160
VIEWPOINT
Chronic fatigue, viruses, and
depression
often complain of persistent fatigue or muscular weakness. A US survey found that generalised chronic fatigue was "a major problem" for 24% of all adults attending primary care clinics, and in a community survey in the UK 25% of women and 20% of men reported that they "always feel tired". The causes of these symptoms are poorly understood and often generate strong differences of opinion both between doctors and between them and their Patients
patients. In some patients the weakness and fatigue developed after epidemics of an obscure illness known in the UK as benign myalgic encephalomyelitis and in the US as epidemic neuromyasthenia, but isolated cases are more common. The Myalgic Encephalomyelitis Association claims that there are 150 000 patients with myalgic encephalomyelitis (ME) in the UK; most of these are sporadic cases rather than part of well-defined epidemics, and Behan has suggested that the condition is as common as multiple sclerosis (about 3 cases per 100 000.4 Whether these sporadic cases are caused by the same putative infection and whether previous viral infection or unrecognised chronic infection are important in the genesis of these states of persistent debility are unresolved issues. The terms "postviral fatigue syndrome" (PVFS), "postviral exhaustion", ME and "chronic Epstein-Barr (EB) virus syndrome" embody an assumption that a viral infection is responsible for the patient’s weakness and
fatigue. Patients with a diagnosis of ME or PVFS have often been found to have a high frequency of unusually high viral antibody titres.4-6 However, as these patients have experienced a recent viral infection more commonly than the rest of the population almost by definition, firm conclusions cannot be drawn. In the US, despite reports of raised antibody titres to Epstein-Barr virus and human herpesvirus type 6, no evidence of persistent viral infection has been found.’ In the UK, two groups have found persistent Coxsackie B virus infection in a proportion of patients with the PVFS.8,9 Confirmation of these claims and the development of a reliable test for persistent Coxsackie infection would have a striking and salutory effect on the management of patients with chronic fatigue. At present, however, claims of abnormally prolonged "jitter values" on single fibre electromyographyl° are unconfirmed and the histology, electrophysiology, and glycolytic enzymes of affected muscles appear to be normal. The development of excessive intracellular acidosis during exercise in a single patient examined by 31P-NMRll also seems to be a non-specific finding.12 That most patients with PVFS find mental exertion as exhausting as physical exertion also suggests that a disorder of skeletal muscle is unlikely to account for all their symptoms.
Although psychiatrists who see patients with these puzzling symptoms often diagnose a depressive illness, this or any other psychiatric diagnosis is frequently unacceptable to them, especially if it has previously been suggested that they have ME. They are unshakably convinced that their symptoms are due to organic illness and refuse antidepressive therapy. It is not sufficiently widely appreciated, even by doctors, that affective illnesses characteristically cause a profound disturbance of energy. Manic patients have boundless energy and are overactive; depressed patients complain bitterly that they have no energy and are notably underactive. Indeed, the disturbance of energy and activity is almost as fundamental as the disturbance of mood. In the (10th) revision of the International Classification of Disease the basic description of a depressive episode begins with the statement that "the subject suffers from lowering of mood, reduction of energy, and decrease in activity. Capacity for enjoyment, interest, and concentration are impaired, and marked tiredness after even minimum effort is common."13 Apart from the absence of any reference to previous viral infection, this description is almost indistinguishable from that of PVFS. Depressive illnesses are also twice as common in women as in men and are uncommon in children, two prominent and otherwise puzzling features of PVFS. Although ME and PVFS are new concepts, there is nothing novel about unexplained chronic fatigue and profound muscular weakness made worse by exercise. Both have been recognised for at least a century. The American neurologist George Beard described what he called neurasthenia in 1867 and attributed it to exhaustion of nerve cells through depletion of their stored nutriment.14 There are stiking similarities between Beard’s neurasthenia and ME: in symptoms, in the social setting in which it presented (predominantly middle classes), in treatment (complete rest was advocated), and in presumed aetiology (a real illness, not a psychiatric disorder) .15 Neurasthenia initially encompassed much of what is now regarded as neurotic illness but by the early years of this century had come to mean unexplained exhaustion and fatigue. There was considerable debate about causation and the relative importance of physical and psychological factors and many therapies were tried, from absolute rest to psychoanalysis. By the 1940s there was general agreement that psychological influences were more important than overwork or endotoxins and, although the diagnosis is now rarely made, neurasthenia has survived as a discrete form of neurotic illness in the International Classification even in the new revision. When patients with chronic fatigue are assessed psychiatrically, between 50 and 80% are found to fulfil operational criteria for psychiatric disorder. 1,7,16,17 Most patients have major depression, others have anxiety or somatisation disorders, and many have an unusually high frequency of depressive episodes before the onset of fatigue. Only one study has failed to find an abnormally high prevalence of current and past psychiatric symptoms, but even here 22 of 48 patients (46%) met criteria for major depression at some stage in their illness.18
