- Email: [email protected]
CHRONIC ALCOHOLIC AND CORTICOSTEROID MYOPATHY
1261 statistical texts, but there is a a handout we use for teaching in this medical school is available on request. In the blood-lead example the test results in a normal deviate of 2-29 (p<0-03) when the 41 retarded children and 36 controls are compared, which is consistent with the Mann Whitney test. I find Dr Moore’s justification for the weighted regression unsatisfactory since it seems to prejudge the existence of a relation between blood and water lead. Also, a marked difference between the mentally retarded and controls having been established, it seems odd to combine them in a single regression. Blood tests could be done on only 77 out of 154 children. Even if there is no obvious selectivity there is still a possibility of bias with so many missing values. In this type of retrospective study a case can be made for the reversal of cause and effect. The mentally retarded might, as a result of, say, lower incomes or lower parental I.Q., be more likely to live in older, poorer housing with high water lead. Such arguments need to be considered before one can declare with any assurance water lead causes mental retardation. is omitted from
elementary
mathematical description’ and
Medical Computing and Statistics Group, Medical School, Edinburgh EH8 9AG
STUART J. POCOCK
CHRONIC ALCOHOLIC AND CORTICOSTEROID MYOPATHY
SiR,—The paper by Dr Rees and his colleagues (April 2,
p.
raises an interesting question about the pathogenesis of chronic alcoholic myopathy,2 a rare complication seen in alcoholic patients. We have seen two young women with clear-cut cushingoid features who had weakness and muscular atrophy associated with excessive drinking of alcohol. Laboratory studies revealed macrocytic anaemia, carbohydrate tolerance, and hepatic impairment. Serum phosphocreatine-kinase and aldolase activities were normal and the serum-lactate-dehydrogenase was slightly raised. In hospital we found an 8 A.M. high plasma-cortisol in both patients (29 and 27 g/dl). Clinical and electromyographic investigation showed myopathy of proximal muscles. Histological examination of deltoid muscle, done in one patient, revealed a diminution in diameter of the fibres with more selective atrophy of type n. Similar findings have been obtained in myopathy of Cushing’s syndrome.3 There thus seems to be a correlation between these two muscular disorders. D. DE GRANDIS Clinica Malattie Nervose e Mentali, A. FIASCHI Centro Ospedaliero Clinicizzato, 37100 Verona, Italy G. TOMELLERI
726)
SEASONAL VARIATIONS IN CARDIAC FAILURE
SIR,-Professor Parry and his colleagues (May 14, p. 1023) right about heat-induced cardiovascular changes being responsible for the seasonal variations of cardiac failure in the Nigerian town of Zaria. However, I wonder if they have paid enough attention to nutritional factors. I have suggested that in Johannesburg Blacks cardiomyopathy, especially peripartal may be
heart-disease, may be a nutritional disorder.4 The finding that peripartal heart-disease, the commonest cause of heart-failure in Zaria, presented most often during the "hungry" season, suggests that malnutrition may also be
an
important factor
1. 2.
Cox, D. R. Analysis of Binary Data; p. 61. London, 1970. Carlsson, C., Dencker, S. J., Grimby, G., Tichy, J. Q. Jl Stud. Alc. 1969,
3. 4.
30, 385. Pleasure, D. E., Walsh, G. O., Engel, W. Seftel, H. C. S. Afr. med. J. 1972, 46, 1823.
K. Archs Neurol. 1970,
22,
118.
