Is there an increased familial prevalence of psychopathology in children with nonverbal learning disorders?(Report)

Learning disabilities (LD) occur in approximately 5% of school-age children (Lyon, 1996), and two major subtypes of LD have been described: children with reading disorders (RD) and children with nonverbal learning disabilities (NLD; Drummond, Ahmad, & Rourke, 2005). Compared to RD, far less research has focused on NLD. Thus, the incidence and prevalence rates of NLD are currently unclear partly due to the difficulty in formulating an inclusive set of classifications that characterizes NLD (Roman, 1998). Most extant research at this point has been descriptive, and the data on treatment outcomes and familial origins of NLD have been less forthcoming. Thus, we know relatively little about potential genetic contributions that may play a role in the development of NLD.

The first documented cases of NLD were elucidated in the 1970s, when researchers began studying children who had discrepancies between their Performance and Verbal IQs on the Wechsler Intelligence Scale for Children--Revised (WISC-R; Wechsler, 1991; see Semrud-Clikeman and Hynd, 1990, for a review of these early studies). The results from these early studies reported that learning disabilities were more heterogeneous than once thought and that various subtypes existed. From these early subtype studies, conceptual underpinnings for a theory of NLD were elucidated. Since this pioneering work, a specific cognitive and behavioral profile has been described in youth with NLD, whose areas of strength include reading, decoding, spelling, and general language skills, yet who have vulnerabilities in math and the visuospatial/perceptual domain that are central to the disorder (Rourke, Ahmad, Hayman-Abello, & Warriner, 2002). Other cognitive NLD symptoms include problems with tactile perception, complex psychomotor skills, and visual perception (Drummond et al., 2005; Johnson & Myklebust, 1971).

Behaviorally, children with NLD are often described as socially inept (Rourke, 1995; Tsatsanis, Fuerst, & Rourke, 1997), and they have significant difficulties related to the processing of nonverbal social information (Badian & Ghubilikian, 1983; Loveland, Fletcher, & Bailey, 1990). Children with NLD may exhibit hyperactivity and are often characterized as being disruptive and unruly (Fuerst, Fisk & Rourke, 1990). As adolescents, individuals with NLD generally encounter progressive socioemotional problems, including difficulty adapting to social situations (Harnadek & Rourke, 1994; Loveland et al., 1990). Adolescents and young adults with NLD are often described as asocial and withdrawn (Rourke, 1995; Rourke, Young, & Leenaars, 1989). Though not specific to NLD, others have demonstrated that children with significantly greater WISC-R Verbal IQ relative to Performance IQ (thought to be a characteristic of NLD) have more aberrant personality characteristics, both disruptive and inhibited (Fuerst et al., 1990). Others (Ikebuchi, Nakagome, Tugawa, & Asada, 1996; Wong & Cornell, 1999) have similarly proposed that lower Performance IQ scores, poor peer relationships, and internalizing symptoms often coexist, interact, and potentiate one another (Nangle, Erdley, Newman, Mason, & Carpenter, 2003).

Despite the literature on emotional and psychiatric functioning in individuals with NLD, there has been little work addressing how genetic variables may contribute to the increased prevalence of psychopathology in this population. This line of investigation may not only hold promise for identifying neuropsychological and behavioral characteristics of disorders that may frequently co-occur, but also be important in guiding a further understanding of the familial and genetic relationships that underlie these disorders. Moreover, integrating heritability with theoretical conceptions that emphasize neuropsychological vulnerabilities may help to advance our knowledge of NLD and, ultimately, enhance our ability to treat the psychopathology that often accompanies this learning disorder (Kibby & Hynd, 2001).

The endophenotype model (Gottesman & Gould, 2003) guided our research design. A shared predisposing vulnerability should be familial, and although not all relatives of children with NLD will have a particular psychiatric disorder (the vulnerability presumably combines with other factors only in some family members to cause the full disorder), we may observe an increased prevalence of certain psychiatric disorders in relatives of children with NLD. This basic premise has been relatively well validated for schizophrenia and ADHD, conditions that share neuropsychological vulnerabilities (i.e., prefrontal mechanisms; Asarnow et al., 2002).

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