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Cluster Headache Help and Support >> Cluster Headache Specific >> Hypothalamus & causation: weeee modification http://www.clusterheadaches.com/cgi-bin/yabb2/YaBB.pl?num=1249417850 Message started by Bob_Johnson on Aug 4th, 2009 at 4:30pm |
Title: Hypothalamus & causation: weeee modification Post by Bob_Johnson on Aug 4th, 2009 at 4:30pm
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>
============================ 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] |
Title: Re: Hypothalamus & causation: weeee modification Post by MJ on Aug 5th, 2009 at 1:30am
"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."
From what I've read this makes a lot more sense than the deformed Hypothalamus thoughts as many readily assume. My interpretive opinion is as allways a chemical balancing act. If the hypothalamus is possibly the correcting factor than whatever feeds it or alters its output is the delaying and instigating factor. Nice find, creates food for thought. |
Title: Re: Hypothalamus & causation: weeee modification Post by Callico on Aug 7th, 2009 at 2:26am
Thanks. Wish I understood it better, but what I understand makes sense.
Jerry |
Title: Re: Hypothalamus & causation: weeee modification Post by campergal on Aug 9th, 2009 at 2:55pm
Thanks Bob,
My doc didn't even want to discuss it. |
Title: Re: Hypothalamus & causation: weeee modification Post by starlight on Aug 10th, 2009 at 12:31pm
Bob, Thanks for the information--very interesting.
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