1. Introduction

Previous research on parental reports and objective measurements taken from actigraphy and polysomnography have shown that ASD children are more prone to sleep problems than children with other neurodevelopmental disorders or children with typical development ^[1][2]. It is estimated that a range of 40% to 93% of the population of ASD children suffer from sleep disorders ^{[3][4][1][5][6]}.

In recent years, an increasing number of studies have reported mixed results on objective and subjective measurements of sleep abnormalities in ASD patients ^{[2][7][8][9][10][11][12]}. The high level of heterogeneity across different studies may be related to biological, social, psychological and environmental factors influencing sleep problems in ASD ^[13].

Research findings over the past two decades have supported a link between sleep states and synaptic plasticity. The term ‘sleep’ is defined as a periodic suspension of the state of consciousness, characterized by the slowing of the neurovegetative functions and by the partial interruption of the sensorimotor relationships of the subject with the environment, essential for brain restoration. The brain state is organized in cycles with two alternating phases: non-rapid eye movement (NREM) sleep, also termed slow-wave sleep (SWS), and rapid eye movement (REM) sleep. SWS is hallmarked by high-amplitude, slow oscillations (less than 1 Hz) and sleep spindles (0.5–2 s bursts of 10–16 Hz), while REM sleep is dominated by low-amplitude, wake-like fast oscillatory EEG activity (4–11 Hz) ^[14].

Recent progress showed that both synapse strengthening and weakening occurs across sleep, highlighting the function of sleep in regulating cortical synaptic plasticity. Different states of sleep affect different aspects of synaptic structural remodeling after the experience, so that memory consolidation and the retention of information can be disrupted by sleep deprivation or reduced sleep quality. This sleep-dependent synaptic plasticity plays an important role in neuronal circuit refinement during development and after learning ^[4][14][15].

2. Development and Findings

This systematic review provides the status of knowledge about the occurrence of sleep problems in children and adolescents with ASD, considering objective parameters from sleep EEG or polysomnography and subjective parameters from sleep questionnaires. Collected data validate literature evidence that, patients with ASD experience a greater rate of qualitative and quantitative sleep disturbances than children and adolescents with typical development.

Considering that sleep problems in ASD are likely to recognize a multifactorial etiology, many possible neurobiological, medical, behavioral, and cultural mechanisms have to be considered in order to correctly understand the meaning of objective and subjective sleep measurement findings.

Sensory integration deficits, ritualistic or self-injurious behaviors, poor communication skills, and limited responsiveness to social cues can exacerbate bedtime resistance, prolonging the amount of time from lights turned off until the onset of any sleep stage, and interfere with sleep continuity. For example, repetitive patterns of behavior, such as going to bed and delayed sleep onset, particularly when ASD children are selectively absorbed by unusual activities during or around sleep (wearing particular pajamas, having a particular toy to play with, performing specific rituals etc.). ASD children with over-sensitivity may have a greater vulnerability to noise, light, and temperature, resulting in environmental discomfort and impairment of sleep quality. Moreover, the ASD phenotype and severity of core symptoms may negatively interfere with symptoms of insomnia, it also happens that a worse quality of sleep impacts daytime behavior problems and the adaptive skill development of ASD children worsens the quality of life of both ASD individuals and their caregivers ^[16][17].

Tessier and Farmer found a decrease of spindle density and duration in ASD children compared to controls, suggesting that this finding may be considered a biomarker of functional anomalies in brain maturation. Spindle activity, originated in the thalamic reticular nucleus, is considered as an electrographic landmark from waking to sleep transition, protecting sleep from being interrupted by external stimuli ^[18][19]. Sleep spindles exhibit an age-dependent pattern, and their developmental modifications are presumably related to the maturation of thalamic-cortical structures, so that spindles are believed to play an important functional role in sleep-dependent synaptic plasticity and memory consolidation ^[20][19][21].

3. Conclusions

As awareness of the critical role of sleep for healthy physical and mental development has grown up, and the study of sleep in neurodevelopmental disorders and particularly in ASD has received more attention. Despite some limitations, the reviewed studies clearly show how objective and subjective sleep abnormalities are recognized in children and adolescents with ASD. These abnormalities can be identified by the polysomnographic analysis of macro- and/or microstructural features of sleep and by the collection of clinical information by parents. Therefore, clinicians should always assess sleep features in the ASD clinical population, given that the identification of sleep difficulties could have implications in the choice of treatment strategies.

Further studies are needed to understand the integrating mechanistic theory of the overlap between sleep disorders and ASD, although there has been progress in understanding the biology underlying disorders, with the involvement of genetic, medical, and behavioral factors. Lastly, whether specific sleep EEG patterns could represent a marker for atypical brain development in ASD is unclear and it needs an ad hoc design for future research.