NOCTURNAL ANGINA

NOCTURNAL ANGINA

903 without neurological deficit, seemed to be due to intensive amphotericin B, both parenterally, intra- treatment with via a ventricular reservoi...

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903 without

neurological deficit, seemed to be due to intensive amphotericin B, both parenterally, intra-

treatment with

via a ventricular reservoir. Infection followed bathing in a chlorinated pool filled from an unfiltered, unchlorinated supply. A sero-positive Naegleria was isolated from the pool and is awaiting confirmation by A period of superchlorination to 10 mouse inoculation. p.p.m. failed to eradicate Naegleria species from the pool, but salination to 0-7% (w/v) has resulted in negative cultures over the past five months.

thecally, and

We are indebted to Dr. Malcolm Fowler and Dr. Rodney Carter for encouragement and advice throughout this period of research. Amoebic Research Unit, Division of Bacteriology, Institute of Medical and Veterinary

Science, Adelaide, South Australia.

KEVIN ANDERSON ADELE JAMIESON.

LEVODOPA IN HUNTINGTON’S CHOREA SIR,-Lakke et aLl withheld levodopa in 2 cases of

Huntington’s chorea because of the outcome of the probenecid test. Therapeutic investigations of levodopa have so far centred mainly on parkinsonism, and reports on its effects in Huntington’s chorea are few. In fact, to our knowledge, in only 2 cases of Huntington’s chorea has levodopa been tried, its effect being briefly mentioned as failing to produce any improvement2 and failing to affect the neurological signs.3 In two other cases of Huntington’s chorea (the juvenile form) the effect of levodopa in reversing the akinesia and rigidity into choreic movements was reported.4 We wish

report a trial of levodopa over twelve months with Huntington’s chorea, and we believe this to be the first case of remarkable improvement in association with levodopa. A 46-year-old married woman, irritable and suspicious by nature, but a good and conscientious mother of 3 daughters, appeared to be well until 1962, when she began to have crying in

a

to

patient

uterine myoma in She was also often depressed. The first neurological signs, appearing in 1968, were swaying on her feet, walking faster than usual without being able to control it, and spilling when eating or drinking, due to jerky movements of the hands. Gradually the choreic movements involved her whole body. The diagnosis of Huntington’s chorea was substantiated by the family history. Treatment with haloperidol, thiopropazate, and chlordiazepoxide gave only temporary relief and her condition deteriorated. During the three months before admission to this hospital on Jan. 13, 1971, she was nursed at home, completely helpless because of severe choreic movements. She was very restless and all her actions were very rapid. She rushed to the toilet a hundred times a day, on her way bumping into everything, and even fell backwards to the floor a few times. She leapt up and fell back to her chair every 5 minutes or so. She was often incontinent of urine and sometimes fxces. She had to be fed and did not speak, except to answer questions very briefly. After a pneumonia, three weeks after admission, she became demented as well, being disoriented in time, place, and person and did not recognise her daughters. We began oral treatment with levodopa on March 4, 1971, the dose being gradually increased until 5 g. a day was reached after fifty-six days, and this dose has been maintained. She also received paraldehyde (8 g.) or chloral hydrate (2 g.) for nocturnal

spells

and headaches. After

an

operation for

although continuing, was intermittent, with recurrence of choreic movements, lasting from a few hours to sometimes a few days. Two months after levodopa was first given, she managed to walk again, having been bedridden since admission, and six months later she was able to look after herself completely. Control of movements returned, and she was able to knit and to do embroidery. We have recorded this motor improvement on film. The other effect of levodopa on the patient was the mental change, the first signs being observed about a week after treatment began. There was a gradual but significant improvement of mental function. Her speech and ability to communicate returned. Her memory improved, with a return to orientation in time, place, and person, and she recognised her children again. She showed interest in herself and in her surroundings. This improvement, however, was accompanied by shorter or longer periods of psychotic behaviour and depression, characterised by paranoid thinking, confusion, hallucinations, and talking and laughing to herself. Twice she made a suicidal attempt. She was also extremely irritable, and this sometimes led to outbursts of anger and aggression. She also had the idea that everything was dirty, having been touched by others. In November, 1971, we decided to counteract these mental disturbances, considered to be side-effects of levodopa,5 with chlorpromazine (25 mg. three times a day) and pericyazine (5 mg. three times daily). These two drugs were successful. For the past three months none of the mental disturbances have been observed, and the motor improvement achieved with levodopa alone has been sustained. For the past two months she has been home every weekend, going shopping, and doing light household duties.

