These abstracts summarize what is now accepted to be the etiology of Clusters.
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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.
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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.
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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]
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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]
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Alcohol is a trigger only when we are in an active cycle/period. But,

some interested, confounding data out of Europe, which has not been explored (as far as I know), indicates that red but not white wine is a trigger, as well as spirits. Hints as some chemical component in red may be involved. In addition, we recognize solvents, some cleaning agents, even as nasal intake, will trigger for some.

Unlike migraine, neither literature or out discussion here, have lead to identification of food triggers in Cluster

I've never seen any hint, suggestion, guess about fat as a trigger, cerainly not causal.

Ok so I used the wrong word - I meant trigger not cause as in fundamental underlying cause.  But keep the replies coming, my PI is a kind of a slave-driver so I don't get a lot of time to do any outside research.  @Batch - I learned that my student insurance which doesn't cover my oxygen will actually cover blood tests so I will definitely check into that, but its these numbers that make the whole thing so complex - only 70%?  That means its somehow related but whether its upstream or downstream is still in question, and obviously 30% of CH patients are able to compensate somehow or the mechanism that causes the deficiency is absent in those - the control of gene expression makes a lot of sense there, but it's a complex problem and its difficult to study.  But I think (I hope?) all of these things - sensitivity to alcohol and vitamin deficiencies - are clues to what the fundamental problem really is.  Not today, and not next year, but someday I'd like the ability to choose my project and when the time comes I think working on CH would be very satisfying.

I really was hoping to hear people's personal experiences, not published data... I did find this, though:

This study shows that eating a high-fat meal leads to dilatation of peripheral conduit arteries and microvessels, as well as to enhanced maximum vasodilator reserve, possibly related to postprandial hyperinsulinemia. In these subjects, flow-mediated endothelium-dependent dilatation remained unchanged after these particular high-fat meals.
[Enhanced peripheral vasodilation in humans after a fatty meal Raitakari et al. J Am Coll Cardiol, 2000; 36:417-422]

So vasodilation is probably the mechanism for the trans fat trigger. 

@Batch- Very helpful!!!! And very interesting.  The homefill system set me back a cool $1500 so I do plan to file the insurance claim, but the most they will pay, if they do, is $600, but as I mentioned before it would cost me more than that to go through two clusters at the tank or rental rates.

@Lenny: I don't know, that's what I'd like to find out!  A LOT of companies have responded to the trans fat stuff and eliminated partially hydrogenated oils from their products. It makes sense that all those big fatty acids tumbling through the veins in high concentrations would exacerbate the issue.  Those headaches were the worst I've ever had - just like people describe with alcohol.  These are no fun, by any means, but they come on slower and progress slower so it's easier to get relief before the beast has fully shown himself.

I've posted the abstracts (reply #1) likely a dozen times and each posting is followed by -- no response, no recognition that this material is at odds with the vascular model which dominates the collective thinking here.

Ricardo as reinforced these abstracts in his comments, but, if the pattern continues, the vascular model will continue to be the dominant explanation.

This is an interesting and oft repeated human experience: once some ideas are embedded in our mind they stick with amazing tenacity! This is one of the key mechanisms behind so many of our prejudices, political positions, and religious beliefs. The fuss over global climate change is only one of the more recent examples of how our thinking habits impede adaptation.

With all that being said, I would not be surprised at all if trans fats triggered a cluster with you, Aurora.  I know I have seen studies that came to the conclusion that a high intake of Trans fat during gestation and Lactation can cause hypothalamus inflammation in offspring. (in rats) Maybe I'm stretching it a bit, but it wouldn't surprise me to see trans fat affecting an already wonky hypothalamus, leading to the actual cluster hit.

-Ricardo

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