Conflict of interest: All authors declare no conflict of interest.
Increased Prepulse Inhibition and Sensitization of the Startle Reflex in Autistic Children
Article first published online: 4 OCT 2013
© 2013 International Society for Autism Research, Wiley Periodicals, Inc.
Volume 7, Issue 1, pages 94–103, February 2014
How to Cite
Madsen, G. F., Bilenberg, N., Cantio, C. and Oranje, B. (2014), Increased Prepulse Inhibition and Sensitization of the Startle Reflex in Autistic Children. Autism Res, 7: 94–103. doi: 10.1002/aur.1337
Funding: This study was supported by The Psychiatric Research Foundation in the Region of Southern Denmark grant 09-5810; Gangsted Foundation grant 1415-8436, and Fru Hermansens Foundation grant 00962-0001.
- Issue published online: 24 FEB 2014
- Article first published online: 4 OCT 2013
- Manuscript Accepted: 3 SEP 2013
- Manuscript Received: 10 DEC 2012
- Psychiatric Research Foundation in the Region of Southern Denmark. Grant Number: 09-5810
- Gangsted Foundation. Grant Number: 1415-8436
- Fru Hermansens Foundation. Grant Number: 00962-0001
- autism spectrum disorders;
- sensorimotor gating;
- auditory processing
The relation between autism spectrum disorders (ASD) and schizophrenia is a subject of intense debate and research due to evidence of common neurobiological pathways in the two disorders. The objective of this study was to explore whether deficits in prepulse inhibition (PPI) of the startle reflex, as usually seen in schizophrenic patients, can be replicated in a group of children with ASD in comparison with a group of matched neuro-typically developed (NTD) controls. An additional aim was to explore possible psychophysiological subgroups within our ASD sample. In a case-control design, 35 ASD patients and 40 matched NTD controls were tested in a psychophysiological test battery. The PPI of the acoustic startle reflex was analyzed in 18 ASD subjects and 34 NTD controls. Habituation and sensitization were analyzed in 23 ASD subjects and 39 NTD controls. In trials with less intense prestimuli (76 dB), patients with ASD did not display the drop in percentage PPI normally found in healthy controls. In addition, ASD patients showed significantly increased sensitization compared with NTD controls. Combined, our results may reflect the hypersensitivity to sensory information in children with ASD. The relation to PPI deficits observed in schizophrenia is not apparent. Future research should study the developmental course of PPI deficits in ASD patients in a longitudinal design. Autism Res 2014, 7: 94–103. © 2013 International Society for Autism Research, Wiley Periodicals, Inc.