Sleep architecture with phase distribution, wake time, arousal and sleep fragmentation could be seen at best only via PSG studies. A major issue in this context is the exclusion of confounding factors such as the effect of medications, co-morbid neurological and psychiatric conditions and, above all, primary sleep disorders. In fact, ADHD children could be generally subdivided in children without sleep disorders, probably less than 50% according to most estimates, and children with sleep disorders.
Many authors claim that in the absence of an abnormal apnea hypopnea index (AHI) or periodic leg movements (PLMs) index, sleep variables in ADHD children are not far from age normative values (Sangal et al., 2005). In a recent thorough metanalysis of polysomnographic (PSG) studies, Sadeh et al. (2006) examined other factors of variance, including age and gender. Age, in fact, reflects maturational changes of neurobehavioral and neurotransmitter systems, which may deeply influence sleep patterns. Females with ADHD usually present less disruptive behaviors, which can also differentially influence sleep attitude and propensity.
Whether or not an adaptation night is performed, it may enable the exclusion of the effects of first night sleep deprivation and adaptation to the lab conditions.
All considered, total sleep time appears to be longer in comparison to controls in ADHD children who underwent an adaptation night. The same subjects also exhibited longer stage 2 than controls (Sadeh et al., 2006); there appears to be a gender-related effect also over time spent in stage 2, but the most consistent effect of TST and stage 1 time was age-related, with a shorter TST and longer stage 1 in younger children (<9 years) compared to older children (>9 years), as if to indicate a more severe sleep impact in the younger group, which is usually also more severely affected in terms of ADHD symptoms, especially as far as hyperactivity is concerned.
A critical review (Bullock & Schall, 2004) examining dyssomnia in ADHD children, reports an overall concordance between authors (O'Brien et al., 2003a; Miano et al., 2006; Silvestri et al., 2009) with respect to a decreased REM percentage and an increased REM latency in ADHD kids. Most reports from France, however, contradict these studies (Lecendreux et al., 2000, Konofal et al., 2001). Furthermore, these data are not confirmed in most studies on HADHD children with nighttime periodic limb movements (Crabtree et al., 2003), as if the REM effect were more consistent with the IADHD type.
Kirov et al. (2004), instead, noticed an increased duration of REM sleep and of the number of sleep cycles in ADHD children compared to controls. Also, REM latency resulted shorter in his subjects as already previously reported by Kahn (1982) and Greenhill (1983), as if a forced REM initiation may have produced a longer REM sleep duration along with an increased number of sleep cycles.
A decreased dopaminergic activity in ADHD may be responsible for cortical dysinhibition of the motor frontal cortices, which would in turn result in the forced ultradian cycle of ADHD with REM-increased propensity. Later on, the same group reported an increased REM drive with shorter REM latency in children with coexisting tick disorders and ADHD, ascribing this type of impact to hypermotor symptoms (Kirov et al., 2007), partially contradicting previous findings (Crabtree et al., 2003) on reduced REM sleep in ADHD children with periodic limb movements.
What almost all authors agree about is an increase of sleep oscillations within the night that contribute to the overall daytime "hypoarousal" phenotype via a possible decrease of sleep efficiency (Gruber et al., 2007). However, while a few authors notice an increase of spontaneous or event-related arousals in their subjects' PSG (Silvestri et al., 2009; O'Brien et al., 2003a), arousals have mostly not been formally identified or reported in ADHD PSG studies. Rather, an increased number of phase shifts has been reported (Miano et al., 2006) with the same clinical significance.
The only dedicated paper in terms of a formal approach to explore the microstructural aspects of sleep in ADHD has been written by Miano et al. (2006) who analyzed the cyclic alternating pattern (CAP) in ADHD children without abnormal AHI or PLMs index. The authors reported an overall reduction of CAP rate, an index of sleep instability, in comparison to normal controls, with ongoing reduction of CAP sequences and A1 index, reflecting hypersynchronous delta waves with a protective effect on sleep continuity. This paper would then reconcile the increased fragmentation and low efficiency seen by other authors in ADHD sleep, with the relative compensatory increase of A2 and A3 subtypes, expressing sleep discontinuity.
A striking CAP similarity between ADHD and narcolepsy (Ferri et al., 2005) has been observed along with increased daytime somnolence on multiple sleep latency tests (MSLT). The latter observation is of seminal importance for the interpretation of ADHD as a primary disorder of vigilance (Weinberg & Brumback, 1990). A deficit of the arousal level fluctuations would underlie the concept and clinical considerations which tend to interpret ADHD as "a hypoarousal state" despite its contradictory daytime paradoxical hyperactivity. Further detailing of this theory and related studies are to follow in the sleep disorders section under "Narcolepsy".
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