there. Absence of clinical changes in nutrition or of variations in haemoglobin does not exclude this possibility. In view of the high incidence of peripartal disease in Zaria perhaps Professor Parry could look at the effects of administering a balanced diet throughout the year to a sample of the female population of childbearing age. This would not be easy but if it could be done the seasonal variations might disappear-and so, eventually, might the disease itself. Medical School, University of the Witwatersrand,
Hospital Street, Johannesburg 2001, South Africa
H. C. SEFTEL
BRIQUET’S SYNDROME OR HYSTERIA? SIR,-You rightly question (May 28, p. 1138) the substitution of Briquet’s syndrome for hysteria and "the surprising aversion (of the St. Louis group) to detecting it in men". The reason why the St. Louis group do not detect it in males is simply because they do not diagnose hysteria but Briquet’s syndrome, in which the male/female ratio (according to Briquet) is 1/20. The frequency of the diagnosis of hysteria in males depends on fashion and semantics. Sydenham, who saw hysteria in 16% of his patients, found it not uncommon in men "leading sedentary life and studying hard", but for etymological reasons (men have no uterus) he preferred to call male hysteria hypochondriasis.I Pierre Marie saw hysteria eight times more frequently in males,2 and Charcot thought that male hysteria is not diagnosed due to a prejudice.3 In Austria they did not believe in male hysteria, and when Freud, under the influence of Charcot, lectured on male hysteria in Vienna, Meynert challenged him to prove his words. (Freudians took their revenge on Meynert posthumously, by disseminating a joke that "Meynert later confessed to Freud on his deathbed that he himself had been a classical case of male hysteria, but always managed to conceal the fact."4) New varieties of male hysteria appeared-"railway spine" in the 1880s in the U.S.A. and, later, "compensation neurosis" in Europe. In private practice it is financially more rewarding to diagnose these conditions as accident neuroses. The question of motivation or gain is often raised in an attempt to find something "positive" in diagnosing hysteria or malingering. Unfortunately, the "gain" discovered by the doctor cannot be confirmed by the hysteric because he or she is not by definition, conscious of it, and it will not be admitted by the malingerer who is too conscious of it. Thus the speculation about the gain is a one-man guessing game. Those who try to define hysteria often avoid the issue of malingering. Both the malingerer and the hysteric behave as if they were suffering from a disease they are trying to imitate. Imitation is "to be (consciously or not) like". The parenthetic expression covers both malingering and hysteria which differ only by the degree of conscious control. If the imitation is conscious, the patient is rejected as a malingerer, if unconscious, he or she is accepted as a bona-fide patient. This distinction is imaginary and cannot be proved with a scientific rigour. "The distinction between hysteria and malingering (is) both impossible in clinical practice and meaningless in law".’ It has also ideological overtones: what is diagnosed as hysteria in St. Louis is called malingering in the U.S.S.R.6 Hysteria can be viewed as unconscious malingering. The malingerer imitates consciously a disease and also the unconscious mechanism (he pretends that he is not aware of his conSydenham, T. in The Works of Thomas Sydenham (edited by G. Wallis); p. 104. London, 1788. 2. Löwenfeld, L. Pathologie und Therapie der Neurasthenie und Hysterie; p. 1.
35. Wiesbaden, 1894. 3. Charcot, J. M. in Clinical Lectures on Diseases of the Nervous System (edited by T. Savill); vol III, p. 273. London 1889. 4. Jones, E. The Life and Work of Sigmund Freud; p. 207. London, 1964. 5. Miller, H. Proc. R. Soc. Med. 1966, 59, 257. 6. Szasz, T. S. The Myth of Mental Illness; p. 76. London, 1972.
elementary
mathematical description’ and
Medical Computing and Statistics Group, Medical School, Edinburgh EH8 9AG
STUART J. POCOCK
CHRONIC ALCOHOLIC AND CORTICOSTEROID MYOPATHY
SiR,—The paper by Dr Rees and his colleagues (April 2,
p.
raises an interesting question about the pathogenesis of chronic alcoholic myopathy,2 a rare complication seen in alcoholic patients. We have seen two young women with clear-cut cushingoid features who had weakness and muscular atrophy associated with excessive drinking of alcohol. Laboratory studies revealed macrocytic anaemia, carbohydrate tolerance, and hepatic impairment. Serum phosphocreatine-kinase and aldolase activities were normal and the serum-lactate-dehydrogenase was slightly raised. In hospital we found an 8 A.M. high plasma-cortisol in both patients (29 and 27 g/dl). Clinical and electromyographic investigation showed myopathy of proximal muscles. Histological examination of deltoid muscle, done in one patient, revealed a diminution in diameter of the fibres with more selective atrophy of type n. Similar findings have been obtained in myopathy of Cushing’s syndrome.3 There thus seems to be a correlation between these two muscular disorders. D. DE GRANDIS Clinica Malattie Nervose e Mentali, A. FIASCHI Centro Ospedaliero Clinicizzato, 37100 Verona, Italy G. TOMELLERI
726)
SEASONAL VARIATIONS IN CARDIAC FAILURE
SIR,-Professor Parry and his colleagues (May 14, p. 1023) right about heat-induced cardiovascular changes being responsible for the seasonal variations of cardiac failure in the Nigerian town of Zaria. However, I wonder if they have paid enough attention to nutritional factors. I have suggested that in Johannesburg Blacks cardiomyopathy, especially peripartal may be
heart-disease, may be a nutritional disorder.4 The finding that peripartal heart-disease, the commonest cause of heart-failure in Zaria, presented most often during the "hungry" season, suggests that malnutrition may also be
an
important factor
1. 2.
