Activation of Pain Fibers to the Internal Carotid Artery Intracranially May Cause the Pain and Local Signs of Reduced Sympathetic and Enhanced Parasympathetic Activity in Cluster Headache
Article first published online: 20 MAY 2005
Headache: The Journal of Head and Face Pain
Volume 31, Issue 5, pages 314–320, May 1991
How to Cite
Hardebo, J.-E. (1991), Activation of Pain Fibers to the Internal Carotid Artery Intracranially May Cause the Pain and Local Signs of Reduced Sympathetic and Enhanced Parasympathetic Activity in Cluster Headache. Headache: The Journal of Head and Face Pain, 31: 314–320. doi: 10.1111/j.1526-4610.1991.hed3105314.x
- Issue published online: 20 MAY 2005
- Article first published online: 20 MAY 2005
- Accepted for Publication: February 2, 1991.
- Cited By
- cluster headache;
- carotid artery;
- trigeminal nerve;
- neurogenic inflammation;
- blood flow
SYNOPSISSeveral clinical and circulatory physiological observations indicate that the internal carotid artery (ICA) with proximal pial and orbital-periorbital branches, as well as external carotid vessels adjacent to the orbital region, are involved in the autonomic symptoms of an attack of cluster headache. Evidence is presented here that an activation of pain fibers innervating the intracranial segment of ICA may cause not only the retroorbital pain of an attack but also, via the mechanical effect of a neurogenic inflammation in the vessel wall, the local symptoms of a sympathetic defect and, via a reflex arc to the parasympathetic pathway along the greater superficial petrosal nerve, the local symptoms from glands and vessels of parasympathetic discharge. Dilation of the intracranial ICA due to activation of this parasympathetic pathway may aggravate pain. Possible mechanisms behind such a local pain fiber activation are discussed.