576
and meningitis can be excluded. An osmotic diuretic should be available if LP is to be done. We thank the Medical Officer of Health, Kilifi District and our colleagues staffof Kilifi Hospital. We are especially grateful to the KEMRI nurses and technical staff and to Dr C. Nevill of the African Medical Research Foundation for their help, and to Dr R. Snow for statistical advice. We thank Dr J. B. 0. Were, Director, Clinical Research Centre, and Dr W. M. Watkins, Director, Wellcome Trust, Nairobi, for their support and encouragement, and Dr C. Newbold, Dr G. Brown, Dr N. White, Prof E. R. Moxon, and Prof B. G. R. Neville for stimulating discussions. We thank the Director of KEMRI, Dr D. Koech, for permission to publish these results. This work was funded by the Wellcome Trust, UK, and formed part of a collaborative study of the pathophysiology of malaria in children. on the
REFERENCES 1. Warrell DA, Molyneux ME, Beales PF. Severe and complicated malaria. Trans R Soc Trop Med Hyg 1990; 84 (suppl 2): 1-65. 2. Molyneux ME, Taylor TE, Wirima JJ, Borgstein A. Clinical features and prognostic indicators in paediatric cerebral malaria: a study of 131 comatose Malawian children. QJ Med 1989; 71: 441-59. 3. Aaslid R, Markwalder T-M, Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg 1982; 57: 769-74. 4. Minns RA, Engleman HM, Stirling H. Cerebrospinal fluid pressure in pyogenic meningitis. Arch Dis Child 1989; 64: 814-20. 5. Kirkham FJ, Levin SD, Padayachee TS, et al. Transcranial pulsed Doppler ultrasound findings in brain stem death. J Neurol Neurosurg Psychiatry 1987; 50:1504-13. 6. Goitein KJ, Amit Y, Mussaffi H. Intracranial pressure in central nervous system infections and cerebral ischaemia of infancy. Arch Dis Child 1983; 58: 184-86. 7. Miller JD, Stanek A, Langfitt TW. Concepts of cerebral perfusion pressure and vascular compression during intracranial hypertension. Prog Brain Res 1972; 35: 411-32. 8. Schmutzhard E, Gerstenbrand F. Cerebral malaria in Tanzania. Its epidemiology, clinical symptoms and neurological long term sequelae in the light of 66 cases. Trans R Soc Trop Med Hyg 1984; 78: 351-53.
Thapa BR, Marwaha RK, Kumar L, Mehta S. Cerebral malana in children: therapeutic considerations Indian Pediatr 1988; 25: 61-65. 10. Warrell DA, Looareesuwan S, Phillips RE, et al. Function of the blood-cerebrospinal fluid barrier in human cerebral malaria: rejection of the permeability hypothesis. Am J Trop Med Hyg 1986; 35: 882-89. 11. Hassler W, Steinmetz H, Gawlowski J. Transcranial Doppler ultrasonography in raised intracranial pressure and in intracranial circulatory arrest. J Neurosurg 1988; 68: 745-51. 12. Tasker RC, Matthew DJ, Helms P, Dinwiddie R, Boyd S. Monitoring in 9.
non-traumatic coma. Part 1: invasive intracranial measurements. Arch Dis Child 1988; 63: 888-94. 13. Brewster DR, Kwiatkowski D, White NJ. Neurological sequelae of cerebral malaria in children. Lancet 1990; 336: 1039-43. 14. Thomas JD. Clinical and histopathological correlation of cerebral malaria. Trop Geogr Med 1971; 23: 232-38. 15. Looareesuwan S, Warrell DA, White NJ, et al. Do patients with cerebral malaria have cerebral oedema? A computed tomography study. Lancet 1983; i: 434-37. 16. MacPherson GG, Warrell MJ, White NJ, Looareesuwan S, Warrell DA. Human cerebral malaria: a quantitative ultrastructural analysis of
parasitized erythrocyte sequestration. Am J Pathol 1985; 119: 385-401. DA, White NJ, Veall N, et al. Cerebral anaerobic glycolysis and
17. Warrell
reduced cerebral oxygen transport in human cerebral malaria. Lancet 1988; ii: 534-38. 18. Jensen MD, Conley M, Helstowski LD. Culture of Plasmodium the role of pH, glucose and lactate. J Parasitol 1983; 69: 1061-67. 19. Lassen NA. The luxury perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 1966; ii: 1113-15. 20. Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B. Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema". J Neurosurg 1981; 54: 170-78. 21. Rosner MJ, Becker DP. Origin and evolution of plateau waves. J Neurosurg 1984; 60: 312-24. 22. Kingston ME. Experience with urea in invert sugar for the treatment of cerebral malaria. J Trop Med Hyg 1971; 74: 249-52. 23. Commey JOO, Mills-Tetteh D, Phillips BJ. Cerebral malaria in Accra, Ghana. Ghana Med J 1980; 19: 68-72.