new
ADDRESS
University Department of Psychiatry, Royal Edinburgh Hospital, Edinburgh, EH105HF, UK (ProfR E Kendell, MD)
161
The relation between PVFS and the symptoms of both depressive illnesses and peripheral neuromuscular disease has been clarified by a prospective study." 47 patients with PVFS, 33 patients with fatiguing neuromuscular disorders—eg, myasthenia gravis and Guillain Barre syndrome, and 26 consecutive admissions with major depression were compared. Even when fatigue was excluded as a symptom, 72% of PVFS patients met operational criteria for psychiatric disorder, mainly major depression. Moreover, the symptoms of the PVFS group and the depressive controls were almost identical. Fatigue brought about by mental and physical exertion was common in both groups. However, 18 of 21 PVFS patients who met criteria for major depression were convinced that their illness had a physical basis. The neuromuscular disorder control patients described little mental fatigue, except in the presence of intercurrent psychiatric disorder, and had fewer somatic symptoms of other kinds. Patients may object to any suggestion that they have depression because such a diagnosis implies that their symptoms are imaginary or "all in the mind".19 Sadly, this assumption, with its crude distinction between real/organic illnesses and psychiatric disorders, seems to be shared by the ME Association and many doctors. Many of the symptoms of patients with ME or PVFS can only be understood as disturbances of cerebral functioning. Impaired concentration and memory, depression, insomnia, and irritability are not attributable to localised muscle disease, even if there is good evidence of muscle abnormalities. Evidence suggests that the whole range of depressive illness, not just endogenous depression, is familial and in part genetically transmitted .20 -21 Antidepressive drugs elevate mood in people who are depressed with little effect in normal people. These facts imply that there must be biological differences, qualitative or quantitative, between people who are prone to depression and those who are not (trait differences) and between people who are currently depressed and those who are not (state differences). These differences must involve, or influence, cerebral function. Depressions are commonly precipitated by stressful circumstances or life events, but the same is true of other diseases such as myocardial infarction. Where then is the fundamental difference between depressive and ’organic’
illnesses?
Irrespective of the role of chronic viral infection, the symptoms of most patients with chronic fatigue states are real, pervasive, and often incapacitating. The only patients whose symptoms can legitimately be described as "all in the mind" are those whose disabilities are learnt behaviour and whose complaints have been moulded and potentiated by the advantages of the invalid role.22 It is important to recognise that, in a society where ME is portrayed as a mysterious, rather glamorous, and disabling illness, people who have acquired this diagnosis may obtain attention and sympathy from friends and relatives, and perhaps also a justification for not fulfilling career ambitions or coping with the demands of everyday life. They may therefore lead less unhappy lives with their symptoms and their diagnosis than they could do otherwise. The statement that someone has a depressive illness is merely a statement about their symptoms. It has no causal implications, despite the fact that depressions that are secondary to a toxic state or metabolic abnormality-eg, Cushing’s disease or drug-induced depression, are usually classified separately. Furthermore, malaise and debility
associated with infection may, by non-specific mechanisms shared with other stressors, help to precipitate episodes of depression. Depression itself may also predispose to subsequent infection by an effect on immune mechanisms and lymphocyte activity." No fundamental distinction can therefore be drawn between depressive illnesses and other kinds of ’real’ or ’organic’ illness. Moreover, depressions have the great merit of being eminently treatable, unlike the chronic viral infections thought to underlie ME and the PVFS. Patients diagnosed as ME or PVFS are almost certainly heterogeneous. Some probably have chronic viral infections that are causally important;8,9 others may have unrecognised disorders of their skeletal musculature. A substantial proportion, however, have depressive illnesses or other well-recognised psychiatric disorders and in some there may be no clear distinction between these three categories. It is essential that a detailed psychiatric assessment is carried out on all such patients, to ensure that a correct diagnosis is made and that appropriate treatment is given. The sudden appearance of symptoms in someone of normal previous personality does not exclude psychiatric disorder. Depressive illness commonly presents in this way. Terms like postinfective fatigue syndrome and myalgic encephalomyelitis, with their unproven assumptions about aetiology, need to be replaced by neutral terms like chronic fatigue syndrome, unless there is hard evidence of persistent viral infection. It is also vital that in future all diagnostic terms are operationally defined. The Centers for Disease Control (CDC) in Atlanta have proposed an operational definition of chronic fatigue syndrome, partly to discourage clinicians from assuming, on inadequate evidence, that their patients have a "chronic EB virus syndrome" .24 The CDC defmition has been made deliberately narrow to maximise the chances of those who fulfil its criteria having a chronic viral infection.Few patients with chronic fatigue meet these requirements.25 Broader definitions will therefore be needed if the majority of patients currently regarded as having ME or PVFS are to be covered. It is likely, though, that these definitions will include many patients who also fulfil criteria for major depression or other psychiatric disorders.
