The objective was to examine the neurophysiological manifestations of auditory hypersensitivity among people with sensory hypersensitivity, according to their sensory profile.

Auditory hypersensitivity is one expression of sensory processing disorders (SPDs) that consists of intolerance to ordinary environmental sounds. The negative impact of hypersensitivity on the person’s performance, participation, and quality of life raises the need to deeply explore its underlying neural mechanisms. This may serve as a platform for developing additional evaluations and adequate treatment. In occupational therapy, event-related potentials (ERPs) have been used to test SPDs, and the results suggest that neural gating is impaired in individuals with SPDs. However, this study included individuals with other comorbidities (e.g., attention-deficit/hyperactivity disorder [ADHD]), and generalizing the results is difficult. The present study aimed to elaborate the knowledge about the central nervous system (CNS) involvement in SPDs by examining cortical responses to sound intensity changes. The N1 and P2 ERP components are associated with auditory perception of stimulus change.

Significant amplitude differences will be found in ERP components N1/P2 between participants with sensory hypersensitivity and the control group in response to changes in intensity.

This study used a prospective cohort design. Thirty-four adults matched by age and gender were assigned according to their cutoff score in the Sensory Sensitivity quadrant of the Adolescent/Adult Sensory Profile. All had bilateral normal hearing and no ADHD, chronic diseases, or learning disability conditions.

The Adolescent/Adult Sensory Profile served for identifying people with hypersensitivity by including those with above normal levels in the Sensory Sensitivity quadrant. ERP was recorded from 21 channels. Average waveforms were computed separately and for each subject and across subjects to obtain grand mean waveforms. ERP analysis included measurement of N1 and P2 amplitudes.

Ethical approval for the procedure was received. All the participants who complied with the inclusion criteria were invited to the clinical center in Haifa University. Measuring the neurophysiological manifestations of auditory hypersensitivity may create a theoretical and practical platform for further exploration, may facilitate the establishment of SPDs as an accepted diagnostic entity in tools such as the Diagnostic and Statistical Manual of Mental Disorders (DSM), and may improve multidisciplinary collaboration.

The analysis used repeated-measures analysis of variance (ANOVA) and t tests. N1 did not exhibit a significant difference or a consistent trend. P2 amplitudes of the SPD group were consistently larger yet did not reach statistical significance. The basic ability to detect change was not statistically different between the groups. However, the response to the early perceived affective attributes of the stimulus was enhanced in the SPD group. This may explain the experiencing of benign sensory stimuli as threatening or painful.

CNS manifestation may include overexcitation and lower adaptation to stimuli and may explain the difficulties in daily life performance. Limitations of the study include a relatively small sample and inclusion of individuals with variable severities of hypersensitivity.