Objectives: We sought to examine the relationship between the response to stressful stimuli in children with ASD both with and without gastrointestinal disorders or significant GI symptomatology. Galvanic skin response (GSR), a measure of eccrine gland activity, and electrocardiogram (ECG), a measure of the electrical signals of the heart, were used as indicators of sympathetic nervous system activation. Data were recorded for a baseline condition as well as in response to auditory and vibrotactile stimulation as well as cold temperature. We hypothesized that the response to stress in children and adolescents with ASD with a GI disorder or significant GI symptomatology would be higher than those with ASD alone. Furthermore, we sought to determine if the response to stress was independent of generalized sensory dysfunction.
Methods: Children and adolescents with an ASD diagnosis with a comorbid GI disorder, as assessed by the Pediatric Questionnaire on Pediatric Gastrointestinal Symptoms (QPGS-RIII), and those with ASD without a GI diagnosis or significant GI symptomatology had GSR and ECG data recorded for a baseline condition as well as independent conditions of auditory, vibrotactile, and cold temperature stimulation. Current sensory functioning in 7 different domains was assessed using a sensory questionnaire completed by the participant’s caregiver.
Results: An omnibus one-way ANOVA across all stress conditions, including baseline exposure to the testing environment, indicated that mean GSR was significantly higher for the ASD GI group. The same effect was revealed for ECG, where mean RR interval was lower (i.e., faster heart rate) for the ASD GI group. Total score on the sensory functioning questionnaire did not differ significantly among the groups. The effects on GSR and ECG remained significant after controlling for the effect of sensory functioning.
Conclusions: Preliminary results from our pilot study suggest that the psychophysiological response to sensory stimuli, as evidenced by GSR and ECG, may differ in those with ASD with a GI disorder or significant GI symptomatology relative to those with ASD alone. Moreover, these differences appear to be largely independent of generalized sensory dysfunction. Although our data indicate differences in physiological responding among the groups, a larger sample size is needed to determine if the effects can be substantiated. Identifying the aspects contributing to GI problems in ASD will be important for optimizing future treatment strategies.
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