Electroencephalographic (EEGS) Abnormalities in Individuals with Autism Spectrum Disorders (ASDS)

Background: ASDs are neurodevelopmental disorders of unknown etiology characterized by social and communication deficits and the presence of restricted interests/repetitive behaviors. Recently, there has been an increasing interest in the occurrence of epileptiform electroencephalograms (EEGs) in ASDs even in the absence of epilepsy (Tuchman, 2011).  Rates as high as 60% have been reported and some investigators proposed that these abnormalities may play a causal role in the autism phenotype (Spence & Schneider, 2009). However, there are not robust evidences concerning specific risk factors in children with ASDs, like for example symptoms severity, which might be used to predict which children will develop epilepsy and/or EEG abnormalities.

Objectives: This study examined the frequency and the nature of EEGs abnormalities in a sample of 57 individuals with ASDs, enrolled at the Center for Pervasive Developmental Disorders in Cagliari (Italy).

Methods: Our sample consisted of 49 males and 8 females, aged 1-17 years (average: 9,05 years), with a diagnosis of ASDs (70% with Autism, 25% with Pervasive Developmental Disorder-not otherwise specified, 5% with Asperger Syndrome). Participants were characterized by borderline intellectual functioning, as measured by different scales, like the Bayley Scales, the Leiter-R, the WPPSI-3 and the WISC-3. The heterogeneity of the measures employed to assess the intellectual functioning was due to the different developmental characteristics of the participants. Each participant was tested whit an “awake-sleep” EEG registration, performed with the System 10-20 of Jasper, after sleep deprivation.

Results: The 58% of the participants showed EEGs abnormalities, in which the anomalies were both nonspecific changes, such as slowing or asymmetry, and epileptiform discharges, consisting of spikes or sharp waves discharges, sharp slow waves, generalized spike-wave, and generalized polyspikes are seen. The EEGs abnormalities were mainly localized in the temporo-occipital region, according with a previous study (Spence and Schneider, 2009) and, less often, in the frontal regions. These anomalies may occur in individuals without seizures, and their presence should not be considered as evidence of epilepsy: rather, these EEG changes are considered to be signs of cerebral dysfunction. The prevalence of epilepsy was the 7%.

Conclusions: The EEG findings in our sample confirm what was found in previous studies, about the rate of EEGs abnormalities in individuals with ASDs and their main localizations (Lee et al., 2011). Since in our sample the rate of EEGs anomalies is higher than the general population, these results suggests that an underlying pathophysiology in ASDs might increase the risk of epileptiform anomalies and epilepsy. It might be of interest to identify specific ASDs phenotype which might be at higher risk of EEGs abnormalities.