The current tendency in the investigation of the aetiopathogenesis of cluster headache is to think of the syndrome as resulting from a hypothalamic derangement with a peripheral neurovascular implication; the hypothalamic central contribution and the peripheral vascular contribution are considered to be equally significant.1"5 In fact the inconsistency of changes in the cerebral vascular blood flow during cluster headache attacks fails to justify the importance usually placed on it. On the other hand, the strong evidence supporting a central hypothalamic mechanism-the periodicity of the attacks, the considerable autonomic involvement which is often most severe on the painful side-seems to suggest that the hypothalamus could be the main site of activation of this disorder.
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