Autism confounds researchers but one way of understanding it is to look through the lens of stress and coping. That is exactly what editors M. Grace Baron, June Groden, Gerald Groden and Lewis P. Lipsitt do in their book Stress and Coping in Autism. Contributions by researchers, clinicians, teachers, and persons living with autism illustrate how it is possible to reduce the impact of stress in autism by understanding both the science and the experience of it. Below we excerpt part of the introduction. To learn more be sure to visit our morning post, Helping Children With Autism Learn.
The construct of stress has expanded our understanding of both typical and atypical human development in a revolutionary way. Research into a number of disorders that are often comorbid with a diagnosis of autism, such as anxiety, shyness, phobias, obsessive-compulsive disorder (OCD), and thought disorder, already include a systematic theoretical and applied analysis of the contribution of stress to the disorder. Autism, in its own right, might also benefit from such a focus for a number of reasons.
Anxiety, an indicator that someone is experiencing stress, was associated with autism as early as Kanner’s (1943) first description of the syndrome. A few early clinical and research reports (e.g., Marks, 1987; Matson & Love, 1990) examined the correlation between fear and anxiety and autism. In 1994, Groden, Cautela, Prince, and Berryman presented the first systematic framework for using the concepts of stress and anxiety to describe and treat autism and proposed that those with autism may, in fact, have a special vulnerability to stress. We now have a better understanding that the clinical problems often associated with stress, such as anxiety, are more prevalent among people with pervasive developmental disabilities than in the general population.
Autism has long been seen as a problem of faulty or different arousal responses to environmental intrusions (Dawson & Levy, 1989). This has given rise to continued speculation about the role of such patterns of arousal as diagnostic markers or even indicators or subtypes of autism. As early as 1979, Piggott’s review of selected basic research in autism suggested that, “Children called autistic probably represent a complex of clinically similar manifestations in a variety of difference physiological disturbance[s]. Objective markers are needed as to allow the demarcation of subgroups of autistic children for further study” (p. 199). More recently, Tordjman, Spitz, Corinne, Carlier, and Roubertoux (1998) offered a stress-based model of autism, integrating biological and behavioral profiles of individuals wish ASD. They propose that stress and anxiety may be core problems of autism and that an analysis of differential responses to stress can lead to the identification of different subtypes. Similarly, Porges’s The Listening Project (2002) documents hyperarousal and vagal disruptions in children with autism and offers a biologically based behavioral intervention designed to stimulate the social behavior of children with autism.
Some of the known biological or behavioral effects of stress (see McEwen, 2002; Sapolsku, 1998) can be seen in persons with autism. For example, there is recent evidence (Krause, He, Gershwin, & Shoenfeld, 2002) of suppressed immune system function in some persons with autism. Under- or oversentivity to pain is a hallmark behavioral symptom for many with autism, and turbulent sensory and perceptual experiences are documented regularly in first-hand reports (e.g., Jones, Quigney, & Huws, 2003). Furthermore, from our clinical experience, some persons with autism when in a state of distress (e.g., in the presence of a feared stimulus, such as a dog) show a sharpening of cognitive-communicative and sensory sills, and may speak in full sentences when this is not the norm. Finally, so many of the behavioral disturbances of autism, especially the problems of self-injury and obsessive routines or stereotypes (as discussed in chapter 6 in this volume) bring a face validity to the assumption that stress may be a critical component of our understanding this disorder.