The functional anatomy of tinnitus

Abstract

We have used positron emission tomography to map the neural systems that mediate subjective tinnitus. In two studies, subjects altered their tinnitus by voluntary jaw muscle contraction or sustained lateral gaze. In the third, tinnitus was altered by intravenous lidocaine. These experiments all linked the loudness of tinnitus with unilateral spontaneous neural activity in auditory cortex. This unilaterality contrasts with the bilaterality of cortical responses during acoustic stimulation, evidence for a noncochlear central origin for tinnitus. Plasticity in the central auditory system, thought to be associated with deafferentation, was demonstrated in hearing-impaired or unilaterally deaf patients by the greater extent of auditory cortex activation by tonal stimuli when compared to normals. Other sensory and motor systems may interact with these aberrant pathways, further upsetting the balance of auditory system activity. This is manifested by patients’ reports of transient voluntary loudness and/or pitch control. In controls, lateral gaze suppressed auditory cortical activity: this cross-modal inhibition was absent in the patients. Subjective tinnitus appears to be due to spontaneous neural activity in aberrant central auditory pathways that have abnormal interactions with other sensory and motor systems. This complexity may explain the unresponsiveness of tinnitus to pharmacological interventions.