Hostname: page-component-5c6d5d7d68-pkt8n Total loading time: 0 Render date: 2024-08-15T17:10:21.719Z Has data issue: false hasContentIssue false
  • English
  • Français

Implications of Individual Differences in Vascular Reactivity for the Management of Migraine

Published online by Cambridge University Press:  06 October 2014

Peter D. Drummond
Peter D. Drummond*
Affiliation:
Department of Neurology, Prince Henry Hospital, and the School of Medicine, University of New South Wales
*
Department of Psychology, Murdoch University, Murdoch W.A. 6150
Get access

Abstract

The view that dilatation of scalp arteries is a major source of pain in migraine was examined in a series of clinical and psychophysiological investigations. Examination of patients during unilateral migraine or tension-vascular headache demonstrated evidence of extracranial vasodilatation in only a minority of patients. Studies of psychophysiological reactivity indicated that the amplitude of superficial temporal artery pulsations increased more on the side habitually affected by headache than on the non-symptomatic side after light exercise, and increased more readily in migrainous subjects than in non-headache controls during psychological stress. In patients who had previously shown thermographic signs of an increase in blood flow at the site of headache, scalp arteries dilated readily to mental arithmetic stress and exercise. Although extracranial vasodilatation sometimes contributes to migraine, it does not appear to be the primary source of pain in the majority of patients. Regulation of scalp artery diameter may be most effective in the subgroup of patients whose scalp arteries contribute to pain.

Type
Research Article
Information
Behaviour Change , Volume 4 , Issue 2 , June 1987 , pp. 20 - 24
Copyright
Copyright © The Author(s) 1987

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

REFERENCES

Bild, R., & Adams, H. E. (1980). Modification of migraine headaches by cephalic blood volume pulse and EMG biofeedback. Journal of Consulting and Clinical Psychology, 48, 51–57.Google Scholar
Blanchard, E. B., Andrasik, F., Appelbaum, K. A., Evans, D. D., Myers, P., & Barron, K. D. (1986). Three studies of the psychologic changes in chronic headache patients associated with bio-feedback and relaxation therapies. Psychosomatic Medicine, 48, 73–83.CrossRefGoogle Scholar
Blau, J. N., & Dexter, S. L. (1981). The site of pain origin during migraine attacks. Cephalalgia, 1, 143–147.CrossRefGoogle ScholarPubMed
Brazil, P., & Friedman, A. P. (1956). Craniovascular studies in headache. A report and analysis of pulse volume tracings. Neurology, 6, 96–102.CrossRefGoogle ScholarPubMed
Cohen, M. J., McArthur, D. L., & Rickles, W. H. (1980). Comparison of four biofeedback treatments for migraine headache: Physiological and headache variables. Psychosomatic Medicine, 42, 463–480.Google Scholar
Drummond, P. D. (1982). Extracranial and cardiovascular reactivity in migrainous subjects. Journal of Psychosomatic Research, 26, 317–331.CrossRefGoogle ScholarPubMed
Drummond, P. D. (1984). Extracranial vascular changes during headache, exercise and stress. Journal of Psychosomatic Research, 28, 133–138.Google Scholar
Drummond, P. D. (1985a). Vascular responses in headache-prone subjects during stress. Biological Psychology, 21, 11–25.CrossRefGoogle ScholarPubMed
Drummond, P. D. (1985b). Predisposing, precipitating and relieving factors in different categories of headache. Headache, 25, 16–22.Google Scholar
Drummond, P. D. (1987). Vascular headache syndromes and their treatment. To appear in: Byrne, D. G. & Caddy, G. (Eds), International Perspectives in Behavioural Medicine. In press.Google Scholar
Drummond, P. D., & Lance, J. W. (1981). Extracranial vascular reactivity in migraine and tension headache. Cephalalgia, 1, 149–155.CrossRefGoogle ScholarPubMed
Drummond, P. D., & Lance, J. W. (1983). Extracranial vascular changes and the source of pain in migraine headache. Annals of Neurology, 13, 32–37.CrossRefGoogle ScholarPubMed
Drummond, P. D., & Lance, J. W. (1984). Facial temperature in migraine, tension-vascular and tension headache. Cephalalgia, 4, 149–158.Google Scholar
Friar, L. R., & Beatty, J. (1976). Migraine: Management by trained control of vasoconstriction. Journal of Consulting and Clinical Psychology, 44, 46–53.CrossRefGoogle ScholarPubMed
Gauthier, J., Doyon, J., Lacroix, R., & Drolet, M. (1983). Blood volume pulse biofeedback in the treatment of migraine headache: A controlled evaluation. Biofeedback and Self-regulation, 8, 427–442.Google Scholar
Graham, J. R., & Wolff, H. G. (1938). Mechanism of migraine headache and action of ergotamine tartrate. Archives of Neurology and Psychiatry, 39, 737–763.Google Scholar
Henryk-Gutt, R., & Rees, W. L. (1973). Psychological aspects of migraine. Journal of Psychosomatic Research, 17, 141–153.CrossRefGoogle ScholarPubMed
Heyck, H. (1969). Pathogenesis of migraine: A contribution. Research and Clinical Studies in Headache, 2, 1–28.Google Scholar
Selby, G., & Lance, J. W. (1960). Observations on 500 cases of migraine and allied vascular headache. Journal of Neurology, Neurosurgery and Psychiatry, 23, 23–32.CrossRefGoogle ScholarPubMed
Tunis, M. M., & Wolff, H. G. (1953). Studies on headache: Long-term observations of the reactivity of the cranial arteries in subjects with migraine of the vascular type. Archives of Neurology and Psychiatry, 70, 551–557.Google Scholar
Wennerholm, M. (1961). Postural vascular reactions in cases of migraine and related vascular headaches. Acta Medica Scandinavica, 169, 131–139.CrossRefGoogle ScholarPubMed
Wolff, H. G. (1953). Stress and Disease. Springfield: Thomas.CrossRefGoogle Scholar