(A) Experimental results suggest that different mechanisms of HHL, myelinopathy (left) and noise exposure resulting in synaptopathy (middle), affects ABR peak 1 (P1) in distinct ways: Myelinopathy increases ABR P1 latency and decreases ABR P1 amplitude, while synaptopathy induced by noise exposure decreases ABR P1 amplitude only, without any change in latency. Combined myelinopathy and synaptopathy induced by noise exposure show additive effects (right, data taken from [8]; *p<0.05, **p<0.01, #p<0.001). Figures in panels (B) and (C) taken from [8] show ABR P1 measures evoked by 11.3kHz sound stimuli at various sound levels for control and myelinopathy cases (*** p < 0.001 by two-way ANOVA). The decrease in ABR P1 amplitude (B) in case of myelinopathy is more pronounced for higher sound levels, whereas ABR P1 latencies (C) are increased for all sound levels. (D) Schematic illustration of type I SGNs, bipolar neurons innervating IHCs via myelinated peripheral projections. (E, F) Simulated peripheral fibers of type I SGNs (SGN fiber) consist of an unmyelinated segment at the peripheral end adjacent to the site of IHC synapses, followed by a heminode and 5 myelin sheaths with 4 nodes between them. Two mechanisms of hidden hearing loss are simulated: (E) synaptopathy, modeled by removing IHC-AN synapses, and (F) myelinopathy, modeled by varying the lengths of the unmyelinated segment (Lu) or the heminode (Lh).