Very little is known about the potential neural abnormalities that exist in the initial stages of autism development. The goal of this project is to identify early neural abnormalities in two- to four-year-old toddlers with autism using whole-night electroencephalography (EEG) recordings in a hospital sleep lab. Toddlers will be recruited from the Negev Autism Center at Ben Gurion University, which includes a well-characterized cohort of over 450 children with autism. Parents of approximately one-third of these children have reported that their children exhibited motor and/or language regression early in life. Ilan Dinstein and his team will compare EEG and sleep abnormalities across toddlers with regressive and classical autism to determine how these two subgroups differ from typically developing toddlers and from each other in their underlying neurophysiology.

Previous studies have suggested that regressive and classical autism may embody different etiologies of autism that emerge at different time points in development for potentially different underlying reasons. For example, it has been proposed that some cases of regressive autism may be caused by early epileptic-like brain activity that may damage cortical circuits and impair development¹. Previous studies on this topic have been performed with older, awake children or adolescents using short EEG recordings. Epileptiform activity, however, is much more prevalent during sleep² and is likely to be more severe early in life. There is, therefore, strong motivation to examine and compare sleep-EEG in two- to four-year-old toddlers with regressive and classical autism.

Dinstein and his team will examine several measures including EEG spectral power and coherence across pairs of electrodes in addition to traditional inspection of recordings for epileptiform activity, assessment of sleep architecture and sleep stability. These measures will enable the team to identify toddlers with specific neural abnormalities and determine whether regressive and classical autism are characterized by distinct neural abnormalities at these very early stages of development.