Two routes revisited fast versus slow change processes in therapy

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The evidence clearly shows that emotion responses can be learned and activated without benefit of neocortex and thought processes . . . This makes them difficult to access and treat through interventions that are strictly cognitive in nature. Emotions acquired through subcortical pathways are difficult to extinguish by any technique. (Izard, 1994, p. 151)

In Izard's further advice to himself and other would-be therapists, he points to the danger of assuming that there is only one route to emotion and that this is modifiable by cognitive psychotherapeutic techniques. Although we may differ about the details of the routes to emotions, we fully concur with Izard that not only must therapists be aware of the potential modular organisation of emotions, they must also be aware of the fact that there are two different routes to emotion and, therefore, that the therapeutic techniques for working successfully with emotional disorders may vary according to the primary route involved in the disorder (Power & Dalgleish, 1999).

As a powerful example of the role of the two routes, we considered David Clark's (1986) model of panic in Chapters 4 and 6. In this model, the person with panic disorder is seen to misinterpret catastrophically certain physiological changes such as a faster-beating heart, dizziness, or shortness of breath, as indicative of impending death or madness. That is, the individual appraises one or more internal signs in a threat-related manner; the high-level schematic model produces extreme fear or panic in the individual. The successful cognitive treatment developed by David Clark in essence provides the individual with an alternative schematic model for the internal signs (cf. Teasdale & Barnard, 1993). Once the more appropriate model has been both accepted and applied, then recovery can occur quickly. Such changes provide an example of the fast change processes that can occur in therapy, in which, for example, it is the appraisal of an internal or external event that provides the primary problem in the disorder. However, the panic-disorder patient will still continue to experience the previously threatening internal signs in the same situations; these are likely to represent the direct activation of threat and will change much more slowly and gradually, that is, they reflect slow change processes in therapy.

The fast and slow change processes can be linked with a number of features of automatic versus controlled processes (Power & Brewin, 1991; Power & Dalgleish,

1999), one of which relates to associative-learning versus rule-learning processes (e.g., Holyoak, Koh, & Nisbett, 1989) and the fact that associative learning is typically slow, but conscious rule learning is typically fast. Cognitive therapy techniques that address schematic models will be successful to the extent that the schematic models are the primary source of the emotional disorder. However, as has been pointed out (Power & Champion, 1986; Power & Schmidt, 2004; Teasdale & Barnard, 1993), if the cognitive therapy technique merely focuses on propositional-level representations, as in the technique of challenging negative automatic thoughts, it may fail to address the higher-order schematic models and, indeed, in some unfortunate circumstances may serve to confirm them. Examples of such problems were given in Chapter 4; thus, if the therapist robustly challenges the patient's statement "I am a failure", this may serve to reinforce the schematic model because the patient now believes that he or she is incapable of carrying out such a task and is inferior to the therapist. The first conclusion, therefore, is that cognitive therapy needs to address high-level schematic models rather than focus on lower-level propositional representations. The second conclusion, however, is that this focus will not work if the source of the problem is via the direct route to emotion.

How therefore should one work with emotional disorders in which the direct associative route to emotion is primarily indicated? In these cases, we suggest, the process of therapeutic change will be slower, because the problems are based on associative-learning mechanisms or other rules of automatisation. This proposal suggests that there are some individuals who, for example, should be more likely to benefit from behavioural exposure techniques in the treatment of anxiety and obsessional disorders. For example, in the case of post-traumatic stress disorder, we noted (Dalgleish, 2004) that it was important to distinguish different types of individuals, including, first, those individuals with extreme beliefs in invulnerability whose schematic models may be "shattered" by the traumatic experience (Janoff-Bulman, 1985) and, second, those individuals in whom extreme cognitive and behavioural avoidance may initially lead to an apparent stoicism in coping with the trauma, but who are more likely to develop late-onset PTSD. Individuals with shattered schematic models should, we predict, benefit more from a cognitive therapy approach, whereas those individuals whose primary problem is the avoidance of associatively generated aversive emotions should do better with exposure techniques. This division is of course somewhat crude and there are many cases in which a combination of cognitive and exposure-based approaches is indicated. Nevertheless, the different challenges in PTSD, in particular, shattered high-level models versus unpleasant low-level intrusions, provide dramatic examples of the different effects of the two routes to emotion in the emotional disorders.

The examples of therapy that we have provided so far have contrasted cognitive versus exposure-based techniques, but we do not in any way mean to imply that slow change processes only occur in the exposure-based treatments. The complexity of therapeutic relationships and the many routes to effective change demonstrate that slow change processes may be set in motion in any form of therapy; for example, the adoption of a new and more appropriate schematic model for panic (a fast change process) should eventually lead to slow change processes, as noted above. A problem is more likely to arise when the therapist aims for schematic model change but the patient wants only lower-level (e.g., symptom) change. Part of the assessment for therapy should therefore consist of the degree to which the patient is satisfied or dissatisfied with self-related schematic models; short-term therapies will have little or no hope of altering schematic models that patients are completely satisfied with, and even long-term therapies are well aware of the limited amount of change possible for ego-syntonic aspects of the self.

Finally, we should note that the existence of two routes for emotion generation provides an account for a number of puzzles that arise in therapy. The first of these is the issue of "intellectual" versus "emotional" change. The SPAARS model would suggest that an "intellectual belief" is likely to be represented at the propositional level, and that change may follow an alteration of one's appraisal of a particular event or situation and no longer lead to the generation of emotion. In contrast, if the direct route still leads to the generation of emotion, the individual will be left with an awareness of a dissociation between the "intellectual" and the "emotional": the two systems are operating in conflict with each other and the individual is aware of the difference between their outputs. The existence of the two routes also provides an explanation for a related problem that people report; namely that they experience their emotional reactions as "irrational", nevertheless the reactions continue to happen out of the individual's control. Again, the SPAARS explanation would be that in such cases no emotion is generated via the appraisal route, only via the direct routeā€”for example, the individual appraises the butterfly to be non-threatening, yet still experiences "irrational" anxiety, that is, anxiety generated by the direct route and, most likely, acquired through an associative learning mechanism. In relation to recommendations for therapeutic practice, we suggest that the presentation of information booklets to patients with emotional disorders should include an amended model of the relation between cognition and emotion. One of the strengths of the cognitive approach has been the educational component which provides the patient with, in Jerome Frank's (e.g., 1982) terms, a strong rationale for the therapeutic approach. However, an amendment of that model would seem warranted, even as presented in handouts to patients.

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