Autism Spectrum Disorder. A Clinical Neurophysiology Approach I

Fig. 4.1

Polysomnography study in a 4-year-old patient with ASD without epileptic seizures. Recordings involve complete electroencephalogram (EEG), chin electromyography, eye movements and electrocardiogram. Note EEG epileptiform abnormality in channels containing the right centroparietotemporal leads, C4, P4, T4, and T6

Relatively few reports of PSG-based sleep studies in children with autism have been published. Overall, these have focused on abnormalities in REM sleep, including immaturity in the organization of eye movements into discrete bursts (Tanguay et al. 1976) , increased muscle twitches during REM sleep (Elia et al. 2000) , and undifferentiated sleep in which features of non-REM and REM sleep are intermixed (Diomedi et al. 1999; Limoges et al. 2005) . The prolonged sleep times, early wake times, and frequent interruptions in sleep noted in the survey literature have not been commented on in these PSG studies. Although subjective sleep parameters appear to be roughly similar in adults and children with ASD, there are inconsistencies in the objective sleep profiles obtained from actual sleep recordings (Elia et al. 2000) .

The characterization of sleep manifestations by specific ASD subtype (preferably by using the International Classification of Sleep Disorders) will help gather better longitudinal data about diagnosis and responses to specific treatments.

4.5 Conclusions

EEG and MEG provide evidence of disrupted brain connectivity in ASD and reveal that gamma-band activity may be crucially involved in aberrant brain functioning in ASD. However, researchers have only recently begun to link patterns of brain activity and connectivity to behavior.

Although there have been relatively few reports of PSG-based sleep studies in ASD, both non-REM and REM sleep abnormalities have been observed, which support the multiplicity of sleep problems in this pathology.

One of the best-known associations with central nervous system dysfunction in ASD is the high risk of epilepsy; though the relationship among epileptiform abnormalities , epilepsy, and regression is not yet well understood. Thus, a greater number of controlled studies are required in order to confirm this relationship. That is why, identification of the early processes that leads to ASD, and to epileptogenicity, or both is a challenge that is worth pursuing.

Acknowledgments

We thank Odalys Morales Chacón for her English assistance. We would also like to thank Abel Sanchez, Daymet Grass, Maydelin Alfonso, and Maria Luisa Rodriguez for their useful cooperation.

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