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. Adjacent perfusion asymmetries involving the frontal, temporal and parietal lobes suggest a interneuronal network resulting in the transition of the sensory to the affect components of the symptom of tinnitus. It is hypothesized that a fundamental function of the amygdala - hippocampal structures is the establishment of a paradoxical auditory memory for tinnitus. It is a result of alteration in auditory masking found in all tinnitus patients. A paradoxical memory for an aberrant auditory signal i.e., tinnitus, is considered to be the initial process in the transition of the sensory to the affect component. 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 phenomena. The overall hypothesis of a final common pathway for tinnitus; the role of the MTLS; and clinical support for this hypothesis is presented.