A Final Common Pathway for Tinnitus - Implications for Treatment

A final common pathway for tinnitus is hypothesized to exist for all patients with tinnitus. Its function is the transition of the sensory to the affect component of the symptom of tinnitus. Single Photon Emission Computerized Tomography (SPECT) with the radio isotope TC99-HMPAO has identified side to side perfusion asymmetries highlighted by that of the amygdala - hippocampal complex. It is hypothesized that a fundamental function of the amygdala - hippocampal structures is the establishment of a paradoxical auditory memory for tinnitus i.e., an aberrant auditory signal. It is a result of alteration in normal auditory masking; and found in all tinnitus patients. Underlying mechanisms are hypothesized to exist and to be highlighted by a diminution of inhibition mediated by gamma aminobutyric acid (GABA) due to disconnection from excitatory (glutamate) inputs. Blockage of GABA mediated inhibition results in Tinnitogenesis, a epileptiform auditory phenomenon. Significant neurochemistry implications for treatment are suggested by the Final Common Pathway for Tinnitus. The overall hypothesis of a final common pathway for tinnitus; and the clinical implications for treatment are presented.