Biological psychiatry in perspective

Transcription

1 MGGelder Oxford University Department of Psychiatry, Warneford Hospital, Oxford, UK Biological psychiatry is a technical term that denotes physiological and biochemical approaches to psychiatric aetiology and, despite the usual wider meaning of the word biological, excludes psychosocial approaches/biological' causes of severe psychiatric disorder have been suspected from the earliest times, and in some periods an excessive focus upon them has led to neglect of psychological and social approaches to treatment, to the detriment of patients. It is important that current research into biological psychiatry should be carried forward in conjunction with the important advances that have been made in psychological and social research.the causes of psychiatric illness are complex and it is unlikely that any single approach, biological or psychosocial, will be sufficient on its own.the great potential of biological psychiatry will be realized only if it is viewed within these wider historical and scientific perspectives. The term biological psychiatry often puzzles those who are working in other branches of science and medicine. The word biology refers to the study of living things and therefore encompasses physiological, biochemical and psychological forms of investigation. In psychiatry, however, it has become conventional to use the term biological to encompass physiological, biochemical and genetic studies in contrast to social and psychological investigations. The general reader who is coming for the first time to the subject of this volume should understand this convention and should view the studies described in this volume in the context of psychological and social investigations. The general reader should also keep in the mind two other perspectives, the historical and the scientific. The historical perspective From the earliest times, it has been recognised that mental disorders have both physiological and psychological causes. In Hippocratic writings of Postal addrets: the 4th century BC, serious forms of mental illness were ascribed mainly Professor M G GeMer, to somatic causes, which were expressed in the then current ideas that n. - ^ ^ T T? health depended on a correct balance of the four body humours (blood, Department of Psychiatry, r. ' \ ' v/ameford Hospital, phlegm, yellow bile and black bile) and imbalance led to illness. Oxford OX3 7JX, UK Depressive disorder was related to an imbalance of black bile, hence the British Medico) BullmHn 1996^2 (No. 3H01-4G7 Tti. British Council 1996

2 Biological psychiatry term melancholia. These ideas were overtaken in the middle ages by the view that mental illness could best be explained in religious terms of sin and evil but in the 17th and 18th centuries interest in physical causes of severe illness revived. The causes were now sought in the brain itself, although the nature of this brain disorder was not understood. Repeated searches failed to show specific pathological changes even with the use of the new science of neuropathology developed in the 19th century. At that time, another aetiological theory came to the fore. It has long been recognized that mental illness tends to run in families, but, in 1809, the French psychiatrist Morel suggested that the disorder became more severe in successive generations of the same family and he suggested that inheritance can interact with certain adverse environmental factors, such as abuse of alcohol, and that the resulting changes could be transmitted to the next generation. This idea, which seems improbable today, was consistent with the then current notions of inheritance of acquired characteristics. These views had two unfortunate effects: they led to therapeutic pessimism and they gave support to the eugenic movement which held that the mentally ill should be separated from society and prevented from reproducing. The story of this period of research is an important reminder that scientific advances uncritically accepted can lead to harmful as well as to beneficial changes in policy. Although ideas concerning the aetiology of severe mental illness were dominated by these neuropathological and genetic theories, it is notable that practising doctors were aware that these ideas could not satisfactorily explain the illness of their patients. For example, the French psychiatrist Esquirol, writing in 1845, recognized the importance of heredity but stressed that psychological and social factors could predispose to or precipitate illness. Among his examples of adverse psychosocial factors were domestic problems, disappointments in love, and 'reversals of fortune', and he recognised also a wide group of physical causes such as the abuse of alcohol, the effects of childbirth and lactation, and epilepsy. The German psychiatrist Wilhelm Griesinger writing later in the century put forward similar views in his influential textbook The Pathology and Therapy of Mental Disorders. He wrote 1 : A closer examination of the aetiology of insanity soon shows that in the great majority of cases it was not a single specific cause under the influence of which the disease was finally established but a complication of several, sometimes numerous causes, both predisposing and exciting. Very often the germs of disease are laid in those early periods of life from which the commencement of the formation of character dates. It grows by education and external influences Bntisb Medical Bulletin 1996;52 (No. 3)

