Abstract
From the time of its delineation as a syndrome, there was little doubt in the minds of most clinicians that cluster headaches are vascular in origin. The persistent unilaterality of the headaches, their paroxysmal nature, their brevity, and their severity were reminiscent of migraine; and their precipitation by vasoactive substances such as histamine, alcohol and nitroglycerin, and occasional amelioration by ergotamine and methysergide reinforced this impression. There was some question of whether cluster headaches are intracranial vascular headaches, extracranial vascular headaches, or both. Some clinicians encountered local tenderness of the external carotid vessels during cluster headaches. Other workers1 established that in some cases the pain of cluster headache could be relieved by raising intracranial (CSF) pressure, a maneuver which would affect only the intracranial circulation. Temple Fay2 demonstrated that stimulation of the carotid artery bifurcation and of the origin of the internal carotid artery could produce pain in the same regions affected by cluster headache.
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Edmeads, J. (1984). Pathophysiologic Aspects of Cluster Headache. In: Mathew, N.T. (eds) Cluster Headache. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-7822-8_6
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DOI: https://doi.org/10.1007/978-94-011-7822-8_6
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