Introduction

The standard diagnostic criteria for OCD have been challenged, and an alternative analysis has been proposed that suggests that no single feature or collection of features is both common and peculiar to all instances of the disorder. Consistent with this position, it was also argued that there is no single way in which OCD may be distinguished either from phobias or from delusional states; and various ways in which OCD may be so distinguished were presented.

The difficulties encountered by the theoretical approaches to OCD that have been reviewed are perhaps more striking than their successes, at least if one attempts to regard any of these approaches as providing a full explanation of the disorder. Nonetheless, some of the accounts that have been considered certainly offer observations and suggestions that concern some OCD patients and that may well be of importance to any valid account of these patients’ psychopathology that eventually emerges. The following observations have been presented as being of possible theoretical importance to an explanation of OCD:

1. OBSERVATION (1) Evolutionary influences may have a role in selecting the content of some OCD symptoms (stressed by some behavioural writers and some of the Pavlovian personality theorists).

2. OBSERVATION (2). The basal ganglia (among other possible biological factors) may have a role in producing at least some cases of OCD.

3. OBSERVATION (3). A neurotic temperament is displayed by many OCD patients (stressed by the Pavlovian personality theorists).

4. OBSERVATION (4). OCD is co-morbid with certain other disorders (stressed by both the Pavlovian personality theorists and Janet's account).

5. […]

Introduction

An increase of interest has recently been shown in biological approaches to OCD, and there are available a number of reviews/discussions of the findings from genetic, neuroanatomical, neurophysiological, neuropsychological and biochemical studies of OCD, as well as from studies of what have been presented as animal models of the disorder (for example, Turner, Beidel and Nathan, 1985; Rapoport and Wise, 1988; Insel, 1988; Pitman, 1989). This chapter will attempt to offer neither detailed comments on the quality of these biological findings, nor a comprehensive review of them. Instead, some of what have been claimed to be the most important of these findings will be briefly outlined, along with some of the suggestions biological theorists have offered regarding the psychological processes at work in OCD. Discussion will then focus on how powerful an argument in favour of a biological account of OCD these findings, if sound, could sustain.

Given the use of supposed animal models of OCD in some biological research, a few remarks concerning such models are in order here. (Animal models of OCD are also offered in other types of research – for example, de Silva, 1988, pp. 206–7). Reed (1985, p. 11) objects to the use of animal models in the study of OCD on the basis of his belief that the defining criteria for the disorder are phenomenological – for a thought or action to be symptomatic of the disorder, according to Reed, it must be experienced as senseless and be resisted, and it is unclear, in the case of any animal behaviour, on what grounds it could be argued that such behaviour has been experienced in this way (although see de Silva, 1988, p. 207).

An outline of the model

The behavioural/learning account of OCD (e.g., Eysenck and Rachman, 1965) is based on Mowrer's (1939,1960) “two factor” theory of learning. This approach provides very similar accounts of both OCD and phobic states. The preoccupations of OCD patients are held by this approach to concern feared stimuli that have acquired anxiety-producing properties by a process of classical conditioning. The behavioural/learning account suggests that the compulsions provoked by these feared stimuli are escape or avoidance behaviour. According to this account, this behaviour reduces or prevents anxiety and is thus reinforced by a process of instrumental conditioning. De Silva (1988) suggests that “the model is essentially one of learned anxiety reduction”. In the case of OCD, as in the case of phobias, the avoidance behaviour may be passive (for example, not approaching objects thought to be contaminated) or active (for example, checking for contamination [Gray, 1982, p. 440]). An example of an OCD escape behaviour is cleaning to remove what is thought to be some contamination.

The model is not substantially altered by the recognition that it is not only anxiety but also other forms of mood disturbance, subsumed under the vaguer term “discomfort” (Rachman and Hodgson, 1980), that is reported by some OCD patients. The maintenance of compulsions is then attributed to learned discomfort reduction (de Silva, 1988).

Consistent with this account, Rachman and his co-workers (e.g., Hodgson and Rachman, 1972; Rachman, de Silva, and Roper, 1976; Rachman and Hodgson, 1980) have shown that compulsions are indeed often provoked by environmental cues, and that when OCD patients are exposed to these cues they experience an increase in anxiety or discomfort.

Introduction

Janet's classic contribution to the literature on OCD (1903) has still not been translated into English. Fortunately, Pitman has provided a highly readable synopsis of Janet's work (1984) as well as an interesting review/commentary (1987a), which will be used as the basis of the discussion here. In his review/commentary, Pitman presents a summary of Janet's ideas in three segments, each of which will be considered in turn here; the points Pitman himself offers will be considered in the course of commenting on Janet's work. Havens (1966) also provides an interesting account of Janet's contribution, some points from which will be briefly discussed in what follows, as will some of Reed's (1985) comments on Janet.

