| Abstract | | One of the most interesting hypothesis on the pathogenesis of cluster headache is that of the involvement of a subset of sensory neurons, with their "dual" functions, efferent (through an antidromic activation) as well as afferent. The involvement of these neurons could explain both the presence of the pain as well as that of the accompanying symptoms. Two big questions arise from this hypothesis. The first concerns the localization of the sensory neurons possibly involved, the other is the cause of this involvement. Concerning the first hypothesis, numerous clues indicate the pterygopalatine fossa as the possible localization of the sensory neurons involved in the pathogenesis of cluster headache. In particularly indirect evidence for the involvement of structures in the proximity of the nasal mucosa is represented by the preventive effect of the nasal applications of capsaicin on cluster headache attacks as well as the acute effect of an application of lidocaine on a single attack. Regarding the second issue, an interesting hypothesis is that of a viral infection which cyclically re-occurs when the immunological surveillance has decreased. The pathogenesis of cluster headache (CH) is still unknown, not withstanding the bulk of research, experimental and clinical, that has been developed regarding this problem. In recent years, a hypothesis has been formulated concerning the involvement of some primary sensitive neurons. In particular, some "C" fibers (amyelinic, slow conduction) containing neuropeptides (substance P, neurokinine A, and CGRP, a peptide relative to the calcitonin gene) have been hypothesized to play a part in the pathogenesis of the syndrome (1,2). The function of this subpopulation of primary sensitive neurons would be that of conducting pain-inducing information generated by thermal or chemical stimuli.(trunc.)
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