IQ scores are volatile indices of global functional outcome, the final common path of an individual's genes, biology, cognition, education, and experiences. In studying neurocognitive outcomes in children with neurodevelopmental disorders, it is commonly assumed that IQ can and should be partialed out of statistical relations or used as a covariate for specific measures of cognitive outcome. We propose that it is misguided and generally unjustified to attempt to control for IQ differences by matching procedures or, more commonly, by using IQ scores as covariates. We offer logical, statistical, and methodological arguments, with examples from three neurodevelopmental disorders (spina bifida meningomyelocele, learning disabilities, and attention deficit hyperactivity disorder) that: (1) a historical reification of general intelligence, g, as a causal construct that measures aptitude and potential rather than achievement and performance has fostered the idea that IQ has special status and that in studying neurocognitive function in neurodevelopmental disorders; (2) IQ does not meet the requirements for a covariate; and (3) using IQ as a matching variable or covariate has produced overcorrected, anomalous, and counterintuitive findings about neurocognitive function.

The authors propose a heuristic model of the social outcomes of childhood brain disorder that draws on models and methods from both the emerging field of social cognitive neuroscience and the study of social competence in developmental psychology/psychopathology. The heuristic model characterizes the relationships between social adjustment, peer interactions and relationships, social problem solving and communication, social-affective and cognitive-executive processes, and their neural substrates. The model is illustrated by research on a specific form of childhood brain disorder, traumatic brain injury. The heuristic model may promote research regarding the neural and cognitiveaffective substrates of children's social development. It also may engender more precise methods of measuring impairments and disabilities in children with brain disorder and suggest ways to promote their social adaptation. Surprisingly little is known about the extent, basis, and consequences of the social problems associated with neurological dys-function and brain insults occurring during childhood, despite the significant long-term implications of social development for children's functioning at home, in school, and in the community (Parker, Rubin, Erath, Wojslawowicz, & Buskirk, 2006;Rubin, Bukowski, & Parker, 2006). Until recently, the lack of measurement tools and articulated models of social functioning has limited our ability to address social outcomes in children with brain disorder. The development of more sensitive measures and explicit models of social functioning would help researchers and clinicians to target children with brain disorders for further study and intervention.Now is an excellent time to consider social outcomes in children with brain disorder. The emerging field of social cognitive neuroscience provides a critical perspective on the social impact of childhood brain disorder. Social neuroscience not only supplies tools needed to better understand the neural substrates and social-cognitive processes associated with social functioning, but also provides a foundation for a multilevel, integrative analysis of the social difficulties arising from neurological insults (Brothers, 1990;Cacioppo, Berntson, Sheridan, & McClintock, 2000;Moss & Damasio, 2001;Ochsner & Lieberman, 2001;Posner, Rothbart, & Gerardi-Caulton, 2001). Although social neuroscience to date has focused primarily on adults, in part because of the inability to study the developing brain in vivo, this no longer need be the case. With contemporary neuroimaging, various elegant methods are available that can inform researchers about brain development and neuropathology in the study of social behavior in children with brain disorder (Toga & Thompson, 2005).The methods and models derived from social neuroscience will be particularly powerful when combined with those associated with the study of social competence in developmental psychology and developmental psychopathology Rubin, Bukowski, & Parker, 2006). The latter approaches reflect a development...

A higher level of spinal lesion in SBM-H is a marker for more severe anomalous brain development, which is in turn associated with poorer neurobehavioral outcomes in a wide variety of domains that determine levels of independent functioning for these children at home and school.

Spina bifida myelomeningocele (SBM), a neural tube defect that is the product of a complex pattern of gene-environment interactions, is associated with naturally occurring, systematic variability in the neural phenotype and in environmental factors that lead to systematic variability in the cognitive phenotype. We characterize the basis for variability in the cognitive phenotype of children with SBM with reference to a model of key biological, cognitive, and environmental events unfolding over the course of development from infancy to middle age. The cognitive phenotype is not domain-specific, but represents manifestations of unobservable constructs involving associative and assembled processing, the latter directly reflecting the impact of the neural phenotype on core deficits involving movement, timing, and attention orienting. The expression of the cognitive phenotype is variable, being moderated by features of the neural phenotype involving secondary CNS insults (such as hydrocephalus) that impair assembled processing, as well as by environmental factors (such as poverty, parenting, and education) that impair associative processing. The preservation of strengths in associative processing depends in part on the severity of the CNS deficits in SBM and the impact of the environment.