For this exercise, I have chosen five different articles related to the literature on potential causes of developmental disorders. I chose this topic, which has been long debated, for two reasons: 1) I am interested in the proliferation of ADHD diagnoses and how psychologists explain them; 2) The topic seems particularly apposite to the model analysis needed for this paper. Thus, five articles will be examined on this topic.
- Gilberg, C. (1992). Autism and autistic-like conditions: Subclasses among disorders of empathy. Journal of Child Psychology and Psychiatry, 33, 813-842).
There are three main causal models used in the field of developmental psychopathology: 1) biology; 2) environment; 3) a combination of the two. Gilberg is the foremost proponent for a biology-based causal model; that is, biology is the formative cause of developmental disorders. Gilberg cites several reasons why biology is the causal mechanism for developmental disorders, which may be ultimately acted on by behavioral factors. The first reason typically given is that a diagnosis of autism usually is related to other physical disease/ sickness. This makes sense due to a biological basis: A biological cause for autism might lead to other conditions that include stomach discomfort, drowsiness, nausea and other symptoms (Gilberg, 1992). Second, there are signs that brain dysfunction accompanies the disease: diagnostic scans using MRI and CRT machines have shown that autistic individuals have a different brain structure than those without autism (Gilberg, 1992). Finally, there are signs that brain damage is related to mental retardation. These point to a model below that posits the cause of autism as a function of biological causes:
In this model, biological factors play the main causal role in the development of the disease. Once the biological origins have started they lead to abnormal brain conditions and a non-functioning brain system.
- Wing, L. (1988). The autistic continuum. In L Wing (Ed.) Aspects of autism: Biological research (pp. v-viii). London: Gaskill and Royal College of Psychiatrists
Although the biological description of autism gained numerous adherents, many scholars felt this causal model, while useful in pointing out the potential role of biology, was incomplete. Indeed, Wing (1988) propounded a new causal model that privileged the role of behavioral aspects in causing developmental disorders. Indeed, while the biological causal model of autism would augur for a similar clinical profile for autistic individuals, this is not observed in practice. Indeed, the wide variance of symptoms and communication abilities among those with autism has brought behavioral explanatory models to the forefront. Wing (1998) proposed a model that stressed the difference that individuals with autism faced: based on his research, the autism “spectrum” was accepted. This model also implemented biological factors as causal units, but stressed the impact of environmental factors in causing variance among those with the diagnosis. This was the second phase in modeling trying to account for developmental disorders.
- Cognition as a mediating factor in developmental disorders
Rutter, M. (1983). Cognitive deficits in the pathogenesis of autism. Journal of Child Psychology and Psychiatry, 24, 513-551.
Firth, U. (1992). Cognitive development and cognitive deficit. The Psychologist, 5, 13-19.
The original dyadic model focusing on biology and environmental factors was formative, but not sufficient in modeling how developmental disorders arose. Indeed, cognition, the process of how individuals perceive and think, is identified as a key moderating factor in developmental disorders. That is, although the biological cause may be similar, it ultimately manifests in different ways due to the moderating factor of cognition. Rutter (1983) was the main theorist to operationalize biological, behavioral and cognitive in one model that looked similar to the one below:
In this model, there are numerous familiar elements. At the top of the model, biological factors act on the brain to cause the developmental disorder. The second element in the model is cognition: In this model, the “C” (representing cognition) is crossed out because the letter represents the level of cognition that is found in individuals without developmental disorders. The crossed out “C” represents that biological factors impact on the brain that makes normal cognition impossible. The lack of cognition moderates the biological impact that then is revealed in various behavioral traits across the spectrum of autism.
Different authors, however, have represented the moderating impact of cognition differently. That is, while most believe that cognition moderates the impact of biology on behavioral symptoms, the moderating effect may not be the same. Indeed, the model below proposed by Firth is postulated below.
This causal model is quite similar to the standard model that implements elements of biological, cognitive, and behavioral. The difference, however, is how the difference in behavioral symptoms is expressed. Where the basic model focuses on the follow from biological through mediation of cognitive to behavioral, this model focuses on explaining why individuals may have more or less severe symptoms based on its expression. That is, the model shows that without cognition the individual has three different symptoms. However, there is a second basis of cognition that this individual has that attenuates the symptoms of S3 to the point of alleviation. Thus, the added detail in this model not only shows how cognition is a moderator of biological symptoms, but also how it can lead to a difference in symptoms at the behavioral level. There are numerous permutations on the biological, cognition, and behavioral models of psycho pathology, but these are the main ones.
5) Barke, E.J. (2001). Causal models of attention-deficit/hyperactivity disorder: From common simple deficits to multiple developmental pathways. Biological Psychiatry, 57(11), 1231-1238.
Barke’s paper is a calculated response to prevailing causal models in the field of ADHD research: core deficits. This literature, which is explored in greater detail above, conceptualizes the onset of ADHD as a function of numerous deficits. Indeed, Barke cites the model (the developmental causal modeling framework) as proposed by Morton and Firth. The model cited in this article differs from the Morton model in two main ways: First, it questions the assumptions made by previous modelers; that is, the authors don’t necessary believe that neurobiologic level build causal chains across the cognitive and neurosphychologic levels of analysis; 2) Second, and related to the first, their causal model is based on the fact that it must be representative of all clinical symptoms (Barke, 2001).
In order to present a new model, however, Barke relaxes these assumptions to present a new type of causal model.
The new model provided above breaks down the constituent variables of biology, cognition, and behavioral into different variables to show how they actually work on the individual. This model is useful in that it does not assume that every theorist is working off the same suppositions in thinking that “biology”, “cognition”, and behavior are the same conceptually across different definitions and models.