Abstract
We reported a 64-year-old male with bilateral vertebral artery occlusion who experienced sudden onset bilateral hearing loss and vertigo.
The patient had no history of hearing impairment and no premonitory symptoms; he was receiving medication for hypertension and hypercholesterolemia.
He had been admitted to a local hospital for colonoscopic polypectomy of a colon polyp. The day after this operation, he suffered bilateral hearing loss, preceded by vertigo and vomiting. The following day, he was transferred to Saku Central Hospital for further evaluation and treatment of the sudden deafness. En route to our hospital, he suffered a respiratory arrest, but voluntary breathing was restored shortly after intratracheal intubation was performed.
On physical examination, the patient's blood pressure was 110/80 mmHg. He had corneal rings and palpebral xanthomas. Neurological examination showed clouding of consciousness. Examination of cranial nerves revealed horizontal gazing nystagmus, predominantly on the right. The patient had severe hearing loss in both ears. Cold caloric stimulation showed severe canal paresis in the left ear and moderate paresis in the right. His speech was scanning and slurred. Deep tendon reflexes were generally hyperactive and pathological reflexes were bilaterally positive, although muscle strength was almost normal. Tests of coordination of the patient's extremities revealed adiadochokinesis and dysmetria, predominantly on the left. He showed truncal ataxia in a sitting position and was unable to walk. He also exhibited dysuria. Laboratory data on admission revealed mild hypercholesterolemia and a diabetic pattern on 75 g OGTT.
Although CT scan on admission revealed small low density areas only in the bilateral cerebellar hemispheres, by the fifth day these lesions were enlarged and new low density areas appeared in the paramedian portion of the mid-to-upper pons and middle cerebellar peduncles. Cerebral angiography of both vertebral arteries (VAs) revealed marked stenosis at the origins and occlusion at the 4th segments. Carotid angiography demonstrated retrograde filling of the basilar artery (BA) and both superior cerebellar arteries, mediating collateral circulation from the anterior and the middle cerebral artery; it was unclear how far the occlusion extended in the rostal direction. Neuroradiological findings suggested that thrombosis extended from the bilateral VA to the middle portion of the BA. Brain-stem auditory evoked potentials (BAEPs), recorded on the 8th day, showed absence of all BAEPs including wave I in both ears, which corresponded to the clinical findings of bilateral hearing loss.
After admission, the patient developed progressive stroke with somnolence, left Horner's syndrome, pseudobulbar palsy, and tetraplegia including facial palsy. Following thrombolytic therapy with urokinase, he improved and was discharged, although bilateral hearing impairment, cerebellar ataxia, mild tetraplegia, and dysuria persisted as sequelae.
Bilateral hearing loss is rarely found as early sign in vertebro-basilar or basilar thrombosis. The BAEPs finding in our case suggested that bilateral hearing loss resulted from damage to the cochlear nerve due to ischemia of its feeder, the internal auditory artery. Sudden onset bilateral hearing loss should be considered a medical emergency which requires immediate evaluation and management, because it may be the initial symptom in critical vertebrobasilar thrombosis.
