Audiologic findings in unilateral deafness resulting from contralateral pontine infarct.

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