Madness Explained
Page 19
More recently, Samuel Guze, a prominent neoKraepelinian, has simply stated that: ‘There can be no such thing as a psychiatry that is too biological.’5 It is clear, therefore, that psychiatrists’ recent preoccupation with biological determinants of psychosis, emphasized in proposition 6 of Gerald Klerman’s manifesto (see Table 3.3, p. 59), was the culmination of a historical trend within the profession.
A curious parallel exists between these assertions and the arguments put forward by some prominent anti-psychiatrists. Both groups, it seems, have assumed that the criterion for disease is some kind of pathology in the brain, and that disputes about the boundaries of madness can therefore be solved by reference to biological data. However, whereas the biological psychiatrists have assumed that neuropathology will inevitably be found in patients (if it has not been found already), the anti-psychiatrists have assumed that it is non-existent. Thomas Szasz, perhaps America’s most controversial critic of psychiatry, is best known for taking this position.
Born in Budapest in 1920, Szasz qualified as a psychiatrist and psychoanalyst in the United States and has been Professor of Psychiatry at the State University of New York, Syracuse, since 1956. He first stated his now infamous position in a 1960 paper entitled ‘The myth of mental illness’,* which was published in the American Psychologist, the professional journal of the American Psychological Association.6 This has been followed by a long series of articles and books that have addressed the same theme in different ways. In contrast to those of Ronald Laing, Szasz’s ideas appear to have been little influenced by his clinical experience; he offers few insights into the nature of psychosis. Rather, his arguments have been directed against the logic and ethics of biological psychiatry. Because Szasz’s opponents have often misunderstood these arguments, it is worth examining them in detail.
The argument outlined in ‘The myth of mental illness’ falls into two parts. Szasz’s first and most important claim is that the concept of mental illness is incoherent. His starting point is the work of the nineteenth-century physiologist Rudolf Virchow, who defined illness in terms of the presence of a lesion in the body. According to this definition, if mental illness is truly illness, it should be associated with some kind of physical pathology, which is most likely to be located in the brain. So far, Szasz’s position is entirely consistent with that of the neoKraepelinians. However, Szasz further notes that, in modern times, disorders of the brain are usually considered to be the province of neurology and therefore that the defining feature of a mental illness is the absence of physical pathology. For this reason, he claims, mental illness cannot be illness in any real sense of the word ‘illness’. On Szasz’s view, talk of mental illness is self-contradictory, in much the same way that describing someone as a ‘married bachelor’ or a ‘meat-eating vegetarian’ would be self-contradictory.
Szasz’s second claim concerns the role that the concept of ‘mental illness’ plays in industrialized societies. Following his argument that this concept is incoherent, Szasz is moved to ask why it has been so readily accepted by mental health professionals and the general public. He argues that a diagnosis of mental illness allows a kind of moral sleight-of-hand, apparently justifying the control of individuals who are a nuisance to others but who are not law-breakers. Once diagnosed as ‘mentally ill’, such individuals can be coerced into undergoing ‘treatment’ so that they will conform more fully to the social norms. On this view, psychiatrists, psychologists and psychiatric nurses belong to a kind of police force that controls and limits the amount of deviance within society.
This second part of Szasz’s argument has often been erroneously identified with the political left. In fact, Szasz’s views build on a tradition of right-wing libertarianism that is familiar to North Americans but which often seems alien to Europeans. Szasz believes that the state should have a minimal role in regulating the conduct of individuals. He therefore argues that recreational drugs should be legalized,7 and that the right to commit suicide should be respected.8 At the same time, he opposes the use of the insanity defence in court cases, because ‘Excusing a person of responsibility for an otherwise criminal act on the basis of inability to form conscious intent is an act of legal mercy masquerading as an act of medical science.’9 Although he has objected to compulsory psychiatric treatment, he has stated that he has no objection to psychiatry between consenting adults.10
Not surprisingly, Szasz’s ideas have earned him the opprobrium of many of his colleagues. Five years after the publication of ‘The myth of mental illness’, Frederick Glaser wrote in the American Journal of Psychiatry: ‘The question will inevitably be raised whether sanctions of some form ought to be taken against Dr Szasz, not only because of the content of his views but because of the manner in which he presents them.’11
Some saw Szasz’s arguments as part of a wider anti-establishment conspiracy. Commenting on the anti-psychiatry movement in general, British psychiatrist Sir Martin Roth (co-author of the 1975 textbook that sought to distance psychiatry from psychology) suggested that:
The anti-medical critique of psychiatry represents one approach within a wider movement which has assumed international proportions and adopts a critical or derogatory stance towards psychiatry’s methods, aims and social role; it is anti-medical, anti-therapeutic, anti-institutional and anti-scientific, either by expressed aims or implicitly through the dogmatic, hortatory, diffuse and inconsistent character of its utterances.12
Of course, these objections are very emotional and tell us little about the merits of Szasz’s position, which deserves a more dispassionate analysis.
