This chapter has been organized around three psychological perspectives on psychiatric problems: biological psychology, information processing approaches, and the cognitive psychology of beliefs. These perspectives reflect three hierarchically related levels on which psychiatric problems can be studied. Human information processing presupposes neural hardware, and beliefs presuppose information processing. When psychiatric phenomena are to be explained in psychological terms, they should be reduced to underlying psychological processes. It is often assumed that the further this reduction is taken, the more respectable and fundamental theories become. On this view, theories focusing on beliefs would be relatively superficial, while theories about neural hardware would be relatively fundamental, if not 'the real thing'. We shall not enter the somewhat philosophical discussion about the merits and necessity of reduction, but reiterate that we do not share the view that the quality of explanations critically depend on the degree of reduction. Rather, it is suggested that the optimal degree of reduction is pragmatic, i.e. the degree of reduction should be dictated by what scientific stance offers the best opportunities for prediction and experimental manipulation of psychopathological phenomena. After all, it would be hard to defend that a certain psychological perspective is superficial when it allows for effective prediction and intervention. The other way round, it would be problematic to claim that perspectives that do not result in precise prediction and intervention nevertheless offer profound understanding.
The merits of neuroscientific contributions to psychiatry are extensively discussed elsewhere in this volume. Technological developments in the field of neuroimaging offer tantalizing prospects of relating disordered behaviour to its neural hardware. It will be particularly interesting to find out what neurophysiological patient-control differences reflect emotions and cognitions of patients, and what brain characteristics represent true pathophysiology. In obsessive-compulsive disorder, for instance, positron emission tomography (PET) scans reveal distinctive brain changes. These changes disapear after successful treatment of obsessive-compulsive disorder, no matter whether the treatment is pharmacological or behavioural.(55) Of course, this suggests that the observed PET scan deviations reflect, rather than cause, obsessive-compulsive pathology. The implication is that normal subjects who are, experimentally, made to feel, think, and act like obsessive-compulsive patients will display the same abnormalities found in patients. Studies like these will no doubt be undertaken and most probably a differentiated picture will occur: just as differences between patients and controls in beliefs may or may not be epiphenomena, visualized differences in brain function may or may not be a mere reflection, rather than a biological cause, of the disorder. Happily , these issues are empirical and can and will be solved by obtaining controlled data.
Theories and paradigms from information-processing approaches have been applied to a wide range of psychopathological phenomena. The emphasis in this chapter was on the selective processing of emotionally valent information. Distinguishing between processing of neutral and negatively valenced information proved to be fruitful; a number of robust processing biases, related to the emotional valence of the information, were identified. There are some indications that such processing biases serve to maintain psychiatric disorders. For instance, relapse after behaviour therapy could be predicted from the tendency of successfully treated patients to see illusory correlations between phobic cues and harm. (93> Also, the occurrence of anxious and depressive problems after severe life stress could be predicted from a tendency to attend selectively to threatening material that was unconsciously perceived. (65)
While explanation of neurotic disorders in terms of beliefs is at odds with popular views about egodystony, the unreliability of introspection, and the epiphenomenal status of beliefs, such 'intentional' explanations have proved remarkably successful. Not only did they generate successful laboratory research, but their clinical implications are straightforward and have made effective treatments available for bulimia, anxiety disorders, and depression, for example. (121125. and 126) Cognitive therapies have recently been developed even for notoriously difficult disorders such as schizophrenia, and results from controlled trials are quite encouraging. (129,,!30)
In clinical psychology, a distinction is commonly made between causal processes in the origin of disorders (aetiology and pathogenesis) and causal factors involved in their maintenance. As to the aetiology, progress in behavioural genetics and in the identification and measurement of stable individual differences in temperament have indicated traits that act as vulnerability factors for the development of psychopathology. In the area of anxiety and affective disorders, so-called 'negative affectivity' is of particular relevance. Meanwhile, although negative affectivity, or 'neuroticism' contributes to the develoment of pathology and while patients with anxiety or affective disorders almost invariably score in the extremes of negative affectivity, the vast majority of people high in negative affectivity do not suffer from Axis I disorders. There is very little data to indicate under what conditions some people at risk develop maladaptive and negative schemas about the self, others, and the outside world. Far more is known about how such schemas or beliefs, once established, are maintained. Processing biases and avoidance, escape, and safety behaviour may act in concert to maintain neurotic disorders. No doubt this picture is very incomplete, but it covers much of the existing data, it has a good record when it comes to experimental validation, and it has therapeutical implications that are encouragingly effective.
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