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.
Highlights
Despite attention-deficit/hyperactivity disorder (ADHD)is one of the most studied developmental disorders from child- to adulthood, the genetic and neuronal factors underlying the development of ADHD are not fully understood[1]
Sleep diary We compared sleep–wake history and caffeine consumption according to sleep diaries between the following groups: ADHD patients who had received stimulant medication in the past but not at the time of their participation in the study (“ADHD-med in past”, n = 6), ADHD patients who had never received stimulant medication (“ADHD-unmed”, n = 11), ADHD patients who received psychostimulants on a regular basis but refrained from taking them during the 24 h prior to the EEG assessment (“ADHD-med day before”, n = 18), ADHD patients who received psychostimulants on a regular basis including the morning of measurement (“ADHD-med measurement day”, n = 10) and healthy controls (n = 86)
We found no group differences neither in the composition of sleep stages, nor in sleep latency or wake after sleep onset, with the exception of that the ADHD group “med-day before” spent significantly less time in stage N1 as compared to the control group (p < 0.05) and that the ADHD group “med-day of measurement” had a longer sleep latency than the groups “ADHD-unmed” (p < 0.01), “ADHD-med day before” (p < 0.01) and healthy controls (p < 0.01)
Summary
Despite attention-deficit/hyperactivity disorder (ADHD)is one of the most studied developmental disorders from child- to adulthood, the genetic and neuronal factors underlying the development of ADHD are not fully understood[1]. A wide range of neuroimaging studies revealed that lower gray matter volumes in different brain regions, e.g. the basal ganglia[2,3], and lower cortical thickness[4,5] are associated with the disorder. A new imaging modality proved useful in tracking brain maturation in humans, i.e. high-density electroencephalography (hd EEG) recordings during sleep[9]. Using this technique, studying sleep EEG slow waves, oscillations of about 1–4.5 Hz characterizing deep non-rapid eye movement (NREM) sleep, offer a promising readout of the functional output of neuronal connectivity[10,11]. During the first two decades of life, SWA follows an inverted U-shaped curve[10,12], similar to gray matter development
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