Journal of the Royal Society of Medicine Volume 85 January 1992

4 Bordelon J, Stone MJ, Frenkel EP. Probable myeloblastic leukemoid reaction with disseminated sarcoidosis. South Med J 1977;70:1378-80 5 Hermann C, Andersen E, Videbaeck AA. Acute myeloblastic leukaemia in sarcoidosis treated with methotrexate. Scand J Haematol 1980;24:234-6 6 Hatake K, Aoyagi N, Takaku F. Acute myelomonocytic leukemia following remission of sarcoidosis. Oncology 1983;40:200-1 7 Reich JM. Acute myeloblastic leukemia and sarcoidosis. Implications for pathogenesis. Cancer 1985;55:366-9 8 Bataille R, Klein B, Luxembourg A, Durie B. Relation entre etats auto-immuns et canc6risation de cellules de la lign6e lymphocytaire B. In: Roux H, Luxembourg A, Roudier J, eds. Immunorhumatologie SOLAL 1990:170-89 9 Hanto DW, Frizzera G, Gajl-Peczalska KJ, Simmons RL. Epstein Barr virus, immunodeficiency and B-cell proliferation. Transplantation 1985;39:461-72

Intestinal tuberculosis We were interested to read the paper by Lingenfelser et al. (July 1991 JRSM, p436) entitled 'Intestinal tuberculosis: an ongoing diagnostic dilemma' but think that some points merit further discussion. The authors state that the rigid criteria for the diagnosis of intestinal tuberculosis have been extended to include an unequivocal response to anti-TB treatment in patients who have 'suggestive' clinical, radiological or operative evidence of intestinal disease and histologically proven TB elsewhere. They also wonder if a therapeutic trial of anti-TB therapy is warranted in patients with suspected intestinal disease alone. In their reported case the diagnosis of pulmonary tuberculosis was eventually made by mediastinal lymph-node biopsy. The idea that intestinal tuberculosis is usually associated with active pulmonary disease is no longer true and the absence of pulmonary involvement should not influence the diagnosis since it has become apparent that greater numbers of patients are presenting with isolated abdominal disease'. In Leicester we have just reviewed 24 cases of intestinal tuberculosis which presented to the General Surgical Department, (unpublished data). In our patient population only two patients (8%) had radiographic evidence.of pulmonary disease and this concurs with the frequency reported by others2. Although as the authors state the diagnosis is ideally made by seeing organisms on microscopy or culture, it is fully justified to instigate a closely monitored trial of chemotherapy in patients in whom the diagnosis is strongly suspected3 and in our series six patients (25%) did not have a histologically proven diagnosis but all made a dramatic improvement on treatment. The authors also state that 'laparotomy remains the definitive investigation in many patients with intestinal tuberculosis'. This statement needs qualification because although laparotomy may eventually be required in many patients other less invasive methods of obtaining tissue for microbiological examination may be employed including laparoscopy and biopsy4 and biopsy of the peritoneum under local anaesthesia5. Consideration should be given to these techniques if appropriate since there is evidence that laparotomy itself may be associated with significant morbidity in these patients6. M J UNDERWOOD M M THOMPSON R D SAYERS


Department of General Surgery, Glenfield General Hospital, Leicester

References 1 National survey of tuberculosis notifications in England and Wales 1978-9. BMJ 1980;281.895-8 2 Kolawole TM, Lewis EA. A radiological study of tuberculosis of the abdomen (gastrointestinal tract). AJR 1975;123:348-58 3 Lambrianides AL, Ackroyd N, Shorey BA. Abdominal tuberculosis. Br J Surg 1980;67:887-9 4 Wolfe JHN, Behn AR, Jackson BT. Tuberculous peritonitis and the role of diagnostic laparoscopy. Lancet 1979,i:852-3 5 Das P, Shulka HS. Clinical diagnosis of abdominal tuberculosis. Br J Surg 1976;63:941-6 6 Bhansali SK. Abdominal tuberculosis: experience with 300 cases. Am J Gastroenterol 1977;67:324-37

