Intellectual abilities in @entity2916 complex: risk factors and correlates from the XXXX 2000 Study.

@entity1 @entity410 @entity73 @entity10622 @entity2916 @entity2473 @entity302 @entity13011 @entity74 @entity717 @entity159
BACKGROUND: @entity2916 ( @entity2916 ) is associated with @entity717 , but the risk pathways are poorly understood. METHOD: The @entity2916 2000 Study is a prospective longitudinal study of the natural history of @entity2916 . One hundred and twenty-five UK @entity1 age 0-16 years with @entity2916 and born between January 2001 and December 2006 were studied. Intelligence was assessed using standardized measures at >= 2 years of age. The age of onset of @entity302 , the type of @entity302 , the frequency and duration of @entity410 , as well as the response to treatment was assessed at interview and by review of medical records. The severity of @entity302 in the early years was estimated using the E-Chess score. Genetic studies identified the mutations and the number of cortical tubers was determined from brain scans. RESULTS: @entity13011 mutations were associated with significantly higher cortical tuber count than @entity10622 mutations. The extent of brain involvement, as indexed by cortical tuber count, was associated with an earlier age of onset and severity of @entity302 . In turn, the severity of @entity302 was strongly associated with the degree of @entity73 . Structural equation modelling supported a causal pathway from @entity74 to cortical tuber count to @entity302 severity to intellectual outcome. Infantile @entity2473 and @entity159 were important contributors to @entity410 severity. CONCLUSIONS: The findings support the proposition that severe, early onset @entity302 may impair intellectual development in @entity2916 and highlight the potential importance of early, prompt and effective treatment or prevention of @entity302 in @entity2916 .
