The crucial point is this: although we may assume that any actual succession of phenomena proceeds according to the laws of nature, it is important to realize that practically no sequence of, say, three or more causally connected concrete events proceeds according to any single law of nature. If the wind shakes a tree and Newton’s apple falls to the ground, nobody would deny that these events can be described in terms of causal laws. But, there is no single law, such as that of gravity, nor even a single definite set of laws, to describe the actual or concrete succession of causally connected events; apart from gravity, we would have to consider the laws explaining wind pressure; jerking movements of the branch; the tension in the apple’s stalk; the bruise suffered by the apple on impact; all of which is succeeded by chemical processes resulting from the bruise, etc. The idea that any concrete sequence or succession of events (apart from such examples as the movement of a pendulum or a solar system) can be described by any one law, or even by a definite set of laws, is simply mistaken.81
This is precisely the situation that we find ourselves in when we try and understand the origins of madness. No doubt this conclusion will seem disappointing – perhaps even nihilistic – to many readers. It implies that we should abandon hope of a quick scientific breakthrough that will curtail madness in the way that antibiotics have curtailed infections. The Nobel Prize that awaits the scientist who discovers the cause of schizophrenia will never be claimed (or worse, it will be awarded to someone who does not deserve it). However, a positive implication can be drawn. Despite the tragedies that we encounter in the psychiatric clinic, most children do not grow up to be disabled by delusions, hallucinations, manic episodes or disordered thinking. In fact, because psychotic complaints seem to require a combination of many factors, even the majority of children of psychotic parents grow up to lead healthy and rewarding lives. Adaptation and triumph over adversity are the norm. Lives that are blighted by insanity are the exception.
19
Madness and Society
Any man who goes to see a psychiatrist should have his head examined.
Samuel Goldwyn1
The first principle in the psychic treatment of mental patients is frankness and unconditional love of the truth. It is just in this point where laymen and doctors make such serious mistakes.
Emil Kraepelin2
The main purpose of this book has been to present a new way of thinking about madness. This has necessitated, first of all, showing that the traditional way of explaining psychosis is fatally flawed, and then bringing together a (hopefully) novel synthesis of research from a wide range of disciplines. Along the way, I have attempted to explain relevant concepts from psychology and the neurosciences in a manner that will allow the layperson to follow my arguments, while at the same time covering relevant findings in sufficient detail to satisfy the curiosity of sceptical psychiatrists and psychologists. Inevitably, this has been a lengthy process and, yet, even at the end, I am aware of so much that I have left out in my attempt to avoid producing a book that (in the nicely ambiguous terminology of my editor) is too ‘monumental’.
It is worth reiterating, in just a few sentences, what I see to be the main benefits of this new way of thinking. Its greatest advantage is that it does not require us to make three dubious assumptions that were central to Kraepelin’s paradigm and its most recent manifestation as the neo Kraepelinian project – that there is an unambiguous dividing line between the psychologically healthy and the psychologically disturbed, that there is a finite and countable number of different mental illnesses, and that these types of illness must be explained primarily in terms of aberrant biology. Second, it allows us to make sense of (in Jaspers’ terminology, both explain and understand) the actual experiences of men and women who receive diagnoses such as schizophrenia and bipolar disorder. (In contrast, Kraepelinian psychiatry had almost nothing to say about why people hear voices, make strange inferences about the actions of other people, become frighteningly excitable or just sit around all day doing nothing.) Third, the account links the experience of madness to processes that are important in ordinary life, and which are reasonably well understood by psychologists (this is in contrast to the old assumption that ‘however much is known about the psychology of the normal individual, in the pathological field new laws will be found to operate’).3 Fourth, I hope the vision I have offered is of a truly ‘joined-up’ psychopathology, in which the findings from various disciplines (anthropology, sociology, developmental and cognitive psychology, developmental biology, genetics and the neurosciences) are linked together in a meaningful way, and in which no single level of explanation (genetic or neurobiological) is seen as somehow ‘trumping’ all the others.
