600

4. Hudson M, Pocknee R, Mowat MAG. D-lactic acidosis in short bowelsyndrome—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 developingcountries. The underlying pathological change, a

progressive degeneration of the central nervous system, ismanifested in various neurological signs-behaviouralchanges, developmental deterioration, ataxia, myoclonicseizures, visual disorders, spasticity, and decerebrate

rigidity. 1 Characteristically, these features appear

insidiously in a child aged five to fifteen who had measlesmany years previously. The doctor in a developing countryhas to make a tentative diagnosis because confirmationrequires the demonstration of high-titre measles antibody inthe cerebrospinal fluid,2 and this test is not usually available.Differential diagnoses include cerebral tumours, other

neurodegenerative conditions, and human immuno-

deficiency virus infection. When antibody tests havebeen applied in developing countries, SSPE has beenshown to account for a substantial fraction of childhood

neurodegenerative conditions. 4-7 Chemotherapy is

ineffective,l and the clinical course is relentlessly downhilluntil death months or years later.SSPE is a rare complication of measles-annual incidence

ranges from under 0.1 cases7,8 to 5 or 6 cases4 per million

population. The wide range partly reflects difficulties indiagnosis and case-finding and also illustrates the relativedegrees of success and failure of measles control achieved bydifferent 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 unfortunatefew children, a long-time (5-10 years) after the acuteinfection.

Children infected in the first 2 years are more at risk andcase-series have consistently shown an excess of boys 49 butthis apparent age and sex bias may merely reflect anothermore important factor concerning the dose of measlesreceived at exposure."A higher incidence of SSPE would be expected in

developing countries because there is more circulatingmeasles10 and attack rates are higher in the first two years oflife. 12 Survey results confirm this suggestion,4-7 althoughfew studies have been conducted in sub-Saharan Africa.13Mass measles vaccination is effective in reducing SSPE

incidence in both developing and industrialisedcountries.9,14,15 Fears that measles vaccine might itself causeSSPE have been shown to be groundless9,15-it is morehazardous to remain unimmunised.1’ SSPE is another

strong reason for promoting mass immunisation, especiallysince the demonstration that high-titre Edmonston-Zagrebmeasles vaccine given in the first year is both safe16 andeffective17 in preventing early measles. The Global AdvisoryGroup of WHO’s Expanded Programme on Immunisationhas recommended that this vaccine is given at six months of

age where early transmission is a hazard.12 SSPE intensifiesthe challenge to governments, programme managers, anddonors in developing countries to apply therecommendation with speed and vigour.

1. Whittle HC, Marshall WC. Measles. In: Weatherall DJ, LedinghamJGG, 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 ofhuman immunodeficiency virus infection in children. Pediatrics 1986;78: 678-87.

4. Cernescu S, Milea S. Epidemiology of subacute sclerosingpanencephalitis in Romania between 1976-1982. Virologic 1983; 34:239-50.

5. Yalaz K, Anlar B, Renda Y, Aysun S, Topcu M, Ozdirim E. Subacutesclerosing panencephalitis in Turkey: epidemiological features. J TropPediatr 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 diseases inBenghazi, Libya. Neuroepidemiology 1988; 7: 159-64.

8. Hinman AR, Orenstein WA, Bloch AB, et al. Impact of measles in theUnited States. Rev Infect Dis 1983; 5: 439-44.

9. Miller CL. Current impact of measles in the United Kingdom. Rev InfectDis 1983; 5: 427-32.

10. Grant JP. The state of the world’s children 1990. Oxford: Oxford

University Press, 1990.11. Aaby P, Bukh J, Lisse IM, Smits AJ. Risk factors in subacute sclerosing

panencephalitis; age and sex-dependent host reactions or intensiveexposure. Ref Infect Dis 1984; 6: 239-50.

12. Hall AJ, Greenwood BM, Whittle H. Modern vaccines: practice indeveloping countries. Lancet 1990; 335: 774-77.

13. Tukei PM, Kenya PR, Ensering J. An epidemiological study of subacutesclerosing panencephalitis in Kenya. East Afr Med J 1983; 60:34-38.

14. Vucenovic V, Vranjesevic D. SSPE—epidemiology and measlesvaccination: our cases. Neurol 1989; 38: 23-31.

15. Bloch AB, Orenmstein WA, Stetler HC, et al. Health impact of measlesvaccination in the United States. Pediatrics 1985; 76: 524-32.

16. Whittle H, Hanlon P, O’Neill K, et al. Trial of high-dose Edmonston-Zagreb measles vaccine in The Gambia: antibody response andside-effects. Lancet 1988; ii: 811-14.

17. Aaby P, Jensen TG, Hansek HL, et al. Trial of high-dose Edmonston-Zagreb measles in Guinea-Bissau: protective efficacy. Lancet 1988; ii:809-11.

NHS NURSING HOMES

The care provided for dependent old people in long-stayhospital wards in Britain is not a source of national pride.Frail elderly individuals who cannot live at home tend to behoused in outmoded buildings, often some distance fromtheir families.! The physical environment can be

depressing-single rooms are rare; bathing and toiletfacilities are usually inadequate; and there is uniformity ofdecor and an unmistakably institutional an-nosphere.’ ZAlthough long-stay wards are home to those who are nursedthere, half have no dining room and it is exceptional forresidents to have items of their own furniture.3 Manycontinuing-care patients are denied basic freedoms. Theyhave to get up early and go to bed at set times, visiting hoursare restricted, and much of the day is spent sitting, doingnothing. Staffing levels are low and the nurses would like tohave better training, support, and recognition. Geriatricianshave not always taken their responsibilities for long-staypatients very seriously.4The 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