Garrett Cardon

The majority of autistic individuals express sensory differences, which can occur in any sensory modality. Unfortunately, the neural underpinnings of sensory atypicalities are not fully understood, especially with regard to modality-specific function. Thus, we aimed to examine neural correlates of modality-specific sensory difficulties across autistic and non-autistic children. We hypothesized patterns of connectivity between supramodal and sensory brain regions, which would correlate with sensory differences in the visual, auditory, tactile, and taste/smell modalities. To this end, autistic (n=30) and non-autistic (n=26) children (6-11 years) underwent resting-state fMRI scans while their caregivers completed the Short Sensory Profile (SSP). Analysis involved computing functional network connectivity patterns between hypothesis-related independent component networks and all other voxels, and their association with behavioral responses. Results largely revealed patterns of connectivity between supramodal and higher order sensory brain regions, such as the cerebellum, medial prefrontal cortex, superior parietal lobule, and supramarginal gyrus, each correlating with questionnaire responses from one or more sensory modalities. Combined, our findings are consistent with a proposed prediction network implicated in sensory processing. We conclude that sensory difficulties, while perhaps underpinned by modality-specific patterns of functional connectivity, may also arise from supramodal neural dynamics, especially those associated with prediction.

Purpose: Autistic individuals frequently experience sensory processing difficulties. Such difficulties can significantly impact important functions and quality of life. We are only beginning to understand the neural mechanisms of atypical sensory processing. However, one established way to measure aspects of auditory function is the auditory brainstem response (ABR). While ABR has been primarily hypothesised thus far as a means of early detection/diagnosis in autism, it has the potential to aid in examining sensory processing in this population. Method: Thus, we investigated standard ABR waveform characteristics in age-matched groups of autistic and typically developing children during various stimulus and intensity conditions. We also examined within ear waveform cross-correlations and inter-aural cross-correlations (IACC) to assess replicability and synchrony of participants’ ABRs, which was a novel approach to ABR analysis in this population. Results: We observed longer peak latencies (esp. wave III and V) and interpeak latencies in the autism and typically developing groups in different conditions. There were no statistically significant results in cross-correlation or IACC. Conclusions: These results suggest that brainstem auditory function may differ slightly, but is mostly similar, between autistic and typically developing children. We discuss these findings in terms of their implications for sensory processing and future utility.

Purpose: Auditory threshold estimation using the auditory brainstem response or auditory steady state response is limited in some populations (e.g., individuals with auditory neuropathy spectrum disorder [ANSD] or those who have difficulty remaining still during testing and cannot tolerate general anesthetic). However, cortical auditory evoked potentials (CAEPs) can be recorded in many such patients and have been employed in threshold approximation. Thus, we studied CAEP estimates of auditory thresholds in participants with normal hearing, sensorineural hearing loss, and ANSD. Method: We recorded CAEPs at varying intensity levels to speech (i.e., /ba/) and tones (i.e., 1 kHz) to estimate auditory thresholds in normal-hearing adults ( n = 10) and children ( n = 10) and case studies of children with sensorineural hearing loss and ANSD. Results: Results showed a pattern of CAEP amplitude decrease and latency increase as stimulus intensities declined until waveform components disappeared near auditory threshold levels. Overall, CAEP thresholds were within 10 dB HL of behavioral thresholds for both stimuli. Conclusions: The above findings suggest that CAEPs may be clinically useful in estimating auditory threshold in populations for whom such a method does not currently exist. Physiologic threshold estimation in difficult-to-test clinical populations could lead to earlier intervention and improved outcomes.