It is also worth emphasizing, for one last time, that the approach I have outlined is genuinely scientific, in the sense that it is evidence-based, so that most of the hypotheses that are components of the framework have been tested by observation or experiment. Critics have very occasionally attempted to dismiss my approach as emotional, self-serving (because I am a psychologist criticizing theories mostly but not exclusively put forwards by psychiatrists), or some kind of throwback to 1960s style anti-psychiatry (as if all criticisms of conventional psychiatry are equivalent). As it is clearly unscientific to cling to the Kraepelinian paradigm, which enjoys almost no evidential support, these kinds of criticisms amount to what Freudians sometimes term projection (the tendency to attribute one’s own faults to other people).
When planning this book, I had originally hoped to discuss at length the many practical implications of the post-Kraepelinian approach. In the end it proved to be impossible to provide a detailed treatment of these implications while, at the same time, keeping this book to a reasonable length. However, I will spend a few pages indicating what I think they are.
Us and Them
The Kraepelinian paradigm encouraged an ‘us’ and ‘them’ distinction between the mad and the sane, whereas the evidence I have described (especially in Chapters 5 and 6) shows that we are mad to varying degrees, that the boundaries of madness are subject to negotiation, and that some of us get on very well despite being (in psychiatric terms) quite psychotic for much of the time.
The ‘us’ and ‘them’ distinction has had a number of very serious negative consequences for those living at the mad end of this spectrum. Most importantly, it has denied them a voice. In the clinical and research literature, this is most evident in discussions of the concept of insight, an absence of which has often been seen to be a cardinal feature of psychosis.
In a famous paper published in 1934, British psychiatrist Aubrey Lewis defined insight as: ‘The correct attitude to morbid change in oneself, and moreover, the realisation that the illness is mental’ (italics mine).4 Elaborating on this idea, Xavier Amador and Henry Kronen-gold, psychologists working at the New York State Psychiatric Institute, have recently suggested that lack of insight has two separate components: unawareness of illness and ‘incorrect attributions’ about the causesofillness.5 Armed with these kinds of definitions, researchers have laboured mightily to discover how common lack of insight really is in psychotic patients (very common, apparently),6 and whether it is related to other variables of interest such as the patient’s neurocognitive abilities or a willingness to take psychiatric drugs. Most of this research has been inconclusive.7 However, the real problem with this kind of approach is that it assumes that psychologists and psychiatrists are privileged possessors of a correct theory of psychosis, which patients are foolish to dispute. It fails to recognize that patients may have good reasons to form hypotheses about their difficulties that are at variance with those accepted by mental health professionals. It also places patients in a terrible double bind, in which their objections to unsatisfactory aspects of psychiatric care are seen by the clinician as further evidence that treatment is imperative. Indeed, the notion that patients lack insight is routinely used to justify cajoling, threatening or misleading patients about their rights in the hope that these strategi
es will pressure patients into accepting treatment. Recent surveys in Europe and North America have confirmed that, even in these enlightened times, coercion is widely regarded as an acceptable and routine strategy in the clinical management of madness.8
Because patients have been denied a voice, they have often been subjected to cruel and ineffective treatments. In the past, these have included insulin coma (which involved patients being injected with the hormone insulin, causing them to fall into a comatose state perilously close to death, whereupon they were revived and the process was repeated), and electroconvulsive therapy (which, before the introduction of muscle-relaxing drugs, sometimes caused patients to suffer spinal fractures). Even more drastic was the prefrontal leucotomy, which was pioneered by the Portuguese neurosurgeon Egas Moniz in the 1930s and practised throughout the developed world until well after the introduction of chlorpromazine.9 This crude brain operation was championed in North America by the manically enthusiastic neurosurgeon Walter Freeman, who, travelling throughout the USA and Canada in the summer of 1951 in a car loaded with equipment, visited mental hospitals to demonstrate his chillingly efficient technique for carrying it out. After administering a jolt of ECT, Freeman would insert an ice-pick-like instrument above the eye of the dazed and convulsing patient, smashing it through the bone of the orbit and into the brain behind. This procedure was cheap and quick; Freeman estimated that he could complete as many as twenty-five operations in a single day, and claimed to have carried out over 5000 during his professional career.10
