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Abstract Summary Autism spectrum disorder is a neurodevelopmental disorder characterized by patterns of delay and deviance in the development of social, communicative, and cognitive skills that arise in the first years of life (Fred et al., 2014). It affects approximately 1 in 88 children and 1 in 54 males (center for disease control, 2012). The causes of ASD are still unclear; however, an etiological factor has been identified in only 15–20% of persons with ASD (Schaefer and Mendelsohn, 2008). Prenatal and perinatal complications are reported more frequently in groups of ASD than in the normal population (Ijichi and Ijichi, 2004). Comorbid psychopathology in ASD as high as 70% (Matson et al., 2010). The most common co-occurring conditions with ASD include ADHD, a variety of anxiety disorders, depression, and oppositional defiant disorder (Leyfer et al., 2006; De Bruin et al., 2007; Simonoff et al., 2008). In addition cognitive impairment, deficits in adaptive functioning, feeding and sleep difficulties, and challenging behaviors(Jang et al., 2011; Kozlowski et al., 2012; Turygin et al., 2013; Yerys et al., 2009) are also common, individuals with ASD are also frequently affected by at least one comorbid psychiatric disorder(Morgan et al., 2003; Bruin et al., 2007; Simonoff et al., 2008). Also 10% of children with ASD had a concurrent medical disorder for example gastrointestinal problems and epilepsy (Rutter, 2005). Summary 75 Using neuroimaging like MRI findings showing some anatomical changes However, these findings had not contributed to any etiological explanation so no consistent association between ASD and different brain abnormalities had been detected (Boddaert et al., 2009). EEG is the primary measure used to capture and characterize epileptiform and abnormal paroxysmal activity through the detection of focal spikes, which occur with increased frequency in ASD (Tuchman and Rapin, 1997, 2002). Multiple EEG abnormalities had been associated with ASD (Levisohn, 2004, Chez et al., 2006). A high rate of seizures and EEG abnormalities in children with ASD was first noted in the 1960s (Tuchman et al., 2009). Subsequently, a large number of studies concerning these combinations had been done (Tuchman and Rapin, 2002, Deonna and Roulet, 2006, Levisohn, 2007). Chez et al. (2006) found that the incidence of abnormal epileptiform activity on EEG occurring as 60–75% of individuals with ASD. There is no agreement on the EEG features of ASD although clinical EEG studies generally agree onthe high prevalence of epileptiform abnormalities inchildren with ASD (Gabis et al., 2005; Chez et al., 2006). So, Additional studies are needed to support and to determine if decreased epileptiform activity is correlated with improved behavioral measures especially if EEG used as a biomarker. |