We believe that levodopa should be given a fair therapeutic trial in Huntington’s chorea. Even if only a small proportion of cases benefit as our patient did, the attempt would be justified. Moreover, at the same time, dopamine metabolism in Huntington’s chorea could be investigated. We determined the homovanillic acid (by the method of Anden s as modified by Gerbode ’) in lumbar cerebrospinal fluid. The results were:e

a

1964, she became paranoid and very irritable.

sedation. The effect of levodopa on the motor system was dramatic, the first signs of improvement being noticed one week after treatment began. The choreic movements gradually subsided, first in her legs and body, the hands and fingers being the last to quieten. During the first six months of treatment the improvement,

Lakke, J. P. W. F., Korf, J., van Praag, H. M. Lancet, 1971, ii, 164. Barbeau, A. Can. med. Ass. J. 1969, 101, 791. Cotzias, G. C., Papavasiliou, P. S., Gellene, R. New Engl. J. Med. 1969, 280, 337. 4. Barbeau, A. Lancet, 1969, ii, 1066. 1. 2. 3.

*

On

chlorpromazine

Delta Ziekenhuis, (Rotterdam Mental Hospital), Poortugaal,

The Netherlands.

and

pericyazine.

B. K. TAN H. J. LEIJNSE-YBEMA H. J. V.D. BRAND.

NOCTURNAL ANGINA SIR,-Iwish to correct the editorial on nocturnal angina (April 1, p. 732), in which I was reported as describing a close relation between episodes of increased blood-pressure and paradoxical sleep in patients with nocturnal angina. We have not in fact made a systematic study of patients with nocturnal angina, but have observed the behaviour of the

blood-pressure during sleep in normal and hypertensive We noted that during rapid-eye-movement (or dreaming) sleep we found the highest as well as the lowest blood-pressures of the night. 8 In Tokyo I reported one patient with a phseochromocytoma which we studied.99 In this middle-aged woman there was a striking correlation between the numbers of rapid eye movements per minute and the simultaneously measured mean arterial pressure.

man.

5. Jenkins, R. B., Groh, R. H. ibid. 1970, ii, 177. 6. Andén, N. E., Roos, B. E., Werdinius, B. Life Sci. 1963, 7, 448. 7. Gerbode, F., Bowers, M. B. J. Neurochem. 1968, 15, 1053. 8. Bristow, J. D., Honour, A. J., Pickering, T. G., Sleight, P. Cardio9.

vasc. Res. 1969, 3, 476. Smyth, H. S. Sleep, Dreams, and Blood-pressure. D.PHIL. thesis, University of Oxford, 1967.

904 What is not clear from the studies carried out so far on nocturnal angina is whether the relation with dreaming sleep is due to a possible increase in the work of the heart occasioned by surges of tachycardia and rises in pressure during dreams, or whether there is general sympathetic discharge at this time causing alterations in the coronary circulation itself or in the metabolic processes in the myocardium. Dr. Turner is quite right in drawing attention to the implication for hypnotic therapy and its cessation on leaving hospital. Although some of the P-blockers seem to be associated with increased dreaming (or at least awareness of dreams), it seems probable that by mitigating the cardiovascular effects of dreaming they might be beneficial during nocturnal angina. This may not always be so, however, for in some patients nocturnal angina is clearly associated with episodes of left ventricular failure at night, and -blockade in this situation would, of course, be harmful unless digitalis had been given beforehand. Radcliffe Infirmary, Oxford OX2 6HE.

