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.

Several 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 are 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.