REFERENCES 1. Kroenke K, Wood DR, Mangelsdorff D, Meier NJ, Power JB. Chronic fatigue in primary care. JAMA 1988; 260: 929-34. 2. Health Promotion Research Trust. The health and lifestyle survey. London: HPRT, 1987. 3. Annual Report. Myalgic Encephalomyelitis Association. Stanford le Hope, Essex: ME Association, 1989. 4. Behan PO, Behan WMH, Bell EJ. The postviral fatigue syndrome—an analysis of the findings in 50 cases. J Infection 1985; 10: 211-22. 5. Straus SE, Tosato G, Armstrong G, et al. Persisting illness and fatigue in adults with evidence of Epstein-Barr virus infection. Ann Intern Med 1985; 102: 7-16. 6. Calder BD, Warnock PJ, McCartney RA, Bell EJ. Coxsackie B viruses and the postviral syndrome: a prospective study in general practice. JR Coll Gen Pract 1987; 37: 11-14. 7. Gold D, Bowden R Sixbey J, et al. Chronic fatigue: a prospective clinical and virological study. JAMA 1990; 264: 48-53. 8. Yousef GE, Bell EJ, Mann GF, et al. Chronic enterovirus infection in patients with postviral fatigue syndrome. Lancet 1988; i: 146-49. 9. Archard LC, Bowles NE, Behan PO, Bell EJ, Doyle D. Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase. J R Soc Med 1988; 81: 326-29. 10. Jamal GA, Hansen S. Electrophysiological studies in the postviral fatigue syndrome. J Neurol Neurosurg Psychiatry 1985; 48: 961-64. 11. Arnold DL, Bore PJ, Radda GK, Styles P, Taylor DJ. Excessive intracellular acidosis of skeletal muscle on exercise in a patient with a post-viral exhaustion/fatigue syndrome. Lancet 1984; i: 1367-69.
162
12. Yonge RP. Magnetic resonance muscle studies: implications for psychiatry. JR Soc Med 1988; 81: 322-25. 13. World Health Organisation Division of Mental Health. ICD-10: 1989 Draft of Chapter V. Mental and Behavioural Disorders. Geneva: WHO, 1989. 14. Beard GM. Neurasthenia or nervous exhaustion. Boston Med Surg J 1969; 3: 217-20. 15.
Wessely S. Old wine in new bottles: neurasthenia and ’ME’. Psychol Med 1990; 20: 35-53.
16. Kruesi MJP, Dale J, Strauss SE. Psychiatric diagnoses in patients who have chronic fatigue syndrome. J Clin Psychiatry 1989; 50: 53-56. 17. Wessely S, Powell R. Fatigue syndromes: a comparison of chronic ’postviral’ fatigue with neuromuscular and affective disorders. J Neurol Neurosurg Psychiatry 1989; 52: 940-48. 18. Hickie I, Lloyd A, Wakefield D, Parker G. The psychiatric status of patients with the chronic fatigue syndrome. Br J Psychiatry 1990; 156: 534-40. 19. Church AJ. Myalgic encephalomyelitis. "An obscene cosmic joke". Med
BOOKSHELF
Renal Tract Stone: Metabolic Basis and Clinical Practice Edited by J. E. A. Wickham and A. Colin Buck. Edinburgh: Churchill Livingstone. 1990. Pp 662. 75. ISBN 0-43038031.
