[Pathophysiology of cluster headache].

The aetiology of cluster headache (CH) is unknown and an unifying pathophysiologic explanation is not available. Based on the clinical features of the disorder, three areas appear to be involved in the pathogenesis and the expression of cluster headache: the trigeminal nociceptive pathways, the autonomic system and the hypothalamus. A brain stem connection may exist between the trigeminal nerve and the cranial parasympathetics. This would explain the reflex trigeminal-autonomic activation but a central nervous system dysfunction located in posterior hypothalamic gray matter is probably pivotal in the process. Such a dysfunction is supported by both posterior hypothalamic activation shown during CH attacks by positron emission tomography and increase of posterior hypothalamic volume shown in magnetic resonance imaging using voxel morphometry. Moreover, such a neurovascular model could be more precise considering some recent experimental and clinical research data as serotoninergic neuromediation involvement, nitric oxide one and a possible genetic predisposition.