A Heuristic Pathophysiological Model Of Tinnitus

1.  Tinnitus pathophysiology should explain both tinnitus distress and tinnitus intensity. 2.  Distress in tinnitus is most likely generated by an aspecific distress network consisting of the amygdala–anterior cingulate and anterior insula. 3.  Tinnitus intensity might be encoded by gamma band activity in the contralateral auditory cortex. 4.  This gamma band activity might result from thalamocortical dysrhythmia. 5.  Tinnitus distress can be seen as phase-synchronized co-activation of the auditory cortex activity and the aspecific distress network. 6.  For tinnitus to be perceived consciously, it requires the auditory cortex activity be embedded in a larger network. 7.  This larger network could be the global workspace, the self-perception network. 8.  The tinnitus network changes in time, hypothetically via an allostatic mechanism. 9.  In chronic tinnitus, the parahippocampus, insula, and dorsolateral prefrontal cortex networks are critical. 10.  The parahippocampus is involved via its auditory sensory gating mechanism, suppressing redundant auditory information.