Deze samenvatting is geschreven in collegejaar 2012-2013.

Inhoudsopgave

A: Cognitive Behaviour Therapy evolution

B: Cognitive behaviour therapy and its scientific foundation

C: Cognition and emotion

D: Panic and social anxiety

E: OCD; Obsessive-compulsive disorder

F: Depression

G: Chronic fatigue syndrome

H: Primary care findings

A: Cognitive Behaviour Therapy evolution

Nowadays Cognitive behavioural therapy is widely accepted and practiced by more and more clinicians: it is the most broad and confidently practiced form of psychological therapy.

CBT evolved in three stages.

1. stage 1: behaviour therapy evolved in UK and US from 1950-1970 with alternate developments.
2. stage 2: growth of cognitive therapy in the US (1960+)
3. stage 3: merging of behaviour and cognitive therapy à cognitive behaviour therapy, late 1980s.

These stages are described in more detail below.

Stage 1: evolution behaviour therapy
The British form of Behaviour Therapy (BT), developed in the early 1950s, and derived mainly from the ideas of Pavlov (classical conditioning), Watson (famous for the Little Albert experiment, behaviorism pioneer) and Hull (drive theory).

Wolpe (systematic desensitization) and Eysenck (among other things, famous for his personality dimensions – neuroticism and extraversion) were the major contributors in the early growing phase of behaviour therapy in the UK.

In the meantime: the ideas of Skinner (operant conditioning) were applied to clinical problems in America. Psychiatric patients shaped their behaviour with use of tangible rewards (the behaviour is thought to be a constructive response) or withhold of rewards (the behaviour is thought to be a destructive response).

The Americans started to work with institutionalized patients with severe problems (like schizophrenia, manic-depressive disorder). They tried to improve the behaviour of people with these problems.

Ayllon and Azrin (1968) came up with the basis for ‘token economy systems’, which started in psychiatric institutions but were later on also introduced in schools, hospitals, hostels etc. In these token economies patients received tokens as reinforcer (originally plastic discs, which could be exchanged for cigarettes, sweets, magazines, etc) for appropriate behaviour and omission of reinforcement for inappropriate behaviour.

To sum up, the American psychologists adopted a Skinnerian style in training and outlook, were behaviourist in their thinking and language, and believed that all psychological/psychiatric disorders originated from false learning. The focus of their work was exclusively on behaviour.

In the United States the work was conducted mainly by psychologists whereas psychiatrists played little part. Unlike the pioneers in the US, in Britain the work on behaviour therapy was conducted by psychologists and psychiatrists. The British group extended their research on to adult neurotic problems, and focused mainly on outpatient samples. They worked mainly on treatments for agoraphobia and other anxiety disorders. They had respect for the ideas of Pavlov and Hull. Hull’s theory provided a possibility of the extension of the theory to clinical problems. Hull’s drive theory, which postulates to predict and control behaviour, contains the following: a stimulus affects an organism and the resulting response depends upon characteristics of both the stimulus and the organism.

The British, who concentrated in London, didn’t ignore genetic contributions, as did the Americans who thought all anxiety disorders resulted from unfortunate conditioning events (e.g. traumas). Their Interest grew for human neuroses. They experimented with neurotic behaviour in animals. Masserman proved the possibility of reducing the fear and abnormal behaviour of animals through conditioning techniques. As an answer Wolpe laid the basis for systematic desensitization (he translated this to a more human form: feeding became relaxation and he added imaginary exposure). Wolpe formulated the theory of reciprocal inhibition: Reciprocal behaviours are competing behaviours. If a situation elicited a certain response, a new introduced stimulus could elicit a different response, and the old response could be weakened. When a subject’s alternate reaction increases, new behaviour is learned and the old behaviour gradually disappears completely. According to this theory in Wolpe’s systematic desensitization, relaxation became the substitute for feeding as the main inhibitor of fear. Wolpe’s theory was helpful but couldn’t explain all of the therapeutic effects people with anxiety disorders experience.

Theorists attempted to explain the persistence of anxiety and unadaptive behaviour to its roots, like Mowrer (1960) who developed a two stage model of fear and avoidance: avoidance behaviour persists because it is successful – especially in the short term. Eysenck made behaviour therapy a leading form of psychotherapy.

Large numbers of people benefited from these developments. The most progress was achieved in reducing anxiety disorders, childhood disorders and improving Quality of Life.

Stage 2: growth of cognitive therapy

Due to the lack of progress in treating depression and the delusional prohibition against the use of cognitive concepts, many therapists read Beck’s work and began to treat depressed patients with cognitive therapy. The remaining inhibitions about cognitive therapy vanished since it was successful, at least, when it was used together with behaviour therapy.

Cognitive pioneers at this time were: Beck and Ellis. They both argued that most disturbances originate from faulty cognitions and/or faulty cognitive processing. The cure has to be found in correcting these cognitive faults. Beck became famous for his treatment for depression: he used cognitive therapy combined with behavioural components. Ellis (around 1960) came up with rational-emotive psychotherapy (RET); emotional or psychological disturbances result from thinking illogically or irrationally. The purpose in RET is to maximize the rational or logical thinking and minimize the irrational or illogical thinking. In order to overcome fears you need 1) insight and 2) action. Ellis incorporated more behavioural components in his RET. Because of Beck’s success in treating depression (mainly because of his famous cognitive triad: pessimistic feelings about the self, the world and the future) he received most attention.

The behavioural therapists liked the cognitive form and visa versa, but the debate continued because of the indefinable interactions between cognitions and behavioural changes (what is the underlying mechanism? Which aspect is more important?).

However, there was still a gap between cognitive therapy and cognitive behavioural therapy at this time.

Stage 3: merging behavioural and cognitive therapy
There was a major shift towards cognitive psychology in psychology in general. The two distinct forms of therapy – the behavioural and the cognitive – were fused together by the successful development of a treatment for panic disorder.

Cognitive therapy was offering content to behaviour therapy. In other words: cognitive concepts had widened the explanatory range of behaviour therapy and helped to fill in the gaps. It has to be said that therapists were a bit too optimistic about the effectiveness of cognitive behavioural therapy (around 1990). The results of studies investigating the effectiveness were open to alternative interpretations: cause, consequence or correlate? What was the working mechanism? For example, Margraf (1991) found that negative cognitions in panic disorder can decline to the same extent in pure exposure treatment as well as in cognitive therapy. So there was no superiority effect of cognitive therapy.

Another obstacle is timing: when does change occur? Cognitive changes can be hard to track. Is it during therapy, during homework assignments? Due to these unclear aspects, it is hard to find the working aspects of treatment.

Explanation for the results of cognitive therapy can be found in treating panic. This is the best supported explanation at this moment (see also chapter D). There is no plausible alternative explanation for the effects of cognitive therapy at the moment of writing this chapter. In the future cognitive analyses will be applied to a wide range of medical-psychological problems (undergoing stressful medical procedures, doctor-patient relationship, and construction of health) and cognitive therapy is expected to expand itself on a variety of non-psychiatric medical problems.

B: Cognitive behaviour therapy and its scientific foundation

Behavioural treatments suffered from skepticism about the scientific basis. In response, there was a retreat from complex clinical patients to psychological dysfunctions in healthy people, like college students. This way, it was possible to show that learning principles could be applied in an informative way to problems which had some resemblance to clinical disorders.

By conducting studies with normal subjects they found an important shortcoming: a failure to take patients’ attitudes and beliefs into account. As a result a search began for ways of incorporating these important elements in treatment. The man with the answer: Beck and his cognitive therapy.

In this chapter, some of the advances of treatment will be reviewed, and for this purpose the experimental studies can be divided into three groups:

1. characterize key cognitions in psychiatric disorders
2. test predictions about the role of these cognitions
3. study factors that maintain cognitions

First some important Models:

Influential models in cognitive therapy:

• Beck’s model of schemata: in depression, schemata are abnormal and negative cognitions arise when a stressful event activates a dysfunctional schema. These schemas persist because people make cognitive errors (e.g. overgeneralization). Beck’s model suggests firstly that thinking becomes more negative when patients are depressed and that this negative thinking maintains the disorder; second that some people who are not depressed have dysfunctional beliefs that make them prone to develop depression during unfavorable circumstances.
• Emotional processing model. This model was invented to account for the clinical observation that the recall of certain memories evokes an emotional response, and that this response diminishes with time and with repeating the recall. Emotional processing has failed when the emotional response persists.

Important cognitions
An attempt is made to reverse certain cognitions in a short time; patterns of thinking that have been established for many years. There are two options to accomplish this: focus treatment on as few as possible cognitions maintaining the disorder (e.g. Clark’s treatment for panic disorder focuses on changing catastrophic cognitions) or use some kind of broad spectrum therapy in which several cognitive and behavioural techniques are combined in an attempt to change a wider range of cognitions and symptoms (Barlow combines cognitive procedures with exposure to interoceptive cues and relaxation training). Several aspects of cognition have been studied in more detail.

Cognition: Thinking

Abnormal thinking is illustrated in panic disorders; patients describe fears that one or more of the physical symptoms of anxiety will lead to a medical emergency. Clinical observations as well as questionnaires and component analysis proved this kind of thinking to be true for patients with panic disorder.

A challenge for panic disorder patients is to recall the thoughts at the time of panic (because these thoughts are not constantly running through the mind, only at times of panic). Clark tried this to ask patients to imagine rapid heart action awareness, and then asked what the patient was thinking.