Urolithiasis:
a
Medical and Surgical Reference
Edited
by Martin 1. Resnick and Charles Y. C. Pak. Philadelphia: Saunders. 1990. Pp 375. /;53.50/$75. ISBN 0-721624391.
The past ten years have seen enormous changes in the of urinary calculus disease. The advent of percutaneous renal surgery in the early 1980s was rapidly followed by the widespread introduction of extracorporeal shock-wave lithotripsy in the second half of that decade. Medical treatment of urinary calculi has not shown such striking advances, but there has been considerable progress in our understanding of the associated metabolic changes. Both these books address our current knowledge of the biochemical abnormalities which lead to urinary calculi, and the therapeutic options now available to urologists. Wickham and Buck’s multi-author volume has contributions from over 60 distinguished clinicians and basic scientists, from both Europe and North America. The editors set out to produce a comprehensive, state-of-the-art text and have succeeded: their many authors thoroughly review all facets of stone disease. Inevitably, the number of contributors has led to some unevenness of style, although this is generally kept under control, and some areas of overlap-but there are not too many of these, and the views expressed by different authors often serve to emphasise the controversies that remain. By contrast, Resnick and Pak have used fewer authors and have a more limited objective: to produce an up-to-date, practical manual for clinicians. They also succeed; not only are recent surgical techniques fully described, but the published results and complications of these treatments are criticallv reviewed. Their approach ensures greater treatment
J Aust 1980; i: 307-09. 20. Andreasen NC, Scgheftner A, Reich T, Hirschfed RMA, Endicott J, Keller MB. The validation of the concept of endogenous depression. Arch Gen Psychiatry 1986; 43: 246-51. 21. Kendler KS, Heath A, Martin NG, Eaves LJ. Symptoms of anxiety and depression in a volunteer twin population. Arch Gen Psychiatry 1986; 43: 213-21. 22. Kendell RE. Hysteria. In: Russell GFM, Hersov LA, eds. Handbook of Psychiatry 4: The neuroses and personality disorders. Cambridge Cambridge University Press, 1983: 232-46. 23. Schleifer SJ, Keller SE, Camerino M, Thornton JC, Stein M. Suppression of lymphocyte stimulation following bereavement. JAMA 1983; 250: 374-77. 24. Holmes GP, Kaplan JE, Gantz NM, et al. Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988; 108: 387-89. 25. Manu P, Lane TJ, Matthews DA. The frequency of the chronic fatigue syndrome in patients with symptoms of persistent fatigue. Ann Intern Med 1988; 109: 554-56.
uniformity of style, but less opportunity for examination of the more controversial metabolic aspects of stone disease. Although they cover the same ground, direct comparisons are perhaps unfair, given the different aims of the editors. Both books are well written and illustrated and both can be safely recommended to anyone who is interested in contemporary medical and surgical treatment of stone disease. Resnick and Pak’s work is perhaps more approachable and less forbidding, but clinicians who also want a comprehensive guide to the more scientific aspects of urolithiasis will find that Wickham and Buck have produced an invaluable reference book. Department of Urology, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK
Prenatal
K. N. BULLOCK
Diagnosis and Prognosis
by Richard Lilford. Guildford: Butterworth Scientific. Pp 245. 39.50. ISBN 0-407010440.
Edited 1990.
