60
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
C DAVIDSON
Department of Cardiology Royal Sussex County Hospital
Brighton
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
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
C DAVIDSON
Department of Cardiology Royal Sussex County Hospital
Brighton
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
