Life-threatening tinnitus

Abstract

A 68-year-old woman presented in October, 1998, with an 8-week history of tinnitus and dizziness. She had no history of cardiovascular, or neurological disease. Computed tomography (CT) scan of the head was not diagnostic. She returned 3 weeks later with new symptoms of altered taste sensation, dysphagia, left-sided numbness, unsteady gait, and diplopia. She had no vertigo, nausea, vomiting, fevers, headaches, or anorexia. There was no history of changes in personality, mood, or cognitive decline, or of seizures. She had lost 7 kg in weight over the past 6 months. Heart rate, blood pressure, temperature, mental state examination and speech were normal. The pupils were reactive and symmetrical. Fundoscopic examination was normal. She had a slow gaze to the left with a 1 syndrome (one eye was fixed in the midline, the other eye could only make abducting movements with horizontal nystagmus in the direction of the abduction). She had decreased left facial sensation and a diminished left corneal reflex. The cranial nerves were otherwise normal. Muscle tone and power were normal. Heel to skin testing was adequate but finger to nose was dysmetric on the left side. She had decreased light touch sensation on the left side of the body. Deep tendon reflexes were normal and symmetrical and the plantar response was flexor bilaterally. The patient’s gait was wide based with severe truncal ataxia. Full blood count, peripheral blood smear, coagulation tests, a biochemistry profile, serum vitamin B12 and folate, thyroid function tests, erythrocyte sedimentation rate, Creactive protein, antinuclear antibodies, antineutrophil cytoplasmic antibody, rheumatoid factor, complement levels for C3 and C4, serum protein electrophoresis, cryoglobulins, and quantitative serum immunoglobulins were normal. Cerebrospinal fluid (CSF) analysis showed protein 0·65 g/L and glucose 4·2 mmol/L, 139 red cells and nine white cells per L (mostly lymphocytes with a few atypical cells). There was no immunological evidence of syphilis (VDRL). CSF cultures and polymerase chain reactions for herpes and cytomegalovirus were negative. Oligoclonal bands were absent. Doppler study of carotid and vertebro-basilar arteries was normal. Gadoliniumenhanced magnetic resonance imaging (MRI) of the head showed bilateral contrast enhancement in the medial aspects of the temporal lobes in the amygdala and hippocampi, as well as in the posterior aspect of the medulla, pons, and midbrain (figure). The imaging was diagnostic for limbic and bulbar encephalitis. CASE REPORT