THE WIDER APPLICATION OF COGNITIVE THERAPY 135

The cognitive framework

Different cognitive levels

It seems clear, on reading these case descriptions and those in other chapters in this book, that although different problems were being addressed, nevertheless the cognitive therapy techniques used share common assumptions about how cognitive factors interact with affect and behaviour to produce symptoms. The authors are clearly working with assumptions about how cognitions can have their effects at various ‘levels’. In this they are following Beck’s model in which cognitive events (thoughts and images of loss, negative interpretations of ambiguous events) arise when a stressor activates an underlying cognitive structure (an attitude, belief, or assumption). These assumptions, such as ‘My value as a person depends greatly on what others think of me’ or ‘If a person I love does not love me, it means I am unlovable’, are not themselves depressive, but when certain events occur (e.g. negative feedback on one’s work in the first case; being jilted by a lover in the second case) they allow a negative inference to be drawn (‘I am nothing’, ‘I am unlovable’).

According to this model, the more underlying dysfunctional assumptions a person has, the more vulnerable they will be to becoming disturbed, since there will be a wider range of situations which will activate one of them. The theory assumes that, once activated, the underlying depressive structures cause biases in memory for past events, in perception of current ambiguous situations, and in anticipation of future events. We can see from the case descriptions given in this book that the sources of ambiguity may be both external and internal to the person. An example of a misinterpretation of an external event is a child smiling at one of Cole’s clients receiving cognitive therapy for offending, or the drug abuse patient, Ted, who responded to a disagreement in a pub with the thought ‘I cannot let anyone treat me unjustly and get away with it’. Examples of ambiguity arising from internal sources occur in Greenberg’s patient where panic symptoms are interpreted in terms of having a heart attack: ‘You don’t really know what is wrong with you and you are just really scared that something could happen, that you could die’. Similarly, the hypochondriacal woman, who feared that she had cancer, found that a number of symptoms would activate this fear: feelings of dryness or pain in her throat, difficulty swallowing, changes in her voice, and lumps or blotches on her skin (Warwick and Salkovskis, Chapter 4).

Finally, by whatever means such negative thoughts, images, and interpretations arise, they have subsequent effects on mood and behaviour. Thus, even in cases where such cognitive phenomena are secondary symptoms, they can still play a causal role in maintaining disturbance of emotion and behaviour. We shall discuss later the increasing evidence that the length of episode and the probability of relapse are partly due to a process whereby mild affective disturbance activates a relatively large amount of negative thinking.

In summary, the cognitive model suggests that cognitive structures (beliefs, assumptions) may render a person more vulnerable to depression in the face of a stressor; that the combination of assumption and stressor causes a number of cognitive events (ideas of loss) to occur with increased frequency and intensity which helps to precipitate a depressive episode; that whether or not this causal sequence occurs, cognitive factors (negative interpretations of ambiguous social situations or ambiguous symptoms) may act to maintain depression. Two questions arise. First, what are the implications of this model for the way in which therapy is conducted? Second, is a levels’ model theoretically cogent?

Implications of a ‘levels’ model for therapy methods

In this book we have seen something of the range of techniques which therapists have brought to bear upon these vulnerability, precipitation, and maintenance aspects of emotional and behavioural disorders. It is important to note that the cognitive model, as set out above, does not imply that the use only of cognitive restructuring techniques by themselves will be sufficient to bring about permanent changes in thought-affect-behaviour links. The cognitive therapy practised here uses both behavioural and cognitive techniques. Figure 10.2 is a diagrammatic representation of this combination which one of us has used (Williams 1984) to illustrate cognitive therapy. This diagram illustrates three points. First, that cognitive therapy consists of both cognitive and behavioural interventions, and not simply techniques dealing with thoughts alone. Second, that in many forms of cognitive therapy, the progression is from the use of a relatively greater proportion of behavioural techniques, at the outset of therapy and/ or when the patient is more seriously disturbed, towards inclusion of more explicitly cognitive techniques. Third, that within both cognitive and behavioural components, therapy progresses from the relatively more simple to the more complex. Within behavioural work, this implies a

136 COGNITIVE THERAPY IN CLINICAL PRACTICE

Figure 10.2 Relative proportion of cognitive and behavioural techniques used as a function of stage in therapy and/or severity of depression

Table 10.1 A hierarchical arrangement of cognitive and behavioural techniques by complexity

progression from graded task assignment to assignment of whole tasks. Within the cognitive component, this implies shifting from a discussion of cognitive events (thoughts, images, particular interpretations) to dealing with underlying beliefs, attitudes, and schemata.

The variation in complexity of the different components of cognitive therapy is important. A more detailed outline is presented in Table 10.1.