Recent technical advances have perhaps outpaced ethical arguments about how we should use information provided by, for example, modem high-resolution ultrasound and DNA technology. The importance of Professor Lilford’s contribution to that debate lies not only in the expertise of the contributors he has brought together, but also in the emphasis given to the need for knowledge about what an observation might mean for prognosis, which transcends the mere diagnosis itself. What is still required is the wisdom to know how to impart that information and to use such
knowledge in the best long-term interests of the individual, couple, or family for whom one is caring. The book begins with three chapters on the antenatal diagnosis of, and prognosis for, a range of fetal structural defects. We are repeatedly reminded that ultrasound appearances are only shadows and images, and must be interpreted with caution. A further three chapters deal with chromosomal anomalies, followed by genetics, DNA technology, diagnostic procedures, and a final chapter on decision analysis-one of the editor’s favourite themes. If I have a criticism it is that the book still places too much weight on calculation and not enough on caring. The proper emphasis on prognosis is a big step in the right direction, but
VIEWPOINT
Chronic fatigue, viruses, and
depression
often complain of persistent fatigue or muscular weakness. A US survey found that generalised chronic fatigue was "a major problem" for 24% of all adults attending primary care clinics, and in a community survey in the UK 25% of women and 20% of men reported that they "always feel tired". The causes of these symptoms are poorly understood and often generate strong differences of opinion both between doctors and between them and their Patients
patients. In some patients the weakness and fatigue developed after epidemics of an obscure illness known in the UK as benign myalgic encephalomyelitis and in the US as epidemic neuromyasthenia, but isolated cases are more common. The Myalgic Encephalomyelitis Association claims that there are 150 000 patients with myalgic encephalomyelitis (ME) in the UK; most of these are sporadic cases rather than part of well-defined epidemics, and Behan has suggested that the condition is as common as multiple sclerosis (about 3 cases per 100 000.4 Whether these sporadic cases are caused by the same putative infection and whether previous viral infection or unrecognised chronic infection are important in the genesis of these states of persistent debility are unresolved issues. The terms "postviral fatigue syndrome" (PVFS), "postviral exhaustion", ME and "chronic Epstein-Barr (EB) virus syndrome" embody an assumption that a viral infection is responsible for the patient’s weakness and
fatigue. Patients with a diagnosis of ME or PVFS have often been found to have a high frequency of unusually high viral antibody titres.4-6 However, as these patients have experienced a recent viral infection more commonly than the rest of the population almost by definition, firm conclusions cannot be drawn. In the US, despite reports of raised antibody titres to Epstein-Barr virus and human herpesvirus type 6, no evidence of persistent viral infection has been found.’ In the UK, two groups have found persistent Coxsackie B virus infection in a proportion of patients with the PVFS.8,9 Confirmation of these claims and the development of a reliable test for persistent Coxsackie infection would have a striking and salutory effect on the management of patients with chronic fatigue. At present, however, claims of abnormally prolonged "jitter values" on single fibre electromyographyl° are unconfirmed and the histology, electrophysiology, and glycolytic enzymes of affected muscles appear to be normal. The development of excessive intracellular acidosis during exercise in a single patient examined by 31P-NMRll also seems to be a non-specific finding.12 That most patients with PVFS find mental exertion as exhausting as physical exertion also suggests that a disorder of skeletal muscle is unlikely to account for all their symptoms.
Although psychiatrists who see patients with these puzzling symptoms often diagnose a depressive illness, this or any other psychiatric diagnosis is frequently unacceptable to them, especially if it has previously been suggested that they have ME. They are unshakably convinced that their symptoms are due to organic illness and refuse antidepressive therapy. It is not sufficiently widely appreciated, even by doctors, that affective illnesses characteristically cause a profound disturbance of energy. Manic patients have boundless energy and are overactive; depressed patients complain bitterly that they have no energy and are notably underactive. Indeed, the disturbance of energy and activity is almost as fundamental as the disturbance of mood. In the (10th) revision of the International Classification of Disease the basic description of a depressive episode begins with the statement that "the subject suffers from lowering of mood, reduction of energy, and decrease in activity. Capacity for enjoyment, interest, and concentration are impaired, and marked tiredness after even minimum effort is common."13 Apart from the absence of any reference to previous viral infection, this description is almost indistinguishable from that of PVFS. Depressive illnesses are also twice as common in women as in men and are uncommon in children, two prominent and otherwise puzzling features of PVFS. Although ME and PVFS are new concepts, there is nothing novel about unexplained chronic fatigue and profound muscular weakness made worse by exercise. Both have been recognised for at least a century. The American neurologist George Beard described what he called neurasthenia in 1867 and attributed it to exhaustion of nerve cells through depletion of their stored nutriment.14 There are stiking similarities between Beard’s neurasthenia and ME: in symptoms, in the social setting in which it presented (predominantly middle classes), in treatment (complete rest was advocated), and in presumed aetiology (a real illness, not a psychiatric disorder) .15 Neurasthenia initially encompassed much of what is now regarded as neurotic illness but by the early years of this century had come to mean unexplained exhaustion and fatigue. There was considerable debate about causation and the relative importance of physical and psychological factors and many therapies were tried, from absolute rest to psychoanalysis. By the 1940s there was general agreement that psychological influences were more important than overwork or endotoxins and, although the diagnosis is now rarely made, neurasthenia has survived as a discrete form of neurotic illness in the International Classification even in the new revision. When patients with chronic fatigue are assessed psychiatrically, between 50 and 80% are found to fulfil operational criteria for psychiatric disorder. 1,7,16,17 Most patients have major depression, others have anxiety or somatisation disorders, and many have an unusually high frequency of depressive episodes before the onset of fatigue. Only one study has failed to find an abnormally high prevalence of current and past psychiatric symptoms, but even here 22 of 48 patients (46%) met criteria for major depression at some stage in their illness.18