These ghastly practices were, of course, exceeded in Germany during the Nazi period, when doctors introduced extermination as a treatment for severe mental illness.11 Inspired by genetic theories which suggested that madness, unless checked, would gradually weaken the Aryan gene-pool, they did not require great encouragement from the state first to compulsorily sterilize and then to kill the most vulnerable members of their society. Gas chambers were constructed in psychiatric hospitals, where tens of thousands of psychotic adults (and many more children said to be suffering from genetic illnesses) were put to death, usually with carbon monoxide, but sometimes by deliberate starvation. As historian Robert Proctor has noted:
It is important to recognise the banality of the operation. In 1941 the psychiatric institution at Hadamar celebrated the cremation of its ten-thousandth patient in a special ceremony, where everyone in attendance – secretaries, nurses, and psychiatrists – received a bottle of beer for the occasion.12
At the beginning of the twenty-first century, it is easy to dismiss these excesses as products of more primitive times. However, the abuses that were perpetrated against psychiatric patients in every country in the West, and which reached a crescendo in Nazi Germany, were made possible by assumptions about psychosis that are the main elements of the Kraepelinian paradigm. Without regarding madness as merely the product of a damaged brain, it would not have been possible to devise a therapeutic system that relied exclusively on physical treatments at the expense of treating people with warmth and humanity. Without the hypothesis that this brain damage is genetically determined, killing would not have been regarded as a rational treatment by a generation of well-trained nurses and physicians in Germany. Above all, without regarding psychosis as ununderstandable (to use Jaspers’ terminology), it would not have been possible to deny psychiatric patients a voice, which might otherwise have been raised in protest against these horrors.
(Of course, I am not suggesting that it was inevitable that Kraepelin’s work would have these consequences. Cruel treatments preceded Kraepelin and, in any case, judgements about what ought to be done to other people are never exclusively determined by beliefs about what is the case. It is perfectly possible to believe that schizophrenia is a genetically determined brain disease while at the same time acting compassionately towards people who receive the diagnosis. But factual beliefs are often used to justify moral intuitions, and the beliefs about psychosis promulgated by Kraepelin and his followers were peculiarly suited to justifying the worst excesses of twentieth-century psychiatric care. In this sense, these excesses were a legacy of the paradigm, a legacy that, in human terms, has been much more costly than the stifling effect that it has had on research.)
Medicines for Madness
Today the assumption that psychosis is a form of brain disease is translated into clinical reality by psychiatric services that rely exclusively on neuroleptic medication, and which make little or no effort to respond to patients’ psychological needs. This bias in the kinds of therapies that are made available to patients reflects systematic misunderstandings about the relative effectiveness of medical and psychological treatments that mirror the misunderstandings about biological and environmental causes of psychosis which I addressed in the previous chapter.
I do not doubt that the accidental discovery of the therapeutic effects of chlorpromazine was a major breakthrough in the treatment of severe mental illness. (It has recently been described as one of twelve defining moments in the history of modern medicine.)13 Clinical trials have consistently demonstrated that patients who take chlorpromazine, or any of the other widely used neuroleptic drugs, experience fewer psychotic complaints and, if they continue to take them when well, fewer relapses than patients who do not take them.14 However, this obvious good news must be qualified by considering the disadvantages of this kind of treatment.
