علائم اوتیسم و اختلال طیف اسکیزوفرنی در جوانان بالینی ارجاع شده به اختلال نافرمانی مقابله ای
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|73088||2012||12 صفحه PDF||سفارش دهید||9894 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Research in Developmental Disabilities, Volume 33, Issue 4, July–August 2012, Pages 1157–1168
Examined autism spectrum disorder (ASD) and schizophrenia spectrum disorder (SSD) symptoms in a clinically referred, non-ASD sample (N = 1160; ages 6–18) with and without oppositional defiant disorder (ODD). Mothers and teachers completed DSM-IV-referenced symptom checklists. Youth with ODD were subdivided into angry/irritable symptom (AIS) or noncompliant symptom (NS) subtypes. Two different classification strategies were used: within-informant (source-specific) and between-informant (source-exclusive). For the source-specific strategy, youth were classified AIS, NS, or Control (C) according to mothers’ and teachers’ ratings separately. A second set of analyses focused on youth classified AIS according to mother or teacher report but not both (source-exclusive) versus both mother and teacher (cross-informant) AIS. Results indicated the mother-defined source-specific AIS groups generally evidenced the most severe ASD and SSD symptoms (AIS > NS > C), but this was more pronounced among younger youth. Teacher-defined source-specific ODD groups exhibited comparable levels of symptom severity (AIS, NS > C) with the exception of SSD (AIS > NS > C; younger youth). Source-exclusive AIS groups were clearly differentiated from each other, but there was little evidence of differential symptom severity in cross-informant versus source-exclusive AIS. These findings were largely dependent on the informant used to define the source-exclusive groups. AIS and NS groups differed in their associations with ASD and SSD symptoms. Informant discrepancy provides valuable information that can inform nosological and clinical concerns and has important implications for studies that use different strategies to configure clinical phenotypes.