Janet on the clinical stages of psychasthenic illness

Janet includes OCD, among other conditions, in the category he terms psychasthenic illness. He divides this category into three stages, these being, from the least to the most severe, the psychasthenic state, forced agitations, and obsessions and compulsions. According to Janet, patients develop the less severe stages of the illness before the more severe and, similarly, lose the more severe stages of the illness before they lose the less severe.

The first stage of the illness – the psychasthenic state – involves the patient's feeling that actions have been unsatisfactorily or incompletely performed. Incompleteness in “perceptions” is also present, consisting of such experiences as derealisation and depersonalisation. Indecision, amnesia, poor control of thoughts, and “emotional insufficiencies” (that is, an inability to experience emotions fully) are reported by patients.

Introduction

Much of the theorising found in psychodynamic approaches tends to pay close attention to the detail of individual patients. This makes it difficult to review thoroughly the whole of the psychodynamic literature on OCD, and in what follows no attempt to do this will be made. To the extent that generalisations across individual patients are possible from this perspective, furthermore, one finds psychodynamic theorists offering a number of different accounts of OCD. It seems unlikely that each of these is intended to apply to a different subgroup of OCD patients, and these accounts thus stand instead as alternative, and perhaps also incompatible, approaches to the disorder.

Given these points, the present discussion will take the following course. Firstly, some of the psychodynamic accounts of OCD that have been offered will be briefly outlined, the emphasis being on exposition rather than criticism. Following this, a single case discussion presented by Malan (1979) will be critically discussed at some length, along with some of Malan's comments concerning psychodynamic theory and therapy. There are two justifications for concentrating critical comment on Malan's case discussion. Firstly, and as already noted, much psychodynamic theorising takes into account the detail of individual patients and is therefore also best discussed with reference to such details. This does not, of course, mean that all of the points raised by any given case will be irrelevant to the evaluation of psychodynamic accounts of other cases, and indeed, it is suggested that some of the themes raised by the case discussion to be considered here (for example, the nature of symbolisation and the role of the unconscious) would be central to many psychodynamic discussions.

Reed's account

Reed's hypothesis of the central problem

A number of authors (for example, Beech and Perigault, 1974; Beech and Liddell, 1974; Carr, 1974; Volans, 1974, 1976; Reed, 1985, 1991) have suggested that a generalised cognitive style or deficit in OCD sufferers may be responsible for the occurrence of OCD symptoms. Reed's ideas represent the most fully worked out contribution from this school. He advances what he terms a “cognitive-structural approach” (Reed, 1985) to explain both the obsessional personality (and personality disorder) and OCD. In what follows, the term obsessional will be used generically, as it is by Reed, to cover OCD, the obsessional personality/personality disorder, and the person who exhibits either of these. Unlike many of the approaches discussed in other chapters of this book, Reed's account has not been subject to widespread critical discussion; particularly detailed consideration of this account is therefore offered here.

What, then, is the central problem in obsessional disorders, according to Reed? His attempts to answer this question in just a few words tend to be a little cryptic. For example, he suggests that obsessional traits and symptoms reflect difficulties in “spontaneous categorizing and integration” (1985, p. 220) leading to attempts to compensate for these difficulties by “the artificial over-structuring of input, of fields of awareness, of tasks and situations” (p. 220); there is, he argues, a “maladaptive over-defining of categories and boundaries” (1969b, p. 787). Reed states that the central phenomenon of these disorders “may thus be seen as a striving towards boundary fixing or the setting of limits in the cognitive/ perceptual modalities” (1985, p. 220).

Introduction and natural history

It is quite common for books on obsessive-compulsive disorder (OCD) to open by offering a brief definition of the disorder. Because the definition of OCD is to be treated here as a major issue in its own right, such an introduction is not possible. Instead, a few examples of symptoms reported by OCD patients are offered. A fuller picture of the symptoms reported by these patients will be provided by the discussion of the definition of the disorder later in this chapter. All the following examples are taken from de Silva (1988, pp. 196–7):

1. (a) thought plus… [mental] image [of the patient's having] knocked someone down with his car

2. (b) impulse…to shout obscenities during prayer or a church service

3. (c) [mental] image of corpses rotting away…

4. (d) repeated and extensive washing of hands to get rid of contamination by germs

5. (e) checking gas taps, door handles, and switches three times [whenever the patient] went past them

6. (f) imagining in sequence…photographs of members of [the patient's] family, his parents, pictures of Jesus Christ and the Virgin Mary, and then photographs of two other persons

Chapters 2 to 7 will review a variety of theoretical approaches to OCD. Although a diversity of work will be covered by this review, including behavioural, cognitive, psychodynamic, and biological approaches to the disorder, the review will not aim to be exhaustive. In particular, it will omit detailed consideration of such important elements as the interesting relationship between OCD and depression (Stengel, 1945; Lewis, 1934), and the phenomenological approach of Schneider (1925), whose classic work on personality disorders includes a discussion of obsessionals, termed by him insecure psychopaths.

