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Electrophysiology of Cranial Nerve Testing: Auditory Nerve

Legatt, Alan, D.

Journal of Clinical Neurophysiology: January 2018 - Volume 35 - Issue 1 - p 25–38
doi: 10.1097/WNP.0000000000000421
Invited Review

Summary: The electrocochleogram and brainstem auditory evoked potentials (BAEPs) are electrophysiologic signals used to assess the auditory nerve. The electrocohleogram includes the cochlear microphonic, the cochlear summating potential, and the eighth nerve compound action potential. It is used predominantly for hearing assessment and for diagnosis of Ménière disease and auditory neuropathy. Brainstem auditory evoked potentials are used for hearing assessment, diagnosis of dysfunction within the cochlea, the auditory nerve, and the brainstem auditory pathways up to the level of the mesencephalon, and intraoperative monitoring of these structures. The earliest BAEP component, wave I, and the eighth nerve compound action potential reflect the same process—the initial depolarization in the distal auditory nerve. Brainstem auditory evoked potential wave II receives contributions from the region of the cochlear nucleus and from the second depolarization in the distal auditory nerve. Wave III and later components are entirely generated rostral to the auditory nerve. Interpretation of BAEP studies is based on waves I, III, and V; auditory nerve dysfunction is manifested as prolongation of the I–III interpeak interval or absence of waves III and V. Eighth nerve tumors can cause a variety of BAEP abnormalities depending on which structures they affect. Adverse intraoperative BAEP changes can have many etiologies, including direct mechanical or thermal injury of tissue, ischemia (including cochlear ischemia or infarction due to compromise of the internal auditory artery), eighth nerve stretch, systemic or localized hypothermia, and artifactual BAEP changes due to technical factors.

Departments of Neurology, Neuroscience, and Medicine (Critical Care Medicine), Montefiore Medical Center and the Albert Einstein College of Medicine, Bronx, New York, U.S.A.

Address correspondence and reprint requests to Alan D. Legatt, MD, PhD, Department of Neurology, Montefiore Medical Center, 111 East 210 St, Bronx, NY 10467, U.S.A.; e-mail:

The author has no funding or conflicts of interest to disclose.

© 2018 by the American Clinical Neurophysiology Society