Another way to investigate catastrophic thinking is by very rapid responses to certain stimuli, for example: complete the sentence “If I had palpitations I could be…….’. Panic disorder patients are primed to expect threatening words, so they don’t only answer faster (more automatically) but also answer faster to threatening words instead of adaptive words like the control groups did.

Beck found certain ways of distorted thinking in depressed patients, as confirmed by other investigations.

Cognition: Attention
In anxiety disorders, there is a general bias towards attention to anxiety-evoking stimuli. Social phobic patients were assumed to attend selectively to the reactions of other people to their behaviour. Experimental studies on social phobic patients show different findings on attention: these patients had more negative self-evaluative thoughts about their own social behaviour. 

Patients with anxiety disorder, depression and obsessional disorder focus more attention on themselves and less attention on their surroundings.

Cognition: Memory
Lloyd and Lishman (1975) were among the first to show that low mood is associated with more rapid recall of unhappy memories as opposed to happy memories. This effect of mood on memory is important because it is likely to maintain low mood by setting up a vicious circle in which low mood leads to recall of unhappy memories which in turn lowers mood further.

Cognition: Visual imagery
Distressing visual imagery may occur in any psychiatric disorder. However it is particularly frequent in post-traumatic stress disorder. Visual images are more persistent than intrusive thoughts because this kind of imagery is more difficult to process emotionally than are verbal recollections of the same event.

Cognition: Worry
Worrying thoughts are associated with less emotional arousal than visual images. However, it may persist because it is a form of avoidance of imagery and therefore anxiety (short-term reward). Worry should lead to less effective emotional processing and therefore to longer term anxiety.

Cognition: Meta-cognition
Meta-cognition refers to beliefs and actions concerned with regulation and interpretation of a person’s own cognitions. There hasn’t been much research on this topic yet, but it could be an important subject to focus on.

Hypotheses testing
To find evidence for hypotheses on the roles of cognitions, experiments are the answer. To illustrate these kinds of experiments, work on panic disorder and depressive disorder are demonstrated as examples.

The Panic disorder hypothesis predicts that

1. panic attacks will occur when a person pays attention to this arousal and attributes it to a physical cause and fears it will have a catastrophic outcome.
2. It also predicts that panic will be produced if catastrophic cognitions are directly activated; and that autonomic arousal will decrease panic, when these catastrophic cognitions are reduced in strength.
3. panic attacks will not occur when cognitions are inactivated at the time when patients are exposed to a stimulus which usually produces panic.

There is evidence for all the predictions: panic can be induced by autonomic arousal arising from any cause (e.g. hyperventilation). Panic could be induced by providing false information that heart rate had increased and when subjects, who had been informed about the consequences and had to breathe CO₂-enriched air didn’t experience as many panic attacks as people who didn’t receive the information.

Depressive disorder is characterized by intrusive thinking. Fennell (1987) showed that when the level of depression was low, distraction had the desired effect of reducing the frequency of depressive thoughts and of producing an associated improvement of mood. However, they failed to find this result in severely depressed patients because

a) low mood increased self-focus,

b) clinical observations suggest that low mood increases the intensity of the intrusive thoughts and

c) it has a different etiology compared to other depressed cases.

Maintaining factors
Cognitions can be changed in two main ways:

1. directly by questioning their logic basis, presenting contrary arguments, or arranging experiences that show that these cognitions are unfounded.
2. indirectly by removing factors that are preventing the changes that normally take place when people are confronted with information and experiences that are incongruent with their beliefs (e.g. patients who expect to faint in a crowded shop and who always avoid/escape from such places, are never able to test the belief that they would have fainted, so the fear of fainting stays because of these ‘safety behaviours’ like avoiding/escaping).

Attempts to suppress thoughts lead, after a short delay, to an increase in the frequency of the previously suppressed thoughts (‘don’t think about white bears’). This finding has not been confirmed by all studies. However, this is important because they suggest that thought suppression could set up a vicious circle which could maintain intrusive thoughts.

These findings indicate the possible importance of maintaining factors in preventing cognitive change. They also suggest that, in treatment, it could be more effective to modify maintaining factors than to attempt to change cognitions directly by reasoning or questioning.

C: Cognition and emotion

The basis idea about emotions consists of the assumption that emotions are mediated through interpretations people give to their experiences (cognitions). Even though this idea sounds plausible, it has some limitations/cautions:

• cognitions as antecedents or consequences of emotions? Is it always true that cognitions are the antecedents of emotions or could it be the other way around? You can think of powerful emotions which produce cognitions. Cognitions could be a consequence of the emotional state as well. In depression this process is well illustrated: depressive mood (emotional state) has a powerful influence on cognitive processes. Once the depressive mood is improved by medicine and/or therapy, negative cognitions disappear as well.

Maybe a better relation between cognitions and emotions is to assume they share a reciprocal relationship. Keep in mind that similar mood states, similar emotions, can have different effects on cognitive processes.

This last assumption finds evidence in research on investigating mood incongruent with memory: most research finds, when inducing a specific mood state (by verbal of musical expressions), congruent mood memory. This implies the following: in depressed moods, subjects have more difficulties recalling positive experiences and are more likely to recall negative experiences, compared to happy moods.

Parrott and Sabini (1990) also investigated this procedure in depressed moods. What they found was surprising: when mood was induced by other means (weather, background music) mood incongruent with memory was observed; depressed moods were more likely to recall positive memories compared to happy moods.

To conclude these findings: depressed moods are not necessarily similar to one another on its effect on cognitions.

• Research concludes that there are various kinds of cognitions; each kind of cognition has different ties with emotion.
• Some researches do not separate emotions and cognitions from each other. This suggests both concepts are intertwined to some extend.
• The maintenance of emotional disorders, like depression, has potential to persist for longer periods even without any environmental input. Negative cognitions can be the explanation for this finding. But how can you explain an ongoing stream of negative cognitions? The book doesn’t provide a clear answer for this, instead it emphases the complicated relationship between cognitions and emotions.

Three different approaches to the concept of ‘mind-in-place’ (a metaphor suggested by Ornstein, 1992) will be discussed in more detail.

1. people don’t have one, but many minds. The dominating one is the current ‘mind-in-place’.
2. mood disorders suffer from persistence from some minds-in-place (patients get stuck in it)
3. cognitive behaviour therapy works by helping patients shift their mind-in-place, with the focus on the shift from the one they got stuck in to other minds.

1. Many minds
The mind consists of a number of distinct ‘minds’, each with its own specialization. The idea behind the ‘mind-in-place’ is that one mind rules at the time. The ruling mind is the one circumstances determines to be required. Alfred serves a perfect example of this phenomenon. Alfred, a man who was standing on the edge of a cliff, about to jump off, didn’t respond to any of the requests his psychiatrist made (‘think about your kids, your wife’). However, when  police a officer came and yelled that the person driving the Pontiac station wagon had to move his car right away because it was standing in the way, Alfred climbed down from the edge and moved his car. This example shows a perfect example of a drastic shift of the mind-in-place. Environmental input can start these shifts, rather than any internal input.

Research suggests the shift doesn’t necessarily have to take place automatically. An experiment showed that triggering certain states (e.g. hostility) adjusts the threshold for using particular constructs. Another experiment delivered more evidence for this suggestion. Subjects, who were primed with achievement words, and were thought of to activate an achievement-state, did better on a scrabble task following the primed achievement words.

2. Mood disorders and mind-in-place
Extension of the fact that depression causes interpretations to be more negative, researchers investigated the influence of these negative cognitions on information-processing. Clinical depression was associated with a rise in accessing unpleasant memories.

According to the associative network theory from Bower: depressed mood puts negative constructs on sharp, so that in interpreting experiences, they will be used more often, and as a result you will get more negative cognitions.

The Interacting Cognitive Subsystems (ICS) framework from Barnard and Teasdale (1991), indicates that the effects of moods, do not operate on a single construct, but on a broader, generic level of representation. The ICS analysis suggests that in depression there is a shift in schematic models (from functional mental models to dysfunctional, different models). In research subjects had to complete certain sentence stems. These sentences were wisely chosen: subjects with dysfunctional models would complete them with positive words and subjects with functional models would complete them with negative words. An example that was used in this study: ‘For everyone to look to me for guidance and advice would make me …….’.

Dysfunctional model-subjects could answer ‘happy’, and functional mood-subjects could answer ‘exhausted’. The results of this study supported the view of the schematic models: depressed subjects gave significantly more positive completions compare to controls. After three months they had to complete the sentences again and the depressed subjects, whose moods had got better in the meantime (because of treatment), completed the sentences with more negative words. In contrast, subjects whose mood had got worse after three months gave more positive words in finishing the sentences.

3. Persistent mind-in-places
If everything goes well, mind-in-place shifts over time as circumstances changes. This process does not happen in mood disorders: patients get stuck in one (dysfunctional) mind. How is this explained?

To answer this, the Interacting Cognitive Sybsystems (ICS) framework, a model by Teasdale and Barnard (1993) will be elaborated. ICS is an information-processing framework. It is not described in detail in the book, so only aspects related to the topic of the book will be addressed. Several elaborations can be found in the book though.

But to understand its core: it is based on the following, basic ideas:

1. There are qualitatively different kinds of information; you can also call these mental codes. Each code represents other sensory experience aspects (e.g. pattern of light, color). There are other codes, which represent repeated pattern (extracted from sensory code patterns created by individuals self over the course of their life). For example: a visual object code captures underlying patterns from patterns in visual sensory codes (e.g. behindness). To make it more complicated, these recurring patterns are themselves represented by codes which represent meanings. The ICS makes a distinction between two kinds of meanings: specific, low-level meanings and generic, high-level meanings. You can refer to the last one as schematic mental models.
2. Information can be transformed from one kind of code to another by certain processes. For example, when you have an input of sound sensory information and a pattern of speech-level code as output.
3. Memory stores all the patterns of information codes.
4. Generic, high-level meanings (which are emotional) play a major role in the production of emotions.

