Figure 4.

Schematic accounting for the symptom cluster triggered by an acoustic shock. The acoustic shock may lead to TTM overuse and injury and inflammatory processes. This activates the trigeminal pathway which is associated with pain and tinnitus (potentially through modulating activity of DCN neurons or stria vascularis). The activation of the TGN can activate the parasympathetic pathway through the parasympathetic-trigeminal reflex. This may explain the autonomic symptoms such as blocked nose and tympanum hyperemia. Moreover, the wide dynamic range neurons of the TCC integrate inputs from the head–neck complex, which may account for referred pain in the temporal and neck region. Finally, the sympathetic system may maintain and amplify pain by interfering with the nociceptor activity. ACC = anterior cingulate cortex, PH = posterior hypothalamus, LC = locus cœruleus, PAG = periaqueductal gray, CN = cochlear nucleus, TGG = trigeminal ganglion; TGN = trigeminal nerve.