Scientific evidence that madness is associated with neuropathology should be problematic for Szasz and other critics of the Kraepelinian paradigm but comforting to neoKraepelinians. Few of Szasz’s early opponents rose to this obvious challenge, perhaps because biological research into madness was still in its infancy at the time that ‘The myth of mental illness’ was written. In the four decades since, however, there have been substantial advances in the technologies available to biological researchers and there can be no doubt that these have provided encouragement to those who have continued to see psychiatry as a branch of physical medicine. It will be helpful to take a look at some of these developments, not only to facilitate our evaluation of the merits of the contrasting positions taken by Szasz and the neoKraepelinians, but also so that we can form an opinion about the achievements of biological psychiatry.
Before commencing this task I should point out that the following review is not intended to be comprehensive. Studies of brain biology have become so complex that it would be difficult to encompass them within a single book, let alone a single chapter. In the present context we must therefore focus more on the implications of biological investigations of psychosis than on the details of individual studies. In particular, what we need to establish is whether studies that point to apparent abnormalities in the brains of psychotic patients leave any room for theories of madness that have a more psychological flavour.
Psychotic Brains
Although it has long been known that the brain is the organ responsible for thought and feeling, its anatomy and physiology only began to be properly appreciated in the nineteenth century, largely as a result of the efforts of the early biological psychiatrists. Their work revealed that the brain consists of billions of small nerve cells, known as neurones, which are connected together into circuits of almost unimaginable complexity. These are surrounded by an even larger number of glial cells, which have metabolic functions, and which help to determine the overall structure of the brain.
At the time of these major advances in neuroscience, it was widely believed that electrical impulses were responsible for the transmission of information within the brain, a belief that had been fostered by Galvani, Volta and others in the eighteenth century, who had shown that nerves could be stimulated by electricity. The invention of the electroencephalogram (EEG) by the German psychiatrist Hans Berger in the 1920s allowed the firs
t recordings of electrical activity from electrodes placed on the human scalp, which appeared to confirm this hypothesis. Our current understanding that the transmission of information within the neurone is electrical, but that neurones communicate by means of chemicals, known as neurotransmitters, is there-fore surprisingly recent. Although Otto Loewi and Henry Dale received the Nobel Prize for medicine in 1936 for their demonstration that the peripheral nervous system utilizes noradrenaline and acetylcholine,13 the idea that neurotransmitters played an important role in the central nervous system only became widely accepted in the 1960s.14
At the moment, neuroscience is again a rapidly expanding field of inquiry, and many different methods of investigation are currently being employed. In what follows I will restrict myself to the three approaches that have been pursued most vigorously by modern biological psychiatrists: studies of the gross anatomical structure of the brain, investigations of activity in different brain regions, and finally examination of the brain’s biochemical composition. I will also focus mainly on studies of schizophrenia patients, as other diagnostic groups within the psychotic spectrum have been much less intensively investigated.
The anatomy of madness
Perhaps the most obvious way of searching for a biological substrate of madness is to look at the brains of mad people. Kraepelin advocated post-mortem studies for this purpose, and encouraged his colleague Alois Alzheimer to pursue this line of research. Although he accepted Alzheimer’s conclusion that the brains of dead psychotic patients looked more or less normal, this did not stop him from asserting that, in dementia praecox, ‘Partial damage to, or destruction of, cells of the cerebral cortex must probably occur, which may be compensated for in some cases, but which mostly brings in its wake a singular, permanent impairment of the inner life.’15
Since Kraepelin’s time, post-mortem studies have been pursued with sporadic enthusiasm but without consistent results. This is no doubt partly because, as we have seen, schizophrenia is an incoherent concept, so that patients who receive the diagnosis are likely to have acquired their symptoms as a consequence of a number of distinct aetiological processes, but also because of the methodological difficulties encountered in this kind of work. The brains studied, which are usually taken from the bodies of elderly patients, may not represent psychotic brains in general, and may have been damaged by whatever factors were responsible for the patients’ deaths. Following death, decay progressively alters brain tissue and these changes become more marked with time. Add in the difficulty of finding comparable brains from ordinary people who died at the same age of similar causes, and which have been stored after death for a similar period under identical conditions, and it is easy to see why repeatable findings have been elusive.16
Interestingly enough, the observation that has been most often replicated is a negative one. At any stage in life after the end of the second trimester of foetal development, neuronal damage (for example, as a consequence of infection or injury) leads to a proliferation of glial cells, accompanied by a rise in associated enzymes and proteins – a process known as gliosis. Most studies that have looked for gliosis in the brains of patients have failed to find it,17 suggesting that damage to the brain after birth is unlikely to play an important role in psychosis. This inference, which is not uncritically accepted by all neuropathologists who agree with the basic observation,18 has in turn led to the suggestion that some kind of foetal brain damage prior to the end of the second trimester may be responsible (a proposal we will consider in detail in a later chapter).
