600

4. Hudson

M, Pocknee R, Mowat MAG. D-lactic acidosis in short bowel

syndrome—an examination of possible mechanisms. QJ Med 1990; 74: 157-63. 5. Thurn JR,

Pierpont L, Ludvigsen CW, Eckfeldt JH. D-lactate encephalopathy. Am J Med 1985; 79: 717-21. 6. Mason PD. Metabolic acidosis due to D-lactate. Br Med J 1986; 292: 1105-06. 7. McNeil I. Nutritional implications of human and mammalian large intestinal function. World Rev Nutr Dietet 1988; 56: 1-42. 8. Dunlop RH, Hammond PB. D-lactic acidosis of ruminants. Ann N Y Acad Sci 1965; 119: 1109-32. 9. van Eys J, Judge MA, Judd J, Hill W, Bozian RC, Abrahams S. A reinvestigation of methylglyoxal accumulation in thiamine deficiency. J Nutr 1962; 76: 375-84.

SSPE IN THE DEVELOPING WORLD Patients with subacute sclerosing panencephalitis (SSPE) present a distressing picture, all too frequent in developing countries. The underlying pathological change, a progressive degeneration of the central nervous system, is manifested in various neurological signs-behavioural

changes, developmental deterioration, ataxia, myoclonic seizures, visual disorders, spasticity, and decerebrate rigidity.1 Characteristically, these features appear insidiously in a child aged five to fifteen who had measles many years previously. The doctor in a developing country has to make a tentative diagnosis because confirmation requires the demonstration of high-titre measles antibody in the cerebrospinal fluid,2and this test is not usually available. Differential diagnoses include cerebral tumours, other neurodegenerative conditions, and human immunodeficiency virus infection. When antibody tests have been applied in developing countries, SSPE has been shown

for a substantial fraction of childhood neurodegenerative conditions. 4-7 Chemotherapy is ineffective,l and the clinical course is relentlessly downhill until death months or years later. SSPE is a rare complication of measles-annual incidence ranges from under 0.1cases7,8 to 5 or 6 cases4 per million population. The wide range partly reflects difficulties in diagnosis and case-finding and also illustrates the relative degrees of success and failure of measles control achieved by different countries."’ The exact pathogenesis is unknown. Some invasion of the central nervous system is common in measles,l but it is unclear why SSPE affects an unfortunate few children, a long-time (5-10 years) after the acute infection. Children infected in the first 2 years are more at risk and case-series have consistently shown an excess of boys 49 but this apparent age and sex bias may merely reflect another more important factor concerning the dose of measles received at exposure." A higher incidence of SSPE would be expected in developing countries because there is more circulating measles10 and attack rates are higher in the first two years of life. 12 Survey results confirm this suggestion,4-7 although few studies have been conducted in sub-Saharan Africa.13 Mass measles vaccination is effective in reducing SSPE incidence in both developing and industrialised countries.9,14,15 Fears that measles vaccine might itself cause SSPE have been shown to be groundless9,15-it is more hazardous to remain unimmunised.1’ SSPE is another strong reason for promoting mass immunisation, especially since the demonstration that high-titre Edmonston-Zagreb measles vaccine given in the first year is both safe16 and effective17 in preventing early measles. The Global Advisory Group of WHO’s Expanded Programme on Immunisation has recommended that this vaccine is given at six months of to account

age where early transmission is a hazard.12 SSPE intensifies the challenge to governments, programme managers, and donors in developing countries to apply the

recommendation with

speed and vigour.