Cox, D. R. Analysis of Binary Data; p. 61. London, 1970. Carlsson, C., Dencker, S. J., Grimby, G., Tichy, J. Q. Jl Stud. Alc. 1969,
3. 4.
30, 385. Pleasure, D. E., Walsh, G. O., Engel, W. Seftel, H. C. S. Afr. med. J. 1972, 46, 1823.
K. Archs Neurol. 1970,
22,
118.
there. Absence of clinical changes in nutrition or of variations in haemoglobin does not exclude this possibility. In view of the high incidence of peripartal disease in Zaria perhaps Professor Parry could look at the effects of administering a balanced diet throughout the year to a sample of the female population of childbearing age. This would not be easy but if it could be done the seasonal variations might disappear-and so, eventually, might the disease itself. Medical School, University of the Witwatersrand,
Hospital Street, Johannesburg 2001, South Africa
H. C. SEFTEL
BRIQUET’S SYNDROME OR HYSTERIA? SIR,-You rightly question (May 28, p. 1138) the substitution of Briquet’s syndrome for hysteria and "the surprising aversion (of the St. Louis group) to detecting it in men". The reason why the St. Louis group do not detect it in males is simply because they do not diagnose hysteria but Briquet’s syndrome, in which the male/female ratio (according to Briquet) is 1/20. The frequency of the diagnosis of hysteria in males depends on fashion and semantics. Sydenham, who saw hysteria in 16% of his patients, found it not uncommon in men "leading sedentary life and studying hard", but for etymological reasons (men have no uterus) he preferred to call male hysteria hypochondriasis.I Pierre Marie saw hysteria eight times more frequently in males,2 and Charcot thought that male hysteria is not diagnosed due to a prejudice.3 In Austria they did not believe in male hysteria, and when Freud, under the influence of Charcot, lectured on male hysteria in Vienna, Meynert challenged him to prove his words. (Freudians took their revenge on Meynert posthumously, by disseminating a joke that "Meynert later confessed to Freud on his deathbed that he himself had been a classical case of male hysteria, but always managed to conceal the fact."4) New varieties of male hysteria appeared-"railway spine" in the 1880s in the U.S.A. and, later, "compensation neurosis" in Europe. In private practice it is financially more rewarding to diagnose these conditions as accident neuroses. The question of motivation or gain is often raised in an attempt to find something "positive" in diagnosing hysteria or malingering. Unfortunately, the "gain" discovered by the doctor cannot be confirmed by the hysteric because he or she is not by definition, conscious of it, and it will not be admitted by the malingerer who is too conscious of it. Thus the speculation about the gain is a one-man guessing game. Those who try to define hysteria often avoid the issue of malingering. Both the malingerer and the hysteric behave as if they were suffering from a disease they are trying to imitate. Imitation is "to be (consciously or not) like". The parenthetic expression covers both malingering and hysteria which differ only by the degree of conscious control. If the imitation is conscious, the patient is rejected as a malingerer, if unconscious, he or she is accepted as a bona-fide patient. This distinction is imaginary and cannot be proved with a scientific rigour. "The distinction between hysteria and malingering (is) both impossible in clinical practice and meaningless in law".’ It has also ideological overtones: what is diagnosed as hysteria in St. Louis is called malingering in the U.S.S.R.6 Hysteria can be viewed as unconscious malingering. The malingerer imitates consciously a disease and also the unconscious mechanism (he pretends that he is not aware of his conSydenham, T. in The Works of Thomas Sydenham (edited by G. Wallis); p. 104. London, 1788. 2. Löwenfeld, L. Pathologie und Therapie der Neurasthenie und Hysterie; p. 1.
35. Wiesbaden, 1894. 3. Charcot, J. M. in Clinical Lectures on Diseases of the Nervous System (edited by T. Savill); vol III, p. 273. London 1889. 4. Jones, E. The Life and Work of Sigmund Freud; p. 207. London, 1964. 5. Miller, H. Proc. R. Soc. Med. 1966, 59, 257. 6. Szasz, T. S. The Myth of Mental Illness; p. 76. London, 1972.