A more promising approach is to study the brains of living patients. Early methods of imaging the living nervous system followed from Röntgen’s discovery of X-rays in 1895.19 These included angiography (in which an X-ray-opaque medium is injected into the cerebral arteries), which was developed in the 1930s by the Portuguese neurosurgeon (and one time foreign minister) Egas Moniz. Moniz’s invention was an important medical breakthrough, because it allowed neurosurgeons to locate cerebral tumours with precision for the first time. The same cannot be said of his more famous invention, the prefrontal leucotomy operation given to thousands of unfortunate schizophrenia patients, for which he was awarded a Nobel Prize in 1949. (In one of the more ironical twists in the history of psychiatry, Moniz was shot dead by a disgruntled leucotomy patient in 1955.)
Godfrey Hounsfield, a British engineer whose work for Electrical and Musical Industries (EMI) Ltd heralded the modern era of brain imaging, was a more deserving recipient of the Prize. In 1970, Hounsfield introduced computed tomography (CT) scanning, which allowed X-ray information taken from different angles to be integrated into a single image depicting a slice through the body. Although this was a revolutionary step forward, the achievements of CT scanning have recently been surpassed by even more advanced technologies, which make similar use of computers to construct complex images. Perhaps the most important of these is magnetic resonance imaging (MRI), which uses strong magnetic fields to provoke a discharge of radio waves from the body, and which is better than CT at imaging the soft tissues of the brain. MRI scans now generate breathtakingly beautiful three-dimensional pictures of the brain that can be rotated and inspected from different angles.
Studies employing these structural imaging technologies have reported a variety of abnormalities in the brains of psychotic patients, including enlargement of the sulci (crevices in the folded tissue of the cortex), focal lesions in different cortical areas, and atypical asymmetries of the cerebral hemispheres. Most researchers, however, have focused their attention on the fluid-filled ventricles in the centre of the brain, perhaps because these were the only anatomical structures that were adequately revealed by early CT scans (see Figures 7.1 and 7.2).
The earliest CT study of psychotic patients was carried out by
Eve Johnstone, Tim Crow and their colleagues at Northwick Park Hospital, near London, who used the first scanner to become available in Britain.20 They reported that a small group of chronically ill schizophrenia patients had significantly larger lateral ventricles than a comparison group of ordinary people. Later studies conducted in several different countries appeared to replicate this finding, implying that schizophrenia patients suffer from some kind of loss of volume in the cerebral cortex.21 As some of these findings were obtained from patients who had only recently become ill and who had not been treated with medication,22 some researchers have inferred that brain disease is present at the very beginnings of psychosis. In the light of the inconsistent neuropathological evidence, it has also been argued that this loss of volume reflects a reduction in the size of neurones and the interconnections between them, rather than a loss of neurones per se.23
Figure 7.1 The cerebral ventricles (reproduced from K. W. Walsh (1978) Neuropsychology: A Clinical Approach. Edinburgh: Churchill Livingstone).
Figure 7.2 CT scans showing the cerebral ventricles in a healthy individual, left, and a patient with a diagnosis of schizophrenia, right (reproduced from N. C. Andreasen (2001) Brave New Brain: Conquering Mental Illness in the Era of the Genome. Oxford: Oxford University Press).
On closer inspection, however, the CT and structural MRI data are more ambiguous. In all studies, substantial variations in ventricular size have been observed in both patients and ordinary people. Moreover, some studies have failed to find evidence of significant ventricular enlargement, presumably because people who receive the diagnosis of schizophrenia form a heterogeneous group.24 However, enlarged ventricles have been recorded in studies of bipolar patients and patients suffering from unipolar (simple) depression, although, again, findings have varied substantially from study to study.25 When mood disorder patients and schizophrenia patients have been compared, little evidence of difference has been found.26 It is therefore unlikely that ventricular enlargement (even if we can be sure that it is present in some patients) is uniquely associated with schizophrenia.
Some of the inconsistencies in the data probably reflect problems that are unique to this kind of research
. For all the precision of CT and MRI, it can be difficult to calculate the exact volume of the cerebral ventricles. A further and perhaps more fundamental obstacle is the difficulty of finding appropriately matched non-psychotic people who are willing to be scanned. In 1986 two Canadian researchers, Geoffrey Smith and William Iacano, highlighted this problem by reanalysing the results from twenty-one studies then available, splitting them into those studies that had found differences between schizophrenia patients and controls and those that had not.27 The average ventricular size of the patients in the two sets of studies was about the same, but the control participants in the studies that did report a difference had smaller ventricles than the control participants in the studies that did not. It seemed that those studies that reported abnormally large ventricles in schizophrenia patients did so because they recruited controls (often patients attending hospital for neurological tests whose brain scans were judged to be normal) who had ventricles that were unusually small! Not surprisingly, later studies, using larger samples and more carefully matched controls, have found more modest differences between patients and ordinary people.28
The importance of recruiting adequately matched controls is underscored by studies which have shown that ventricular volume is affected by factors such as sex, age, head size, educational achievement, social class, ethnicity, alcohol consumption, water retention and even pregnancy.29 As some of these sources of variation can change with time, it should not be surprising that ventricular volume can vary between one occasion and another. A recent study found that some psychotic patients who at first appeared to have large ventricles showed a reduction of ventricular volume to within normal limits when scans were repeated at a later date.30