Abstract
The intracranial internal carotid artery (ICA) is strongly implicated in the pathogenesis of cluster headache.Angiography has demonstrated a dilated ICA with branches from the cavernous sinus level during active periods A and a narrowed lumen of the proximal (extracavernous) ICA toward the end of an attack. Sympathetic fibers to the human ICA and its branches originate in the superior cervical ganglion and run as the internal carotid nerve along the ICA. Immediately after entering the skull cavity, fibers diverge to form a terminal plexus in the intracranial ICA wall.Parasympathetic fibers reach the human intracranial ICA with rami orbitales from the sphenopalatine ganglion, and with the greater deep petrosal nerve from a ganglion along the greater superficial petrosal nerve, and possibly from the otic ganglion.Sensory fibers reach the human intracranial ICA within the cavernous sinus through short branches from the ophthalmic trigeminal division,with a contribution from the maxillary division at least in the monkey.s The question arises whether this innervation exerts a vasomotor action locally. Such action might explain the angiographic findings in cluster headache.
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Hardebo, J.E. (1994). Importance of Cerebrovascular Receptors in Cluster Headache. In: Bevan, R.D., Bevan, J.A. (eds) The Human Brain Circulation. Vascular Biomedicine. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0303-2_35
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DOI: https://doi.org/10.1007/978-1-4612-0303-2_35
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