ResearchMEG event-related desynchronization and synchronization deficits during basic somatosensory processing in individuals with ADHDColleen Dockstader1 , William Gaetz2 , Douglas Cheyne1,2 , Frank Wang1 , F Xavier Castellanos3 and Rosemary Tannock1,4  1Neurosciences and Mental Health Program, The Hospital for Sick Children, Toronto, Canada 2Department of Diagnostic Imaging, The Hospital for Sick Children, Toronto, Canada 3Child Study Center, New York University, New York, USA 4Human Development & Applied Psychology, Ontario Institute for Studies in Education, Toronto, Canada author email corresponding author email
Behavioral and Brain Functions 2008,
4:8doi:10.1186/1744-9081-4-8
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| Published: |
12 February 2008 |
Abstract
Background
Attention-Deficit/Hyperactivity Disorder (ADHD) is a prevalent, complex disorder which is characterized by symptoms of inattention, hyperactivity, and impulsivity. Convergent evidence from neurobiological studies of ADHD identifies dysfunction in fronto-striatal-cerebellar circuitry as the source of behavioural deficits. Recent studies have shown that regions governing basic sensory processing, such as the somatosensory cortex, show abnormalities in those with ADHD suggesting that these processes may also be compromised.
Methods
We used event-related magnetoencephalography (MEG) to examine patterns of cortical rhythms in the primary (SI) and secondary (SII) somatosensory cortices in response to median nerve stimulation, in 9 adults with ADHD and 10 healthy controls. Stimuli were brief (0.2 ms) non-painful electrical pulses presented to the median nerve in two counterbalanced conditions: unpredictable and predictable stimulus presentation. We measured changes in strength, synchronicity, and frequency of cortical rhythms.
Results
Healthy comparison group showed strong event-related desynchrony and synchrony in SI and SII. By contrast, those with ADHD showed significantly weaker event-related desynchrony and event-related synchrony in the alpha (8–12 Hz) and beta (15–30 Hz) bands, respectively. This was most striking during random presentation of median nerve stimulation. Adults with ADHD showed significantly shorter duration of beta rebound in both SI and SII except for when the onset of the stimulus event could be predicted. In this case, the rhythmicity of SI (but not SII) in the ADHD group did not differ from that of controls.
Conclusion
Our findings suggest that somatosensory processing is altered in individuals with ADHD. MEG constitutes a promising approach to profiling patterns of neural activity during the processing of sensory input (e.g., detection of a tactile stimulus, stimulus predictability) and facilitating our understanding of how basic sensory processing may underlie and/or be influenced by more complex neural networks involved in higher order processing. |