Madness Explained
Page 27
It should be emphasized that nothing in this dimensional account of emotion detracts from the fact that we are able to use a sophisticated emotional vocabulary. Presumably, our choice of emotion words when experiencing positive or negative affect is influenced by additional information that is available at the time. This information may include some of the physiological cues we considered earlier (for example, the butterfly sensation in our stomach that we associate with fear), our knowledge of our recent history (we are unlikely to feel ashamed unless we know that we have transgressed a moral code or caused insult to others), together with various environmental stimuli (for example, the behaviour of other people who are present).
The emotional circumplex and abnormal mood
As I noted at the beginning of this chapter, most psychiatrists and clinical psychologists have uncritically accepted the theory of basic emotions as reflected in the English language. For example, the neuroses have traditionally been divided into depression and anxiety disorders in much the same way that ordinary English distinguishes between being depressed and being anxious. In the past few years, this classification of the neuroses has been challenged by a number of researchers in Britain and the United States who have used arguments similar to those I employed in Chapter 4 when criticizing the neo-Kraepelinian account of the psychoses.36 For example, patients rarely experience depression or anxiety alone, and clinical studies using questionnaire37 and interview measures38 have consistently found that these symptoms are highly correlated. Moreover, when patients have been studied over long periods of time, mood symptoms often shift so that what seems to be mainly depression at the outset may later appear to be an anxiety disorder or vice versa.39 Not surprisingly, as we have seen, parallel observations have been made by researchers interested in the moods experienced by schizophrenia patients. Although some researchers have focused on depression and others on anxiety, high levels of both emotions are usually reported during psychotic episodes and also during the prodromal phase that precedes them.
David Watson and his colleague Lee Anna Clark have argued that these problems of classifying abnormal mood can be explained by locating them on the emotional circumplex.40 All negative emotions, they have argued, involve strong negative affect or dysphoria. Feelings of anxiety typically also involve physical tension (the body’s natural preparation for fight or flight in the face of an emergency). Depression, on the other hand, usually involves not only the presence of negative affect, but also the absence of positive affect. Psychiatric patients who have been administered questionnaires designed to measure these different components of emotion have been found to score as the theory predicts.41
Do Some Psychotic Patients Lack Emotions?
Although the experiences of patients diagnosed as suffering from bipolar disorder provide the most obvious point of contact between madness and theories of normal emotion, I will focus in the remaining parts of this chapter on symptoms more usually attributed to schizophrenia. The apparent absence of emotions sometimes observed in patients with this diagnosis presents an obvious but hopefully not insuperable difficulty for my claim that emotion plays a central role in psychosis.
Schizophrenia patients’ apparent lack of emotional expression is sometimes described as flat affect or affective blunting. However, patients sometimes complain of a lack of subjective pleasure, known as anhedonia. These symptoms are usually included in the broader class of negative symptoms that emerges from factor-analytic studies such as those we considered in the first part of this book. The appearance of these symptoms in the same factor suggests that they occur together in real life, so that someone who complains of anhedonia is also likely to show flat affect, and vice versa.
However, they are separable phenomena nonetheless. The Scale for Assessment of Negative Symptoms (SANS), a widely used symptom-rating scale devised by American psychiatrist Nancy Andreasen,42 describes the following features of flat affect: unchanging facial expression (‘the patient’s face appears wooden, mechanical, frozen’); decreased spontaneous movements; paucity of expressive gestures (‘the patient does not use his body as an aid in expressing his ideas’); poor eye-contact; affective non-responsivity (‘failure to smile or laugh when prompted’) and lack of vocal inflections (‘speech has a monotonic quality, and important words are not emphasized through changes in pitch or volume’). All of these descriptors concern the expression of emotion.
In contrast, the same scale describes anhedonia-asociality as comprising a lack of recreational interests and activities; a loss of sexual interest and activity; an inability to feel intimacy and closeness; and impoverished relationships with friends and peers. This description emphasizes the failure to obtain subjective pleasure from relationships, a phenomenon that is sometimes called social anhedonia to differentiate it from the inability to experience physical pleasure, known as physical anhedonia. Psychologists Loren and Jean Chapman of the University of Wisconsin have devised questionnaires for measuring these types of anhedonia separately in both patients and ordinary people and have shown that they are usually highly correlated.43
It is also important to note that flat affect and anhedonia do not exhaust the negative symptoms commonly attributed to schizophrenia patients. For example, other negative symptoms listed in the SANS manual include alogia (impoverished thinking); apathy; and attentional deficits. With the exception of the last of these, which we considered in the previous chapter, these symptoms have been the subject of almost no psychological research, and so I will say almost nothing more about them in the present context.
The status of negative symptoms
Before proceeding to consider flat affect and anhedonia in detail, it is worth briefly considering the status of the negative symptoms in general.
