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Autism and the pervasive developmental disorders (PDDs) are highly complex and variable in their clinical presentation and manifestations. For example, symptoms and characteristics change with developmental maturity and vary with the degree of associated cognitive impairment (Filipek et al., 1999a). This evolving pattern of clinical features can make the differential diagnostic process very difficult in some cases. Nonetheless, the defining feature of autism is the presence of a distinctive impairment in the nature and quality of social and communicative development (influenced by the specific biological and environmental circumstances of the individual). It is this impairment that distinguishes autism from other neurodevelopmental conditions (e.g., mental retardation, developmental language disorders, specific learning disabilities). For example, whereas mental retardation is characterized by a pervasive developmental delay, autism is characterized by a distinctive impairment in the nature of social-communicative development. The prognostic significance of this autistic social dysfunction is underscored by preliminary studies that report a negative correlation between the severity of this social impairment and treatment responsiveness, at least with regard to social and linguistic growth following intensive, behaviorally based early intervention (Ingersoll, Schreibman, & Stahmer, 2001).

Additional complexity in the differential diagnosis of autism and related PDDs results from a wide range of accompanying abnormalities within cognitive, adaptive, affective, and behavioral domains of development, including mental retardation (Volkmar, Cook, Jr., Pomeroy, Realmuto, & Tanguay, Volkmar & Klin, 1999), deficits in executive functions (Liss, Fein, et al., 2001; Ozonoff, 1995, 1997; Pennington et al., 1997), limitations in adaptive skills (especially in socialization and functional communication; Liss, Harel, et al., 2001), learning disabilities (e.g., nonverbal learning disability; Rourke, 1995), mood instability (Di Martino & Tuchman, 2001; Hellings, 1999; Hollander, Dolgoff-Kaspar, Cartwright, Rawitt, & Novotny, 2001), stereotypic and self-injurious behaviors (King, 2000), anxiety disorders (Kim, Szatmari, Bryson, Streiner, &: Wilson, 2000), and aggression (Hollander et al.; King, 2000).

During the past decade, the reported prevalence of autism-related conditions has risen markedly (Bryson, Clark, Sc Smith, 1988; Fombonne, Du Mazaubrun, Cans, & Grandjean, 1997; Fombonne, Simmons, Ford, Meltzer, & Goodman, 2001; Wing & Potter, 2002; Yeargin-Allsopp et al., 2003), in part as a result of a broadening of the diagnostic concept to include milder and more atypical variants. This has led to the increasingly frequent use of the term autism spectrum disorder (ASD) within clinical and educational settings (Filipek et al., 1999b), consistent with prior conceptions of autism, including the broader autistic spectrum (Wing & Gould, 1979) and ASD (Allen, 1988).

Recent genetic studies lend support to this concept, because it appears that the heritable factor in autism is not the specifically defined disorder itself, but rather, subtle weaknesses in social interaction and interpersonal discourse (Bailey, Palferman, Heavey, & Le Couteur, 1998; Le Couteur, Bailey, Goode, Pickles, et al., 1996). The literature suggests that the genetic liability for autism may be associated with limited interest in social interaction, few close confiding friendships, impaired socioemotional responsivity (a less robust finding), language delays, conversational impairments, problems in communication planning, and possibly anxiety and rigidity (Bailey et al., 1998). The boundaries of the behavioral phenotype for autism has been examined in same-sex twin pairs (28 monozygotic [MZ] and 20 dizygotic [DZ]), one of whom had autism (Le Couteur et al., 1996). Among the discordant co-twins (those without autism), findings included language impairments in childhood and social deficits persisting into adulthood. This broader phenotype was much more common among MZ pairs than DZ pairs, indicating a strong genetic influence. Behavioral and cognitive characteristics of autism appear to be less genetically based because no differences were found within and between MZ twin pairs. . .

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