NO RELATION BETWEEN CEPHALIC VENOUS DILATATION AND PAIN IN MIGRAINE

Citation
D. Daugaard et al., NO RELATION BETWEEN CEPHALIC VENOUS DILATATION AND PAIN IN MIGRAINE, Journal of Neurology, Neurosurgery and Psychiatry, 65(2), 1998, pp. 260-262
Citations number
15
Categorie Soggetti
Psychiatry,"Clinical Neurology",Surgery
ISSN journal
00223050
Volume
65
Issue
2
Year of publication
1998
Pages
260 - 262
Database
ISI
SICI code
0022-3050(1998)65:2<260:NRBCVD>2.0.ZU;2-2
Abstract
Evidence for the involvement of the cranial arterial system in migrain e is plentiful, but it is unclear whether the cranial venous system ma y be involved in the mechanism of migraine pain. Venules are the prefe rentially involved vessels in the neurogenic inflammation animal model of migraine. The cranial and cerebral veins and sinuses are pain sens itive and receive sensory innervation from the trigeminal nerve. If th e veins are involved in migraine pathogenesis, a venous dilatation wou ld presumably be painful. The effect of a short lasting cranial venous dilatation, induced by applying pressure on the internal jugular vein s (Queckenstedt's manoeuvre), was therefore compared with a placebo pr ocedure, consisting of an equal pressure applied on to the lateral asp ect of the neck. In each procedure pressure was applied for 10 seconds . The study used a single blind, randomised, cross over design, and 20 patients with an acute attack of migraine without aura participated. After each procedure, headache intensity was rated on a standardised f ive point scale. After Queckenstedt's manoeuvre 40% of the patients re ported no change in headache intensity, 25% a worsening, and 35% an im provement of their headache. No significant difference between the hea dache intensity ratings during Queckenstedt's manoeuvre and the placeb o manoeuvre was found (p=0.22). The findings make it unlikely that the cephalic venous system is of major importance in migraine pain mechan isms and, therefore, also less likely that neurogenic inflammation pla ys a significant part in humans during attacks of migraine without aur a.