5.3 Causal links and models
There seems little doubt that genetic factors and atypical functioning of one or more areas of the brain and nervous system accompanies some or all ASDs. But this tells us little about the role of these influences in a ‘causal chain’ leading to autism.
As we saw, genetic defects may play a major initiating role, perhaps affecting the development of specific brain areas and systems, which in turn hinder development of specific socio-cognitive functions. The idea that similar brain damage may result from birth hazards, as suggested by Folstein and Rutter, or even from other sources, has not been conclusively disproved. Shattock and Savery (1997) maintain that brain damage in autism is secondary to metabolic disorders in which the chemical break down and digestion of certain food substances releases poisonous bi-products into the blood stream, and ultimately into the brain. Shattock further suggests that the rising incidence of autism noted in Section 2 is due to the effects of raised toxin levels in the environment and foods. Currently such causal claims are highly controversial, though this does not rule out atypical metabolism as a side effect of autism. Rutter et al. (1999) have documented a striking incidence of autistic-like symptoms in children adopted from Romanian orphanages, who were subjected to extreme emotional and physical deprivation in the early months of their lives. It is conceivable that this deprivation affected brain function. However, unlike children with classic autism, many of these children showed marked diminution of symptoms once in a nurturing environment.
Equally challenging is to explain how organic influences affect functioning at the biological, socio-cognitive and behavioural levels. Section 5.2 identified a number of major and distinct brain areas. Can these different areas be meaningfully linked, given that each has multiple functions, and given the difficulties pointed out by Ozonoff of identifying primary and secondary influences? How do you extrapolate from such biological links to the difficulties that people with autism experience and manifest?
Baron-Cohen and colleagues (1999; 2000) have offered a model that attempts to address some of this complexity, building on Baron-Cohen's developmental account of mind-reading in Section 4. As we saw, early developing behaviours such as following someone's gaze, or looking where they are pointing are thought to constitute a mechanism that ‘kick starts’ the capacity to ‘read’ mental states such as beliefs and emotions from people's behaviour, and particularly from their eyes. Baron-Cohen et al. suggest that in typically developing children, this mechanism is served at the biological level by an integrated brain system involving the amygdala, together with specific sub-areas of the temporal lobe (the superior temporal gyrus) and of the frontal cortex (the orbito-frontal cortex). These structures were shown in Figure 8. The theoretical rationale for these ideas derives from a proposal by Brothers (1990) that these parts of the brain have evolved as a ‘module’ specialised for the processing of socially significant stimuli. The essential idea is that part of the brain is specialised for ‘social intelligence’. The researchers draw on a wide range of evidence to argue that early influences on this system result in atypical brain functioning that produces the characteristic ‘mind-reading’ deficits seen in autism. An experimental test of the model is featured in Box 10.
Box 10: Testing predictions of the ‘amygdala model’
The experiment involved two participant groups:
ASD group: six adult participants with a diagnosis of high functioning autism or Asperger's syndrome;
Control group: twelve non-autistic control participants.
The participants in both groups were matched for mean age, IQ, educational level, handedness and socio-economic status.
Participants were presented with a series of photographs of eyes, such as those shown below in Figure 9, and asked to perform the following tasks. fMRI scanning was carried out while each participant performed the tasks.
Task A: press one of two buttons to indicate whether the person shown is male or female.
Task B: press one of two buttons to indicate which of two emotions shown at the bottom of the photograph is portrayed by the eyes.
Both faces in Figure 9 are female. The emotions portrayed are a) concerned, and b) sympathetic.
Both participant groups performed the two tasks with considerable accuracy, though the control group performed better than the ASD group on the ‘mind-reading’ task. The main interest of the researchers lay in the areas of the brain that were activated while performing the ‘mind-reading’ tasks. In the non-autistic group, the areas activated included the left amygdala. In the participants with ASDs, the amygdala was not activated at all, and other areas, such as the superior temporal gyrus, were activated more strongly than in the control participants.
The experimenters concluded that the different parts of the brain used by ASD and control participants when responding in Task B reflected the use of different processing strategies. In particular, failure to activate the left amygdala meant that the ASD participants were not engaging with the faces as emotional stimuli. Their reliance on brain areas such as the superior temporal gyrus meant that they were treating the task as a kind of face recognition, i.e. they were assessing the emotional expressions in an atypical ‘non-emotional’ way.
As a theoretical model, Baron-Cohen's approach has several appealing features:
it focuses on specific sub-areas of the brain known to have specialised functions, rather than on global areas that have multiple functions;
it builds on anatomical knowledge of neuronal connections to integrate different sub-areas of the brain into a single functional system;
it builds on neuropsychological findings to predict how atypical system functioning will affect the socio-cognitive skills of people with ASDs.
Such experimental results as those in Box 10 also provide a biological basis for Happé's (1994) finding that some people with ‘high functioning’ autism or Asperger's syndrome pass Theory of Mind tasks without having full social understanding. The suggestion that they learn ‘solutions’ in an atypical way is supported by the present findings suggesting that different brain functioning is involved. A difficult challenge for such an approach is to explain differences in functioning across the spectrum: on the one hand, the majority of people with autistic spectrum disorders fail Theory of Mind tasks, and the Baron-Cohen et al. result does not bear directly on their failure. On the other, the notion that elements of the cognitive phenotype for autism are present in ‘normal’ individuals outside the spectrum (see Section 4.5) begs the difficult question of whether their brain function is also atypical.
Another problem is that the amygdala model makes no mention of structures such as the cerebellum and frontal lobes, which have been implicated in autism by other researchers. Does this mean that separate models are required to explain the role of these structures? Answers to these questions are beyond the scope of this course, but they indicate that current understanding of brain functioning in autism is provisional.
The problem of reconstructing the developmental trajectory also re-surfaces here. Studies of adult brain dysfunction do not tell us what biological influences were at play before or at birth, how they might have altered the typical course of brain development and the individual's interactions with his/her environment. Observed atypicalities of brain function may even develop as a result of autism. Though the notion of neural plasticity is usually associated with beneficial change to the nervous system as a result of experience, it can also imply detrimental change. In an elegant and wide-ranging article, Schore (2001) argues that healthy development of brain structures like those in Baron-Cohen's model occurs during a critical period in the child's infancy subject to the regulating effects of the child's interactions with his/her caregiver. It is therefore possible that the impoverished social interaction experienced by autistic children over time induces negative plastic changes. This controversial idea does not preclude the infant entering the world with an innate difficulty in social engagement. However, it does echo Hobson's (1993) idea that such a starting point could trigger a ‘negative spiral’ in which the capacity for social engagement becomes progressively more flawed. According to Schore's model, this spiral constitutes a complex cycle of interaction involving behaviour, social cognition and brain function.
Superior temporal gyrus: A folded area on the outside of the temporal lobes. Thought to have an active role when a person is monitoring another's direction of gaze.
Orbito-frontal cortex: The area on the under surface of the frontal lobes. Thought to have a role in exercising judgement.