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January-February 2008
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< previous | 1 | 2 | 3 | 4 At the time of Kanner’s discovery, mainstream psychiatry was in the thrall of Freudian theory, which attributed most childhood disorders to family environment rather than biology. Autism came to be viewed as an extreme and rare condition—the result of profound emotional (and specifically, maternal) neglect. For most of the latter half of the twentieth century, clinicians used the diagnosis only in cases where no other label was possible. As Margaret Bauman, associate professor of neurology and director of the Learning and Developmental Disabilities Evaluation and Rehabilitation Services (LADDERS) in Wellesley, recalls: “The majority of the cases we see today would not have been labeled autistic when I was a resident in pediatrics [in the late 1960s]. The autistic kid was a kid who sat in the corner, rocking back and forth, and made no eye contact. The rest were labeled ‘mentally retarded’ or ‘childhood schizophrenia.’” It wasn’t until the early 1980s that a new understanding of autism began to emerge. The catalyst was an article published by British autism expert Lorna Wing that described a little-known syndrome called Asperger’s Disorder. Hans Asperger was an Austrian-born pediatrician who studied children in a psychiatric hospital in Leipzig, Germany, in the late 1930s—the same time that Kanner was conducting his research in Baltimore. Asperger documented a condition in boys that he termed “autistic psychopathy,” characterized by “a lack of empathy, little ability to form friendships, one-sided conversation, intense absorption in a special interest, and clumsy movements.” His patients differed from Kanner’s in that they did not exhibit developmental delays in language or cognition (Asperger in fact referred to them as “little professors”), yet they shared key impairments in social interaction, reciprocal communication, and imagination (i.e., repetitive behaviors and interests). Wing’s 1981 paper brought Asperger’s findings to the attention of the English-speaking world and showed how the core features of autism could occur in a wide range of people, some severely mentally retarded and others highly intelligent. In the ensuing years, the predominant view of autism as a discrete psychoemotional condition gave way to the idea of a continuum of biologically based autistic syndromes, requiring greater diagnostic specificity. By 1994, the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) listed detailed criteria for five “pervasive developmental disorders” (PDDs), including Asperger’s, that comprised the “autism spectrum.” * * The pervasive developmental disorders (PDDs) comprising the autism spectrum share core deficits in social interaction, language, and range of interests or behaviors. They differ in degree of severity, number of areas of impairment, pattern of onset, and rate of prevalence. Autistic disorder (the most common) is four times more common among males than females and generally involves mental retardation. Rett’s disorder, a rare condition that occurs only in females, usually involves severe mental retardation. Childhood disintegrative disorder (CDD), involving a precipitous loss of abilities after at least two years of normal development, appears rarely, and more often among males. Asperger’s disorder, diagnosed five times more frequently in males than females, involves pronounced social deficits but no significant cognitive or language acquisition impediments. Pervasive developmental disorder not otherwise specified (PDD NOS), a “subthreshold category,” applies to cases in which some criteria for autistic disorder are present and the onset of symptoms doesn’t fit other PDD diagnoses. For details, visit www.nimh.nih.gov/..., posted by the National Institute of Mental Health. The increased awareness of autism’s related conditions and their symptoms corresponded to a steep rise in diagnoses in the early 1990s. Many parents became convinced that the escalating numbers of cases stemmed from exposure to thimerosal, a mercury-based preservative used in childhood vaccines. Another theory linked the measles/mumps/rubella (MMR) vaccine, in particular, to the onset of autistic symptoms. Numerous epidemiological studies have failed to substantiate these claims, and in 2004 the Institute of Medicine of the National Academies found no causal relationship between either mercury or MMR vaccine and autism. But even though it is not possible to get an accurate count of real cases prior to the early 1990s, there is a growing sense among researchers and clinicians that the real incidence of autism is on the rise and that environmental triggers likely play a role. The potential factors range from chemicals in food and cosmetics to parental age, stress, and reproductive technologies—offering no clear indication of where epidemiological studies might begin. Before scientists can isolate possible external causes, they need a clearer understanding of the biological pathways that lead to the combinations of traits and deficits along the autism spectrum. Genetic ComplexityA 1977 study of twins provided the first evidence of a genetic basis for autism. If one twin had the disorder, the other was far more likely to have it if he or she was identical rather than fraternal. (Because identical twins share their entire DNA, while fraternal twins share only half on average, a disease that tends to co-occur in identical pairs indicates genetic influence.) The discovery helped undermine the prevailing psychoanalytic theories that blamed autism on bad parenting and, in particular, on cold, unaffectionate, “refrigerator” mothers. 1 | 2 | 3 | 4 | continued >  
 
 
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