Audiologic findings in unilateral deafness resulting from contralateral pontine infarct KAREN JO DOYLE, MD, PhD, CYNTHIA FOWLER, PhD, and ARNOLD STARR, MD, Irvine and Long Beach, California F o c a l brain stem infarction has been uncommonly associated with unilateral sensorineural hearing loss (SNHL). Kumar et al. (1986) 1 found a single case of brain stem infarction among 200 cases of unilateral SNHL. Previous case reports of unilateral S N H L after brain stem infarct have been the result of lesions of the ipsilateral cochlear nuclei in the dor- solateral medulla. 2,3 Wada and Starr (1983) 4 deter- mined that an experimentally produced lesion of the lateral lemniscus produced a unilateral contralateral abnormality in the N 3 portion of wave III of the auditory brain stem response (ABR) in guinea pigs. We report a case of unilateral S N H L after a con- tralateral focal pontine infarct verified by magnetic resonance imaging (MRI) and A B R testing. CASE REPORT A 63-year-old man with a history of hypertension was admitted to the Veterans Administration Medical Cen- ter-Long Beach in June 1994 with a urinary tract infec- tion. During his admitting physical examination, a neuro- logic examination was performed that revealed a right- sided hearing loss. The neurologic examination was otherwise normal. He reported that he had had a stroke in April 1994 and had spent several days in another hospital. The records and MRI scans from that hospital- ization were obtained. The admission physical examina- tion from April revealed a blood pressure of 170/86, a central right facial palsy, a right-sided hearing loss, nys- tagmus (direction not given), and unsteady gait. Labora- tory examination revealed normal cerebrospinal fluid chemistries and cell counts and negative VDRL. The MRI From the Divisions of Otolaryngology-Head and Neck Sur- gery and Audiology (Drs. Doyle and Fowler), Veterans Administration Medical Center; and the Departments of Otolaryngology-Head and Neck Surgery (Drs. Doyle and Fowler) and Neurology (Dr. Starr), University of California Irvine. Received for publication April 28, 1995; revision received June 27, 1995; accepted July 17, 1995. Reprint requests: Karen Jo Doyle, MD, PhD, Department of Otolaryngology-Head and Neck Surgery, University of Cali- fornia Irvine Medical Center, Bldg. 25, Route 81, 101 The City Dr., Orange, CA 02668. OTOI.A~YNGOI. HZAO NECK SUnG 1996;114:482-6. from April 1994 demonstratd a dorsally located infarct involving the medial left portion of the upper pons, as well as ischemic changes of the periventricular deep white matter (Figs. 1 and 2). He was referred 3 weeks after the stroke to the Audi- ology Department for evaluation of his right-sided hearing loss. Audiogram revealed a fiat, severe SNHL in the right ear and a moderate high-frequency SNHL above 2000 Hz in the left ear (Fig. 3). Speech discrimination was 0% in the right ear and 92% in the left ear. Acoustic reflexes were absent in the right ear. ABR was performed with condensation and rarefaction dicks presented 10/second at 95 dB nSL (Fig. 4). In the left ear, all components were identified, and their intercomponent times were within normal limits. In the right ear, wave I was present for condensation clicks at 1.98 msec, and no other waves were identified. Transient and distortion-product otoacoustic emissions (OAEs) were performed. In the right ear, tran- sient emissions were present with energy present through 3000 Hz with 81% reproducibility, similar to those ob- tained from the left ear (Fig. 5). Distortion-product OAEs (2F2 - F1 = 1.221; F1 = 70 dB SPL; F2 = 70 dB SPL) were present across frequencies in the right ear and through F2 = 3000 Hz in the left ear. Repeat MRI with gadolinium of the internal auditory canals was performed, and they were normal. DISCUSSION Although we used the combined term sensorineu- ral hearing loss, the majority of patients with S N H L have lesions of the sensory apparatus, whereas neu- ral lesions, including spiral ganglion degeneration, eighth nerve lesions, and central auditory pathway lesions from the cochlear nuclei to the temporal cortex, are found less frequentlyJ A m o n g the causes of hearing loss, cerebrovascular infarction of the auditory pathways has been described infrequently. A 1986 report of 200 cases of unilateral S N H L found 42 individuals with confirmed retrocochlear lesions, of which there was one lesion adjacent to the co- chlear nucleus and a second patient with a pontine lesion? The most commonly found central lesions in that study were cerebellopontine angle tumors, cen- tral nervous system lues, and multiple sclerosis. Lownie and Parnes (1991) 2 found two cases of ipsi- lateral S N H L caused by infarcts of the cerebellum
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