The traditional designation of cluster headache as a vascular headache disorder is probably inappropriate; the vascular alterations that occur appear to be epiphenomenal, as they are in migraine, resulting from a primary CNS discharge. The hypothalamus may well be the site of such activation, containing posterior cells that regulate autonomic functions and anterior nuclei that serve as the major circadian pacemaker in mammals (Moore-Ede et al, 1983), both of which are necessary to explain the clinical symptoms and the uncanny periodicity of cluster headache attacks. The biologic clock is serotonergically modulated (Mason, 1986) and is connected anatomically to the eye (Sadun et al, 1984).The drugs effective in the treatment of the cluster headache syndrome enhance serotonergic neurotransmission, as also occurs in the treatment of migraine.This suggests that unstable serotonergic neurotransmission, at different loci, may be common to both disorders. In this section, we will review, among other data, the evidence supporting the tantalizing speculation that the cluster headache syndrome may be the result of an antidromically discharging biologic pacemaker
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