PETER SLEIGHT

CLINICS FOR THE TREATMENT OF EPILEPSY AND CONVULSIONS SIR,-In a debate in the House of Lords,l Lord Aberdare stated in reply to a question concerning the Reid report on people with epilepsy that professional opinion was by no means unanimous over the question of providing special epilepsy clinics. There seem to be certain misunderstandings about such clinics, especially about whether they should be diagnostic or follow-up, and anxiety has been expressed to me over the referral to such clinics of patients who have had their first fit, it being felt that such patients are better seen at the general outpatient clinics of physicians, neurologists, and pxdiatricians. Doubts are also expressed about the feasibility of multidisciplinary clinics as envisaged in the Reid report. I think it is important that the protagonists in the discussion on special epilepsy clinics should publish their views before the impending discussions about implementation of the Reid report, and that some figures should be provided in support of these views. I have been in charge of an epilepsy clinic, mainly for " adults, for about 18 years, and I have held a convulsions clinic " in a children’s hospital for some years, though I am not a pxdiatrician. This latter clinic has recently become multidisciplinary, my colleagues being a consultant poediatrician particularly interested in neurology, a consultant in developmental medicine, and a consultant in subnormality. This arrangement has advantages to all concerned. A survey of patients seen at my adult clinic in 1965 showed that only 15% of 117 consecutive patients were referred by their general practitioner because of a first attack, and nearly half of them did not have epilepsy. Of the remaining cases 27% were referred by another consultant, and 39% of the cases referred by general practitioners had already seen another consultant at some time. Thus 66% of all cases had already seen another consultant because of their epilepsy. Review of the current situation at the two clinics is as follows:

It is, of course, most important to avoid attaching an incorrect label of epilepsy because of the social and psychological difficulties which face all who receive this label. It 1. Hansard

(Lords), Jan. 27, 1972, col.

485.

is of interest that a fifth of the patients referred to thetwo clinics did not appear to be suffering from epilepsy. Both clinics are " open ", and this seems essential since it is important to see some new patients. I consider that a special epilepsy clinic should be both diagnostic and

follow-up. I think that the best service to the patient with epilepsy will be provided by any doctor who is particularly interested in epilepsy, whether he be (in alphabetical order) a clinical

neurophysiologist, neurologist, neurosurgeon, paediatrician. physician, or psychiatrist, as is at present the case. 42 Westfield

Road, Edgbaston, Birmingham B15 3QG.

P.

M. JEAVONS.

BARBITURATE COMA AND BLISTERS SIR,-Another type of blister not mentioned in your editorial (April 1, p. 733) is that seen in diabetes mellitus. Clinically, they are the same as the blisters associated with barbiturates and other drugs, though they are often more serious because of an associated ischsemic limb.l Histological examination2 showed intraepidermal splitting without acantholysis, and, as in the barbiturate blister, dermal

change was slight. Although the presence of peripheral neuropathy in diabetes has been thought to be associated with these blisterswe suggested that an intraepidermal metabolic change, with associated hypoxia, might be the underlying cause, related to poor control of hyperglycxmia. The clinical similarity to the barbiturate blisters may indicate that

hypoxia is

common to

both types of blister.

Belfast City Hospital, Belfast BT9.

G. E. ALLEN.

Royal Victoria Hospital, Belfast BT12.

D. R. HADDEN.

DIARRHŒA INDUCED IN HUMANS BY GLUCAGON PLUS GASTRIN SiR,—Both glucagon and pentagastrin have been shown to stimulate intestinal secretion in dogs.44 Glucagon and pentagastrin given simultaneously by constant intravenous infusion produced an explosive cholera-like diarrhoea in

dogs. Neither glucagon nor pentagastrin had such an effect on their own.5 We have extended the study of the effect of these hormones

to human patients. Glucagon (Eli Lilly & Co.) (45 {1.g. per kg. per hr.) and pentagastrin (I.C.I.) (6 {1.g. per kg. per hr.) were given simultaneously to 3 fasting human volunteers by continu-

intravenous infusion for four hours. In the 1 patient was usually constipated) the test had to be stopped when he passed a very large loose stool. The other 2 patients passed loose, or watery, stools immediately after a meal eaten at the end of the four-hour hormone infusion. The role played by the meal is uncertain. Neither patient had diarrhaea before the test. 2 of these 3 patients were given glucagon alone in the same dose; neither had diarrhoea. Another patient with histologically proven ZollingerEllison syndrome, and known to have high blood-gastrin levels, was given an infusion of glucagon alone. This induced a profuse watery diarrhoea which was different in character and severity from his usual loose stool. Glucagon and pentagastrin may be implicated in the pathogenesis of diarrhoeas characterised by excessive intestinal secretion in man, and more particularly with certain

ous

(who

1. Allen, G. E. Practitioner, 1969, 203, 189. 2. Allen, G. E., Hadden, D. R. Br. J. Derm. 1970, 82, 216. 3. Rocca, F. F., Pereyra, E. Diabetes, 1963, 12, 220. 4. Barbezat, G. O., Grossman, M. I. Science, N.Y. 1971, 174, 422. 5. Barbezat, G. O., Grossman, M. I. Lancet, 1971, i, 1025.