Sleep EEG slow-wave activity in medicated and unmedicated children and adolescents with attention-deficit/hyperactivity disorder

Abstract

Slow waves (1–4.5 Hz) are the most characteristic oscillations of deep non-rapid eye movement sleep. The EEG power in this frequency range (slow-wave activity, SWA) parallels changes in cortical connectivity (i.e., synaptic density) during development. In patients with attention-deficit/hyperactivity disorder (ADHD), prefrontal cortical development was shown to be delayed and global gray matter volumes to be smaller compared to healthy controls. Using data of all-night recordings assessed with high-density sleep EEG of 50 children and adolescents with ADHD (mean age: 12.2 years, range: 8–16 years, 13 female) and 86 age- and sex-matched healthy controls (mean age: 12.2 years, range: 8–16 years, 23 female), we investigated if ADHD patients differ in the level of SWA. Furthermore, we examined the effect of stimulant medication. ADHD patients showed a reduction in SWA across the whole brain (−20.5%) compared to healthy controls. A subgroup analysis revealed that this decrease was not significant in patients who were taking stimulant medication on a regular basis at the time of their participation in the study. Assuming that SWA directly reflects synaptic density, the present findings are in line with previous data of neuroimaging studies showing smaller gray matter volumes in ADHD patients and its normalization with stimulant medication.

Sleep Power Topography in Children with Attention Deficit Hyperactivity Disorder (ADHD)

“…This study expands our previous findings on normalized sleep power topography in ADHD children, which pointed to a relative increase of SWA power over centro-parietaloccipital regions in these subjects compared to TD children 18 . Here, we investigated systematically both absolute and normalized power density maps in all traditional frequency Correlation between power and total sleep time in children with attention deficit/hyperactivity disorder (ADHD).…”

“…Spectral analysis was performed using all artifact-free 6-s epochs (Welch's averaged modified periodogram with a Hamming window, 8 segments with 50% of overlap) on the average-referenced signal. For topographic analysis, average signal power (across epochs) was computed for 6 classical frequency ranges [32]: delta/SWA (1-4 Hz), Theta (4-8 Hz), Alpha (8-12 Hz), Sigma (12-16 Hz) Beta (16)(17)(18)(19)(20)(21)(22)(23)(24)(25), low Gamma (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40). Both topographic maps of absolute average-referenced and normalized data (z-score across channels of the same participant) were examined.…”

“…Older studies, which commonly focused only on one arbitrarily selected EEG channel, showed no abnormalities in the lower frequencies range (0.5–4.5 Hz) during non-rapid eye movement (NREM) sleep [ 12 , 13 , 14 , 15 ]. However, three later studies [ 16 , 17 , 18 ] have been performed in children with ADHD during sleep using high-density EEG (HD-EEG), which allows a higher level of spatial resolution of electrocortical activity in comparison to standard EEG. While two out of three studies found higher slow wave activity (SWA) over a centro-posterior cluster of electrodes [ 16 , 17 ], one found a global decrease in SWA in ADHD children compared to TD peers [ 18 ].…”

“…However, three later studies [ 16 , 17 , 18 ] have been performed in children with ADHD during sleep using high-density EEG (HD-EEG), which allows a higher level of spatial resolution of electrocortical activity in comparison to standard EEG. While two out of three studies found higher slow wave activity (SWA) over a centro-posterior cluster of electrodes [ 16 , 17 ], one found a global decrease in SWA in ADHD children compared to TD peers [ 18 ]. According to a recent meta-analysis, these apparently discrepant results might be explained by the negative association between SWA and both mean age and the use of medications [ 11 ].…”

What Is the Link Between Attention-Deficit/Hyperactivity Disorder and Sleep Disturbance? A Multimodal Examination of Longitudinal Relationships and Brain Structure Using Large-Scale Population-Based Cohorts

“…Particularly, the neuroanatomical associations of sleep disturbances were mediated to a greater extent by ADHD symptoms in subcortical regions with higher gene expression levels of these pathways ( Figure S16 in Supplement 1 ). Therefore, if a given ADHD treatment targets one of these pathways, it might reduce the ADHD component in sleep disturbances ( 109 ). However, approximately half of the brain-sleep association was not mediated by ADHD symptoms, suggesting that not all GMV reductions common to ADHD and dyssomnia stem from ADHD itself.…”