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Carotid artery compression
ARTICLES
12 Msuya FH, Curtis CF. Trial of pyrethroid impregnated bednets in an area of Tanzania holoendemic for malaria. Part 4: effects on incidence of malaria infection. Acta Trop 1991; 49: 165–71. 13 Stich AH, Maxwell CA, Haji AA, et al. Insecticide-impregnated bed nets reduce malaria transmission in rural Zanzibar. Trans R Soc Trop Med Hyg 1994; 88: 150–54. 14 Winstanley P, Watkins W, Muhia D, Szwandt S, Amukoye E, Marsh K. Chlorproguanil/dapsone for uncomplicated Plasmodium falciparum malaria in young children: pharmacokinetics and therapeutic range. Trans R Soc Trop Med Hyg 1997; 91: 322–27. 15 Nzila AM, Mberu EK, Sulo J, et al. Towards an understanding of the mechanism of pyrimethamine-sulfadoxine resistance in Plasmodium falciparum: genotyping of dihydrofolate reductase and dihydropteroate synthase of Kenyan parasites. Antimicrob Agents Chemother 2000; 44: 991–96. 16 Nzila AM, Nduati E, Mberu EK, et al. Molecular evidence of greater selective pressure for drug resistance exerted by the long-acting antifolate pyrimethamine/sulfadoxine compared with the shorteracting chlorproguanil/dapsone on Kenyan Plasmodium falciparum. J Infect Dis 2000; 181: 2023–28. 17 Marsh VM, Mutemi WM, Muturi J, et al. Changing home treatment of childhood fevers by training shop keepers in rural Kenya. Trop Med Int Health 1999; 4: 383–89. 18 Goodman CA, Coleman PGA, Mills AJ. Cost-effectiveness of malaria control in sub-Saharan Africa. Lancet 1999; 354: 378–85. 19 Hyde JE. The dihydrofolate reductase-thymidylate synthetase gene in
the drug resistance of malaria parasites. Pharm Ther 1990; 48: 45–59. 20 Wang P, Sims PF, Hyde JE. A modified in vitro sulfadoxine susceptibility assay for Plasmodium falciparum suitable for investigating Fansidar resistance. Parasitology 1997; 115: 223–30. 21 Triglia T, Wang P, Sims PF, Hyde JE, Cowman AF. Allelic exchange at the endogenous genomic locus in Plasmodium falciparum proves the role of dihydropteroate synthetase in sulfadoxine-resistant malaria. EMBO J 1998; 17: 3807–15. 22 Triglia T, Menting JG, Wilson C, Cowman AF. Mutations in dihydropteroate synthetase are responsible for sulfone and sulfonamide resistance in Plasmodium falciparum. Proc Natl Acad Sci USA 1997; 94: 13944–49. 23 Basco LK, Tahar R, Keundjian A, Ringwald P. Sequence variations in the genes encoding dihydropteroate synthase and dihydrofolate reductase and clinical response to sulfadoxine-pyrimethamine in patients with acute uncomplicated falciparum malaria. J Infect Dis 2000; 182: 624–28. 24 Watkins WM, Mberu EK, Winstanley PA, Plowe C. The efficacy of antifolate antimalarial combinations in Africa: a predictive model based on pharmacodynamic and pharmacokinetic analyses. Parasitol Today 1997; 13: 459–64. 25 Watkins WM, Mosobo M. Treatment of Plasmodium falciparum malaria with pyrimethamine-sulfadoxine: selective pressure for resistance is a function of long elimination half–life. Trans R Soc Trop Med Hyg 1993; 87: 75–78. 26 White NJ, Nosten F, Looaresuwan S, et al. Averting a malaria disaster. Lancet 1999; 353: 1965–67.
Uses of error: Carotid artery compression 20 years ago, when I was a PhD student, I was involved in a research project on the source of pain in migraine. At the time, we thought that pain arose primarily from the distention of the scalp arteries, and that constriction of these arteries accounted for the therapeutic effect of ergotamine compounds. However, supporting evidence was weak, so we embarked on a search for signs of cranial vessel involvement in migraine and other types of headache. I applied sufficient manual pressure to the superficial temporal artery to occlude its flow, to see whether the patients’ headaches decreased. To eliminate other cranial vessels as a source of pain, I also applied pressure briefly over the carotid artery below its bifurcation in the neck. All went well for the first 185 patients, but then a 60year-old woman developed aphasia and hemiparesis shortly after carotid artery compression. Fortunately, emergency assistance was close at hand, and she made a full recovery after anticoagulant treatment. I discontinued this procedure immediately, but did not think to include a description of the adverse event in the paper that was eventually accepted for publication. The full force of this omission struck me recently, when I learnt that at least one clinician used compression of the carotid artery to identify “vascular” headaches. Time has moved on, and it seems likely now that cranial vessels are only a secondary source of pain in migraine. Selecting a course of treatment following a careful medical history and examination is obviously better than putting patients at risk by compressing their carotid arteries. Peter D Drummond School of Psychology, Murdoch University, Western Australia 6150, Australia
THE LANCET • Vol 358 • October 13, 2001
1223
For personal use. Only reproduce with permission from The Lancet Publishing Group.