3 This statement still rings true today and could form a useful background to the studies described in this volume. Despite these wise and balanced views, many of the doctors who cared for the mentally ill in the second half of the 19th century took a simplistic organic view. The problem was recognised by Adolf Meyer, a Swiss doctor who became the dominant figure in American psychiatry in the late 19th and early 20th century. In the course of medical training in Switzerland, Meyer had been taught to think of aetiology in the tradition of Griesinger. When he began work in American psychiatric hospitals, he was disturbed by the narrowly organic views about aetiology and the consequent therapeutic nihilism. Meyer set out to promulgate the idea that mental illness had multi factorial causes and that, even in cases with the most obvious organic aetiology, there were additional psychosocial factors which could often be modified to the benefit of the patient. Meyer called this balanced approach psychobiology, a name that resembles the modern term biological psychiatry but had an altogether wider meaning embracing a detailed knowledge of each patient's biography and the educational and external influences that Griesinger had emphasized. Meyer's psychobiology had a beneficial effect on the practice of psychiatry by bringing about more active programmes of rehabilitation and resettlement and a better understanding of the psychological and social causes of mental illness. Its effects on research were less desirable, because psychobiology was so general and all-embracing it did not provide a clear guide to priorities in research. In the 1930s, neuroscience was in an early stage of development and this approach to psychiatric research together with Meyer's psychobiology were overtaken by psychoanalysis, which seemed at the time to provide answers to clinical problems which more scientific approaches could not rival. The gradual development of better methods of investigation, coupled with the discovery of drugs with powerful effects in the psychoses, led to a growing interest in the biological psychiatry which eventually expanded rapidly as new techniques of brain investigation became available. These few landmarks in the history of ideas about the causes of mental illness point to an important general conclusion. Each generation has based ideas of aetiology on the scientific approaches that were most active and seemed most plausible at the time. This sometimes led to a narrow view of aetiology, in which other factors, less easy to investigate, were neglected. Although, as the above quotations show, observant clinicians have always been aware of the complexity of the causes of psychiatric disorders in their patients, others have neglected the wider causes to the detriment of their patients. This volume reflects the wider viewpoint for it contains articles on psychological approaches as well as genetic, biochemical and physiological methods. Nevertheless, the reader Bnh(hMei cat Bulletin (No. 3) 4 0 3

4 Biological psychiatry should bear in mind the wealth of research into social and psychological causes of severe mental illness that cannot be reviewed here. The scientific perspective Three features of causation in psychiatry create difficulties for biological research: causes may be remote in time; one cause may have several effects; and one effect may have many causes. The causes of psychiatric illness are often remote in time. It has long been recognized that experiences in childhood can affect personality development and response to stress and it now seems possible that events before or soon after birth may be a primary cause of schizophrenia acting perhaps upon the development and maturation of the brain. The details of the process cannot be explained at present, but the general model has an obvious parallel in epilepsy in which trauma to the brain may result in disorder many years later. Nevertheless, it is very difficult to carry out direct scientific tests of associations so far apart in time. In the case of schizophrenia, indirect evidence has been called upon, for example the absence of gliosis in areas of the brain showing structural changes, a finding which suggests a pathological change before or around the time of birth 2. A second source of indirect evidence is the study, in the brains of schizophrenics dying of other causes, of genes known to be involved in brain development (see for example 3 ). A second difficulty for biological research is that in psychiatry a single cause can have multiple effects. This is illustrated by the consequences of syphilitic infection of the brain. When neurosyphilis was common, psychiatrists recognized that it could lead to dementia, affective symptoms, or a features resembling those of schizophrenia. Similarly, Huntington's chorea, which is due to a disorder involving a single gene and causing movement disorder and dementia, is associated also with psychiatric disorder including bipolar disorder 4. With this diversity of manifestations of known single causes, it is difficult to decide what range of disorders should be included in an aetiological investigation. It has been suggested, on the one hand, that the whole spectrum of psychoses may have a common cause (see for example 5 ) and, on the other, that these aetiological studies should consider specific subgroups within schizophrenia or manic depressive disorder. A third difficulty is that one effect may have multiple causes. There are predisposing, precipitating, and maintaining causes of psychiatric disorder; and there are usually psychological and social causes interacting with one or more genetic or biochemical cause of the same disorder. For example Kendler et al 6 calculated that about half the liability to major 404 Britith M»< cal Bulletin }996fi2 (No. 3)