new
ADDRESS
University Department of Psychiatry, Royal Edinburgh Hospital, Edinburgh, EH105HF, UK (ProfR E Kendell, MD)
161
The relation between PVFS and the symptoms of both depressive illnesses and peripheral neuromuscular disease has been clarified by a prospective study." 47 patients with PVFS, 33 patients with fatiguing neuromuscular disorders—eg, myasthenia gravis and Guillain Barre syndrome, and 26 consecutive admissions with major depression were compared. Even when fatigue was excluded as a symptom, 72% of PVFS patients met operational criteria for psychiatric disorder, mainly major depression. Moreover, the symptoms of the PVFS group and the depressive controls were almost identical. Fatigue brought about by mental and physical exertion was common in both groups. However, 18 of 21 PVFS patients who met criteria for major depression were convinced that their illness had a physical basis. The neuromuscular disorder control patients described little mental fatigue, except in the presence of intercurrent psychiatric disorder, and had fewer somatic symptoms of other kinds. Patients may object to any suggestion that they have depression because such a diagnosis implies that their symptoms are imaginary or "all in the mind".19 Sadly, this assumption, with its crude distinction between real/organic illnesses and psychiatric disorders, seems to be shared by the ME Association and many doctors. Many of the symptoms of patients with ME or PVFS can only be understood as disturbances of cerebral functioning. Impaired concentration and memory, depression, insomnia, and irritability are not attributable to localised muscle disease, even if there is good evidence of muscle abnormalities. Evidence suggests that the whole range of depressive illness, not just endogenous depression, is familial and in part genetically transmitted .20 -21 Antidepressive drugs elevate mood in people who are depressed with little effect in normal people. These facts imply that there must be biological differences, qualitative or quantitative, between people who are prone to depression and those who are not (trait differences) and between people who are currently depressed and those who are not (state differences). These differences must involve, or influence, cerebral function. Depressions are commonly precipitated by stressful circumstances or life events, but the same is true of other diseases such as myocardial infarction. Where then is the fundamental difference between depressive and ’organic’
illnesses?
Irrespective of the role of chronic viral infection, the symptoms of most patients with chronic fatigue states are real, pervasive, and often incapacitating. The only patients whose symptoms can legitimately be described as "all in the mind" are those whose disabilities are learnt behaviour and whose complaints have been moulded and potentiated by the advantages of the invalid role.22 It is important to recognise that, in a society where ME is portrayed as a mysterious, rather glamorous, and disabling illness, people who have acquired this diagnosis may obtain attention and sympathy from friends and relatives, and perhaps also a justification for not fulfilling career ambitions or coping with the demands of everyday life. They may therefore lead less unhappy lives with their symptoms and their diagnosis than they could do otherwise. The statement that someone has a depressive illness is merely a statement about their symptoms. It has no causal implications, despite the fact that depressions that are secondary to a toxic state or metabolic abnormality-eg, Cushing’s disease or drug-induced depression, are usually classified separately. Furthermore, malaise and debility
associated with infection may, by non-specific mechanisms shared with other stressors, help to precipitate episodes of depression. Depression itself may also predispose to subsequent infection by an effect on immune mechanisms and lymphocyte activity." No fundamental distinction can therefore be drawn between depressive illnesses and other kinds of ’real’ or ’organic’ illness. Moreover, depressions have the great merit of being eminently treatable, unlike the chronic viral infections thought to underlie ME and the PVFS. Patients diagnosed as ME or PVFS are almost certainly heterogeneous. Some probably have chronic viral infections that are causally important;8,9 others may have unrecognised disorders of their skeletal musculature. A substantial proportion, however, have depressive illnesses or other well-recognised psychiatric disorders and in some there may be no clear distinction between these three categories. It is essential that a detailed psychiatric assessment is carried out on all such patients, to ensure that a correct diagnosis is made and that appropriate treatment is given. The sudden appearance of symptoms in someone of normal previous personality does not exclude psychiatric disorder. Depressive illness commonly presents in this way. Terms like postinfective fatigue syndrome and myalgic encephalomyelitis, with their unproven assumptions about aetiology, need to be replaced by neutral terms like chronic fatigue syndrome, unless there is hard evidence of persistent viral infection. It is also vital that in future all diagnostic terms are operationally defined. The Centers for Disease Control (CDC) in Atlanta have proposed an operational definition of chronic fatigue syndrome, partly to discourage clinicians from assuming, on inadequate evidence, that their patients have a "chronic EB virus syndrome" .24 The CDC defmition has been made deliberately narrow to maximise the chances of those who fulfil its criteria having a chronic viral infection.Few patients with chronic fatigue meet these requirements.25 Broader definitions will therefore be needed if the majority of patients currently regarded as having ME or PVFS are to be covered. It is likely, though, that these definitions will include many patients who also fulfil criteria for major depression or other psychiatric disorders.
