Assessment & Research

Interaction of finger representations in the cortex of individuals with autism: a functional window into cortical inhibition.

Coskun et al. (2013) · Autism research : official journal of the International Society for Autism Research 2013
★ The Verdict

Adults with autism show normal fast finger-inhibition in MEG, so the “low cortical inhibition” marker needs an age and method check.

✓ Read this if BCBAs who assess sensory processing in teens or adults with autism.
✗ Skip if Clinicians only working with young children or non-autistic populations.

01Research in Context

01

What this study did

The team used MEG to watch brain waves in young adults with autism. They tapped two fingers very fast and looked for a sign of cortical inhibition. The same test was done with neurotypical adults for comparison.

02

What they found

The slope of the brain response was the same in both groups. There was no sign of weak cortical inhibition in the autism group. The old idea of “low inhibition” in the somatosensory cortex did not hold up.

03

How this fits with other research

Rojahn et al. (2012) saw dampened brain waves in children with autism, but those kids were only 8-11 years old. The new study tested adults, so the clash may simply mark a developmental shift, not a true conflict.

Taylor et al. (2017) and Sapey-Triomphe et al. (2019) both found lower GABA in the sensorimotor cortex of people with autism. The new MEG data do not deny those GABA drops; they just show the drop does not break the fast finger-inhibition circuit you can measure with MEG.

Tannan et al. (2008) first claimed tactile disinhibition in adults using a touch-adaptation task. The null MEG result updates that claim: the cortex can still inhibit, at least when probed by rapid finger taps.

04

Why it matters

If you screen sensory issues, do not assume every adult with autism has a fixed “low inhibition” brain mark. A quick MEG finger test may not be the biomarker we hoped for. Keep watching GABA and behavior, but drop the blanket label.

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Pair any sensory questionnaire with a simple timed tactile task instead of assuming a brain-based inhibition deficit.

02At a glance

Intervention
not applicable
Design
quasi experimental
Population
autism spectrum disorder, neurotypical
Finding
null

03Original abstract

An established neural biomarker of autism spectrum disorder (ASD) has the potential to provide novel biological and pharmacological targets for treatment. Lower level of inhibition in brain circuits is a leading biomarker candidate. A physiological investigation of the functional levels of inhibition in the cortex of individuals with autism can provide a strong test of the hypothesis. The amplitude of cortical response to the stimulation of adjacent fingers is controlled by the level of cortical inhibition and provides just such a test. Using magnetoencephalography, we recorded the response of the somatosensory cortex to the passive tactile stimulation of the thumb (D1), and index finger (D2), and to the simultaneous stimulation of both fingers combined (D1,D2) of the dominant (right) hand of young subjects with and without autism. For each participant, we measured the response to the stimulation of both fingers combined (D1,D2) relative to the post hoc sum of the responses to the stimulation of each finger alone (D1+D2) in multiple different ways and linearly regressed the ASD and neurotypical (NT) groups' responses. The resulting slopes were then compared: Smaller slope values imply attenuated response to paired finger stimulation, and enhanced levels of inhibition. The short-latency M40 and mid-latency M80 response slopes of the group with autism obtained in different ways were either significantly smaller, or statistically indistinguishable from NT. The result does not support reduced inhibition in the somatosensory cortex of individuals with autism, contrary to the seminal hypothesis of reduced inhibition. Implications are discussed including refinements of current theory.

Autism research : official journal of the International Society for Autism Research, 2013 · doi:10.1002/aur.1314