'Hysteria', 'functional' or 'psychogenic'? Drs Mace and Trimble (August 1991 JRSM, p 471) raise important though largely unacknowledged problems. The first is that psychiatric diagnosis by exclusion is logically indefensible'. That so many doctors do it doesn't make it right but merely demonstrates how uncritically they accept a practice which expediently places the blame for diagnostic failure upon the

victim2. Second, the terms used in ascribing the putative mental illness supposedly responsible for the patient's symptoms - 'hysteria', 'neurotic', and the like - are not merely diagnostic dustbins for disposing of patients with normal test results; they have specific technical meanings. People to whom they validly apply must display certain positive diagnostic features; to use them when these features are lacking or when their presence has not been ascertained is to use them figuratively rather than in their technical sense. The figurative use oftechnical terms, or metaphor, poses no intrinsic problems; they only arise when metaphor is passed off as if it represented technical usage, which is effectively what happens when a patient's speculatively ascribed 'neurosis' is accorded the undeserved status of a properly reached diagnosis. Third, although such pseudodiagnoses cannot long survive critical scrutiny3, they possess considerable face validity. As the authors note, 'however arrived at, the neurologist's opinions in these cases [are] likely to be of lasting influence'. It is worrying that as many as 36 000 British neurological patients per year may be relegated to the disadvantaged status of ascribed mental illness because of systematic abuse of the doctor's diagnostic authority. Finally, there is the problem that psychogenic dismissal4 may cause lasting psychological damage to patients traumatized by the experience. This dismissal injury appears to be an iatrogenic variant of post-traumatic stress disorder6. If doctors admitted inability to diagnose a patient, these problems wouldn't arise. V RIPPERE

61 Queen Alexandra Mansions, Hastings Street, London

References 1 Rippere V. Anatomy of a nonsense, or the common medical practice of dismissing the neurotic., Newsletter of the Society for Environmental Therapy 1989,9:160-7 2 Rippere V. Blaming the patient: the Flat Earth Society guide to successful medical practice. Newsletter of the Society for Environmental Therapy, 1990;10:1f61-9'3 Slater E. The diagnosis of hysteria. BMJ 1965;i:1395-9



Journal of the Royal Society of Medicine Volume 85 January 1992

4 Vickery K. Foreword to Richard Mackarness. Chemical Victims. London: Pan, 1980 5 Rippere V. The mental state of dismissed patients - an enquiry into dismissal injury. I. A very peculiar practice. Newsletter of the Society for Environmental Therapy 1991;11(in press)

Myocarditis - a controversial disease In the editorial (January 1991 JRSM, p 1) the need to evaluate more specific treatments for viral myocarditis was mentioned. We agree, assessment of treatment is difficult, however we would like to report our experience of a patient with varicella-zoster myocarditis treated with acyclovir, as occasionally a treatable cause may be found. A 38-year-old man with no previous cardiac history presented with a 24 h history of periumbilical pain, nausea, fever and rigors. One week previously, his daughter had suffered from chickenpox and his son had developed a rash 24 h prior to his father's admission. On examination, he was pyrexial (39°C), pulse rate 70 irregular, blood pressure 110/70, normal heart sounds. A rash characteristic of chickenpox was noted. His ECG revealed ventricular trigemini with T wave inversion and ST depression in leads I, II, III, AVL and V4 to V6. A chest X-ray showed an enlarged, globular heart, cardiothoracic ratio (CTR) 14/27. A diagnosis of varicella-zoster was made and intravenous acyclovir was commenced at 750 mg 8 hourly. Following 3 days of treatment, the ectopics settled and repolarization changes disappeared. Oral acyclovir, 200 mg four times a day was continued for a further week. One month later, a chest X-ray showed a CTR 13.5/27, an ECG showed mild left ventricular hypertrophy but no repolarization abnormalities. A 24-h tape showed only occasional ventricular ectopics. Acyclovir has been previously used in the treatment ofvaricella-zoster myocarditis in a child with complete heart block', and it was considered that acyclovir may have induced recovery of myocardial function. In our patient, early treatment with acyclovir was associated with a rapid recovery and no long term sequelae. M APPLEBY P KON


