Abstract
An hypothesis regarding the possible role of the carotid body in the pathogenesis of cluster headache is presented. It states: 1. The pathways concerned with cyclic cluster periods may begin centrally involving specific areas in the hypothalamus. The major influence of this physiological change is proposed to be an inhibition of the sympathetic and disinhibition of parasympathetic supplies to the carotid body. The result, whether due to increased vasomotor tonus or interruption of intrinsic sympathetic stimulation, is suggested to cause diminished peripheral chemoreceptor activity. 2. The pathway concerned with onset of spontaneous or induced attacks begins, as proposed, with oxygen desaturation--which, upon reaching threshold levels may induce a hyperactive chemoreceptor response, and stimulate through afferent pathways the nuclei of the 7th and 10th cranial nerves and respiratory centers, via the nucleus solitarius. 3. The consequence of this excitation may involve the third suggested pathway resulting in stimulation of peripheral secretory and other receptors innervated by the cranial nerves.
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