A subtle development in the theory of how the hypothalamus is involved in CH (last sentence). Nothing here will affect us now--but I'm posting this abstract to make the point that developments are often painfully slow in good science and we need to keep our desires for magic under control! <bg>
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Lancet Neurol. 2009 Aug;8(8):755-64.
Pathophysiology of trigeminal autonomic cephalalgias.

Leone M, Bussone G.

Headache Centre, Neuromodulation Unit and Neurological Department, Fondazione Istituto Neurologico Carlo Besta, Milano, Italy.

Cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) are primary headaches recently classified together as trigeminal autonomic cephalalgias (TACs). The causes of these headaches have long been debated, with "peripheral" hypotheses in opposition to "central" hypotheses.

THE AVAILABLE INFORMATION INDICATES THAT THE PAIN ORIGINATES FROM WITHIN THE BRAIN IN CLUSTER HEADACHE. THE HYPOTHALAMIC ACTIVATION OBSERVED DURING TAC ATTACKS BY USE OF FUNCTIONAL NEUROIMAGING, AND THE SUCCESS OF HYPOTHALAMIC STIMULATION AS A TREATMENT, CONFIRM THAT THE POSTERIOR HYPOTHALAMUS IS CRUCIAL IN THE PATHOPHYSIOLOGY OF THESE HEADACHES.

The posterior hypothalamus is now known to modulate craniofacial pain, and hypothalamic activation occurs in other pain disorders, SUGGESTING THAT THIS BRAIN AREA IS LIKELY TO HAVE A MORE COMPLEX ROLE IN THE PATHOPHYSIOLOGY OF TACS THAN THAT OF A MERE TRIGGER. HYPOTHALAMIC ACTIVATION MIGHT PLAY A PART IN TERMINATING RATHER THAN TRIGGERING ATTACKS, AND MIGHT ALSO GIVE RISE TO A CENTRAL PERMISSIVE STATE, ALLOWING ATTACKS TO TAKE PLACE.

PMID: 19608101 [PubMed]

Thanks.  Wish I understood it better, but what I understand makes sense. 

Jerry

Bob,  Thanks for the information--very interesting.