It is possible for sensory input to have a direct effect on emotion production (through the synthesis of high-level affect-related meanings). The transformation processes have been divided in nine cognitive subsystems, each with its own specialization.

In one ‘mind’, all these processes take place. Now it is time to try to formulate an answer to: how does the persistency of certain minds work (in mood disorders)?

In depression for instance, a depressive mood depends on continuing production of schematic depressive models.

Why is this production an ongoing process?

• Because in depression, a continuing stream of negative events may happen which keep producing depressive schematic models (but this is hardly ever the case in depressed individuals).
• Because the cause of negative input are negative thoughts one produces on its own. So the depressive mind will maintain itself. This process is well illustrated in the model below (based on Teasdale and Barnard, 1993). For further elaborations of the model, see page 81. Key features of this model of the mind:

1. two cognitive subsystems deal with meanings (schematic model and negative specific meanings)
2. depression results from depressive high-order meanings directly and indirect from negative specific meanings
3. it is a dynamic system; for depression to be maintained, a continuous stream of depressive high-order meanings has to be provided. When this process is blocked, the depression will neutralize.
4. Functional ‘minds’ focus on reducing depression. However, in this ‘mind’ the cognitive strategies are dysfunctional and the depression is maintained.

There are three aspects of the process configuration that contribute to being stuck in one mind:

1. Cognitive system feedback loop (thin lines in the model); depressive-related schematic models produce specific negative meanings, and on their turn contributes to depressive schematic models.
2. Bodily sensations feedback loop; depression generates physical sensations (bodily effects), which causes input for depressive schematic model.
3. Schematic models give priority to limited processing resources; information associated with depression gets priority treatment. A term used for this idea is: cognitive imperialism.

How to change the mind-in-place?
According to the outcomes of social experiments (where people were asked to put a huge sigh in their front lawn, most people didn’t agree, but 60% of people who were previously asked to put up a more subtle sign and agreed to do this, did agree with the view-blocking sign in their front lawn) it appears that humans have a memory for minds. When a certain mind was once the mind-in-place in a certain context, in similar contexts, that mind has a tendency to knock on the mind-in-place door again.

The ICS framework suggests a special memory system for all the created schematic models. Cues, as with all types of information, can retrieve a specific schematic model.

This basic idea can be applied to depression, where certain depressive models will be dominant in the mind-in-place. How can that be changed? A distraction task will have temporarily effects but cannot offer a long term solution. The key is to create provision for alternative schematic models. The alternative models should have some similarities to the depressive models in order to respond to the same cues and/or context, but on the other hand, these models should differ enough in order to prevent (more) depression.

Depression treatment
Psychological treatment for depression: cognitive and/or behavioural approaches, should focus for long-term success on creating a stock of memories of alternative schematic models. By implementing homework assignments, patients get the chance to create these models in a wide range of contexts, so that accessing these new models can more easily be provided by these contexts.

Clinical observations show that cognitive therapy can lead to a shift of schematic models to certain themes like: depression-as-a-psychological-mood-in-which-I-see-no-positive-future, instead of ‘the-future-is-hopeless’. Investigations on cognitive therapy versus medication use for treating depression, favours cognitive therapy for long-term effectiveness. The major challenge in depression treatment is to prevent relapses after treatment is finished.

Research that explored the meta-awareness (having a wider perspective on feelings and thoughts) showed that patients, receiving cognitive therapy and medication, had a significant increase in meta-awareness compared to patients receiving only medication. To see if these findings are indicative for preventing relapse a follow up has to be conducted, and at time of writing, no follow up had been completed yet.

Meanings in cognitive therapy
The ICS recognizes two different kinds of meanings:

• Specific, or low-order meanings refer to specific concepts and their relationships (propositional code).
• Generic, or high-order meanings refer to schematic mental models of experience (implicational code).

Conclusions from these different meanings are the following:

1. Both meanings cannot be reduced to one another.
2. Intervention forms used for the two kinds of meanings should be different
3. ICS suggests that emotions are only linked to the generic meanings.

What does this mean for effective treatment? First, the major goal of treatment should be, as noted before, to change the schematic mental models. This could be accomplished by changing specific meanings which contribute to the models. One technique for this is evidence schemas (considering evidence for and against beliefs). But it is not always sufficient to change the schematic mental model. You should also include actual experiences in which new beliefs/models are created. One way of achieving this is by behavioural experiments. Because the most effective way of changing cognition is by changing behaviour.

D: Panic and social anxiety

Phobic disorders and OCD were considered to be the result of conditioning: in phobias, one of the maintaining factors was avoidance; in obsessive-compulsive disorder it was the compulsive behaviour.

What are panic disorder and social phobia?
Both disorders have been recognized for many years in the DSM.

Panic disorder
The essential feature of a panic disorder is the occurrence of panic attacks (sudden onset period of intense fear) which cause discomfort associated with at least four symptoms (e.g. dizziness, palpitations). You only get the panic disorder diagnosis if you suffer from recurrent panic attacks, where at least some of them come unexpected.

Social phobia
The essential feature of social phobia is a marked and persistent fear of social or performance situations due to the individual’s belief that he/she will act in a way which will be embarrassing or humiliating.

Treatment overview
In the beginning exposure therapy was used as treatment, but it focused only on agoraphobia. In the mid 1970s repeated in vivo exposure had been shown to effectively treat agoraphobic fear and avoidance. Both therapies (in vitro and in vivo exposure) seem to be effective but have several limitations. A sizeable proportion of patients either fail to respond or show only partial improvement. Nowadays there is cognitive behavioural therapy for both disorders. Both specific CBT-forms for panic disorder and social phobia will be described in detail further on.

Dominating models
Before discussing the models, some general assumptions are made:

• individuals become anxious in response to certain stimuli because they interpret the stimuli as much more dangerous than they really are.
• These unrealistic interpretations persist because patients engage in cognitive and behavioural strategies that are intended to prevent the feared event from occurring
• The symptoms of the anxiety itself are additional sources of perceived danger, producing a series of vicious circles which have the potential to further contribute to the maintenance of the disorders.

Panic disorder
The cognitive model of a panic disorder states that individuals who experience recurrent panic attacks do so because they have a relatively strong tendency to interpret certain bodily sensations in a catastrophic fashion. The catastrophic misinterpretations involve: making sensations more dangerous and interpret the sensations as indicators of immediate disaster.

Below you can find a model (based on the model from Clark, 1986) with the sequence of events in a panic attack:

Once an individual has developed a tendency to interpret catastrophically bodily sensations, there are two processes which could contribute to the maintenance of panic disorder:

1. patients become hyper vigilant and repeatedly scan their body
2. safety behaviours tend to maintain patients’ negative interpretations

The critical event is: the misinterpretation of bodily sensations.
It is important to keep in mind that 7%-28% of the normal population experience an occasional unexpected panic attack.

Social phobia
Social phobics develop a series of assumptions about themselves and social situations, and as a result they interpret normal social interactions in a negative way. The negative interpretation (e.g. someone you’re talking to is looking away, the interpretation: ‘I’m being boring’) triggers a state of anxiety which consists of three components (illustrated in the model below based on the model of Clark and Wells (1995):

1. somatic and cognitive symptoms of anxiety that are triggered by the perception of danger.
2. safety behaviours to try to reduce threat and prevent feared outcomes from occurring.
3. shift in attention; from thinking of being in danger of negative evaluation by others to detailed monitoring and observation of themselves

A social phobic’s’ distress is not restricted to times when they are in social situations.

Empirical status of the cognitive models

In this section several correlational and experimental studies will be considered. For the entire description, see page 129 and further.

Panic disorder – misinterpretations of bodily sensations

1. Hypothesis: individuals with panic disorder will be more likely to interpret bodily sensations in a catastrophic fashion.

à difference between internal and external events (panic patients more negative interpretations of internal, social phobic’s of external events)

à panic patients react more heavily to false auditory feedback indicating an increase in heart rate.

à panic patients showed a greater increase in anxiety and panic while reading certain combinations of words (bodily sensations + catastrophes).

2. Hypothesis: sustained improvement after the end of treatment will depend on cognitive change having occurred during the course of therapy.

à misinterpretation of bodily sensations at the end of treatment was a significant predictor of panic/anxiety at follow up.

à within patients who were panic-free at the end of treatment, there was a significant correlation between misinterpretation of bodily sensations at the end of treatment and subsequent relapse.

Panic disorder – cognitive change preventive factors

1. role of interoception in the maintenance of panic disorder

à panic patients were more accurate in their heartbeat perception than controls

2. role of safety behaviours

à panic patients engaged in safety behaviours of the sort which could maintain their negative beliefs.

Social phobia – negative thinking

1. Hypothesis: social phobics interpret social situations in a more threatening fashion

à when possible, social phobics were significantly more likely to choose negative interpretations of ambiguous situations.

à social phobics were more likely to choose catastrophic interpretations of mildly negative social events.

2. Hypothesis: in-situation safety behaviours play a role in maintaining social phobia

à exposure and dropping of safety behaviours produced significantly greater reductions in anxiety and belief ratings for feared outcomes.