It is hard to think of any significant aspect of our lives that is not influenced by what we have learned in the past. The world looks and sounds the way it does because as infants we learned to partition it up in certain meaningful ways: we see familiar faces rather than meaningless blobs of colour and hear words rather than noise. Similarly, we behave in the ways we do because we have learned from past experience that our various actions have certain specific consequences. Like many topics of psychological inquiry, the importance of learning can perhaps best be realised by considering what life is like for people who have learning difficulties. Consider the case of Greg, a patient described by Sacks (1992), who became profoundly amnesic as a result of a benign brain tumour that was removed in 1976. Although his memory for events from his early life was almost completely normal, Greg remembered virtually nothing that had happened to him from 1970 onwards and appeared quite unable to learn anything new. He continued to believe, for instance, that Lyndon Johnson was the American President. In 1991 he was taken to a rock concert given by a group that he had been a great fan of in the 1960s, and despite sitting through the concert in rapture and recalling many of the songs, by the next morning he had no memory of the concert. More distressingly, when told of his father's death he was immeasurably sad but forgot the news within a few minutes. He was unable to learn that his father was no longer alive, and relived his grief anew every time he was told the news.

In the Introduction I argued that human associative learning can best be understood by considering three questions. What does the system do? How, in broad informational terms, does it do it? And how is this achieved at the mechanistic level? We have answered the first question by suggesting that to a first approximation the system does what a statistician would do: that is to say, it computes the degree of conditional contingency between events as defined by the metric ΔP. The second question is answered (again to a first approximation) by reference to the memorisation of instances, with stimuli being represented in a multidimensional psychological space and with interstimulus similarities being an exponential function of distance in the space. We now turn to our final question: what is the mechanism of learning? What sort of mechanism computes contingency, and represents associative knowledge in terms of memorised instances? In this chapter we will examine how contemporary associationist learning systems attempt to answer this final question.

I also pointed out in the Introduction that enthusiasm for associationist accounts of human learning waned somewhat in the 1960s and 1970s. Partly, this was due to impatience with the highly constrained tasks that researchers in the verbal learning tradition employed, but partly it was also due to the apparent inability of associationist theories to cope with more complex examples of human learning and cognition. For instance, a number of extremely sophisticated analyses had been undertaken of the difference between novices and experts performing various skills such as playing chess or remembering strings of digits (e.g. Chase and Ericsson, 1981; Chase and Simon, 1973).

If we take the commonsense view that the human associative learning system has evolved for adaptive purposes, then it is immediately clear that the major benefits learning affords an organism are the ability to make predictions about events in the environment and the ability to control them. If it is possible to predict that a certain event signals either impending danger such as a predator, or imminent reward such as access to food, then appropriate action can be taken to avoid the danger or extract maximum benefit from the reward. It has been common, particularly in discussions of animal conditioning, to interpret learning from the perspective of the benefit it brings the organism.

Of course, this is not to say that learning is always beneficial, and the high incidence of maladaptive behaviours, such as phobias in humans that can be traced to prior learning episodes, attests to this fact. Nevertheless, it seems plausible that such learned behaviours emerge from a system that fundamentally exists to exploit and benefit from regularities that exist in the world, whether they be signal–outcome or action–outcome regularities. For instance, when Pavlov's dogs learned to salivate to a bell that signalled food, it is likely that they benefited from the increased digestibility and hence nutritional benefit of the food. When a child learns that saying ‘juice’ reliably produces a rewarding drink, it has acquired the ability to control a small but important aspect of its environment.

In this chapter we will try to establish the degree to which human learning is appropriately adapted to the environment.

The picture of concept learning that emerges from the previous chapters is of a rather passive process in which instances are encoded in memory as a result of weight adjustments in an adaptive network system. This is passive in the sense that so long as the subject attends to the stimuli, the hypothesised processes operate automatically on the incoming information. But it has commonly been argued that in some circumstances a different, active process can operate whereby a person considers various hypotheses concerning relationships between events, modifies or rejects inadequate hypotheses, and in short tries to induce a rule describing the relationship between stimuli and outcomes. In this chapter we consider the evidence that the account of associative learning discussed in the previous chapters is incomplete and needs to be supplemented by an additional and possibly independent rule-learning mechanism.

Before considering the evidence and nature of this rule-learning process, it is necessary first to consider what exactly we mean by a ‘rule’. This concept has, to put it mildly, been a source of some debate and confusion amongst psychologists and philosophers. On the surface, the definition of a rule seems unproblematic: we simply say that a rule is a principle that specifies definitively whether an object or event is of a particular sort or not. For instance, if an object has four sides of equal length lying in a plane and with right-angles between them, then it is a square. Any object conforming to this principle is a square, and any object that violates the principle is not a square.