HC, Marshall WC. Measles. In: Weatherall DJ, Ledingham JGG, Warrell DA, eds. Oxford textbook of medicine, 2nd ed. Oxford: Oxford University Press, 1987: 5.89-93. 2. Norrby E. Measles virus. In: Lenette EH, Balows A, Hausler WJ, Shadomy HJ, eds. Manual of clinical microbiology. Washington, DC: American Society of Microbiology, 1985: 772. 3. Epstein LG, Sharer LR, Oleske JM, et al. Neurologic manifestations of human immunodeficiency virus infection in children. Pediatrics 1986; 1. Whittle

78: 678-87. 4. Cernescu S,

Milea S. Epidemiology of subacute sclerosing in Romania between 1976-1982. Virologic 1983; 34:

panencephalitis 239-50. 5. Yalaz K, Anlar

B, Renda Y, Aysun S, Topcu M, Ozdirim E. Subacute sclerosing panencephalitis in Turkey: epidemiological features. J Trop

Pediatr 1988; 34: 301-05. 6. Bakir TM, Hossain A, Ramia S, Sinha NP. Seroepidemiology of mumps, measles and subacute sclerosing panencephalitis in Saudi Arabia. J Trop Pediatr 1988; 34: 254-56. 7. Radhakrishnan K, Thacker AK, Maloo JC, Gerryo SE, Mousa ME. Descriptive epidemiology of some rare neurological diseasesin Benghazi, Libya. Neuroepidemiology 1988; 7: 159-64. 8. Hinman AR, Orenstein WA, Bloch AB, et al. Impact of measles in the United States. Rev Infect Dis 1983; 5: 439-44. 9. Miller CL. Current impact of measles in the United Kingdom. Rev Infect Dis 1983; 5: 427-32. 10. Grant JP. The state of the world’s children 1990. Oxford: Oxford

University Press, 1990. Aaby P, Bukh J, Lisse IM, Smits AJ. Risk factors in subacute sclerosing panencephalitis; age and sex-dependent host reactions or intensive exposure. Ref Infect Dis 1984; 6: 239-50. 12. Hall AJ, Greenwood BM, Whittle H. Modern vaccines: practice in developing countries. Lancet 1990; 335: 774-77. 13. Tukei PM, Kenya PR, Ensering J. An epidemiological study of subacute sclerosing panencephalitis in Kenya. East Afr Med J 1983; 60:34-38. 14. Vucenovic V, Vranjesevic D. SSPE—epidemiology and measles

11.

vaccination: our cases. Neurol 1989; 38: 23-31. 15. Bloch AB, Orenmstein WA, Stetler HC, et al. Health impact of measles vaccination in the United States. Pediatrics 1985; 76: 524-32. 16. Whittle H, Hanlon P, O’Neill K, et al. Trial of high-dose EdmonstonZagreb measles vaccine in The Gambia: antibody response and side-effects. Lancet 1988; ii: 811-14. 17. Aaby P, Jensen TG, Hansek HL, et al. Trial of high-dose EdmonstonZagreb measles in Guinea-Bissau: protective efficacy. Lancet 1988; ii: 809-11.

NHS NURSING HOMES

provided for dependent old people in long-stay in Britain is not a source of national pride. wards hospital Frail elderly individuals who cannot live at home tend to be housed in outmoded buildings, often some distance from their families.! The physical environment can be depressing-single rooms are rare; bathing and toilet facilities are usually inadequate; and there is uniformity of decor and an unmistakably institutional an-nosphere.’Z Although long-stay wards are home to those who are nursed there, half have no dining room and it is exceptional for residents to have items of their own furniture.3 Many continuing-care patients are denied basic freedoms. They have to get up early and go to bed at set times, visiting hours are restricted, and much of the day is spent sitting, doing nothing. Staffing levels are low and the nurses would like to have better training, support, and recognition. Geriatricians have not always taken their responsibilities for long-stay The

care

patients very seriously.4 The Health Care Research Unit at Newcastle University has published its evaluation of an alternative model of long-term nursing care.5,6 The first three National Health

SSPE in the developing world.

600 4. Hudson M, Pocknee R, Mowat MAG. D-lactic acidosis in short bowel syndrome—an examination of possible mechanisms. QJ Med 1990; 74: 157-...
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