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like ignoring a hair-line split in a brake pipe of a car. The pipe may work perfectly well under normal driving conditions, but under extra load of sudden fierce braking, it may give way.

If this is correct, then the time to assess vulnerability is when there is likely to be some small amount of affective disturbance (Teasdale 1988). For example, if two patients, on completing treatment, have the same level of mood disturbance but the mood of the first is associated with greater dysfunctional attitude than is the mood of the second, then the first should be more vulnerable to relapse. There is indeed evidence from outcome trials of depression (Simons et al. 1986) that people who respond equivalently to the acute phase of treatment (in terms of their behavioural and emotional recovery) have different probabilities of relapse depending on the level of their dysfunctional attitudes at treatment termination. Whether a similar point can be made about other disorders is not yet clear.

There are important implications of these findings for how to test the cogency of any theory which sees dysfunctional attitudes as vulnerability factors. In testing the model in other clinical disorders, it may prove insufficient merely to measure such attitudes at the beginning and end of treatment and during remission. Dysfunctional attitudes may appear normalised during times of low stress. Vulnerability consists of the tendency for fast and extensive recruitment of dysfunctional attitudes when stress levels begin to increase. This predisposition may well be a relatively permanent aspect in some patients, and future research must work towards clarifying how such a predisposition is activated.

Future Research

Basic research on cognitive processes

In this section we examine just one example of the way in which basic research can help our understanding of cognitive processes: research on depression and autobiographical memory. It has been known for some time that depressed people are more likely to retrieve negative than positive events from the past (Lloyd and Lishman 1975). Further research has shown that this is not due simply to having more negative events in one’s past or to a tendency to misclassify neutral and positive events as negative (Teasdale and Fogarty 1979). Recently we have found an additional subtle deficit in the memory of depressed people. Their memory for emotional events (both positive and negative) tends to be less specific. That is, in respose to an instruction to remember a specific episode when given a cue word (e.g. happy, angry), they are more likely to refer to categories of events (e.g. ‘birthday parties’ or ‘the times he argued with me’). Patients are especially poor at recalling specific positive memories— which reverses the normal tendency in non-depressed control subjects to be more specific in positive memories (Williams and Broadbent 1986; Williams and Scott 1988). Why does this occur?

Retrieval from autobiographical memory is a staged process in which a general description of the memory required is generated, plus mnemonic cues to help search for specific examples of the general description. For example, in searching for a happy memory, one is likely first to recall the sort of activities or people or places that make one happy, then to search for specific examples. We believe that depressives are particularly likely to stop at this general stage, partly because it is effortful to be more specific, but partly because these patients store emotional events in long-term memory (LTM) in overgeneral categories, making it more difficult to retrieve specific instances.

The significance of this difficulty in recalling specific memories can be seen in therapy where a person fails to give specific examples of times when they have been happy. Without such ready recall of concrete examples of coping successfully with life in the past, solving current problems is made even more difficult. The lack of specificity exists even if they are able to report in general terms that their lives are happy. They are then in the cognitively confusing position of believing their lives should be happy, but having little ready access to specific evidence. The resulting guilt only adds to the depressive’s problems.

Neither is it much help that their memory of unhappiness is also more overgeneral (though to a lesser extent than positive memories). Successful problem solving requires an ability to recall relatively detailed pictures of past problems so that possible ways around obstacles can be more easily seen. For example, Wahler and Afton (1980) found that mothers under stress who had relationship problems with their children tended to use global blameful statements to describe their children’s behaviour. They found it difficult to retrieve specific examples of the children’s bad behaviour. As part of a parent training programme mothers who were able to learn to be more specific to describe their children’s behaviour were also those mothers who responded best to the therapy.

What is the importance of these results for cognitive therapy? First, diaries which record activities or thoughts may be of therapeutic benefit in part by encouraging patients to be specific in looking at their problems. Second, Wahler and Afton imply that diary keeping is a skill which may take time for patients to learn, since it involves a degree of specificity of description which is particularly hard for such patients to achieve spontaneously. When depressed patients fail to keep diaries, therapists often interpret this to mean that patients are not motivated to use the technique, or, even worse, are trying to undermine the therapy. There may be such patients, of course, but these hypotheses ought not to be considered until one has rejected the

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skill-deficit hypothesis. One would not blame a dyslexic child for not being able to spell. Neither should one expect a depressed patient to be able to identify, write down, or recall specific examples until this deficit in their cognitive processing has been explicitly addressed as part of treatment.

