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
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.