Department of Cardiology Royal Sussex County Hospital


Reference 1 Ettedgui E, Ladusans E, Bamford M. Complete heart block as a complication of varicella. Int J Cardiol 1987;14:362-5

Another look at holistic medicine Dr Bourne (July 1991 JRSM, p 446) believes that I, '... ignore the fact that every GP must practice Holistic Medicine . . .', in spite of the fact that, in agreement with Dr Hall (October 1990 JRSM, p 676) I say, '. . . I have long since preferred to deal with patients, rather than with bits ofthem!' (March 1991 JRSM, p 183). Further, I did not suggest that specialists failed to consider differential diagnosis. He refers to fibromuscular pain, a matter which illustrates one of the real difficulties in this field; the existence of 'muscle pain syndromes', like fibrositis and trigger points, is not as yet wholly supported by

proof, remaining for the time being to some extent controversial. Of course I agree that local injections may be of benefit, as he will discover when he reads the book he mentioned', but I do not recollect any '. . . account ofthe uselessness of every one of the 30 therapies . . .'. What I did say was, '. . . it is rare indeed to be able to predict therapeutic outcome.' This is a very different statement, and the current evidence in its support seems overwhelming. L'Ilot, Les Fitayes, J K PATERSON 13640 La Roque d'Antheron, France

Reference 1 Burn L, Paterson JK. Musculoskeletal medicine - the spine. London: Kluwer, 1990

Neuroleptic malignant syndrome and catatonia other diagnostic considerations I read with interest the article by Sagar (August 1991 JRSM, p 500) 'Neuroleptic malignant syndrome: a diagnostic dilemma'. Prominent amongst all three cases was the clinical sign ofcatatonia which indeed is a difficult differential diagnosis. As rightly mentioned by the author, it poses a diagnostic dilemma. Catatonia and neuroleptic malignant syndrome may not actually be different disorders biochemically' although some authors consider it to be so, at least clinically2. In addition to schizophrenia, neuroleptic malignant syndrome and neuroleptic induced catatonia there are hosts of other causes (mostly organic) which should be kept in mind while debating the differential diagnosis of catatonia. Many of them can result in lability of autonomic functions as well, thus presenting clinically not very differently than neuroleptic malignant syndrome. These include cerebral tumours (eg tuberous sclerosis, subdural haematoma), cerebrovascular disorders (eg cerebral artery aneurysms), degenerative (eg Parkinson's disease, cerebral atrophy), other drugs (eg amphetamines, phencyclidine, adrenocorticotrophic hormone, morphine, aspirin) endocrine, metabolic, infective and others3. Another interesting disorder Gjessing's Periodic Catatonia4 presents as periodic episodes of catatonic excitement or stupor associated with vegetative disturbances including alteration in pulse rate, blood pressure and temperature. Berrios5 discriminated between organic stupors which are on the nornal consciousness-coma spectrum and those that result from lesions in the brainstemdiencephalon axis. It is the latter group which presents diagnostic problems. The clinical features of such disorders suggest a psychogenic syndrome and because ofthe involvement of diencephalon there may also be lability of hypothalamic functions (eg blood pressure, pulse and temperature). Another disorder which shows marked overlap with the neuroleptic malignant syndrome clinically is Strauder's lethal catatonia. This disorder also progresses to agitation, mutism, hyperthermia and dehydration and as the name suggests, may be lethal, but is suggested to be of viral aetiology'. In both these disorders there seems to be diencephalic dysfunction which results in suppression of thermoregulatory mechanisms. D K ARYA

Department of Psychiatry, Queen's Medical Centre, Nottingham NG7 2UH

'Hysteria', 'functional' or 'psychogenic'?

Journal of the Royal Society of Medicine Volume 85 January 1992 4 Bordelon J, Stone MJ, Frenkel EP. Probable myeloblastic leukemoid reaction with dis...
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