Sensorimotor Gating Variability in ASD with and without Epilepsy Comorbidity May Indicate a Sensory Treatment Target.

Oral Presentation
Friday, May 11, 2018: 11:20 AM
Grote Zaal (de Doelen ICC Rotterdam)
J. J. Sprengers1, E. Juarez2, D. M. van Andel1, C. Vlaskamp3, K. Linkenkaer-Hansen4, H. Bruining5 and B. Oranje3, (1)Brain Center Rudolf Magnus, Department of Psychiatry, UMC Utrecht, Utrecht, Netherlands, (2)CNCR, VU Medical Center, Amsterdam, Amsterdam, Netherlands, (3)Department of Psychiatry, Brain Center Rudolf Magnus, NICHE Lab, University Medical Center Utrecht, Utrecht, Netherlands, (4)Department of Integrative Neurophysiology, CNCR, VU University Amsterdam, Amsterdam, Netherlands, (5)Brain Centre Rudolf Magnus, Amsterdam, Netherlands

An increasing role for sensory dysfunctions is indicated in the pathogenesis of Autism Spectrum Disorder (ASD). The nature and severity of these dysfunctions in ASD may indicate specific subtypes and treatment targets. Event related potential (ERP) EEG paradigms in relation to clinical manifestations of ASD offer a framework to characterize and dissect sensory dysfunctions. Sensorimotor gating is an unconscious early sensory processing mechanism and found abnormal earlier in children with epilepsy. As proof of principle, we tested whether sensory gating deficits are influenced by focal EEG abnormalities and epilepsy comorbidities in ASD.


To test the association between sensorimotor gating abnormalities and epilepsy comorbidity in children with ASD.


90 children aged 7-12 with an IQ above 70 and atypical sensory behavior (60 diagnosed with autism spectrum disorder (ASD), 30 diagnosed with epilepsy and ASD comorbidity) and 30 typically developing children aged were investigated. Sensory behavioral abnormalities (SP-NL, ABC-I, ADOS and SRS), quantitative and qualitative EEG parameters (p50, resting state and focal abnormality grading) were assessed. Comparative statistical analyses were used to test whether abnormal p50 suppression coincided with epilepsy diagnosis or focal abnormality grades and associated with different behavioural outcomes.


Sensory gating abnormalities were more frequent amongst children diagnosed with epilepsy and in children who showed focal EEG abnormalities. Presence of p50 abnormalities or epilepsy comorbidity seemed not to associated with autism severity or sensory abnormalities.


Sensory gating abnormalities seem to be more frequent in ASD patients with epilepsy comorbidity. This association may elude to common mechanisms between ASD and epilepsy syndromes as has been hypothesized previously. Future studies may attempt to correct sensory gating deficits in ASD with antiepileptic treatment, especially when epielptiform abnormalities are noted in the EEG of children with ASD.