated nystagmus appears to activate the cuneus and cerebellar vermis. These sites were found in addition to an extensive network that included frontal eye fields and other sites in frontal, parietal, and temporal cortex that were activated by lateral gaze in seven control subjects and the patients. The unilateral deafness in patients with GET was associated with expansion of auditory cortical areas responsive to tones delivered to the good ear. In addition to GET, unilateral deafness, end-gaze nystagmus, and facial nerve dysfunction were common.

CONCLUSIONS: Patients with GET have plastic changes in multiple neural systems that allow neural activity associated with eye movement, including those associated with the neural integrator, to stimulate the auditory system. Anomalous auditory activation is enhanced by the failure of cross-modal inhibition to suppress auditory cortical activity. The time course for the development of GET suggests that it may be due to multiple mechanisms.




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