falciparum:
Cutaneous vasoconstrictor response to glucocorticoids in asthma
The aim of the study was to find out whether asthma patients whose airways obstruction is sensitive (CS) or resistant (CR) to corticosteroid treatment also differ in their cutaneous vasoconstrictor response to a potent topical glucocorticoid. Corticosteroid resistance was defined by failure of forced expiratory volume in 1 s (FEV1) and peak expiratory flow rate to improve by at least 15% after a 2-week trial of corticosteroids (prednisolone 20 mg daily for 1 week, then 40 mg daily for 1 week) despite more than 15% improvement with inhaled beta agonists. Beclomethasone dipropionate in concentrations of 3 µg/ml, 10 µg/ml, 30 µg/ml, and 100 µg/ml was applied to forearm skin; the site was occluded under plastic and the degree of blanching assessed after 18 h. CS asthmatic subjects (n=31), asthma patients with mild airways obstruction (n=26), asthma patients taking long-term prednisolone (n=13), and healthy volunteers showed similar vasoconstrictor responses. In CR asthmatic subjects
(n = 15), the response (expressed in terms of either blanching intensity or the proportion of patients showing a positive response) was significantly lower than that in the CS group at concentrations of 3 µg/ml (p
and meningitis can be excluded. An osmotic diuretic should be available if LP is to be done. We thank the Medical Officer of Health, Kilifi District and our colleagues staffof Kilifi Hospital. We are especially grateful to the KEMRI nurses and technical staff and to Dr C. Nevill of the African Medical Research Foundation for their help, and to Dr R. Snow for statistical advice. We thank Dr J. B. 0. Were, Director, Clinical Research Centre, and Dr W. M. Watkins, Director, Wellcome Trust, Nairobi, for their support and encouragement, and Dr C. Newbold, Dr G. Brown, Dr N. White, Prof E. R. Moxon, and Prof B. G. R. Neville for stimulating discussions. We thank the Director of KEMRI, Dr D. Koech, for permission to publish these results. This work was funded by the Wellcome Trust, UK, and formed part of a collaborative study of the pathophysiology of malaria in children. on the
REFERENCES 1. Warrell DA, Molyneux ME, Beales PF. Severe and complicated malaria. Trans R Soc Trop Med Hyg 1990; 84 (suppl 2): 1-65. 2. Molyneux ME, Taylor TE, Wirima JJ, Borgstein A. Clinical features and prognostic indicators in paediatric cerebral malaria: a study of 131 comatose Malawian children. QJ Med 1989; 71: 441-59. 3. Aaslid R, Markwalder T-M, Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg 1982; 57: 769-74. 4. Minns RA, Engleman HM, Stirling H. Cerebrospinal fluid pressure in pyogenic meningitis. Arch Dis Child 1989; 64: 814-20. 5. Kirkham FJ, Levin SD, Padayachee TS, et al. Transcranial pulsed Doppler ultrasound findings in brain stem death. J Neurol Neurosurg Psychiatry 1987; 50:1504-13. 6. Goitein KJ, Amit Y, Mussaffi H. Intracranial pressure in central nervous system infections and cerebral ischaemia of infancy. Arch Dis Child 1983; 58: 184-86. 7. Miller JD, Stanek A, Langfitt TW. Concepts of cerebral perfusion pressure and vascular compression during intracranial hypertension. Prog Brain Res 1972; 35: 411-32. 8. Schmutzhard E, Gerstenbrand F. Cerebral malaria in Tanzania. Its epidemiology, clinical symptoms and neurological long term sequelae in the light of 66 cases. Trans R Soc Trop Med Hyg 1984; 78: 351-53.
