Besides having persistent language difficulties, children with Developmental Language Disorder (DLD) frequently experience symptoms that are associated with various neuropsychiatric disorders. However, the extent to which children with DLD develop such neuropsychiatric symptoms is variable. A better understanding of the relationship between early language ability and the occurrence of neuropsychiatric symptoms, might improve our ability to identify those children with DLD who have the highest risk to develop neuropsychiatric symptoms, and therefore potentially most benefit from targeted intervention. One factor that may hinder progress in understanding this relationship in DLD, is the etiological heterogeneity that characterizes this population, implying that the origin of DLD varies from child-to-child. Studying a population with a homogeneous etiology could therefore provide a unique opportunity to study the relationship between language difficulties and co-occurring neuropsychiatric symptoms. The central approach that was used in this dissertation was the comparison of children with DLD to such an etiologically homogeneous group: children with the 22q11.2 deletion syndrome (22q11DS). Similar to DLD, 22q11DS is associated with early language difficulties and increased prevalence rates of a variety of neuropsychiatric symptoms. However, children with 22q11DS have a shared etiology, being a missing piece of DNA on chromosome 22q11DS. Results of this dissertation provide new insights on the impact of language difficulties on the occurrence of neuropsychiatric symptoms in 22q11DS, which might provide leads for future research and clinical care for 22q11DS and DLD, and might also be of relevance to other clinical populations.
