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. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: Neurosci Biobehav Rev. 2020 Dec 4;121:1–17. doi: 10.1016/j.neubiorev.2020.11.030

Figure 1.

Figure 1.

(A) Schematic of ascending information pathway in the central auditory system. Descending and recurrent connections have been omitted for simplicity. (B) Hypothesized model of enhanced central gain and hyperacusis in autism resulting from impaired brainstem transmission. Homeostatic upregulation of gain in the inferior colliculus (IC) results in excessive sound-evoked activity in the higher structures of the auditory system, including primary/secondary auditory cortex, the putative source of enhanced loudness perception. (C) Alternate model of enhanced central gain and hyperacusis in autism as a result of excitation/inhibition imbalance in the IC, thalamus, and/or auditory cortex. Notably, enhanced auditory cortical activity is likely sufficient to cause hyperacusis, and while other central auditory structures may contribute, pathology could feasibly be limited to cortical areas. SOC = Superior Olivary Complex.