Future strategies for clinical research

Ultimately the efficacy of cognitive therapy with each of the client groups discussed in this book can only be tested by a properly controlled outcome study. In such studies random assignment of clients to different groups, using clearly defined patient groups diagnosed by internationally recognised criteria, are essential. Good outcome studies are very difficult to do (hence their scarcity) but at least, as a minimum, they need to have the following characteristics. First, there must be an appropriate control condition. Sometimes it is permissible for this control condition to be a treatment-as-usual condition (as, for example, used by Teasdale et al. 1984). This is more appropriate where cognitive therapy is being used for the first time specifically for that group. However, the case for using a treatment-as-usual control group must be made on each occasion, for it does not control the quality of the control therapies that are given (e.g. the length of time they spend with a therapist).

A second aspect of cognitive therapy which will need to be taken into account in an outcome trial is the quality of the therapy being delivered. It will be important to make tapes of sessions and to have them assessed by experienced cognitive therapists to check (1) that the therapy format conforms to the cognitive therapy model in general, and (2) that the quality of the particular cognitive therapy being used is adequate. Without these reassurances, any failure to produce the predicted effects may too easily be put down to the poor quality of the therapy. If cognitive therapy does not work very well for a particular client group we need to know that sooner rather than later, without escaping into excuses about the quality of the cognitive therapy.

Third, an outcome trial needs comprehensive assessment of behavioural, affective, and cognitive variables. These need to be made not only by self-ratings but by an independent assessor. Ideally they should be combined with some measures which assess self-schema or attention or memory biases which have been derived from experimental cognitive psychology. In a recent book on the application of cognitive psychology to emotional disorders, Williams et al. (1988) suggest that the measures of outcome should be matched to the type of psychopathology. Thus, for example, it is more appropriate, for anxiety-based disorders, to use outcome measures which assess biases in automatic aspects of encoding and retrieval. Conversely, it is more appropriate to use, as a measure of outcome in depression-based disorders, procedures which assess strategic or effortful aspects of cognitive processing, as most tests of memory do.

Fourth, there needs to be adequate follow-up for at least one or two years after the initial acute phase of treatment. An important aspect of this follow-up is that it should not merely be a single assessment to see how well each group of patients is still faring. Cognitive therapy claims to be a treatment which will not only be effective in the acute phase but also prevent relapse. The follow-up phase is a crucial aspect of the study and should be built into the design. This means that the numbers of patients in each group should be sufficient so that if the predicted proportion of relapses occur in the cognitive therapy and control groups, then the comparison between the groups will have sufficient power to show the difference to be attributable to the therapy rather than to chance. For example, one might expect a control group to have a relapse rate of 50 per cent. One may be quite happy if the cognitive therapy was able to cut the relapse rate by half to 25 per cent. Indeed, that would seem to be a very good outcome. However, to be able to confirm that this difference did not occur by chance one would need sufficient numbers. If there were forty-eight responders in the trial evenly split between the two groups (twenty-four in each), then in the control group twelve people would relapse, leaving twelve improved. In the cognitive therapy group six people would relapse leaving eighteen improved. Analysis of these data yields a chi-square of 3.2 which has not achieved statistical significance at the 5 per cent level. One could not be sure that this result did not occur by chance. Increasing the number of responders in the trial to sixty (thirty in each group) allows statistical significance to be achieved at a 5 per cent level (with a similar breakdown of results), with fifteen out of the thirty relapsing in one group and seven out of the thirty relapsing in the other.1

Another aspect of building the follow-up into the design at the outset of the study is that one can define relapse pre rather than post hoc. Many studies which perform naturalistic follow-ups (that is, waiting to see which patients return for treatment) also incur the problem that people may return to treatment for different reasons and at very different levels of symptoms. Some may not return for treatment at all, and yet have very severe symptoms. Others return with very mild worries. Thus it is necessary, if the follow-up is to be adequate, to build in some repeated assessment of the frequency and intensity of signs and symptoms. Such repeated assessment will also take into account the occurrence of further negative life events and chronic difficulties. One would not wish to judge two (otherwise similar) patterns of relapse as being truly equivalent if the first followed an extremely severe life event and the second seemed to occur unprecipitated.

Third, a follow-up which is built into the design at the outset of the study will have some proper hypotheses about which patients are most likely to relapse. For example, as we have seen above, the cognitive model would predict that those people who, despite the fact that they are symptom-free at the end of the treatment, nevertheless continue to express dysfunctional attitudes, are the most likely to relapse.