5 depression could be accounted for by four factors: recent stressful life events; genetic factors; previous history of major depression; and neuroticism. The factors appeared to interact with 60% of the effect of genetic factors directly related to risk of developing major depression, and 40% expressed through increased liability to experience stressful events and to have high neuroticism. Despite these complexities, recent advances in neuroscience have led to major advances in the understanding of psychiatric aetiology and promise to reveal much more. Psychiatric research has benefited both from advances in basic science and from technological developments. There is now a wide span of scientific approaches to mental illness, including structural and functional imaging of the brain, molecular genetics, cell biology and metabolic studies. The contributions of these methods to the study of psychiatric aetiology is illustrated in several of the articles of this volume. (For example those by Craddock and Owen on modern genetic approaches and on clinical imaging techniques, by Smith and Jobst, and by Frangou and Murray.) Findings from these methods applied to patients have to be evaluated against a knowledge of the range of normal variation and some of the new techniques have not been in use for long enough for it to be certain how great is this variation, so that the extent and specificity of abnormality may sometimes be overestimated as it has been in the past. For example, when studies of the chromosome abnormalities began, the frequency of the XYY abnormality appeared to be particularly great among highly aggressive patients, but subsequent studies showed that the frequency of the abnormality in the general population was greater than had been supposed and the association with aggressive behaviour was correspondingly weaker 7. Also, some associations between biological abnormalities and psychiatric disorders turn out to be due to normal psychological reactions to the core abnormality. For example, it seems that in panic disorder the greater part of the psychological changes are due to a fearful reaction to autonomic symptoms which may arise from a primary disorder of autonomic regulation 8. Advances in neuroscience have not depended solely on new techniques, there have been important theoretical developments as well. Some of these new ideas, which are highly relevant to psychiatric aetiology, are discussed by Friston and Cowen who consider connectionist accounts of brain function and the important concepts of neural networks, neural modulation and neural plasticity, which provide different ways of conceptualizing the pathological basis of mental disorder. While reading about these striking advances in biological research, it is important to remember that some productive approaches to psychiatric aetiology fall outside the conventional confines of biological psychiatry and, therefore, are not described in this volume. Clinical psychology is flnhjfi Mtdical Bulletin 1996J2 (No. 3) 4 0 5

6 Biological psychiatry one of these approaches (though one aspect of the discipline - cognitive neuropsychology-is represented in this volume by the article by Frith). Sociological studies have been important in showing how the core features of functional psychosis can be added to by those of institutionalism, a key finding for those who are searching for the link between brain and behaviour. Such studies have also demonstrated the role of social stressors ('life events') in provoking and maintaining schizophrenia and affective disorders (see 9 ). Psychiatric epidemiology has been highly important in showing that the major mental disorders occur in a wide variety of different societies (arguing strongly against the view that schizophrenia is a product of social conditions) and epidemiological methods have been used effectively in the studies of population genetics which have laid the framework for molecular genetic investigations. Conclusions The scientific perspective reminds us that the findings described in this volume must be considered in the context of equally important discoveries from social and psychological research into psychiatric disorder. Psychosocial factors interact with biochemical and physiological factors in the aetiology of these conditions, and some of the findings of 'biological' studies may even be secondary to psychological disturbances. The historical perspective reminds us of the danger of focussing clinical practice too closely on current scientific advances because many aspects of the care of patients cannot be measured or investigated scientifically. Many of the important advances in knowledge described in this volume will doubtless lead to improvements in treatment, but it is important in the meantime that they do not result in neglect of other, less scientific, aspects of care. With this caution in mind, there is much in this volume that gives hope for the future understanding and treatment of psychiatric disorder. References Griesinger W. Mental Pathology and Therapeutics (2nd edn 1867, translated from the German by C. Lockhart Robertson and J. Rutherford). London: New Sydenham Society, 130 Bruton CJ, Crow TJ, Frith CD et al. Schizophrenia and the brain: a prospective clinico neuropathological study. Psychol Med 1990; 20: Bloom FE. Advancing a neurodevelopmental origin for schizophrenia. Arch Gen Psychiatry 1993; Peyser CE, Folstein SE. Depression in Huntingdon disease. In: Sarkstein SE, Robinson RG. (Eds) Depression in Neurological Disease. 1993; Britith Mtdical Bulletin 1996;52 (No. 3)

7 Crow TJ. The demise of the Kraepehn binary system as a prelude to genetic advance. In: Gershon ES, Cloninger R. (Eds) Genetic Approaches to Mental Disorders. Washington: American Psychiatric Press, 1994 Kendler KS, McGuire M, Gruenberg AM et al. The Roscommon family study. (1) Methods, diagnosis of probands and risk of schizophrenia in relatives. Arch Gen Psychiatry 1993; 50: Witkin HA, Mednick SA, Schulsinger F. CnminaUty and XYY and XXY man. Science 1976; 193: Clark DM, Salkovskis PM, Hackmann A, Middleton H, Anastasiades P, Gelder MG. A comparison of cognitive therapy, applied relaxation and imipramine in the treatment of panic disorder. Br J Psychiatry 1994; 164: Brown GW, Harris TO. Social Origins of Depression. London: Tavistock, 1978 British Mtdkal Bulletin }996$2 {No. 3) 407