The proposition that schizophrenia may arise from a neurodevelopmental deficit takes us back to our consideration of development, design, and intentional causal processes. If the deficit is present at an early stage, what might be the consequences in childhood? Further neuropsychological hypotheses are of great interest in this respect. Frith (1992) has argued that the deficit in schizophrenia is in the link between willed intentions and the monitoring of actions. There are similarities between Frith's model and that of Gray et al. (1991) in that both imply disruptions to the sense of self (Hemsley 1998). Under experimental conditions schizophrenic patients have been shown to be poorer than other individuals at correcting their actions when they are unable to see their effects, which suggests that their central monitoring is poorer (Mlakar et al. 1994). A consequence of such a deficit is likely to be that the schizophrenic sufferer does not recognize that he is the cause of his own actions, and this may form the basis of the experience of having ones actions controlled by another agent, and by analogy with action, the experience of thoughts being controlled. There is a failure of (meta)representation of the individual's own mental activities. Frith has also emphasized that a problem for many schizophrenics is to understand context. In human communication it is necessary to understand the meaning of the words, and also the way in which they are being used in a particular context, and schizophrenics tend to be bad at this. In other words they have difficulties in identifying metacommunications accurately. If these hypotheses are correct, and at this stage they must be viewed as informed speculations, the person with schizophrenia suffers from deficits in processes which in infancy appear to be crucial to the development of the self, and its metarepresentational capabilities. The linking of memory to event provides a sense of continuity over time, the sense of agency repeated over time and place creates continuity, and the accurate identification of context links self to different circumstances.
If it is hypothesized that the neurodevelopmental deficit is present in infancy, is it possible that analogous psychological deficits might be present also early in development? If so what would be the implications for the infant's experience of the caregiver, and the caregiver's experience of the infant? We do not know the answer to these questions, but our speculations will focus on information processing and the development of the self. We may guess that the infant whose capacity to generate internalized regularities and to detect and enjoy novelty is impaired might appear rather puzzled and unresponsive, which might impede the development of pleasurable, rhythmic, face to face interactions which are so characteristic of the first months of life, and appear to form the basis of subsequent forms of communication and relating. Difficulties in understanding interpersonal context might have similar consequences. We do not know whether the hypothesized deficit might be overcome, at least in part, by the use of appropriate strategies. Clearly the generation of expectations and departures from them arises both from the capacity of the infant, and the nature of the stimuli, provided predominantly in infancy by a caregiver. Might some parents be more able than others to provide sufficient scaffolding on which to create such internalized rules, perhaps through substantial repetition, or more marked variations against such a background? Conversely might some parents give up the task of close sustained interactions in the face of an apparently uncomprehending infant? Such ideas suppose that limitations in generating expectancies, and in selecting salient cues are present in the child from an early age, and the role of parents is to find ways of compensating for them. However, we have reviewed in the last chapter mechanisms whereby early experience may undermine the metarepresentational system. We argued that where caregivers create confusion as to what kind of rules apply in interactions, the infant may have difficulty organizing representations of experience into coherent domains of social interaction, hence undermining effective social action. We suggested also that some infants and young children may achieve a 'solution' to this problem through simplified metarepresentational systems, such as those underpinning controlling attachment. However if such a resolution is not achieved, and especially if the child is exposed to persistent disrupted communications, a chronic deficit in the capacity to understand social contexts may arise. This possibility has not been tested directly, however recent studies of risk factors for psychosis suggest there may be routes that involve severe childhood adversities such as loss or trauma (Agid et al. 1999; Garety et al. 2001). Consideration of such possibilities highlights the way in which the development of representations and metarepresentations might be impeded or facilitated. They entail variants of the design stance explanation, in the sense outlined in Chapter 7. The common strand is the acquisition of the rules for the interpretation of events. The extent to which these are hard-wired, how pervasive they are, and extent to which they are open to modification is not prejudged.
We should be clear that there are other possibilities. For instance it could be argued that the neurodevelopmental deficit, whilst present from early childhood, is not expressed until the time when schizophrenia is commonly first seen, in adolescence, perhaps as a result of neuronal maturation at that age. Then our analysis might not apply. It seems, however, that at least a significant number of children who are at risk for schizophrenia do show differences from other children. Studies of the children of parents with schizophrenia have shown that they have more attentional deficits, and that these are associated with subsequent social insensitivity, social indifference, and social isolation (Cornblatt et al. 1992). Clearly studies such as this are complicated by the presence of parents with schizophrenia who might have the same or similar hypothesized deficits as their children, however they provide some preliminary evidence that deficits may be present in childhood which could disrupt early parent-child interactions, with implications for subsequent development.
In our discussion of the design stance it was emphasized that even where intentional causal processes are hard-wired, in humans the 'wiring' may be influenced by experience. If the development of the visual system is influenced by visual experience then why not information processing? In rats the phenomenon of latent inhibition is not seen if they have not been handled during the first days of life (Weiner et al. 1987) which suggests that early experiences may have long-term structural implications. This does not lead us away from the role of genetic influences, but rather to an interactive theory in which the information-processing capacity is central and the origins are in genetically determined variability and contributions from early intentional causal processes.
Further indirect support comes from studies where both inheritance and environment have been assessed. In the Finnish Adoption Study the rate of schizophrenia or schizophrenic spectrum disorders in the adopted children of schizophrenic parents was 30% compared with 15% in a control group. However these differences were apparent only in a comparison of adopting families which were rated (without knowledge of the adopted children's mental health) as disturbed (Tienari 1990). In the context of a developmental interactional account the capacity for multiple representational systems may be important to outcome. Thus the infant with the hypothesized deficit may as a result of a parent's ability to compensate, develop a secure attachment relationship, which will increase the chances of instrumental and interpersonal competence. This may act as a protective factor in relation to a persistent deficit and the risk of psychosis. Conversely the development of insecure attachment may increase the risk. Children who as infants have been classified as 'insecure', later in life elicit fewer supportive responses from their teachers than those rated 'secure'. If a similar effect applies between parents and children, and if the vulnerability of infants makes it more difficult for parents to establish a secure attachment relationship, then these parents might later be less supportive and more critical of their children.
If the developmental processes of the kind described here are important then schizophrenia may appear after many years of mismatched and unsatisfactory interactions. There is ample evidence that the emotional atmosphere in the home, and especially the level of criticism, hostility, and over involvement, (which together are termed 'expressed emotion') influences the course of schizophrenia (Bebbington and Kuipers 1994; Butzlaff and Hooley 1998). Mueser et al. (1998) found high rates of traumatic events in patients with schizophrenia and bipolar disorder, and Garety et al. (2001) reported that severe trauma was associated with psychotic symptoms unresponsive to medication. The mechanism is unclear, but probably entail interactional processes with mutual influences between parental and (adult) child behaviours.
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