Different psychiatrists have emphasized the negative features of psychosis to varying degrees. For example, Kraepelin’s account of dementia praecox clearly emphasizes the intellectual and emotional deficits he observed in his patients, whereas Schneider placed much more emphasis on what we now regard as positive symptoms. Modern theories of negative symptoms, which, in the absence of a substantial volume of psychological research, have sometimes tended to be rather speculative, have turned on two controversies. First, some psychologists and psychiatrists have debated whether negative symptoms are products of some kind of underlying intrinsic (in medical terms, morbid) process and, second, others have debated whether they can be distinguished from depression. These debates are not entirely unconnected as, clearly, if negative symptoms are just an unusual variant of depression they are less mysterious than they might otherwise appear.
The problem of whether negative symptoms are caused by some kind of process intrinsic to the individual is raised by the suspicion that they may be environmentally determined or iatrogenic (doctor-caused) conditions. Until recently, patients commonly spent many years languishing in large hospitals where they received very little stimulation. Not surprisingly, many patients treated in this way fell into a state of learned helplessness, in which they lacked the skills to interact with others or the motivation to look after themselves. In the 1970s, British social psychiatrist John Wing, working with the sociologist George Brown, observed that providing institutionalized patients with appropriate support and stimulation could bring about a reduction in what we now call negative symptoms, although they cautioned that over-stimulating patients might cause an exacerbation of their delusions and hallucinations.44 More recently, some authors have made comparisons between the fate of institutionalized patients and other marginalized or victimized individuals such as the long-term unemployed or the victims of concentration camps.45 Psychiatrist and anthropologist Richard Warner, based at the University of Colorado, has examined historical records to show that recovery rates in psychotic patients are lower in periods of poor economic opportunity such as the Great Depression of the 1930s, so this comparison may not be entirely far-fetched.46 However, not all studies have found an association between institutionalization and
negative symptoms. Eve Johnstone, Tim Crow and others failed to find differences in negative symptoms between patients living in the community and those who had experienced long-term hospitalization.47
Whereas evidence on the relationship between negative symptoms and an adverse environment is inconsistent, the evidence that negative symptoms can be exacerbated by the medications administered to patients is clear-cut. Although biological psychiatrists have been slow to recognize the negative psychological impact of their treatment methods, a neuroleptic-induced deficit syndrome (NIDS), characterized by emotional blunting and reduced motivation, has been well documented. It is often difficult to distinguish between this syndrome and negative symptoms that are not drug-induced.48 As neuroleptics are also known to make some patients depressed, side effects of medication may also contribute to the difficulty in distinguishing between negative symptoms and depression. In a study conducted by psychologist Martin Harrow and his colleagues at the University of Illinois, schizophrenia patients were studied for a period of five years. Patients who were taking neuroleptics, in comparison with those who were not, were more likely to experience both depression and anhedonia during the follow-up period, even when initial levels of symptomatology were taken into account.49
Other researchers have concluded that negative symptoms, while overlapping with depression, cannot simply be explained by negative mood. In the study by Ross Norman and Ashok Malla described earlier, depression was more closely associated with positive than negative symptoms.50 In another study, carried out by psychiatrist Steven Hirsch and others in London, in which a group of schizophrenia patients who were currently depressed was compared with a group that was not currently depressed, no difference was found in the SANS scores of the two groups.51 If these findings seem inconsistent with those reported by Martin Harrow and his colleagues it is perhaps because they have not been interpreted in the context of a well-thought-out theory of emotion. As we will see later, when researchers have focused specifically on patients’ emotional responses, a clearer picture of the mechanisms responsible for some negative symptoms has begun to emerge.
The discovery that some of the cognitive deficits found in schizophrenia patients are specifically associated with negative symptoms might seem to be consistent with the notion that they are intrinsic characteristics of the individual. In the last chapter we saw, for example, that negative symptom patients perform particularly poorly on high-load versions of the Continuous Performance Test. However, as we have also seen, test performance may not be a reliable indicator of an intrinsic morbid process. Indeed, there is nothing implausible about the idea that cognitive deficits arise from an impoverished environment. (Remember David Shakow’s observation that the performance of schizophrenia patients on psychological tests could match that of ordinary people if they received an appropriate level of support and encouragement.) Better evidence that negative symptoms are more than just an adverse reaction to an unsupportive environment is the finding that they are sometimes present during the earliest stages of psychosis, especially in those patients whose premorbid functioning (as reflected by occupational or school reports) is poor.52 This observation suggests, first, that there is a continuum between poor social functioning and negative symptoms and, second, that whatever mechanisms are responsible for negative symptoms may be present before the onset (and treatment) of full-blown psychosis.