3. Hypothesis: social phobics use interoceptive information to construct an impression of themselves which they assume reflects what other people observe and this information is relatively more important than observation of others’ actual behaviour.

à social phobics reported more negative self-evaluative thoughts.

à social phobics have a reduced awareness of the details of a social interaction

à social phobics’s estimates of the dangerousness of social situations are partly based on the perception of their own emotional response.

4. Hypothesis: socially anxious individuals will selectively retrieve negative information about how they may appear to others when anticipating a social interaction

à high FNE (fear of negative evaluation) subjects showed a bias towards recall of negative, rather than positive, public self-referent words.

Specific cognitive behavioural treatments

Treatment for both disorders involves a mixture of cognitive and behavioural techniques which are intended to help patients identify and modify their distorted, anxiety-related thoughts and beliefs. Particular emphasis is placed on reversing the maintaining factors identified in the models.

Panic disorder – treatment overview

1. reviewing a recent panic attack with the patient to identify main sensations and negative thoughts.
2. cognitive procedure: identify possible triggers for unexpected attacks (make use of diaries/discussion).
3. cognitive procedure: help patients to understand the significance of past events which are inconsistent with their negative beliefs.
4. cognitive procedure: education about the nature of anxiety.
5. cognitive procedure: deal with images of feared outcomes (in the same way as you deal with negative thoughts).
6. behavioural experiments: these fall into two classes; either induce feared situations in order to demonstrate possible causes of symptoms or to stop safety behaviours.

Social phobia – treatment overview

1. reviewing recent episodes of social anxiety with the patient to identify main sensations, safety behaviours and the interoceptive part
2. behavioural experiments: changing safety behaviours is often the best way to start.
3. obtain realistic information about how the patient actually appears by using video and audio feedback (make use of homework assignments for practicing purposes)
4. test predictions about negative evaluation by others through behavioural experiments (intentionally perform behaviour that patient falsely believe will lead to negative evaluation).
5. social phobics tend to make ‘post-mortem’ of their social interaction: the post-mortem provides further, incorrect, evidence of social failure (patients make things worse afterwards). Discuss this with the patient to ban the post-mortem.
6. modify assumptions (through the use of Socratic questioning)

Treatment efficiency

Panic disorder
Cognitive therapy is effective, and the success is not entirely attributable to non-specific therapy factors. Another study shows cognitive therapy superior to relaxation and imipramine (medicine). Cognitive therapy seems to be the better choice, also for better long term maintenance of improvement.

Several studies share these results (actually four out of five say cognitive therapy is superior).

Because of these positive outcomes, there have been attempts to develop a successful but brief therapy treatment. Clark managed to develop a seven-session cognitive therapy treatment with the same positive long term results.

Barlow developed the panic control treatment (PCT), a form of CBT, which is different from cognitive therapy, but PCT shares many common procedures. This form appears effective as well.

Social phobia
Based on earlier cognitive behavioural models, several treatments have been developed for social phobia:

• Butler and colleagues’ anxiety management training (AMT)
• Heimberg’s cognitive behavioural group treatment (CBGT)
• Mattick and Peter’s combined group exposure and cognitive restructuring treatment

Comparisons between these psychological interventions indicate that each of these treatments has a specific effect, but there is room for improvement in effectiveness. Clark and colleagues developed a new treatment, based on the model described in this chapter, which has to prove its effectiveness in the future.

E: OCD; Obsessive-compulsive disorder

OCD is a major disabling anxiety disorder. Individuals with OCD have to learn how to live with it, rather than hope for a 100% cure. Psychosurgery is still considered to be appropriate in the most severe cases. Prevalence of OCD is between 1% and 3% of the general population. CBT is widely applied as treatment for OCD.

OCD – core problems
OCD is an anxiety disorder that causes feelings of extreme panic, fear and guilt and compels the individual suffering from it to perform certain actions. Recurrent thoughts, images and impulses or compulsive behaviours are characteristic for OCD. The compulsions can be overt (hand washing) or covert (thought rituals). To distinguish obsessions from other psychotic phenomena, the individual with OCD has to recognize the intrusiveness of the obsessions, created by their own mind. Intrusive thoughts are always ignored, suppressed or neutralized.

Compulsions are repetitive behaviours which the individual with OCD performs in response to obsessional thoughts or in order to fulfil a certain rule they came up with (like switching the light on and off 17 times). These compulsive behaviours must be aimed to reduce distress or the chances of a certain feared outcome.

In order to be diagnosed with OCD, the obsessions and/or compulsions must interfere with the individuals’ daily life and cause distress. This criterion is crucial, because a lot of people (around 90%) experience intrusive thoughts without meeting the OCD diagnosis.

Treatment developments
The learning theory provides the basis of current behavioural therapy for OCD. The two factor model of fear by Mowrer (1947) is described in the OCD context: fear of specific stimuli has developed through classical conditioning, and operant conditioning maintains the fear because the individual reduces aversive stimuli initially by escaping or (later on) avoiding the feared stimuli. Another important observation by Solomon and Wynne (1960) was that avoidance responses continued long after the conditioned stimuli had ended. This is typically the case in obsessions.

Meyer came with the first success stories of behavioural treatment for obsessions. He tackled avoidance behaviour directly. Rachman adapted his treatment method and added in vivo exposure.

Behaviour theory
Behavioural treatment of individuals with OCD is based on the Behavioural theory. This theory suggests that obsessive thoughts are associated (through conditioning processes) with anxiety, and fail to cease. The avoidance behaviours prevent anxiety from decreasing.

This is why behavioural therapy is known as exposure and response prevention (ERP). The focus in this therapy is on:

• expose the individual to obsessional response evoking stimuli
• help to prevent avoidance responses to occur

Research supports, first of all, that obsessions were associated with anxiety. Second, that avoidance behaviour decreased the anxiety. Third, that if the avoidance compulsions were delayed, anxiety spontaneously decreased (not immediately) and fourth, that when the rituals were not performed, the anxiety level in the next feared situation was lower than when the ritual was performed.

ERP in practice
Effectiveness rates of behavioural treatment seem to be around 75%. Effectiveness is not equal to ‘cured’, but you have to think of it in terms of improvement. OCD treatment has to deal with dropouts and treatment refusals as well. This could be due to other psychological disorders that play a major contribution to the individual like depression.

So despite the seemingly good effects ERP can have, there is room for a lot of improvement. Because of this and the cognitive basis for obsessions, cognitive therapy entered the OCD treatment approach. Some researchers thought of OCD as a general cognitive deficit disorder. This is not surprising given the cognitive restrictions OCD individuals share: memory problems, intrusive thoughts, bizarre behaviour, problems with decision making and generalized mood disturbances.

Cognitive deficit theories have been developed and are based on either the view that obsessive individuals have a general failure in cognitive control or they have poor general memory and decision making abilities.

One problem with these theories is that they do not account for the highly specific problems with memory and decision making. Research supports the specificity of these two concepts.

The cognitive behavioural hypothesis proposes the problem to be a specific one instead of some general deficit. It suggests that obsessions are the result of patterns of specific responses to stimuli where the individual is emotionally sensitive about. Another way of stating the hypothesis is by explaining that obsessive patients try too hard to control their own cognitions and as a result other cognitive functions suffer because of the competition for resources for processing.

In effectiveness of therapy treatment the general cognitive deficit theories find no grounds. Only the behavioural and cognitive theories provide a basis for the OCD phenomenology.

Cognitive theory
Obsessive individuals tend to make attempts to neutralize the thoughts/images/impulses. Neutralizing means to voluntarily take action with the intention to reduce the perceived responsibility. Neutralizing can be overt or covert (e.g. compulsions or thought rituals). Because neutralizing is avoidance behaviour, it maintains the obsessions, makes them even more frequent and as a result the urge to neutralize increases.

The Cognitive theory hypothesizes that the interpretation of the obsessional thoughts is responsible for a lot of effects OCD individuals experience:

• increased anxiety, discomfort, and even depression
• the original thought and other associated ideas are more easily accessible
• neutralizing responses attempts to avoid or escape responsibility

Cognitive theory thus hypothesis that it’s not poor mental control which causes OCD, but misinterpretation of mental functioning. The reason OCD individuals experience discomfort is because they appraise the content and occurrence of the intrusive thoughts. Due to the avoiding behaviours (overt and covert) motivated by the appraisal, the frequency of the thoughts increases. The appraisals made by the individuals are focused around responsibility, which leads to mental efforts (preoccupation and over-control). The term responsibility implies that the individual thinks he/she is, or may come to be, the cause of harm unless he/she takes action to prevent or restore this. Without this feeling of responsibility, obsessional episodes would not occur (even though no obsessional episodes will be caused, it does not take responsibility to experience feelings of anxiety and depression).

Because obsessive individuals try too hard to control their mental processes and activity (over-control), it can cause a lot of distress. There are several reasons why distress occurs:

1. direct conscious attention to what’s going on inside the mind could modify the contents of your consciousness
2. trying to control something which is hard to control causes failure and has the opposite effect
3. trying to prevent harm and responsibility for harm makes individuals more alert to harm concerns
4. neutralizing works as safety behaviour; it prevents the individual from ever knowing that the harm would probably not occur without the neutralizing behaviour.

Experiments intrusive thoughts
Some ‘recent’ (1989 – 1994) experimental studies are described in detail.
Let’s start with the measurement instruments. Responsibility was measured with two different approaches. One assessed general attitudes and beliefs which reflected responsibility, the second assessed specific self-reported responsibility interpretation.