Thapa BR, Marwaha RK, Kumar L, Mehta S. Cerebral malana in children: therapeutic considerations Indian Pediatr 1988; 25: 61-65. 10. Warrell DA, Looareesuwan S, Phillips RE, et al. Function of the blood-cerebrospinal fluid barrier in human cerebral malaria: rejection of the permeability hypothesis. Am J Trop Med Hyg 1986; 35: 882-89. 11. Hassler W, Steinmetz H, Gawlowski J. Transcranial Doppler ultrasonography in raised intracranial pressure and in intracranial circulatory arrest. J Neurosurg 1988; 68: 745-51. 12. Tasker RC, Matthew DJ, Helms P, Dinwiddie R, Boyd S. Monitoring in 9.
non-traumatic coma. Part 1: invasive intracranial measurements. Arch Dis Child 1988; 63: 888-94. 13. Brewster DR, Kwiatkowski D, White NJ. Neurological sequelae of cerebral malaria in children. Lancet 1990; 336: 1039-43. 14. Thomas JD. Clinical and histopathological correlation of cerebral malaria. Trop Geogr Med 1971; 23: 232-38. 15. Looareesuwan S, Warrell DA, White NJ, et al. Do patients with cerebral malaria have cerebral oedema? A computed tomography study. Lancet 1983; i: 434-37. 16. MacPherson GG, Warrell MJ, White NJ, Looareesuwan S, Warrell DA. Human cerebral malaria: a quantitative ultrastructural analysis of
parasitized erythrocyte sequestration. Am J Pathol 1985; 119: 385-401. DA, White NJ, Veall N, et al. Cerebral anaerobic glycolysis and
17. Warrell
reduced cerebral oxygen transport in human cerebral malaria. Lancet 1988; ii: 534-38. 18. Jensen MD, Conley M, Helstowski LD. Culture of Plasmodium the role of pH, glucose and lactate. J Parasitol 1983; 69: 1061-67. 19. Lassen NA. The luxury perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 1966; ii: 1113-15. 20. Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B. Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema". J Neurosurg 1981; 54: 170-78. 21. Rosner MJ, Becker DP. Origin and evolution of plateau waves. J Neurosurg 1984; 60: 312-24. 22. Kingston ME. Experience with urea in invert sugar for the treatment of cerebral malaria. J Trop Med Hyg 1971; 74: 249-52. 23. Commey JOO, Mills-Tetteh D, Phillips BJ. Cerebral malaria in Accra, Ghana. Ghana Med J 1980; 19: 68-72.
falciparum:
Cutaneous vasoconstrictor response to glucocorticoids in asthma
The aim of the study was to find out whether asthma patients whose airways obstruction is sensitive (CS) or resistant (CR) to corticosteroid treatment also differ in their cutaneous vasoconstrictor response to a potent topical glucocorticoid. Corticosteroid resistance was defined by failure of forced expiratory volume in 1 s (FEV1) and peak expiratory flow rate to improve by at least 15% after a 2-week trial of corticosteroids (prednisolone 20 mg daily for 1 week, then 40 mg daily for 1 week) despite more than 15% improvement with inhaled beta agonists. Beclomethasone dipropionate in concentrations of 3 µg/ml, 10 µg/ml, 30 µg/ml, and 100 µg/ml was applied to forearm skin; the site was occluded under plastic and the degree of blanching assessed after 18 h. CS asthmatic subjects (n=31), asthma patients with mild airways obstruction (n=26), asthma patients taking long-term prednisolone (n=13), and healthy volunteers showed similar vasoconstrictor responses. In CR asthmatic subjects
(n = 15), the response (expressed in terms of either blanching intensity or the proportion of patients showing a positive response) was significantly lower than that in the CS group at concentrations of 3 µg/ml (p