REFERENCES 1. Kroenke K, Wood DR, Mangelsdorff D, Meier NJ, Power JB. Chronic fatigue in primary care. JAMA 1988; 260: 929-34. 2. Health Promotion Research Trust. The health and lifestyle survey. London: HPRT, 1987. 3. Annual Report. Myalgic Encephalomyelitis Association. Stanford le Hope, Essex: ME Association, 1989. 4. Behan PO, Behan WMH, Bell EJ. The postviral fatigue syndrome—an analysis of the findings in 50 cases. J Infection 1985; 10: 211-22. 5. Straus SE, Tosato G, Armstrong G, et al. Persisting illness and fatigue in adults with evidence of Epstein-Barr virus infection. Ann Intern Med 1985; 102: 7-16. 6. Calder BD, Warnock PJ, McCartney RA, Bell EJ. Coxsackie B viruses and the postviral syndrome: a prospective study in general practice. JR Coll Gen Pract 1987; 37: 11-14. 7. Gold D, Bowden R Sixbey J, et al. Chronic fatigue: a prospective clinical and virological study. JAMA 1990; 264: 48-53. 8. Yousef GE, Bell EJ, Mann GF, et al. Chronic enterovirus infection in patients with postviral fatigue syndrome. Lancet 1988; i: 146-49. 9. Archard LC, Bowles NE, Behan PO, Bell EJ, Doyle D. Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase. J R Soc Med 1988; 81: 326-29. 10. Jamal GA, Hansen S. Electrophysiological studies in the postviral fatigue syndrome. J Neurol Neurosurg Psychiatry 1985; 48: 961-64. 11. Arnold DL, Bore PJ, Radda GK, Styles P, Taylor DJ. Excessive intracellular acidosis of skeletal muscle on exercise in a patient with a post-viral exhaustion/fatigue syndrome. Lancet 1984; i: 1367-69.
162
12. Yonge RP. Magnetic resonance muscle studies: implications for psychiatry. JR Soc Med 1988; 81: 322-25. 13. World Health Organisation Division of Mental Health. ICD-10: 1989 Draft of Chapter V. Mental and Behavioural Disorders. Geneva: WHO, 1989. 14. Beard GM. Neurasthenia or nervous exhaustion. Boston Med Surg J 1969; 3: 217-20. 15.
Wessely S. Old wine in new bottles: neurasthenia and ’ME’. Psychol Med 1990; 20: 35-53.
16. Kruesi MJP, Dale J, Strauss SE. Psychiatric diagnoses in patients who have chronic fatigue syndrome. J Clin Psychiatry 1989; 50: 53-56. 17. Wessely S, Powell R. Fatigue syndromes: a comparison of chronic ’postviral’ fatigue with neuromuscular and affective disorders. J Neurol Neurosurg Psychiatry 1989; 52: 940-48. 18. Hickie I, Lloyd A, Wakefield D, Parker G. The psychiatric status of patients with the chronic fatigue syndrome. Br J Psychiatry 1990; 156: 534-40. 19. Church AJ. Myalgic encephalomyelitis. "An obscene cosmic joke". Med
BOOKSHELF
Renal Tract Stone: Metabolic Basis and Clinical Practice Edited by J. E. A. Wickham and A. Colin Buck. Edinburgh: Churchill Livingstone. 1990. Pp 662. 75. ISBN 0-43038031.