Let’s continue by discussing briefly some experiments which had been conducted to look for evidence to support the cognitive theory. The research purpose was to show an increase in frequency of intrusive thoughts after avoiding, escaping, or other strategies. Some contradicting results were found, but this was mostly due to the experimental factors. Other experiments did find an increase in frequency of intrusive thoughts, right after suppression periods and in OCD individuals this increase in frequency continued. The importance of responsibility appraisal has also been found in research.

Thinking errors
The reason for discussing cognitive thinking errors is due to the fact that cognitive hypotheses suggest that OCD individuals can be characterized by their thinking pattern, from which the most typical thinking is: any influence over the outcome of a situation equals feeling responsibility for the outcome.

Investigations about the role of responsibility and omissions show that OCD-individuals are more sensitive to omissions. Normally (without OCD) people are sensitive to omission under two circumstances:

• when it is believed one has a special duty to be aware of consequences from omission
• when one has foreseen the negative consequences as a result from the omission.

For OCD-individuals both circumstances play a major part. Some OCD individuals see foreseeing negative consequences as a duty.

When OCD-individuals do not see any dangerous objects they don’t feel responsible or foresee harm. But when a possible dangerous situation is spotted (for example, a piece of glass in the middle of a classroom), they have to decide what to do with it. Deciding not to act (omission of acting), will result in feeling responsible for what will happen with it.

Implications for treatment of the cognitive theory
Given the cognitive theory, Cognitive behavioural therapy is aimed to help OCD-individuals realize that their obsessive thoughts are very distressful but irrelevant to further action.

The OCD individuals have to learn how to control intrusive thoughts. This is helpful only when they realize that their interpretation has to be changed. In order to learn to control the obsessive thoughts, OCD individuals have to learn that exercising control is pointless.

A second aim of therapy is to modify beliefs into less threatening beliefs. The OCD individual has to realize his/her problem as a thinking problem, instead of a ‘real’ problem.

An example of how to carry out this aim is to ask a patient to think: ‘I will make myself die right now’. In this manner you can test and understand the obsessive thought. Patients will hopefully see it is the thinking problem which causes the OCD.

Cognitive behavioural therapy was an answer to the ERP problems (high drop-outs and non responsive patients). It is also argued that cognitive therapy brings more complete and thorough change in OCD individuals. Due to the engagement style in treatment, chances of drop-outs and refusal is reduced. 

Cognitive behavioural therapy is one of the few therapeutic treatments which seem to be effective in ruminators. The therapy focuses on appraisal and maximises exposure to make response prevention easier. This last focus is done with the help of an audiotape loop, a certain technique where obsessive thoughts are provoked. The cognitive hypothesis suggests that various psychological problems share certain broad consistencies. A panic attack-individual and a social phobic, for example, both share some consistencies, but specific models of their particular psychological problems will guide them further in therapy.

Treatment strategies in OCD
A general strategy involves the engagement of the OCD individuals in their therapy. It is crucial for them to understand the psychological basis, and thereby understand the reality of their thoughts. It would not help therapy improvement if someone was still thinking he/she would murder his/her children. The patient also has to be agreeing with the fact that therapy focuses on reducing the worries and thoughts instead of reducing the risks that comes with the thoughts. A collaborative relationship is required for effective treatment.

With the help of guided discovery, the maintenance of the obsessive problems will be evaluated and a specific ‘model’ for each individual will be developed to understand the maintenance of his/her problems. Specific treatment elements are finding evidence for and against certain beliefs, and behavioural experiments, to look for further evidence. By doing this, and with the use of cognitive and behavioural interwoven elements in general, patients will learn to adopt more functional and less frightening beliefs.

Other specific elements of therapy are self-monitoring and identification of obsessive thoughts and the appraisal OCD individuals give to these thoughts. By the using exercises (e.g. by keeping a daily record of the obsessive thoughts), they learn how to modify the beliefs and the responsibility that comes with their thoughts.

Therapists also use discussion techniques, which can be extremely helpful, because the patient instead of the therapist will guide him/herself to certain insights about the OCD problems.

Behavioural experiments, previously mentioned, could be carried out within sessions, or in-between sessions. Most of the behavioural experiments fall into either one of the following two classes:

1. behavioural experiments to assess in what way and to what extent certain processes play a role in maintaining obsessive thoughts/fears.
2. Exposure exercises to get used to feared stimuli without having the chance to perform neutralizing behaviours.

To show patients the counter-productive effects of suppressing thoughts, therapists ask them to keep a diary of their thoughts and let them experiment (this could be done as homework and/or in therapy sessions itself) with conscious suppressing and letting thoughts come without trying to neutralize them. This will show the patients that neutralizing (suppression) will only make the thoughts worse and more frequent. By showing this, some longer term effects (a whole day without worrying too much) are established. Therefore it could be a powerful method of demonstrating the way suppression works.

Exposure exercises come in handy for the negative appraisals OCD individuals make. The way patients react in these exercises are observed and evaluated against possible explanations of the problems. Two possible explanations have been identified:

1. the problem is of actual harm and someone’s responsibility.
2. the problem is the worry about that harm and feeling responsible for the prevention. 

Underlying assumptions should also be dealt with. Some dysfunctional assumptions are identified and modified. Due to the crucial impact misinterpretation has on OCD individuals, it is of great importance to pay attention to the misinterpretation and help the patients find other more functional ways to interpret. For patients, there could be two explanations for their thoughts and feelings: reality of their thoughts or a ‘thinking’ problem.

Example of treatment
The treatment strategies in obsessive ruminations are described in detail, divided in six stages.

Stage 1:

This is the assessment stage where the therapist focuses on the following aspects:

• description of recent episode of rumination and the specific sequence of rumination
• identify how intrusive thoughts/beliefs are interpreted and responsibility level of patient
• identify impact of interpretation on efforts to suppress, neutralize, or control the thoughts
• impact of these efforts are emphasized

At the end of the first stage, a formulation of the problem should be agreed on and the goals of therapy should have been established. Goals can be short-term, mid-term or long-term.

To sum up: stage 1 is all about assessment and goal-setting.

Stage 2:

By using several strategies, further clarification of the formulation is determined. The patient has to understand the treatment rationale and why their problems are maintained. The strategies used in this stage are the following:

1. Discussion about the intrusive thoughts (are they helpful? Can violent intrusive thoughts be helpful in some situations? Etc).
2. Discuss the relationship between the intrusive thoughts and the patients’ appraisal. Identifying of normal circumstances where neutralizing takes place.
3. Examine patients’ own ideas about things that could go wrong.
4. Consider the ways in which positive thought could be negatively interpreted. Demonstrate the importance of appraisal of the content and occurrence of certain thoughts instead of the thoughts itself.
5. Discuss what it means to think certain things. What does that say about yourself or someone else if you think ‘I will kill my children’?
6. Identify the problem-solving and intrusive thoughts link. The thoughts can be positive, neural of negative. Explain that it is very useful to have negative intrusive thoughts in unusual circumstances (for example, when you’re being attacked and robbed, it is useful to think violent thoughts)
7. Ask the patient how it would be if no intrusive thought would ever come to mind.

The second stage is about normalizing and considering non-threatening alternative explanations.

Stage 3:
Stage 3 is about reconsideration of the problems. The two alternative views will be compared with each other. Differences and similarities will be discussed. Emphasis is placed on how to experience the intrusive thoughts without feeling distressed. Remind the patient that it is not the goal to eliminate the thoughts; most of the time this is not possible and certainly not desirable.

Stage 4:
With the use of audiotape exposure belief modification is started. Through a tape loop, intrusions are elicited. Responsibility appraisals and the need to neutralize are identified. Response prevention is dealt with by helping the patient challenge their appraisal of the intrusions. This stage involves homework and continuing with this process. Homework consists of using the tape at home, and then at certain intrusive thought eliciting places, finally the tape is played in response to actual intrusions.  

Stage 5:
Stage 5 consists of further behavioural experiments with the tape, and in the end in vivo. Elaboration of the audiotape method is provided by the use of the tape as a response to intrusions. At this time, the patient should be aware of his/her beliefs, the effect, his/her responses, effect of appraisal and responsibility and how to cope with the intrusions. The goal of therapy is not to decrease intrusive thoughts, but because of the patients’ reappraisal, a decrease in intrusive thoughts is a desired side effect of therapy.

Stage 6, final stage:
The sixth stage covers any remaining problems, but its focus is on relapse prevention. Identify possible obstacles in the future and discuss ways of dealing with them. The therapists’ role has shrunk to a minimum and the patients’ efforts are central so that patients can take responsibility for their own actions and thoughts.

Effectiveness
Not enough research has been done yet (at this point in time), but CBT for OCD individuals seems to be very effective, maybe even superior to exposure treatments.

F: Depression

To some extent, depressive mood is a common experience among all individuals. Everyone feels depressed once in a while and perceives the world in a pessimistic manner. But when a depression continues, the pessimistic feelings get worse and more intense. It affects emotions (sadness, hopelessness), cognitions (guilt, memory, self-esteem, concentration), behaviour (agitated), motivation (no interests in activities) and physical aspects (sexual problems, sleep problems, energy loss). Five or more of the symptoms, experienced longer than two weeks will lead to the diagnosis of major depression.

Even though 50% recovers in less than three months, patients often develop a clinical course of chronic depression.

