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Carotid artery compression

Drummond, P.D.ORCID: 0000-0002-3711-8737 (2001) Carotid artery compression. The Lancet, 358 (9289). p. 1223.

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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 60-year-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.

Item Type: Journal Article
Murdoch Affiliation(s): School of Psychology
Publisher: Elsevier
Copyright: Elsevier
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