LONDON, SATURDAY 6 MARCH 1976

BTISH

MEDICU1\TAL After stroke, what? Stroke is common: the annual incidence of acute cerebrovascular accidents in Britain lies somewhere between 1 8 and 2-0 per thousand population.' The amount of severe disability caused is probably greater than from any other medical condition.2 Management in the acute stage is concentrated on preserving life by orthodox intensive measures and the early recognition of syndromes, such as subarachnoid haemorrhage and extracranial causes of acute stroke, which are amenable to early neurosurgical intervention.3 Diagnostic accuracy can be vastly improved by the use of computer-assisted axial tomography, which has revolutionised the management of stroke in those hospitals equipped with an EMI-scanner.4 Even so, predicting outcome in the individual patient remains difficult, though a poor functional prognosis may be identified within a few days.5 Early death is common, and almost half of all patients with strokes die within the first three to four weeks.6 Of the survivors, a further half are, dead within the next four to five years. If disability is defined as dependence on another person for one or more of the activities usually considered essential for daily living,7 then stroke survivors have a spectrum of impairment. One-third will recover, one-third will be completely dependent and bedfast, and the remaining third will have some degree of residual functional incapacity.8 In a health district of 250 000 there will be 350-400 acute strokes each year, and this should leave between 170 and 200 survivors after six weeks, whose numbers will drop further during the next six months to between 150 and 170. Of these, some 50 will have dense hemiplegia with little outlook for further functional recovery. Fifty will have fully recovered (but still be at risk); so that only the remaining 50 out of the original 350 are likely to benefit from any efforts at rehabilitation. There is, moreover, no evidence that physiotherapy influences neurological outcome in the early stages.9 Several trials have failed to find any difference between the results of complex treatment techniques such as proprioceptive neuromuscular facilitation and simpler methods.'0 11 It can, however, be shown12 13 that patients' ability to cope with daily living can be improved by exercises designed to improve their general fitness and to train their remaining functions to compensate for the losses sustained. Such a programme may be difficult to achieve in an outpatient rehabilitation department because of problems of transport; indeed, this may be the most important reason for the success of residential units.'4 0 BRITISH MEDICAL JOURNAL 1976. All reproduction rights reserved.

Lesions of the non-dominant hemisphere often have a poorer functional prognosis and respond less well to efforts of rehabilitation than lesions of the dominant hemisphere. This difference is thought to be due to the associated disorders of body image, and no way has yet been found to overcome these problems. 5 In general, rehabilitation of patients with stroke requires a practical outlook. The most successful programmes have concentrated on exercises; functional movement; preventing deformity; and the appropriate use of aids, appliances, and, infrequently, surgery.'6-'8 Dysphagia in their victims is also the subject of current debate.'9 20 Formal speech therapy may have a part to play in its management, but the amount and intensity of treatment needed are being evaluated.2' 22 Much disability after stroke is due to omission rather than commission-contractures, stiff and painful shoulders, bed sores, and loss of morale may all be preventable. Physical treatment of victims of completed stroke, unenthusiastically applied at infrequent intervals over a long period in a vain attempt to achieve unrealistic goals, will lead only to unnecessary invalidism and depression. It also leads to loss of morale in the therapist. In contrast, common-sense measures given in the early stages after the patient has completed his medical treatment are likely to lead to as great a degree of functional improvement as any more esoteric methods of management. World Health Organisation, Technical Report Series, 1971, No 469, Cerebrovascular Diseases; Prevention, Treatment and Rehabilitation. Geneva, World Health Organisation, 1971. 2 Royal College of Physicians of London, Report of the Geriatric Committee Working Group on Strokes. London, Royal College of Physicians, 1974. 3 Oxbury, J M, British Medical_Journal, 1975, 4, 450. 4 British Medical Journal, 1976, 1, 483. 5 Russell, R W R, and Harrison, M J G, British Journal of Hospital Medicine, 1973, 10, 244. 6 Weddell, J M, Rehabilitation After Stroke-A Medico-Social Problem. Offprint of paper presented at Scandia symposium, Stockholm, 1974. 7 Office of Population Censuses and Surveys, Handicapped and Impaired in Great Britain, pts I and II by A I Harris. London, HMSO, 1971. 8 Gresham, G E, et al, New England J7ournal of Medicine, 1975, 293, 954. 9Newman, M, Stroke, 1972, 3, 702. 10 Stern, H, et al, Archives of Physical Medicine and Rehabilitation, 1970, 51, 526.

1' Feldman, D J, et al, Journal of Chronic Diseases, 1962, 15, 297. 12 Rehabilitation Study Group, Stroke, 1972, 3, 375.

Millard, J B, Annals of Physical Medicine, 1965-6, 8, 244. Beer, T C, et al, British Medical Journal, 1974, 1, 226. Hurwitz, L J, and Adams, G F, British Medical Journal, 1972, 1, 94. 16 Gordon, E E, and Kohn, K H, Journal of Chronic Diseases, 1966, 19, 3. 17 Somerville, J G, The Rehabilitation of the Hemiplegic Patient. London, British Council for the Rehabilitation of the Disabled, 1970. 13

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542 18 Roper, B A, British JIournal of Hospital Medicine, 1973, 9, 85. 19 Department of Education and Science, Speech Therapy Services. London, HMSO, 1972. 20 Hopkins, A, Health Trends, 1975, 7, 58. 21 Sarno, M T, Silverman, M, and Sands, E, Journal of Speech and Hearing Research, 1970, 13, 607. 22 Wepman, J M, JIournal of Speech and Hearing Disorders, 1972, 307, 203.

