The relation between Autism Spectrum Disorders (ASD) and Schizophrenia is a matter of intense debate and research, considering evidence of common neurobiological pathways in both disorders. A growing number of systematic studies on ASD report co-occuring psychiatric symptoms and disorders to be common in these patients, and from follow up studies we know that a significant number of patients within years after diagnosis develop psychosis or even schizophrenia. The diagnostic boundaries of autism and schizophrenia have moved outward over the years and similar to autism some authors also describe “a schizophrenia spectrum”. It seems to be that especially the broader phenotypes of these spectra may overlap. A large amount of literature reports on schizophrenic patient’s inability to discriminate relevant from irrelevant sensory information, a phenomenon termed “sensory filtering” (or sensory gating). Similarly, individuals with autism often demonstrate abnormal reactivity to sensory stimuli, a phenomenon that is pervasively present throughout life. One of the paradigms thought to reflect filtering of sensory information is the prepulse inhibition of the startle reflex (PPI), a psychophysiological paradigm which is believed to assess so called sensorimotor gating.
The aims of this study were to investigate whether schizophrenia-like deficits in sensorimotor gating, habituation and sensitization of the acoustic startle reflex are present in a group of children with ASD by comparing them with a group of matched neurotypically developed controls. An additional aim was to explore possible psychophysiological subgroups within our ASD population.
In a case-control design 35 ASD children, 8-12 years old, diagnosed according to DSM-IV-TR criteria and 40 matched NTD controls were tested with a psychophysiological tests battery. Parents to all participants completed the Social Communication Questionnaire (SCQ), Social Responsiveness Scale (SRS) and the Child Behaviour Checklist (CBCL).
PPI of the acoustic startle reflex was analyzed in 18 ASD cases and 34 NTD controls. Habituation and sensitization was analyzed in 23 ASD cases and 39 NTD controls. Patients with ASD did not display the usual drop in percentage PPI in trials with less intense prestimuli (76dB/120ms) as normally found in healthy controls. In addition, ASD cases showed significantly increased sensitization compared to controls.
Combined, our results may reflect the hypersensitivity of children with ASD to sensory information. The relation to PPI deficits as observed in schizophrenia is not apparent, although it cannot be excluded that a constantly hypersensitive filter in some ASD children might eventually collapse, resulting in sensory overload of higher brain processes as currently widely believed to be the case in schizophrenia patients. Future research should therefore study the developmental course of PPI deficits in ASD patients in a longitudinal design.