Long-term outcome studies suggest that today’s psychiatric patients do not do much better than the patients of Kraepelin’s era.15 Although most modern recipients of psychiatric care find that neuroleptics to some extent control their symptoms, it is doubtful whether any are cured by this kind of treatment, and a substantial minority obtain no benefit whatsoever. Despite extensive research, no one has found a way of predicting in advance which patients will respond to neuroleptic treatment.16 However, there is very good evidence that patients who fail to benefit from one type of neuroleptic will fail to respond to any other.17 These persistent ‘neuroleptic non-responders’ would almost certainly do better if given no neuroleptic treatment whatsoever, yet drug-free strategies for managing symptoms are almost never considered by modern psychiatric services.
The distressing and sometimes dangerous side effects caused by conventional neuroleptics add to the difficulty in forming a balanced opinion about their value. The most obvious of these are the ‘extra-pyramidal’18 side effects, which include Parkinsonian symptoms (the patient becomes stiff or suffers from uncontrollable tremors, experienced by about 25 per cent of patients), akathisia (a very unpleasant subjective feeling of restlessness and agitation) and tardive dyskinesia (spasmodic movements of the jaw and tongue, which are unsightly and, once established, are sometimes irreversible even after the medication has been discontinued; now thankfully very rare). Side effects that are less obvious to the observer but which cause considerable distress to patients include sexual dysfunction19 (experienced by over a third of patients)20 and severe weight gain (probably the consequence of an increased craving for carbohydrates;21 experienced by about 50 per cent of patients).22
The psychological side effects of neuroleptics can be very distressing.* Akathisia is often accompanied by a type of depression sometimes described as neuroleptic dysphoria,23 which can persist for many years.24 In the long term, taking neuroleptics can also lead to a profound lack of motivation, known as the neuroleptic induced deficit syndrome, which is almost impossible to distinguish from negative symptoms.25 In one clinical trial it was found that patients treated with neuroleptics, although less symptomatic, achieved fewer life goals than patients treated with a placebo.26
Effects that are life-threatening but fortunately less common include sudden heart failure (psychotic patients are about twice as likely to die this way than ordinary people);27 the neuroleptic malignant syndrome (a disorder characterized by muscular rigidity, fever and fluctuating consciousness, which is often mistaken for a bacterial infection, and which is fatal if drugs are not promptly discontinued);28 and agranul
ocytosis (a loss of white blood cells, which is also fatal unless treated promptly).29 There are also hidden risks of death associated with neuroleptic medication that are difficult to calculate. For example, because obesity increases the risk of myocardial infarction and stroke, patients who experience neuroleptic-induced weight gain presumably suffer an increased risk of dying from these illnesses, but such deaths are never recorded as drug reactions.30 Similarly, there is evidence that severe akathisia can provoke patients to attempt suicide,31 but patients’ suicides are rarely regarded as drug-induced.
Because of these many adverse effects, neuroleptics, if used indiscriminately, can cause more harm than good. Biological psychiatrists should therefore have been strongly motivated to establish the safest and most effective dose of this kind of treatment. It is therefore all the more remarkable that the first experiments to address this question were not published until 1990 – approximately 40 years after the drugs were first introduced.32 The results of these studies surprised many psychiatrists, because they showed that no additional clinical benefits were obtained for doses equivalent to more than about 350 milligrams of chlorpromazine a day, a much lower dose than was commonly used in routine practice. The same studies provided clear evidence of a simple linear relationship between dose and side effects – the higher the dose the more likely it is that patients will experience side effects that are severe and very distressing.33 The inescapable conclusion that follows from these findings is that the overzealous use of neuroleptic medication has led to a worldwide epidemic of avoidable iatrogenic illness, causing unnecessary distress to countless vulnerable people, and no doubt sending some to early graves. Astonishingly, this problem continues at the time of writing. Despite advice to the contrary from organizations such as the Royal College of Psychiatrists in Britain34 and the US National Institute of Mental Health,35 surveys show that psychiatrists continue to treat many of their patients with bizarrely high doses of neuroleptic drugs.36
Madness Explained Page 57