Antidepressants are most often the first attempt to solve the depressive problems. They provide an easy and cheap method for dealing with depression. But to prevent the recurrence of other, new episodes of depression, patients should continue with taking their medication. Research supports the effectiveness of this approach. However, there is a need for effective psychological treatments because:

• some patients do not accept medication
• there is a preference for psychological treatments
• medication has severe side effects
• some antidepressants could be dangerous for cardiac patients
• overdoses of some antidepressants are cardio toxic

All these reasons stress the need for effective psychological treatment for depression.

Learning theories & social skills
Many theories have been developed concerning depression. It started with the view of depression as ‘extinction’. According to the ‘loss of reinforcer’ theory by Costello (1972) reinforcers in the environment of depressed individuals lost their potential as reinforcers.

However, Lewinsohn’s (1970) theory is the most influential behavioural theory. According to this theory depression is caused by a low rate of response-contingent positive reinforcement. As a consequence, respondent behaviour of depressed individuals could provide a sufficient explanation for decreased behavioural output. When depression kicks in, reinforcement from others maintains the depressive symptoms. When close friends and family later on stop rewarding the depressive behaviour (by avoiding the depressed individual), available rewards are reduced further in the environment of depressed individuals’.

One of the major treatment targets at that time was training social skills. This led to an interesting discussion whether depressed individuals indeed had deficient social skills. Some studies show decreases in social skills in depressed individuals, other studies found no deficits in measures of social behaviour.

The suggested conclusion was that it depends on the content of the depressed individuals conversation.

The content of their speech causes the alienating effect depressed individuals can have on others. When a depressed individual talks inappropriate, they could enter an awkward social situation where only advanced social skills would rescue the particular awkward social situation. Depressed individuals often do not possess such social skills and the result is withdrawal from these, and other social situations. So the focus in treatment should not be on social skills alone, but on the content of communication.

Rehm’s theory of self-control (1977)
This theory states that depressed individuals pay selective attention to negative aspects. In evaluating themselves, their criteria are biased so that they could never achieve what they set for themselves. In response to this, rewards are rarely assigned. This results in self-blame, as a lack of self-rewards. Several studies show that depressed individuals do indeed punish and reward themselves differently from non-depressed subjects.

Beck
Three main components of Beck’s cognitive theory of depression are:

1. negative automatic thoughts

• often perceived as 100% true by depressed individuals

2. systematic logical errors, or cognitive errors.

• Seven different categories have been identified:

1. Arbitrary inference: in the absence of sufficient evidence, drawing conclusions about something.
2. Overgeneralization: drawing a conclusion on the basis of one aspect of a situation.
3. Selective abstraction: focusing on one aspect of a particular situation, and ignoring more important, relevant aspects.
4. Minimalization: discounting positive effects of an event
5. Maximalization: exaggerating the importance of events
6. Personalization: linking external events to oneself, even when there is no reason for making such a link.
7. Dichotomous thinking: all-or-nothing thinking. For example: ‘What the point! I can never succeed because I’m only third in this class. I’m not first. So I’m a complete failure’.

3. depressive schema’s

• persisting assumptions about the world, the self and the future.

The theory suggests that these depressive schemas develop over a longer period of time and can be triggered by a combination of certain stressful circumstances.

Beck’s cognitive behaviour therapy deals with the negative thoughts first. Other core techniques of the therapy are:

• behavioural experiments: reality testing of fixed negative beliefs
• homework assignments: to get the patients involved in activities they avoided
• catching thoughts: make depressed individuals aware of the depressive thoughts, automatic thought, schema’s
• cognitive rehearsals: discover possible obstacles, imagine how it feels to succeed in something
• dealing with underlying assumptions and fears: how did the depressive schemas develop and how does it influence patients’ today life?
• Alternative therapy: let the depressed individual imagine an upsetting situation and then think of coping strategies.

Effectiveness therapy
Several conclusions can be drawn from the reviews about the effectiveness of cognitive behaviour therapy.

1. CBT is effective for a variety of populations (think of social class, culture).
2. Antidepressants + CBT are more effective than CBT alone.

Not only CBT is effective in treating depression. In particular approaches which combine cognitive and behavioural procedures, together with cognitive therapy and interpersonal psychotherapy (IPT), seem to be most effective in treating depression.

Effectiveness study in detail
One study is discussed into detail. For the whole elaboration, see page 268 and further. In summary, psychotherapy (either interpersonal psychotherapy or CBT) was no more nor less effective than a certain drug plus clinical management. For the psychotherapies: none of the therapies were significantly more effective than the others on depressive symptoms and overall functioning.

Keep in mind that this study was conducted in 1989!

Relapse and recurrence prevention

The term relapse refers to:

• (finished) successful treatment and
• Recurrence of depression (either measured by cut off scores, for instance on the Hamilton Depression scale or the BDI, or by returning to treatment).

Rates of relapse vary between 22% - 92%, dependent on type of treatment, medication, duration, etc. Studies suggest that relapse rates can be halved by maintaining medication. But to rely solely on medication is not advised for several reasons: addiction, overdoses danger, side-effects. So the question remains: can cognitive therapy help decrease relapse?

Studies found that when cognitive therapy had been added to antidepressant medication during the treatment, relapse rates dropped significantly. An interesting idea that remains speculative: are depressed individuals who respond successfully to cognitive therapy different from depressed individuals who respond to medication? Maybe those individuals responding to cognitive therapy are less likely to relapse anyway. Differences between them and those responding to medication could then be explained by those individual variations, instead of treatment effects.

This idea remains speculative, because no evidence has been presented to support it yet.

To conclude this section: cognitive therapy is not less effective than medication and studies support the finding that cognitive therapy is more effective in preventing relapse. Cognitive therapy is one of the most influential contributions to treatment for depression.

Change mechanisms
As previously described, CBT is just one of the various therapies effective in treating depression. It is suggested that  this view is due to shared therapeutic strategies like providing feedback and new experiences. More specific for depression, therapies share some effective techniques:

• elaborate rationale that provides structure and patients’ belief in controlling their own behaviour and depression
• skills training
• emphasizes importance of these skills outside therapy context
• encouragement to attribute mood improvement to patients’ own efforts, rather than to the efforts of the therapist.

The same treatment outcomes like increased problem-solving abilities and elevated mood, can be produced by many different factors, which may share a final common pathway. After following cognitive therapy, an individual could experience a new depressive episode, but is likely to have learned to prevent the mood from activating negative thoughts and ignore it in interpreting the validity of current beliefs. For both changes it is important to have the ability to retrieve specific, imaginable, concrete and alternative information.

The suggestion is that when individuals are not able to come up with these alternatives, they will respond more slowly to treatment and have a higher chance of relapse.

Depression and autobiographical memory
A study which has an interest in the role of autobiographical memory as a source of information, is discussed in detail. The focus of this study is on the finding that depressed individuals have problems in retrieving specific information. Before discussing the study, is it necessary to understand a couple important consequences that follow deficits in personal memories:

• impairment of reinterpretation of old memories
• obscuration of links between thoughts, mood and behaviour
• preventing generation of alternative coping strategies when one encounters problems

Autobiographical memory is biased in depressed individuals: remembering positive events takes longer than remembering negative events. Another finding is that depressed individuals are more likely to be over-general in their own memories (e.g. specific memory of ‘going for a walk with the dog last Friday’ is over generalized in ‘going for walks with the dog’). The same findings are revealed during cognitive therapy: ‘I can’t do anything right’, ‘I’m a failure’ are common, over generalized statements patients make. Retrieving specific memories is hard for depressed individuals. This is true for both negative as positive events.

Memories can be illustrated as layers. The upper layers are general and act as indices for the specific detailed lower layers. For example: for the cue word ‘happy’, the upper layer could be ‘my girlfriend’ (because this is in general associated with happiness). Depressed individuals get stuck at this level. A term for this phenomenon is mnemonic interlock. Mnemonic interlock is most likely to occur with self-references instead of specific events memories.

Effects of mnemonic interlock or over-generalization memory

1. over-general memory may inhibit reinterpretating and reschematizating the past. For example, when someone didn’t say hello to you, an upper layer of ‘disliking me’ can be created and in order to interpret this event differently, lower layers with the specifics of the event must be retrieved.
2. The ability to keep track of aspects of daily life is fundamental for cognitive therapy. In diaries for instance. Difficulties in doing this will interfere with therapeutic progress.
3. Problem-solving is hampered by over-general memory. Problem solving involves several steps:
   
   1. General orientation to a certain problem
   2. Generation of as many alternative solutions as possible
   3. Weigh pros and cons of each solution
   4. Select the best alternative
   5. Implement this alternative
   6. Evaluate the outcomes

Depressed individuals have a hard time accomplishing problem solving the way it is intended. They tend to use only their upper layers for generating solutions. These layers lack specificity, which is necessary for satisfying solutions.

As was said before: over-general memory slows down therapy progress.

Future research focuses not only on the effect of memory problems on the persistence of depression, but also on relapse and recurrence probabilities.

G: Chronic fatigue syndrome

This chapter covers the cognitive behavioural approach to chronic fatigue and chronic fatigue syndrome.

Chronic fatigue – nature and history
The symptom fatigue
Many variations of fatigue exists, most often the main focus has been on reduced performance. In this chapter, fatigue is considered to be a subjective feeling of exhaustion or lack of energy. Lots of people experience fatigue once in a while, almost 1 out of 4 adults experience fatigue as a problem.

The illness fatigue
Fatigue is one of the most common symptoms presented in primary care. The fatigue can be part of many diseases, but most of the time the fatigue remains undiagnosed. The illness fatigue, without any organic cause, has been described for more than a hundred years. The diagnosis of neurasthenia would be applied to what we now consider chronic fatigue. When the neurasthenia faded away, chronic fatigue was considered to be part of depression for psychiatrists, and part of other organic diseases for physicians.