Urolithiasis:
a
Medical and Surgical Reference
Edited
by Martin 1. Resnick and Charles Y. C. Pak. Philadelphia: Saunders. 1990. Pp 375. /;53.50/$75. ISBN 0-721624391.
The past ten years have seen enormous changes in the of urinary calculus disease. The advent of percutaneous renal surgery in the early 1980s was rapidly followed by the widespread introduction of extracorporeal shock-wave lithotripsy in the second half of that decade. Medical treatment of urinary calculi has not shown such striking advances, but there has been considerable progress in our understanding of the associated metabolic changes. Both these books address our current knowledge of the biochemical abnormalities which lead to urinary calculi, and the therapeutic options now available to urologists. Wickham and Buck’s multi-author volume has contributions from over 60 distinguished clinicians and basic scientists, from both Europe and North America. The editors set out to produce a comprehensive, state-of-the-art text and have succeeded: their many authors thoroughly review all facets of stone disease. Inevitably, the number of contributors has led to some unevenness of style, although this is generally kept under control, and some areas of overlap-but there are not too many of these, and the views expressed by different authors often serve to emphasise the controversies that remain. By contrast, Resnick and Pak have used fewer authors and have a more limited objective: to produce an up-to-date, practical manual for clinicians. They also succeed; not only are recent surgical techniques fully described, but the published results and complications of these treatments are criticallv reviewed. Their approach ensures greater treatment
J Aust 1980; i: 307-09. 20. Andreasen NC, Scgheftner A, Reich T, Hirschfed RMA, Endicott J, Keller MB. The validation of the concept of endogenous depression. Arch Gen Psychiatry 1986; 43: 246-51. 21. Kendler KS, Heath A, Martin NG, Eaves LJ. Symptoms of anxiety and depression in a volunteer twin population. Arch Gen Psychiatry 1986; 43: 213-21. 22. Kendell RE. Hysteria. In: Russell GFM, Hersov LA, eds. Handbook of Psychiatry 4: The neuroses and personality disorders. Cambridge Cambridge University Press, 1983: 232-46. 23. Schleifer SJ, Keller SE, Camerino M, Thornton JC, Stein M. Suppression of lymphocyte stimulation following bereavement. JAMA 1983; 250: 374-77. 24. Holmes GP, Kaplan JE, Gantz NM, et al. Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988; 108: 387-89. 25. Manu P, Lane TJ, Matthews DA. The frequency of the chronic fatigue syndrome in patients with symptoms of persistent fatigue. Ann Intern Med 1988; 109: 554-56.
uniformity of style, but less opportunity for examination of the more controversial metabolic aspects of stone disease. Although they cover the same ground, direct comparisons are perhaps unfair, given the different aims of the editors. Both books are well written and illustrated and both can be safely recommended to anyone who is interested in contemporary medical and surgical treatment of stone disease. Resnick and Pak’s work is perhaps more approachable and less forbidding, but clinicians who also want a comprehensive guide to the more scientific aspects of urolithiasis will find that Wickham and Buck have produced an invaluable reference book. Department of Urology, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK
Prenatal
K. N. BULLOCK
Diagnosis and Prognosis
by Richard Lilford. Guildford: Butterworth Scientific. Pp 245. 39.50. ISBN 0-407010440.
Edited 1990.
Recent technical advances have perhaps outpaced ethical arguments about how we should use information provided by, for example, modem high-resolution ultrasound and DNA technology. The importance of Professor Lilford’s contribution to that debate lies not only in the expertise of the contributors he has brought together, but also in the emphasis given to the need for knowledge about what an observation might mean for prognosis, which transcends the mere diagnosis itself. What is still required is the wisdom to know how to impart that information and to use such
knowledge in the best long-term interests of the individual, couple, or family for whom one is caring. The book begins with three chapters on the antenatal diagnosis of, and prognosis for, a range of fetal structural defects. We are repeatedly reminded that ultrasound appearances are only shadows and images, and must be interpreted with caution. A further three chapters deal with chromosomal anomalies, followed by genetics, DNA technology, diagnostic procedures, and a final chapter on decision analysis-one of the editor’s favourite themes. If I have a criticism it is that the book still places too much weight on calculation and not enough on caring. The proper emphasis on prognosis is a big step in the right direction, but
