Common Sensory Endophenotypes Spanning Sensory Processing Disorder and the Autism Spectrum

Thursday, May 12, 2016: 1:45 PM
Room 307 (Baltimore Convention Center)
J. J. Foxe1,2 and S. Molholm3, (1)Albert Einstein College of Medicine, Bronx, NY, (2)Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, NY, (3)Neuroscience and Pediatrics, Albert Einstein College of Medicine, Bronx, NY

Sensory-processing anomalies constitute a hallmark symptom domain of the ASDs, but similar sensory symptoms are often observed in other neurodevelopmental disorders (e.g. Obsessive Compulsive Disorder, Attention Deficit Hyperactivity Disorder), suggesting some shared genetic liability and the possibility of common endophenotypes. There is also emerging recognition amongst clinicians and researchers that there exists a substantial cohort of children who do not meet diagnostic criteria for a categorical neurodevelopmental disorder, but nonetheless manifest clinical levels of hypo- or hyper-sensitivity to sensory inputs. These otherwise typical children with sensory processing disorder (SPD) are of specific interest to the research community in that the restriction of their pathology to the sensory processing domain allows for study of a relatively “purified” phenotype.


To assess both basic unisensory and multisensory processing in SPD with the use of psychophysics and high-density electrophysiological recordings of brain activity, and compare with unisensory and multisensory processing in neurotypical controls and individuals with ASD.

Methods: N/A


Study 1: Somatosensory evoked potentials (SEPs) to trains of stimuli delivered at varying presentation rates (ISIs ranging from 150ms to 1050ms) were examined to determine whether differences in the initial registration and processing of tactile inputs might account, in part, for aberrant reactions to the sensory environment. Thirteen children with SPD (5.3 - 15.2 years) and 13 matched neurotypicals produced SEPs that were similar in their temporal and spatial properties.  Clear between-group differences in SEP amplitude as a function of stimulation rate were observed, and these were most apparent in later phases of sensory processing (130-195ms).  Response slopes as a function of ISI suggested a steeper slope for the SPD group, due to greater increase in response amplitude as ISI increased.  These findings suggest a potential neural mechanism for the increased reactivity to tactile inputs observed in SPD.

Study 2: High-density ERPs interrogated multisensory integration (MSI) in three groups of fourteen age- and IQ-matched children: those with ASD, those with SPD, and neurotypical individuals. Participants responded as quickly as possible to unisensory-visual, unisensory-auditory or bisensory-audiovisual stimuli. Probing the behavioral data for evidence of MSI (i.e., race model violation) indicated clear separation between the two clinical groups and the TD children, and analysis of the electrophysiological data subtly distinguished children in the ASD group from their peers in the TD and SPD groups.

Study 3: It is now well-established that children with an ASD show severe deficits in their ability to integrate seen and heard speech. Children with SPD do not show the social communication deficits that are part of the diagnostic criteria for an ASD.  Here we asked whether they would also show deficits in multisensory speech integration under noisy environmental conditions. Monosyllabic words were presented in different levels of noise, which were sometimes accompanied  by videos of the person articulating the word.   Comparing performance measures of 12 SPD children to 12 matched neurotypical controls, we find a clear deficit in multisensory speech integration.


Collectively, these studies point to clear anomalies in sensory processing across three modalities in SPD children.