does anyone know how to stop the headaches? Does anyone know the cause? Does anyone know why they happen? I don't understand it. Can they ever be stopped for good?

Yes, maybe, sort of, me either, maybe. ;)

Most research points to a defect in our hypo-thalamus. Which helps to explain the clockwork like nature of CH as your hypo-thalamus controls your circadium rhythms.

To stop the pain it's critical you attack the mechanism of the pain, and nt the pain itself. Pain killers, short of rendering you knocked out, just won't help. Breathing pure oxygen, at a rate to support hyper-ventilation, started at the first sign of an attack, will completely abort the whole attack for most. Imitrex injectables, and for some the nasal spray version, will accomplish the same thing.

I don't understand it. Many of the better educated types on this board study the interactions of various brain chemicals and hormones, pre and post attack, and during the attacks. Most of that is a bit over my head. I stick with the high percentage abortives and preventatives.

Some people grow out of them, typically in their 50's and 60's. That being said we have people in their 70's on this board still getting attacks. That's why i say maybe.

The closest thing I've seen to a "cure", and it's not a cure but it works better then anyhting else I've seen:

Clusterbusters.com

Hang in there. The mnore you learn, the less beasty runs your life.

joe

There is still a huge amount about CH that is currently not well understood, so time and the efforts of those doing research will advance the understanding of what causes CH, what causes them to be triggered, why some are epidsodic and others chronic, what triggers an episode and what stops it, etc....

However, as Joe explained, there has been some good work done that has identified multiple different ways to prevent CHs and other ways to kill off a CH when it arrives. I expect that in time we'll see even more work done in this area, although at the moment most of the research work is being done around migraines and then the treatments are also found to work for CH too (e.g. imitrex).

Thank you Joe,

Now thats how you anwser a post!!!
There is a light... and i may not be doomed to live in the stone age for life.

In it to win it..
Coach Bill

Hey there, cluster2. I know it's hard to read intent or emotion in a quick post, but I have to say yours sound to me like someone who is reaching out, but hasn't found the right words to say. I'm only saying we're here for you, and if you'd let us in, we may be able to help a bit. This site means you do not have to struggle alone anymore. We do understand. And we bring years of experience with both failures and successes. So...if you want, you can open up some. Let us know wha't going on. Blessings. lance

Guiseppi wrote on Jan 22^nd, 2012 at 7:32pm:

Most research points to a defect in our hypo-thalamus.

Hi

While I know studies have found CHs to have" more grey matter" in the hypo-thalamus, I've never read any conclusion about the nature of this surplus. Is it proven to be a defect?

There are some answers to your questions in these two articles--BUT--that doesn't mean most us us can understand them! <bg>

My grasp of such material is: There is growing understanding of the PROCESSES involved in the origin and experience of Cluster--but that the first-cause is not yet understood. That is, why the abnormal gray matter, in the first place.

While I share your interest in your questions, I long ago concluded that the best we can do is work to understand how best to treat outselves, given the volume of understandable information which we have available to us.
=======================
Headache:lessons learned from functional imaging
British Medical Bulletin 2003; 65: 223-234

Arne May
Department of Neurology, University of Regensburg, Regensburg, Germany

Using PET in a larger patient series, significant activations ascribable to the acute cluster headache were observed in the ipsilateral hypothalamic grey matter when compared to the headache-free state44. This highly significant activation was not seen in cluster headache patients out of the bout when compared to the patients experiencing an acute cluster headache attack45. In contrast to migraine25, no brainstem activation was found during the acute attack compared to the resting state. This is remarkable, as migraine and cluster headache are often discussed as related disorders and identical specific compounds, such as ergotamine and sumatriptan, are currently used in the acute treatment of both types of headache46. These data suggest that while primary headaches such as migraine and cluster headache may share a common pain pathway, the trigeminovascular innervation, the underlying pathogenesis differs significantly as might be inferred from the different patterns of presentation and responses to preventative agents46.
Just as it is striking that no brainstem activation occurs in contrast to acute migraine, no hypothalamic activation was seen in experimental pain induced by capsaicin injection into the forehead47. This is important because injection of the forehead would activate first (ophthalmic) division afferents which are the trigeminal division predominantly responsible for pain activation in cluster headache. Thus two other types of first division of trigeminal nerve pain, while sharing neuro-anatomical pathways with cluster headache, do not give rise to....