Transfusion malaria in developing countries Transfusion malaria remains a problem in developing countries, and Edrissian' has reviewed 111 cases of transfusion malaria recorded in Iran from 1963 to 1972, while Wickramasinghe2 has recently dealt with 16 cases of accidental transfusion malaria that occurred in Sri Lanka. Cases have been reported from a large number of countries, some of the early accounts having come from China.3 There is little doubt, however, that transfusion malaria is still grossly underreported. The incubation period of blood-induced infection is quite different from that of mosquito-transmitted malaria, since in the former there are no tissue stages in the liver. Both the interval between infection and the appearance of parasites in the blood-the prepatent period-and the presymptomatic period depend on four factors: the number of parasites introduced; the method of inoculation; the susceptibility of the recipient; and the length of blood storage before transfusion. Reviewing a series of over 100 cases of transfusion malaria in Rumania, Lupascu et a14 pointed out that 86% of all cases occurred when the blood was stored for less than five days; cases after 7-12 days were rare, while infections with the blood stored for 13 or more days were exceptional. In addition to infection from blood transfusion accidental transmission of malaria may also occur with plasma if some stray red blood cells happen to contain plasmodia5 or as a result.of leucocyte transfer.6 Most reported cases of transfusion malaria are due to Plasmodium malariae, followed by P vivax and Pfalciparum. Neither systematic screening-with various serological techniques-nor premedication of suspected donors is a practical solution in developing countries. The generally accepted procedure in areas where non-immune persons may receive blood that may possibly contain scanty malaria parasites is the prophylactic administration of antimalarial drugs to the recipients.7 8 As there is no likelihood of true relapses occurring after blood transmission of P vivax, P malariae, or P ovale, radical treatment with an 8-aminoquinoline such as primaquine is not required. A single dose of 600 mg base chloroquine to the recipient 24 hours before or on the day of transfusion seems to protect from induced malaria. It may be prudent, however, not to rely on a single dose of chloroquine but to give all non-immune recipients the standard three-day course of antimalarial treatment. 9 10 In parts of the world where strains resistant to the 4-aminoquinolines are known to occur, such as SE Asia and S America, the preventive administration of sulfadoxine, 1-5 g, together with pyrimethamine, 75 mg (Fansidar), is advisable. Once again it may be prudent to give a full three-day course of curative treatment-quinine (four doses, 540 mg each dose, given at intervals of 12 hrs) and then a single dose of sulfadoxine-pyrimethamine.11 A detailed account of the problem of blood transfusion and the whole range of tropical diseases

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(including malaria) is available in the comprehensive review by Bruce-Chwatt.12 Edrissian, G H, Transactions of the Royal Society of Tropical Medicine and Hygiene, 1974, 68, 491. Wickramasinghe, F A, Tropical Doctor, 1976, 6, 4. 3Wang, C W, and Lee, C U, Chinese Medical Journal Shanghai, 1936, 50, 241. 4Lupascu, G, et al, Bulletin of the World Health Organisation, 1967, 36, 485. 5 Vostokova, K K, and Andreeva, M I, Medskaya Parazit, 1964, 33, 724. 6 Dover, A S, and Guinee, V F,3Journal of the American Medical Association, 1971, 218, 1830. 7Edington, G M, and Gilles, H M, Pathology in the Tropics, 2nd edn. London, Edward Arnold, 1976. 8 Vargas, L, Gaceta Medica de Mexico, 1971, 101, 691. 9 Baba, S, Transfusion, 1963, 6, 145. 10 Kane, Y, and Kane, 0, Transfusion, 1963, 6, 151. 11 Hall, A P, British Medical_Journal, 1976, 1, 323. 12 Bruce-Chwatt, L J, Tropical Diseases Bulletin, 1972, 69, 825. 2

Screening for presymptomatic coronary disease Coronary artery disease has been shown to be the cause of death in four out of every 10 men in studies with high necropsy rates.' Yet while clinical procedures and simple laboratory tests permit recognition of traits associated with increased risk of coronary disease,2 they may not identify its presence in any one individual-let alone whether it represents a danger to him (or to others). One American man in five3 may expect to have symptoms from a coronary lesion by age 60, but not all of those with symptoms of coronary disease will die from it, and half of those who do will never have had recognised symptoms. In these cases of unexpected sudden death there is commonly serious obstructions of two or three major coronary arteries,4 so that it follows that angina is both a poor guide to risk and an insensitive marker of underlying coronary obstructive disease. Follow-up studies after coronary angiography have shown that risk of death is closely related to the severity of coronary obstruction,5 6 and that the 25% or so patients with clinically diagnosed angina but normal coronary arteries7 have a normal (or better than normal)

prognosis.6 Most coronary deaths are due to sudden ventricular fibrillation without infarction or occur within an hour of onset of infarction,8 but even myocardial infarction may not be a clinical event. The Framingham study showed that onequarter of the individuals who developed electrocardiographic evidence of myocardial infarction had not been recognised as having had an infarct by their doctors. 9 Short of coronary angiography, then, recognising coronary disease is not always possible. An abnormal electrocardiogram may falsely suggest ischaemia, and one in four ECGs reverts to normal after actual infarction.9 Nevertheless, certain ECG abnormalities are associated with a high incidence of coronary disease. Most important of these is left ventricular hypertrophy,10 but other pointers include intraventricular conduction defects and non-specific ST and T wave changes. Changes in the ECG during or after effort lack specificity11 if an ST segment depression of 0 5 mm is accepted, and show inadequate sensitivity ifthe measure is set at 2 mm: at present 1 mm is the usual criterion. Unfortunately, the exercise ECG also suffers from lack of reproducibility: tests may vary between

Editorial: After stroke, what?

LONDON, SATURDAY 6 MARCH 1976 BTISH MEDICU1\TAL After stroke, what? Stroke is common: the annual incidence of acute cerebrovascular accidents in Bri...
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