الفهرس 
acknowledgmentOnly 14 pages are availabe for public view
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Abstract
A unifying pathophysiologic explanation of cluster headache is not yet available. For
any hypothesis to be complete, it must account for the three major features of the
syndrome, which include the trigeminal distribution of the pain, the ipsilateral autonomic
features, and the tendency for attacks to cluster with striking circadian and circannual
consistency, which is the signature feature of cluster headache.
Based on the clinical features of the disorder, three conclusions can be drawn. First,
because the pain of cluster headache is invariably centered around the eye and forehead, it
is probable that the ipsilateral trigeminal nociceptive pathways are integrally involved.
Second, the ipsilateral autonomic features suggest activation of the cranial parasympathetic
system (lacrimation and rhinorrhoea) and dysfunction of the ipsilateral sympathetic nerves
(ptosis and miosis). The cavernous carotid artery was suggested as a likely site of
involvement, since it is here that the trigeminal, parasympathetic, and sympathetic fibers
converge. Finally, the remarkable and often clockwork consistency and seasonal
predilection of attacks strongly suggest that a central pacemaker (the suprachiasmatic
nucleus) must be integrally involved in the genesis of this disorder. (52)