VASCULAR HEADACHE: ARE BLOOD VESSELS INVOLVED?

Taking these observations on acute cluster headache together with what has been observed in experimental head-pain and migraine, the data establish that migraine and CLUSTER HEADACHE, FAR FROM BEING PRIMARILY VASCULAR DISORDERS, ARE CONDITIONS WHOSE GENESIS IS TO BE FOUND IN THE CENTRAL NERVOUS SYSTEM IN PACEMAKER OR CIRCADIAN REGIONS SPECIFIC TO THE SYNDROME. If further studies confirm these findings, a better understanding will be gained of where and how acute and preventative therapy can be targeted.
=====
Interesting to note that he is saying that the primary mode of action is NOT as a vasoconstrictor but on its effect on the central nervous system. Doesn't change our appreciation of this class of meds but suggests we need to change how we think about the nature of CH.
==============================
Handb Exp Pharmacol. 2007;(177):129-43.   


Serotonin receptor ligands: treatments of acute migraine and cluster headache.


Goadsby PJ.

Institute of Neurology, Queen Square, London WC1N 3BG, UK. peterg@ion.ucl.ac.uk

Fuelled by the development of the serotonin 5-HT(1B/1D) receptor agonists, the triptans, the last 15 years has seen an explosion of interest in the treatment of acute migraine and cluster headache. Sumatriptan was the first of these agonists, and it launched a wave of therapeutic advances. These medicines are effective and safe. Triptans were developed as cranial vasoconstrictors to mimic the desirable effects of serotonin, while avoiding its side-effects. IT HAS SUBSEQUENTLY BEEN SHOWN THAT THE TRIPTANS' MAJOR ACTION IS NEURONAL, WITH BOTH PERIPHERAL AND CENTRAL TRIGEMINAL INHIBITORY EFFECTS, AS WELL AS ACTIONS IN THE THALAMUS AND AT CENTRAL MODULATORY SITES, SUCH AS THE PERIAQUEDUCTAL GREY MATTER. Further refinements may be possible as the 5-HT(1D) and 5-HT(1F) receptor agonists are explored. Serotonin receptor pharmacology has contributed much to the better management of patients with primary headache disorders.

PMID: 17087122 [PubMed]
=================================================================
J Clin Neurosci. 2010 Mar 11.

What has functional neuroimaging done for primary headache ... and for the clinical neurologist?
Sprenger T, Goadsby PJ.

UCSF Headache Centre, Department of Neurology, University of California, 1701 Divisadero St, Suite 480, San Francisco, CA 94115, USA.

Our understanding of mechanisms involved in primary headache syndromes has been substantially advanced using functional neuroimaging.

THE DATA HAVE HELPED ESTABLISH THE NOW-PREVAILING VIEW OF PRIMARY HEADACHE SYNDROMES, SUCH AS MIGRAINE AND CLUSTER HEADACHE, AS BRAIN DISORDERS WITH NEUROVASCULAR MANIFESTATIONS, NOT AS DISORDERS OF BLOOD VESSELS.

PMID: 20227279 [PubMed]

Zeitgeist wrote on Jan 24^th, 2012 at 10:55am:

Guiseppi wrote on Jan 22nd, 2012 at 7:32pm: Most research points to a defect in our hypo-thalamus. Hi While I know studies have found CHs to have" more grey matter" in the hypo-thalamus, I've never read any conclusion about the nature of this surplus. Is it proven to be a defect?

I think the pain proves it pretty conclusively!

Regards,
Jim

Kilowatt3 wrote on Jan 25^th, 2012 at 6:46am:

I think the pain proves it pretty conclusively!

Hi Jim.
Unfortunately it is not that simple.