Recently there has been more attention to what we now call chronic fatigue syndrome.

Chronic fatigue syndrome
In 1988 the syndrome got consensus for its existence. Chronic fatigue syndrome is characterized by fatigue as the dominant complaint. To receive the diagnoses of CFS the patient needs to suffer from the symptoms for at least six months. It has to be medically unexplained and associated with significant decrease in functioning. The main criteria for chronic fatigue syndrome are:

1. Clinically evaluated, medically unexplained fatigue. At least six months suffering from this fatigue.
2. Four of more symptoms should be experienced (headache, muscle pain, joint pain, memory impairment, etc)
3. Several exclusion criteria exist for CFS (psychotic disorders, dementia, anorexia/bulimia nervosa, obesity, melancholic or bipolar depression, active unresolved disease).

As with any relatively new diagnostic criteria, it remains controversial. Due to the major overlap with other disorders (like depression) and medical illnesses, CFS is difficult to diagnose properly.

When chronic fatigue is the main complaint patients suffer from, the diagnosis of CFS is very useful. Once the diagnoses CFS is given, patients can be further evaluated according to other clinical relevant aspects like coping behaviour, physiological state, social situation, mood and illness beliefs.

Etiology CFS
CFS is unlikely to have a single cause. CFS is suggested to be an interplay between physiological, psychological and social factors. Debate has been going on about which factors (physical of psychological) play the biggest role in the cause and maintenance of CFS.

Physical
Neurasthenia, a proper diagnoses resembling CFS, was a physical disease. Good old Freud considered CFS as a result of excessive masturbation and thus a physical disease. But as years went by these arguments fell out of favor.

In the following decades, various physical causes were raised. But until now, no single physical cause has been established.

Psychological
In the early 1900’s psychological causes were proposed, most often as a combination with physical causes or as a vicious circle.

Later on, more psychological fatigue models were raised, without physical contributions. Much of these models theorized about CFS as an aspect of depression. There were some who focused on fatigue as a symptom itself. In the 40’s, chronic fatigue was considered to be a consequence of chronic conflict and frustration according to the psychodynamic view.

In a more recent psychodynamic perspective, chronic fatigue is argued to be a result from overwork, which is a result of attempting to compensate for low self-esteem.

Psychological versus physical
The debate is still going. Another illustrative example of a disease with a similar debate questions is myalgic encephalomyelitis (ME). The advantage of chronic fatigue can be integrated in physical, psychological and social views and transcended into a coherent model of these factors combined.

Treatment
None of the treatments developed for chronic fatigue have been generally accepted as an effective treatment.

Physical treatments
Rest was the main component of physical therapies. In more recent therapies, rest is also the big contributor to the healing process.

Due to its association with depression and according to the view of chronic fatigue as a result from biological processes, antidepressant drugs are used as treatment strategy.

Psychological treatments
One of the earliest forms of psychotherapy for chronic fatigue consisted of encouragement and persuasion by the physician, this type of therapy was called rational persuasion.

Later on, when psychological factors were more and more accepted, the physical therapies had to make way for psychotherapy and activity increases.

An early form of cognitive behavioural therapy was developed. Concerning the activity increases, patients had to gradually increase their activity in order to challenge the view that fatigue was an inevitable consequence of activity.

The problem of acceptability arose with psychological therapies for somatic complaints. Majority of patients prefer a medical approach.

Cognitive behavioural approach
To overcome the physical attribution of the chronic fatigue, attempts have been made to identify and modify physical and psychological factors perpetuating the chronic fatigue problems.

The modern approach of cognitive behavioural therapy is based on:

• both somatic symptoms and physiological state as psychological factors (mood, cognitions, behaviour) are included
• an interacting model of the illness

Typical components of chronic fatigue patients
Clinical experience and systematic descriptions of chronic fatigue patients show characteristic patterns of thinking, feeling and behaving.  

Thoughts
Patients often believe in an organic cause for their symptoms. They might even diagnose themselves with having ME. They have a hard time attributing the disease to psychological factors. Believing that there is a disease explanation for their chronic fatigue is associated with greater disability and worse outcome. This illustrates the need for more psychological consensus about chronic fatigue.

The patients’ biggest concern seems to be performance abilities. Attitudes like ‘I should try harder’ and ‘ I must cope’ function as a compensation for vulnerable self-esteem.

Behaviour
Patients find themselves unable to be active due to the exacerbation of fatigue and other symptoms. Their response is to avoid activities. The more avoidant patients are, the more the disability. However, most patients do not maintain a constant (low) level of activity. Occasionally they have outbursts of activity, which will stop when fatigue symptoms arise. This results in chronic expanded activity levels from very low activity to very intense activity.

Mood
Depression and anxiety are the most common mood influences chronic fatigue patients experience. But the one reported most by patients is frustration. Patients are very reluctant to express distress and acknowledge depression.

Physiology
Symptoms which occur in CFS, could be the result of sympathetic arousal of the nervous system. Disturbed sleep patterns are common complaints among chronic fatigue patients. Due to prolonged inactivity, patients show physiological deconditioning and reduced tolerance of exercise. Fortunately this process can be reversed.

Interpersonal and social factors
Chronic work stress often precedes the onset of CFS. A contributing factor to interpersonal and social factors is the concern patients have about what others belief the cause of their CFS is. Patients’ beliefs can be (wrongly) shaped by reading available (media) information. The same can be said for the role doctors play in shaping patients’ views on CFS.

Cognitive behavioural conceptualization
A generic model of all the above mentioned contributing factors to the perpetuation of CFS is illustrated below.

The model is based on Sharpe, 1997.

Specific model
As a guide in therapy, you can apply the more specific model of chronic fatigue syndrome (Wessely and colleagues). In this cognitive behavioural model you can find a vicious circle of interacting physical and psychological factors.This model has certain limitations: the model does not explain all aspects of clinical presentation of CFS.

1. beliefs/thoughts about performance and coping are excluded.
2. the model offers no explanation why some people are more vulnerable to develop CFS.

In order to rectify these limitations, Surawey et al. (1995), have proposed a more complex model of chronic fatigue syndrome.

Several additions have been added, compared to the first specific model.

1. This model includes two interacting cycles:

1. on cycle is based on catastrophic misinterpretation of symptoms. This will lead to distress and avoidance of acitivity.
2. the other cycle is based on ‘should’ statements (‘I should try harder’). These statements will lead to frustration and bursts of activity.

2. Another aspects added to this expanded specific model is the incorporation of frustration.

3. Patients’ attitudes about performing correctly and coping are incorporated.

Utilization of the model
The cognitive behavioural perspective offers some advantages over the medical and other psychological models:

• The important factors in perpetuating CFS are apparent from clinical assessment and complex investigation of those factors is not required.
• The model can be individually applied to patients. In this way, the model covers the heterogeneity among CFS patients.
• The model integrates physical, social and psychological aspects.

The question remains whether this perspective, can lead to effective treatment. This will be discussed in the next section.

Cognitive behaviour therapy
The main aim of therapy is to break the vicious circles. Patients have to learn to reappraise their understanding of the chronic fatigue and to cope more effectively. The therapy approach which is carried out in Oxford is described. It consists of five stages:

Stage 1:    Assessment and formulation

Stage 2:    Experiment with increase in activities / reevaluation of illness beliefs

Stage 3:    Reviewing unhelpful attitudes / beliefs

Stage 4:    Problem-solving practical difficulties

Stage 5:    Review and planning for future

General assessment procedures

Medical
Organic diseases have to be excluded first. Then a proper diagnosis should be given. It is important for the patient not to receive a wrong diagnosis (like ME) or let the patient leave without any attribution of the symptoms. CFS is therefore the label to compromise between possible diseases on the one hand and a acceptable label for the patient on the other hand.

Referral to a psychologist or psychiatrist should be made with a positive attitude, to overcome any reluctance of the patient.

Psychiatric
The mental state should be assessed in order to find any psychological disorders and to diagnose depressive and anxious symptoms. By the use of a structured interview any other important aspects have to be assessed.

Assessment procedures and aspects will be discussed more into detail.

cognitive behavioural assessment: includes an interview with the patient and significant other(s), patient-completed questionnaires and diaries.

• current problems should be assessed first. Both the physical and psychological and social factors
• cognitions about the illness are important to assess. A good way of assessing the cognitions is through the use of diaries.
• Emotions are often hard to express for chronic fatigue patients. Certain questionnaires can help in assessing the severity of emotional distress (for example the Hospital Anxiety Depression Scale (HAD).
• Behaviour related to the illness should be assessed. How does the patient cope? What does he/she do to prevent it? A clear picture of someone’s daily life should be established.
• Physiological changes cannot be ignored. For example, exercise tolerance.
• Interpersonal and social factors have to be attended to.

The next step is to develop a cognitive behavioural formulation, individualized for each patient in order to design the most effective treatment plan. The formulation is a hypothesis and can be adjusted if necessary.

Keep notion on the fact that the therapeutic relationship has to be positive and collaborative in order for the therapy to be effective.

Engagement: share your formulation with your patient to establish a collaborative relationship and get the patient engaged in treatment. Be careful with patients who attribute their symptoms to a pure physical cause.

Therapy planning: estimate how much therapy a patient needs; some patients need only one phone call, while others can only improve by hard core therapy and lots of encouragement.

Goal setting:  goal setting will give therapy some direction to work towards. The goals should be specific, achievable and realistic.

