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. 2008 Feb 12:4:8.
doi: 10.1186/1744-9081-4-8.

MEG event-related desynchronization and synchronization deficits during basic somatosensory processing in individuals with ADHD

Affiliations

MEG event-related desynchronization and synchronization deficits during basic somatosensory processing in individuals with ADHD

Colleen Dockstader et al. Behav Brain Funct. .

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.

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Figures

Figure 1
Figure 1
Grand Mean Contralateral SI localization for Control (blue) and ADHD (red) Based on SAM Differential Analyses.
Figure 2
Figure 2
SI Group Differences in Frequency and Power During Random Presentation of a Somatosensory Stimulus. (A) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for control subjects. In both control subjects and subjects with ADHD the plot was baselined using the average spectral energy observed in the pre-stimulus period (-100 – 0 ms). (B) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for subjects with ADHD. (C) Group mean differences of the group TFRs. (D) Statistically significant values remaining once group differences were thresholded to p </= 0.05. (E) Divergence of early response to the stimulus in controls and ADHD. (F) Divergence of power in beta rebound in the latter portion of the trial between controls and ADHD.
Figure 3
Figure 3
SI Group Differences in Frequency and Power During Predicted Presentation of a Somatosensory Stimulus. (A) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for control subjects. In both control subjects and subjects with ADHD the plot was baselined using the average spectral energy observed in the pre-stimulus period (-100 – 0 ms). (B) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for subjects with ADHD. (C) Group mean differences of the group TFRs. (D) Statistically significant values remaining once group differences were thresholded to p </= 0.05. (E) Groups show no divergence of early response to the stimulus in controls and ADHD. (F) Divergence of power in beta rebound in the pre-stimulus period between controls and ADHD.
Figure 4
Figure 4
Grand Mean contralateral SII localization for control (blue) and ADHD (red) based on SAM differential analyses.
Figure 5
Figure 5
SII Group Differences in Frequency and Power During Random Presentation of a Somatosensory Stimulus. (A) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for control subjects. In both control subjects and subjects with ADHD the plot was baselined using the average spectral energy observed in the pre-stimulus period (-100 – 0 ms). (B) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for subjects with ADHD. (C) Group mean differences of the group TFRs. (D) Statistically significant values remaining once group differences were thresholded to p </= 0.05. (E) Divergence of the ERD response to the stimulus in controls and ADHD. (F) Divergence of power in beta rebound in the latter portion of the trial between controls and ADHD.
Figure 6
Figure 6
SII Group Differences in Frequency and Power During Predicted Presentation of a Somatosensory Stimulus. (A) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for control subjects. In both control subjects and subjects with ADHD the plot was baselined using the average spectral energy observed in the pre-stimulus period (-100 – 0 ms). (B) Grand Mean TFR of the individual, virtual channel, spatially-filtered single trials for subjects with ADHD. (C) Group mean differences of the group TFRs. (D) Statistically significant values remaining once group differences were thresholded to p </= 0.05. (E) Divergence of the ERD response to the stimulus in controls and ADHD. (F) Divergence of power in beta rebound in the latter portion of the trial between controls and ADHD.

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