Under conditions of profound sensory deprivation, the brain has the propensity to reorganize. For example, intact sensory modalities often recruit deficient modalities’ cortices for neural processing. This process is known as cross-modal reorganization and has been shown in congenitally and profoundly deaf patients. However, much less is known about cross-modal cortical reorganization in persons with less severe cases of age-related hearing loss (ARHL), even though such cases are far more common. Thus, we investigated cross-modal reorganization between the auditory and somatosensory modalities in older adults with normal hearing (NH) and mild-moderate ARHL in response to vibrotactile stimulation using high density electroencephalography (EEG). Results showed activation of the somatosensory cortices in adults with NH as well as those with hearing loss (HL). However, adults with mild-moderate ARHL also showed robust activation of auditory cortical regions in response to somatosensory stimulation. Neurophysiologic data exhibited significant correlations with speech perception in noise outcomes suggesting that the degree of cross-modal reorganization may be associated with functional performance. Our study presents the first evidence of somatosensory cross-modal reorganization of the auditory cortex in adults with early-stage, mild-moderate ARHL. Our findings suggest that even mild levels of ARHL associated with communication difficulty result in fundamental cortical changes.

Objective: Auditory neuropathy spectrum disorder (ANSD) affects approximately 5–15% of children with sensorineural hearing loss (SNHL). ANSD is characterized by the presence of otoacoustic emissions (OAE) and an absent or abnormal auditory brainstem response (ABR). The purpose of this study was to investigate the prognostic value of slow-rate ABR in predicting the auditory cortical development and auditory speech perception outcomes in case studies of children with ANSD. Design: ABR waveform characteristics were collected at slow stimulation rates (5.1 clicks/second) and a fast stimulation rates (>11–31.1 clicks/second, rates typically used in a clinical setting) in three case reports of children with ANSD. P1 CAEP responses and measures of auditory speech perception using the Infant Toddler Meaningful Auditory Integration Scale (IT-MAIS) were also collected in these children. Retrospective analysis was performed to evaluate the prognostic value of slow- versus fast-rate ABR in predicting P1 CAEP responses and auditory speech perception outcomes in these children. Study sample: Participants included case reports of three paediatric participants with a clinical diagnosis of ANSD. Results: Slow-rate ABR did not elicit significant improvements in waveform morphology compared to fast-rate ABR. P1 CAEP results were present in 2 out of 3 cases and were consistent with auditory speech perception outcomes. Conclusions: Even when ABR stimulation rates were slowed, ABR responses in these children with ANSD did not display any characteristic or replicable pattern, and ABR responses were not predictive of cortical auditory maturation or behavioural performance. In contrast, P1 CAEP responses provided valuable information regarding the maturational status of the auditory cortex and P1 CAEP responses were consistent with behavioural measures of auditory speech perception. Overall, results highlight the high prognostic value of P1 CAEP testing when used in conjunction with behavioural measures of auditory speech perception in children with ANSD.

Sensory dysfunction is a core symptom of autism spectrum disorder (ASD), and abnormalities with sensory responsivity and processing can be extremely debilitating to ASD patients and their families. However, relatively little is known about the underlying neuroanatomical and neurophysiological factors that lead to sensory abnormalities in ASD. Investigation into these aspects of ASD could lead to significant advancements in our general knowledge about ASD, as well as provide targets for treatment and inform diagnostic procedures. Thus, the current study aimed to measure the covariation of volumes of brain structures (i.e., structural magnetic resonance imaging) that may be involved in abnormal sensory processing, in order to infer connectivity of these brain regions. Specifically, we quantified the structural covariation of sensory-related cerebral cortical structures, in addition to the cerebellum and amygdala by computing partial correlations between the structural volumes of these structures. These analyses were performed in participants with ASD (n = 36), as well as typically developing peers (n = 32). Results showed decreased structural covariation between sensory-related cortical structures, especially between the left and right cerebral hemispheres, in participants with ASD. In contrast, these same participants presented with increased structural covariation of structures in the right cerebral hemisphere. Additionally, sensory-related cerebral structures exhibited decreased structural covariation with functionally identified cerebellar networks. Also, the left amygdala showed significantly increased structural covariation with cerebral structures related to visual processing. Taken together, these results may suggest several patterns of altered connectivity both within and between cerebral cortices and other brain structures that may be related to sensory processing.