Click-evoked auditory brainstem responses and autism spectrum disorder: a meta-analytic investigation of disorder specificity.

Background Click-evoked auditory brainstem response (ABR) alterations are associated with autism spectrum disorder (ASD), but the specificity of these findings to the disorder is unclear. We therefore performed a meta-analysis on ABRs and attention-deficit/hyperactivity disorder (ADHD), a neurodevelopmental disorder that shares some etiologic and symptom overlap with ASD. Methods Seven papers compared ABR latency components (I, III, V, I-III, III-V, and I-V) between participants with and without ADHD. We used random-effects regression to generate component-specific estimates (Hedges's g) that adjusted for study sample sizes and the number of studies contributing to each estimate. We compared these estimates to our recently published meta-analysis of ABRs and ASD. Results All ADHD studies employed cross-sectional designs. ADHD was associated with longer latencies for waves III and V (g = 0.6, 95% confidence interval (CI) 0.3, 1.0 and g = 0.6, 95% CI 0.3, 0.9) and waves I-III and I-V (g = 0.7, 95% CI 0.2, 1.3 and g = 0.6, 95% CI 0.3, 1.0). Effect sizes from the ASD and ADHD meta-analyses did not differ from each other. Conclusions Similar patterns of ABR alterations are observed in ADHD and ASD. However, studies rarely screen for middle ear dysfunction or hearing loss and rely upon cross-sectional designs. Addressing these issues will inform the viability of ABRs as a prognostic and/or etiologic biomarker for these disorders. Impact Click-evoked ABR alterations are associated with ASD, but the specificity of these findings to the disorder is unclear. We therefore performed a meta-analysis of the association between ABRs and ADHD, a disorder that shares some etiologic and symptom overlap with ASD. ADHD was associated with longer ABR latencies for several components. These components are identical to those implicated in ASD. Effect sizes were similar in magnitude across disorders. The viability of ABRs as prognostic and/or etiologic biomarkers for neurodevelopmental risk requires addressing limitations in the literature (e.g., cross-sectional data, non-standardized ABR protocols, minimal characterization of symptom heterogeneity).