Semi-Automated Analysis of Peak Amplitude and Latency for Auditory Brainstem Response Waveforms Using R.

Many reports in the last 15 years have assessed changes in the auditory brainstem response (ABR) waveform after insults such as noise exposure. Common changes include reductions in the peak 1 amplitude and the relative latencies of the later peaks, as well as increased central gain, which is reflected by a relative increase in the amplitudes of the later peaks compared to the amplitude of peak 1. Many experimenters identify the peaks and troughs visually to assess their relative heights and latencies, which is a laborious process when the waveforms are collected in 5 dB increments throughout the hearing range for each frequency and condition. This paper describes free routines that may be executed in the open-source platform R with the RStudio interface to semi-automate the measurements of the peaks and troughs of auditory brainstem response (ABR) waveforms. The routines identify the amplitudes and latencies of peaks and troughs, display these on a generated waveform for inspection, collate and annotate the results into a spreadsheet for statistical analysis, and generate averaged waveforms for figures. In cases when the automated process misidentifies the ABR waveform, there is an additional tool to assist in correction. The goal is to reduce the time and effort needed to analyze the ABR waveform so that more researchers will include these analyses in the future.

Mutation of Foxo3 causes adult onset auditory neuropathy and alters cochlear synapse architecture in mice.

Auditory neuropathy is a form of hearing loss in which cochlear inner hair cells fail to correctly encode or transmit acoustic information to the brain. Few genes have been implicated in the adult-onset form of this disease. Here we show that mice lacking the transcription factor Foxo3 have adult onset hearing loss with the hallmark characteristics of auditory neuropathy, namely, elevated auditory thresholds combined with normal outer hair cell function. Using histological techniques, we demonstrate that Foxo3-dependent hearing loss is not due to a loss of cochlear hair cells or spiral ganglion neurons, both of which normally express Foxo3. Moreover, Foxo3-knock-out (KO) inner hair cells do not display reductions in numbers of synapses. Instead, we find that there are subtle structural changes in and surrounding inner hair cells. Confocal microscopy in conjunction with 3D modeling and quantitative analysis show that synaptic localization is altered in Foxo3-KO mice and Myo7a immunoreactivity is reduced. TEM demonstrates apparent afferent degeneration. Strikingly, acoustic stimulation promotes Foxo3 nuclear localization in vivo, implying a connection between cochlear activity and synaptic function maintenance. Together, these findings support a new role for the canonical damage response factor Foxo3 in contributing to the maintenance of auditory synaptic transmission.

Sensory filtering phenomenology in PTSD.

Disrupted sensory filtering, or problems with suppressing irrelevant environmental sensory stimuli, has been reported in individuals with posttraumatic stress disorder (PTSD). However, the relationship of sensory filtering deficits to specific PTSD symptoms versus an association with general trauma exposure is unclear. These relationships were examined by administering self-report measures of trauma exposure, PTSD, and sensory gating phenomenology to undergraduate participants with PTSD (n=32), with trauma history but without PTSD (n=144), and with minimal trauma history (n=153). Subjects with PTSD reported greater filtering disruption than individuals in the trauma only and low trauma groups, who did not differ. Individuals endorsing reexperiencing and numbing symptoms, and females endorsing hypervigilance, reported disrupted sensory filtering phenomenology. These results suggest that impaired filtering differentiates between individuals with PTSD symptoms and asymptomatic individuals exposed to multiple traumas and low-trauma controls.

P50 sensitivity to physical and psychological state influences.

Although P50 is described as a largely preattentive process, increasing evidence suggests that the psychological state of a participant may influence P50 and its suppression. A paired-stimulus paradigm was used to examine the contributions of variability in stimulus parameters and state factors, such as expectancy and vigilance, on P50. Results obtained from 34 healthy subjects indicate that stimulus intensity and background stimulus intensity influenced P50 amplitude whereas stimulus duration had no significant impact. Importantly, P50 suppression varied with fluctuations in P50 amplitude to the first stimulus, and both P50 and its suppression reflected possible declines in attention or vigilance over the course of the session. Findings from this study suggest that P50 is not entirely preattentional and may reflect the psychological state of a participant. Implications of these results for research with schizophrenia patients are discussed.