Treatment process: the aim of therapy is to work with the patient collaboratively in order to help him/her attain a more realistic and helpful formulation of the illness and develop ways to cope. Treatment components are:

1. behavioural interventions; stabilize and then increase activity gradually.

2. cognitive interventions; the aim is to let the patients see that improvement is possible through their own efforts and confidence building in the function abilities. There is a possibility for some cognitions to interfere with therapy:

   1. task-interfering cognitions like ‘Activity is harmful for people like me’.

   2. After increasing the level of activity, patients can become increasingly concerned about the increase of fatigue and/or pain (which comes along with the increased activity level). If they misinterpret these increases as relapses, patients will refrain themselves from any form of activity.

   3. More general attitudes like perfectionism.

3. reducing distress and depression: to take the underlying worry away, make sure patients understand their illness as best as possible, so the worrying can be reduced, and thus the distress. Other problems related to depression can be tackled during therapy, or by using antidepressants.

4. normalizing physiology: the reduction of distress plus a stabilized activity level will lead to normalizing physiology. Attention can be paid to other physiological aspects, like sleep disturbances.

5. overcome external obstacles; this can be overcome by learning the patient more effective coping styles and to involve (more) significant others in therapy, in order to minimize the aversive effects the patient can have on them.

End of treatment: The result of the collaborative relationship should be a final formulation. Guidelines and ideas about how to continue in the future (and deal with relapse) should be considered.

Some administrational notes of therapy:

• individual therapy is the most commonly practiced form of therapy but group therapy is also possible. It has the advantage of interaction with other patients, but the disadvantage of reinforcing dysfunctional illness beliefs.
• An average of 10 – 20 sessions per patient is usual.
• Informational aids to help the patient get the most out of their therapy are tapes (recorded during therapy), written summaries of certain therapy concepts (for example cognitive behavioural therapy) and books/articles.

Effectiveness
Five different studies investigated the effectiveness of cognitive behavioural treatment approach to chronic fatigue syndrome. A detailed description of the studies will be omitted, but the overall conclusion is: 

• CBT is significantly more effective in treating chronic fatigue patients
• To achieve patient compliance, illness beliefs should be addressed in a collaborative way.

Future research
The current definition of chronic fatigue syndrome has many limitations. In the future, useful sub-classifications must be designed.

The cognitive and behavioural aspects also deserve more attention in the future. Specific topics that need to be further elaborated:

• role of attitudes and assumptions in the perpetuation of chronic fatigue syndrome
• (potential) role of cognitive avoidance concerning depression and anxiety
• underlying symptom production and aggravation that occurs with activity

Treatments
Brief treatment for widespread use is needed to provide more and effective treatment in primary care. More effective treatment should be developed for resistant patients.

Young presented schema-based therapies (1990), which seemed to be appropriate for difficult patient groups, but these methods require empirical investigation first.

Practitioners
Treatment for chronic fatigue syndrome should be provided by professional trained therapists. The development for integrated medical/psychological services should be continued.

H: Primary care findings

For this chapter in particular: keep the timeframe in mind when this chapter was written.

Almost everyone in the general population has a general practitioner (GP). When diagnosed with psychiatric problems, 95% were treated by their GP, the rest by psychiatrists (these numbers are valid for the UK). It is safe to say that things have changed in the last 20 years, at least in the Netherlands!

Whoever treats patients, it is important the treatment is carried out correctly and effectively. One particular psychological treatment, namely problem-solving, will be described in detail later. Problem-solving techniques improve coping skills in schizophrenic patients. This illustrates how effective problem-solving skills can be. Most patients, seen by primary care practitioners, have the age between 45- 64, women represents the majority of them. To bring in the economic point of view: disorders are very expensive. This is one of the reasons why the field has to be as effective as possible.

Most reported psychiatric symptoms in patients with mental disorders, were: worry, anxiety, sadness, fatigue, somatic symptoms and sleep disturbances.

Several studies, with the shared aim to investigate psychological treatments as an alternative treatment to medication, are discussed in this chapter.

Study 1: no medication prescription
The aim of this study was to figure out if anxiolytic medication could be withheld from patients with emotional disorders without causing unwanted consequences. In order to figure this out, two groups, both with anxiety as the dominant symptom were compared. The first group received only medication. The second group only brief counseling from their GP. The counseling consisted of four stages: listening and assessment, symptoms explaining, reassuring and advising.

Results and conclusions:

• No significant outcome differences between both groups were found. So, withholding medication is possible for achieving the same results as psychological treatment.
• Patients did not feel dissatisfied by medication withholding.

Study 2: patients with poor prognosis
The first study confirms the result that about one-third of patients with a neurotic disorder, did not improve within six months. This led to the aim for the second study: to figure out the outcomes of treating this group with a treatment especially designed for them. The psychological treatment that was chosen to treat this group was problem-solving. This treatment was chosen for several reasons:

• it was likely to be effective due to the personal and social focus, which are important in maintaining emotional disorders
• it’s a brief and non-specialized treatment, which is helpful to carry this out in general practice.
• Problem-solving can be learned fast.

The main components of problem-solving are: assessing symptoms and problems, explain symptoms, reassure the patient about effectiveness of problem-solving and problem-solving should be carried out according to six stages. It starts with clarification and ends with evaluation of progress.

Two groups were formed: poor prognosis patients were randomly allocated to one of the following groups: usual treatment by their GP or problem-solving treatment.

Results and conclusions:

• After 7 weeks, both groups improved significantly, but the problem-solving group improved most.
• After 28 weeks (final assessment), the problem-solving group showed further improvement, however, not significant compared to the first findings.
• Overall conclusion: problem-solving, given by a professional, was effective and feasible as a treatment for emotional disorders for poor prognosis patients in primary health care.

Study 3: major depression treatment
The question whether problem-solving treatment would be effective for major depression arose since it was effective for depressive disorder seen in general practice. From all patients in primary care 1 out of 10 suffers from depressive disorder, and 1 out of 20 suffers from major depression.

Even though antidepressant can be effective in treating depression, several disadvantages can be mentioned. Think about side-effects, the passing of psychological problems and the basis of depression, which often are social and psychological problems.

Considering the previously mentioned advantages of problem-solving treatment, it sounds plausible to investigate the effectiveness of problem-solving treatment to patients with major depression.

Two research questions ought to be answered in this study:

• Is problem-solving treatment effective?
• Is problem-solving treatment feasible?

A randomized controlled clinical trial compared three treatment groups: problem-solving treatment, antidepressant (amitriptyline) with standard clinical management and drug placebo with standard clinical management.

Results and conclusions:

• problem-solving treatment was significantly more effective than placebo treatment, but not antidepressant treatment.
• Patient recovery were highest among the problem-solving treatment (60%). The antidepressant showed recovery rates of 52%, and the placebo group 27%.
• Concerning the feasibility;
  
  • Duration of problem-solving was very brief.
  • GP’s can be well trained to give problem-solving therapy as effectively as psychiatrists.
  • Only two drop-outs show that the problem-solving treatment was acceptable for patients.

Study 4: problem-solving treatment for major depression
To elaborate further on these findings, the question whether problem-solving treatment combined with medication is more effective than either one alone still required an answer. At time of writing, the researchers were in the middle of answering this question..

Future research
Two new directions can be seen in developing research:

1. evaluating problem-solving treatment for depressive disorders in the elderly.
2. evaluating problem-solving treatment in culturally different communities.

Problem-solving treatment in a nutshell
Problem-solving treatment is described as an example how to conduct this kind of treatment.

The treatment consists of seven stages:

1. explaining treatment and treatment rationale

2. problem clarification and definition

3. goal setting (achievable goals)

4. solutions generating

5. choose one preferred solution

6. implement this solution

7. evaluate

The typical course of problem-solving treatment will be described below. For the detailed description, see page 425 and further.

Session 1:
Motivating the patient is very important to achieve positive outcomes.

The aims of the first session are to:

1. List symptoms and problems and find a link between them.
2. Explain treatment and treatment rationale.
3. Use a specific example to illustrate the stages.

The first six stages are then implemented.

• Stage 1 consists of three sub-steps: recognition of emotional symptoms, recognition of problems and acceptance of a link between these symptoms and problems. It is important to emphasize the active role of the patient.
• Stage 2 is twofold: first you have to list the problems in a clear and concrete form and pick one problem you will be focusing on. This problem should be as specific as possible. The next step is to break this problem down into smaller parts. This way the problem will consist of several, more manageable, smaller parts.
• Stage 3 involves goal picking. When choosing an achievable goal, take notion of the patients’ strengths and weaknesses. When a short term goal can be reached, this develops a sense of achievement.
• Stage 4 is about listing as many solutions as possible to the problem.
• Stage 5 is about choosing the preferred solution after weighing the pros and cons of the solutions first.
• Stage 6 involves implementation of the preferred solution. If patients find it difficult to carry out this step, break the solution down into smaller achievable steps.

Homework can be assigned to practice with these stages.

Session 2:
This session usually starts with stage 7: the evaluation of the patients’ progress. It is important to praise any efforts taken by the patient to solve certain problems. Discuss any encountered difficulties. Together you can decide to try another solution first if the original preferred one causes too much trouble.

The rest of the session covers the task planning before the next session.

Session 3 and further:
Review the original problems and consider progress. Pay attention to any difficulties. Once the problem-solving skills are mastered by the patient, you can emphasize the use of these skills in future arising problems as well. The more sessions, the less active the therapist should be. Patients need to feel their own contribution to the treatment success.