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Please cite this article in press as: Guest, H., e stem-response measures to avoid audiomet In Guest et al. (2017), we tested for associations between tinnitus and electrophysiological measures of cochlear synaptopathy in young humans with normal hearing sensitivity. Tinnitus and control groups were matched closely for age, sex, and audiometric thresholds up to 14 kHz. The groups did not differ significantly in auditory-brainstem-response (ABR) or envelopefollowing-response (EFR) measures of synaptopathy. The matching of audiograms at extended high frequencies (EHFs) was intended to prevent confounding effects of EHF audiometric loss on brainstem-response measures. Such effects are, in our view, a potential pitfall in synaptopathy research, which tends to employ high stimulus levels that likely elicit contributions from the extreme cochlear base (for example, 120 dB pSPL in Gu et al., 2012; 130 dB peSPL in Liberman et al., 2016). Derived-band responses in humans indicate that ABR wave I is dominated by high-frequency generators, including those above 8 kHz (Don and Eggermont, 1978; Hardy et al., 2017), and increasingly so at high stimulus levels (Eggermont and Don, 1980). Hardy et al. (2017; personal communication, 10/02/17) recently demonstrated that both wave I amplitude and the ratio of wave I amplitude to wave V amplitude are reduced when noise high-pass filtered at 8 kHz is added to remove contributions from EHF regions. Their findings raise questions about apparent evidence for cochlear synaptopathy in humans, since such evidence has often been accompanied by EHF audiometric deficits (Gu et al., 2012; Liberman et al., 2016; Schaette and McAlpine, 2011), or even deficits at standard audiometric frequencies (Bramhall et al., 2017). However, it has come to our attention that control of audiometric factors in our tinnitus study might have come at a cost. Hickox et al. (2017) note that many animal models of synaptopathy additionally produce some degree of basal hair-cell loss. Liberman et al. (2016) posit that “high-frequency threshold elevation will be correlated with mid-frequency cochlear synaptopathy”. If this expectation is justified, then over-matching of audiometric thresholds in our study might have risked obscuring genuine differences in auditory nerve function between groups. Future research might usefully address this issue by allowing variation in EHF audiometric thresholds and preventing their direct influence on proxymeasures of synaptopathy through the application of high-pass masking