The important implication of the cognitive model for how these techniques are used in the therapy sessions described in this book is that they are not all simply added together to form a collection of individual cognitive and individual behavioural techniques. We have already pointed out how therapists working within the cognitive model in this book use the cognitive framework right at the outset to guide the questions which elicit information from the client about their long-term and short-term

THE WIDER APPLICATION OF COGNITIVE THERAPY 137

past, and about their current functioning. It is important to make this point lest studies which purport to test cognitive therapy for some client groups be misinterpreted. For example, there have been five outcome studies which have examined some forms of cognitive interventions with anxious patients, summarised by Stravynski and Greenberg (1987). However, each of these studies takes one or two cognitive techniques (e.g. self-instructional training which attempts to change the internal self-talk of a person; or cognitive restructuring which challenges and repeatedly exposes the fallacious thinking of the anxious patient) and either compares these with behavioural exposure or adds them to a package of behavioural methods to see how much they make a difference. It comes as no surprise to find that nothing much is added by ‘cognitive’ techniques, thus delivered. According to the cognitive model as developed by Beck, setting out to compare cognitive and behavioural tasks in this way misses the point. The cognitive model used by the therapists in this book suggests that behavioural assignments are themselves a potential way of changing the cognitive biases in patients with emotional and behavioural disorders. The important element of the cognitive model is its assertion that behavioural exposure is not sufficient unless it changes these cognitive biases. If behavioural exposure does not produce cognitive change, the model predicts that the patient will relapse. Is such a theory likely to be correct?

Theoretical cogency of a ‘levels’ model

Two issues arise here. First, is there any evidence for entities such as ‘underlying dysfunctional attitudes’ in the various client groups described here? Second, do these attitudes play the role the model ascribes to them as factors which outlast any particular episode of a disorder and render a person vulnerable for another episode?

The first question appears easier to answer. The chapters of this book have uncovered much evidence of dysfunctional attitudes in the various types of patients. Just two examples will suffice. Consider the assumptions of Warwick and Salkovskis’s patient about her health: ‘If I get an illness it will be unbeatable’; ‘Both sides of the body must be absolutely identical or there is something wrong’; ‘Symptoms inside the body are more serious than ones on the outside’; ‘Symptoms always mean something or they wouldn’t be there’. The predictions of the cognitive model are clear and unambiguous in this case. They suggest that if this patient is treated with a therapy which successfully deals with her anxiety about current symptoms, even if it reduces the frequency and intensity of intrusive thoughts about her health, it will not prevent relapse if she retains these dysfunctional underlying assumptions. Sooner or later they will be activated again, and symptoms will return.

Another example is given by Greenberg’s patient who suffers from panic attacks. She was able to identify four levels at which his fears could be represented. First, the fear of the physical effects of panic; second, fear of affect itself; third, the reactions to family and significant others; and fourth, the view of himself as inadequate and incompetent. Once again the cognitive model makes the clear prediction that even if one were able to deal with his fear of the physical effects of panic and thus reduce his symptomatology, nevertheless leaving him with the underlying attitude to himself as ‘inadequate and incompetent’ would leave him with a continued vulnerability for further breakdown.

Biran (1987) illustrates treatment of a single case of agoraphobia which suggests that the treatment of agoraphobia may need to take dysfunctional attitudes into account. The first stage of the treatment was exposure with some attempt to change surface cognitions. A great deal of progress was made, but careful assessment revealed that at the end of this phase many core dysfunctional attitudes remained which were tackled in a second phase of therapy. Nine-month follow-up revealed no relapse. This result needs to be followed up by the inclusion of specifie hypotheses about relapse in future outcome studies.

The answer to the second question is more difficult. Do dysfunctional attitudes, if untreated, act as relatively permanent vulnerability factors, as Biran clearly assumed? Has not the evidence from studies which show normalisation of dysfunctional attitudes on recovery from depression revealed that what we once thought were vulnerability factors have turned out to be merely state-dependent variables (Wilkinson and Blackburn 1981; Lewinsohn et al. 1981; Simons et al. 1984)? If so, patients will have many permanent-looking dysfunctional attitudes when distressed, but these will disappear when the distress remits.

There are indications that this conclusion is premature, however. According to Teasdale (1983), an important maintaining factor in depression is the extent to which any amount of affective disturbance produces cognitive changes. These assumptions are examined in a further paper by Teasdale and Dent (1987) in which recovered depressives and ‘never depressed’ controls were given mood induction and the extent of cognitive change examined. They found that for equivalent degrees of mood shift, the recovered (and presumably more vulnerable) group showed greater tendency to rate themselves negatively. Vulnerability for depression may thus be defined in terms of the amount of affective disturbance needed to make people react with global negative self-evaluations. If a relatively small affective disturbance causes a large cognitive reaction there is a greater likelihood of the negative spiral twisting more deeply. Notice that these notions overcome the problems that arise from the negative findings in the research literature. For example, one would not necessarily be able to measure this vulnerability in the complete absence of current depressed mood, so that testing recovered patients may often show little cognitive differences (Wilkinson and Blackburn 1981; Lewinsohn et al. 1981). The vulnerable people may nevertheless be those who react to small mood disturbance with more ‘catastrophic’ cognitions. To deny that these people are vulnerable is