There are a number of key points that we wish to highlight and carry forward in the way that we have done in previous chapters. Although many of the theories of emotional disorder that we have reviewed began life specific to a particular disorder, the more successful theories (such as cognitive therapy) have subsequently been applied to a range of other emotional disorders. It is often in the course of such extensions that some of the features of the original model become altered.
1 Several different types of theories (e.g., learned helplessness/hopelessness, cognitive therapy, and the social-cognitive theories) point to the key role that significant events play in the emotional disorders. However, it is not simply that such events occur, but rather the types of explanation that individuals make (see also the discussions in Chapters 2 and 3 about interpretation and appraisal). Dysfunctional explanations are more likely to occur the more negative or severe the event is, but seem to be less important for more trivial events or for positive events. In contrast to Seligman, however, the focus should not only be on how an individual explains the causes of events—there are a range of other factors that must be considered as part of an overall explanation. Such factors include how an individual perceives the consequences rather than causes of events, how the events impact on important domains or areas of investment, and so on. We would also note that the learned helplessness/hopelessness approach has often seemed to focus excessively on conscious appraisal of events, whereas we would concur with many of the theorists discussed in Chapter 3 that the relevant appraisal processes can be either conscious or unconscious.
2 Most of the models that we have reviewed in this chapter have been diathesis-stress models in which a pre-existing vulnerability factor has interacted with subsequent stressors to produce the particular disorder. That is, most models began life as onset models. The slings and arrows of outrageous clinical and experimental data, however, have frequently led to these models being revised so that they fall somewhere between onset models, maintenance and recovery models, and relapse models, obviously in the hope that enough of the model will survive intact. The problem lies with the fact that the key evidence in favour of a putative vulnerability factor is typically obtained from currently disordered individuals obtaining higher scores than non-disordered individuals on Factor X; thus, the evidence is typically cross-sectional and correlational and the disputes centre around the old statistical chestnut of how to interpret correlations. It seems more than likely, however, that we will need different models and different weightings of factors to account for the onset of a first episode of an emotional disorder, maintenance and recovery from a first episode, relapse, and future recurrence of subsequent episodes.
3 An adequate cognitive account of emotion requires at least two levels of semantic representation; for example, a propositional level and a mental model level (e.g., Power & Champion, 1986) or Implicational level (Teasdale & Barnard, 1993). In fact, these multiple levels of representation may need to be even more complex in order, for example, to account for how the self-concept can change so dramatically both within and between episodes of depression and mania. The complex varying hierarchical relationships that exist within the self-concept seem to require more than a "monolithic" approach in which the individual is either positive or negative.
4 The age-old problem of the supposed illogicality and irrationality of the emotions is nowhere more strongly in evidence than in relation to the emotional disorders. For example, the cognitive therapy approach initially assumed that normal thinking was logical and rational and that one of the key problems of depression was a breakdown in logical thinking. However, the fact that evidence was obtained for the opposite proposal—namely that depressed individuals appeared sometimes to be more rational or realistic than their non-depressed counterparts—highlights the problems with these two opposite proposals: How can we explain the fact that there is evidence for both? Our interpretation is that the proposals for depressive distortion and depressive realism present only one view of the proverbial elephant (see Chapter 7) and that both proposals are true, though under different circumstances. Indeed, the same arguments can be applied to normal thinking, which can be shown to be accurate and realistic under certain circumstances but considerably distorted under others. Of course, the demonstration that both normal thinking and "emotional thinking" can be rational or can be distorted still leaves open the question of whether there is an inherent mental logic in which distortions arise from, say, performance limitations, or whether the mind's achievements are at best quasi-logical but there is no inherent mental logic (e.g., Evans, 1989). The jury is still out on this issue. What is clear, though, is that "emotional" thinking should not be equated with "irrational" thinking; thinking can short-cut rationality under numerous different circumstances (e.g., Solomon, 2003).
5 Theories that have predicted global cognitive biases or that have searched for global vulnerability factors in the emotional disorders need to be revised, because the evidence suggests that more specific biases are implicated. This evidence converges from a number of directions. For example, predictions from Beck's and from Bower's models were that biases should occur in a wide range of cognitive processes, whereas the evidence now points more strongly to mnemonic biases being implicated in depression and attentional biases in anxiety. In a similar manner, measures of global attributional style, dysfunctional beliefs, and self-esteem also need to address more specific content domains because, for example, the global scores are often too contaminated with symptom measures.
6 The idea of loops and locked systems has become more evident in models of the emotional disorders. Whereas the initial cognitive therapy model had a simplistic linear model of cognition causing emotion, there have been a number of subsequent qualifications of this idea (Clark, 1986; Greenberg & Safran, 1987; Teasdale, 1999) in which circular causal models of the cognition-emotion link have been considered. Indeed, as noted in Chapters 2 and 3, it should now be clear that cognition does not cause emotion, nor vice versa, because cognition is part of the emotion. We also note with interest an additional type of loop included within Teasdale and Barnard's (1993) ICS framework in which two different levels of representation, the Implicational and the Propositional subsystems, may serve to maintain a disorder through becoming locked in a loop. In the next chapter we will consider an extension of this idea—the possibility that basic emotions may become coupled under appropriate circumstances and that the continued reactivation of one emotion by another may serve to maintain an emotional disorder.
7 The cognitive and the social-cognitive theories have all highlighted the importance of social factors in the emotional disorders, although to varying degrees. For example, in Beck's and Seligman's theories there are key roles for the occurrence of stressful events many of which are social in nature, and also the key role of the early caretaker-child relationship for the development of a depressogenic attributional style or underlying dysfunctional assumptions. By definition, the social-cognitive theories have focused on the importance of interpersonal roles and goals and the possibility, for example, that overinvestment in one particular role or goal will leave the individual vulnerable in the face of adversity. We must emphasise, however, that we would disagree with an extreme social constructionist position (e.g., Harre, 1987) which argues that emotions are the enactment of certain interpersonal roles.
8 Again we emphasise that an adequate model of mental functioning must be able to account for a range of inhibitory phenomena in relation to emotion. For example, it has been clear from Freud and Janet onwards that individuals may inhibit certain traumatic memories and that these may remain in a form that is not integrated into the core belief system (see Davies & Dalgleish, 2001). These unintegrated traumatic memories may, in Freud's words, form a "pathogenic nucleus" (Breuer & Freud, 1895) around which subsequent related material is organised. The more recent interest in "emotional processing" has rejuvenated this issue, because of its importance for understanding the emotional disorders. In this respect, we should emphasise that it may not simply be traumatic memories that are inhibited, but also particular emotional states that the individual may attempt to inhibit or which may be experienced as a "loss of self" if inhibition fails. This possibility will form one of the key points that will be included in the integrative model to be presented in Chapter 5.
Towards an integrated cognitive theory of emotion: the SPAARS approach
THE PICTURE SO FAR 130 SOME THEORETICAL REMARKS
CONCERNING A THEORY OF MIND 135
THE FORMAT OF MENTAL REPRESENTATIONS 140 EMOTION GENERATION VIA SCHEMATIC
MODELS 146 ADDITIONAL CONSTRAINTS AND
PROCESSES WITHIN SPAARS 158
A NOTE ON COMPLEX EMOTIONS 166
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