A preliminary transcranial magnetic stimulation study of cortical inhibition and excitability in high-functioning autism and Asperger disorder
Article first published online: 29 MAR 2010
© The Authors. Journal compilation © Mac Keith Press 2010
Developmental Medicine & Child Neurology
Volume 52, Issue 8, pages e179–e183, August 2010
How to Cite
ENTICOTT, P. G., RINEHART, N. J., TONGE, B. J., BRADSHAW, J. L. and FITZGERALD, P. B. (2010), A preliminary transcranial magnetic stimulation study of cortical inhibition and excitability in high-functioning autism and Asperger disorder. Developmental Medicine & Child Neurology, 52: e179–e183. doi: 10.1111/j.1469-8749.2010.03665.x
- Issue published online: 8 JUL 2010
- Article first published online: 29 MAR 2010
- PUBLICATION DATA Accepted for publication 2nd February 2010. Published online
Aim Controversy surrounds the distinction between high-functioning autism (HFA) and Asperger disorder, but motor abnormalities are associated features of both conditions. This study examined motor cortical inhibition and excitability in HFA and Asperger disorder using transcranial magnetic stimulation (TMS).
Method Participants were diagnosed by experienced clinicians strictly according to DSM-IV criteria. Participants with HFA (nine males, two females; mean age 16y 8mo, SD 4y 5mo) or Asperger disorder (11 males, three females; mean age 19y 1mo, SD 4y 2mo) and neurotypical participants (eight males, three females; mean age 19y 0mo, SD 3y 1mo) were administered a paired-pulse TMS paradigm intended to assess motor cortical inhibition and excitability. Responses to TMS were recorded by electromyography.
Results Cortical inhibition was significantly reduced in the HFA group compared with both the Asperger disorder (p<0.001) and neurotypical (p<0.001) groups, suggesting disruption of activity at gamma-aminobutyric acid A (GABAA) receptors. There was no group difference in cortical excitability.
Interpretation Cortical inhibition deficits may underlie motor dysfunction in autism, and perhaps even relate to specific clinical symptoms (e.g. repetitive behaviours). These findings provide novel evidence for a possible neurobiological dissociation between HFA and Asperger disorder based on GABAergic function.