12 Msuya FH, Curtis CF. Trial of pyrethroid impregnated bednets in an area of Tanzania holoendemic for malaria. Part 4: effects on incidence of malaria infection. Acta Trop 1991; 49: 165–71. 13 Stich AH, Maxwell CA, Haji AA, et al. Insecticide-impregnated bed nets reduce malaria transmission in rural Zanzibar. Trans R Soc Trop Med Hyg 1994; 88: 150–54. 14 Winstanley P, Watkins W, Muhia D, Szwandt S, Amukoye E, Marsh K. Chlorproguanil/dapsone for uncomplicated Plasmodium falciparum malaria in young children: pharmacokinetics and therapeutic range. Trans R Soc Trop Med Hyg 1997; 91: 322–27. 15 Nzila AM, Mberu EK, Sulo J, et al. Towards an understanding of the mechanism of pyrimethamine-sulfadoxine resistance in Plasmodium falciparum: genotyping of dihydrofolate reductase and dihydropteroate synthase of Kenyan parasites. Antimicrob Agents Chemother 2000; 44: 991–96. 16 Nzila AM, Nduati E, Mberu EK, et al. Molecular evidence of greater selective pressure for drug resistance exerted by the long-acting antifolate pyrimethamine/sulfadoxine compared with the shorteracting chlorproguanil/dapsone on Kenyan Plasmodium falciparum. J Infect Dis 2000; 181: 2023–28. 17 Marsh VM, Mutemi WM, Muturi J, et al. Changing home treatment of childhood fevers by training shop keepers in rural Kenya. Trop Med Int Health 1999; 4: 383–89. 18 Goodman CA, Coleman PGA, Mills AJ. Cost-effectiveness of malaria control in sub-Saharan Africa. Lancet 1999; 354: 378–85. 19 Hyde JE. The dihydrofolate reductase-thymidylate synthetase gene in
the drug resistance of malaria parasites. Pharm Ther 1990; 48: 45–59. 20 Wang P, Sims PF, Hyde JE. A modified in vitro sulfadoxine susceptibility assay for Plasmodium falciparum suitable for investigating Fansidar resistance. Parasitology 1997; 115: 223–30. 21 Triglia T, Wang P, Sims PF, Hyde JE, Cowman AF. Allelic exchange at the endogenous genomic locus in Plasmodium falciparum proves the role of dihydropteroate synthetase in sulfadoxine-resistant malaria. EMBO J 1998; 17: 3807–15. 22 Triglia T, Menting JG, Wilson C, Cowman AF. Mutations in dihydropteroate synthetase are responsible for sulfone and sulfonamide resistance in Plasmodium falciparum. Proc Natl Acad Sci USA 1997; 94: 13944–49. 23 Basco LK, Tahar R, Keundjian A, Ringwald P. Sequence variations in the genes encoding dihydropteroate synthase and dihydrofolate reductase and clinical response to sulfadoxine-pyrimethamine in patients with acute uncomplicated falciparum malaria. J Infect Dis 2000; 182: 624–28. 24 Watkins WM, Mberu EK, Winstanley PA, Plowe C. The efficacy of antifolate antimalarial combinations in Africa: a predictive model based on pharmacodynamic and pharmacokinetic analyses. Parasitol Today 1997; 13: 459–64. 25 Watkins WM, Mosobo M. Treatment of Plasmodium falciparum malaria with pyrimethamine-sulfadoxine: selective pressure for resistance is a function of long elimination half–life. Trans R Soc Trop Med Hyg 1993; 87: 75–78. 26 White NJ, Nosten F, Looaresuwan S, et al. Averting a malaria disaster. Lancet 1999; 353: 1965–67.
Uses of error: Carotid artery compression 20 years ago, when I was a PhD student, I was involved in a research project on the source of pain in migraine. At the time, we thought that pain arose primarily from the distention of the scalp arteries, and that constriction of these arteries accounted for the therapeutic effect of ergotamine compounds. However, supporting evidence was weak, so we embarked on a search for signs of cranial vessel involvement in migraine and other types of headache. I applied sufficient manual pressure to the superficial temporal artery to occlude its flow, to see whether the patients’ headaches decreased. To eliminate other cranial vessels as a source of pain, I also applied pressure briefly over the carotid artery below its bifurcation in the neck. All went well for the first 185 patients, but then a 60year-old woman developed aphasia and hemiparesis shortly after carotid artery compression. Fortunately, emergency assistance was close at hand, and she made a full recovery after anticoagulant treatment. I discontinued this procedure immediately, but did not think to include a description of the adverse event in the paper that was eventually accepted for publication. The full force of this omission struck me recently, when I learnt that at least one clinician used compression of the carotid artery to identify “vascular” headaches. Time has moved on, and it seems likely now that cranial vessels are only a secondary source of pain in migraine. Selecting a course of treatment following a careful medical history and examination is obviously better than putting patients at risk by compressing their carotid arteries. Peter D Drummond School of Psychology, Murdoch University, Western Australia 6150, Australia
THE LANCET • Vol 358 • October 13, 2001
1223
For personal use. Only reproduce with permission from The Lancet Publishing Group.