In an attempt to resolve the debate about the intrinsic nature of negative symptoms, psychiatrist William Carpenter and his colleagues at the University of Maryland have proposed that only a proportion of patients suffer from what they describe as a core deficit syndrome.53 They have argued that the symptoms that define the deficit syndrome are enduring features of the patient that are not caused by extrinsic factors such as depression or demoralization. The six symptoms which they believe often meet these requirements are: restricted emotion as evidenced by facial expression, gestures and vocal inflection; diminished subjective emotional range; poverty of speech; curbing of interests; a diminished sense of purpose; and diminished social drive. However, the crucial feature of their definition is the exclusion of possible causes such as anxiety, depression or drug side effects, which they argue can be achieved with a high degree of reliability if information about the long-term course of an illness can be obtained from a suitable informant, for example a close relative of the patient.54 Although this approach is surely an important advance on previous attempts to make sense of negative symptoms, it suffers from disadvantages that we have already encountered in other categorial classification schemes. First, the division of patients into those with or without the deficit syndrome does not allow for the possibility that patients suffer from deficit symptoms by degrees (that is, that deficit symptoms, like other symptoms we have considered, may lie on a continuum with normal functioning). Second, the approach does not help us understand the role of psychological processes in negative symptoms. It is possible that these problems can be avoided by focusing on particular symptoms with out trying to prejudge, for the moment, their causes.
Flat affect
The danger of equating outward expression with the subjective experience of emotion was vividly illustrated by a remarkable paper written by Jean Bouricius, a retired social worker and mother of a 32-year-old schizophrenia patient.55 Suspicious that objective ratings of psycho-pathology failed to capture adequately her son’s experiences, she asked five professionals (two doctors, two social workers and a psychologist) who knew him well to assess his symptoms using the SANS. All five returned moderately high ratings, especially for affective blunting. However, Ms Bouricius was able to show that her son’s diary notes for the same period were rich with emotional material. For example, he described a visit to his doctor in the following manner:
Went to see my doctor but couldn’t talk. Kept saying, ‘I don’t know,’ to his questions. Started crying. Felt pity and love for Rhoda [a friend] because she has fear, because she has to take medication, because she is a mental patient like me, because I want to marry her, but I think I never can. I started saying that I had lost my memory. Then I got up and left.
And a few days later:
Rhoda asked me if I were spoiled and I angrily said no, but I feel hurt, as if I was born for a purpose I hide from, covering myself with warm blankets. Go to hell, World! I cannot die in peace and safety. I cannot face the slightest breath of real life or death or ugliness. But I hurt for being such a coward. I was always a coward – socially, physically, mentally, sexually, emotionally. If I go insane, am I brave? I will, because then, and only then, I am brave, not a coward. I hate all people. They compete and want stimulation. I hate them all, all. None loves, none cares, none understands or ever will understand. I am dead, dead – very, very limited, afraid and hurt. Go to hell, World!
The relationship between flat affect and patients’ subjective experience of emotion has been more formally investigated in a number of studies which have broadly supported Ms Bouricius’ observations. Howard Berenbaum and Tom Oltmanns showed emotionally blunted schizophrenia patients, non-blunted schizophrenia patients, depressed patients and ordinary people film clips that had been selected for their ability to elicit emotional reactions. The participants were asked to report the extent to which they felt happy or disgusted by the content of each clip. As expected, the blunted patients were rated as less expressive than the normal controls when watching both positive and negative clips. They were also less expressive than the non-blunted schizophrenia patients, but only when watching the positive clips. However, when the participants’ subjective ratings of their emotions were examined, the blunted patients did not differ from those of any of the control groups.56
Ann Kring, Sandra Kerr, David Smith and John Neale of the State University of New York at Stoney Brook carried out a very similar experiment, but studied patients who were drug-free in order to exclude the confounding effects of neuroleptic medication. Using a questionnaire designed to measure positive and negative affect as def
ined by Watson and Tellegren’s circumplex model, they also found that their schizophrenia patients experienced just as much positive and negative emotion as ordinary people, despite being less emotionally expressive.57 More recently, a group of researchers at the University of Maastricht in Holland have taken the study of patients’ subjective emotions out of the laboratory and into everyday life by using a technique known as experience sampling, in which a small electronic device is used to prompt patients to fill in simple diaries at random points in the day; in this study, schizophrenia patients as a whole were found to experience more intense and variable negative emotion than healthy controls, and emotionally blunted patients did not differ from patients who were not showing evidence of flat affect.58
The overall picture that emerges from these studies is of normal subjective emotion in schizophrenia patients. Flat affect, therefore, appears to reflect a difficulty of expressing rather than feeling emotions. Consistent with this hypothesis, Cecile Sison, Murray Alpert and others at the New York University Medical Center have observed that patients with flat affect show more hesitations in their speech, and less activity in their facial muscles (as measured by electromyography), than schizophrenic patients without flat affect, or depressed patients.59