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pathophysiology of CH's? (Read 1437 times)
kika
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pathophysiology of CH's?
Jun 29th, 2008 at 1:23am
 
i am trying my hardest, not easy having been on topamax recently, to understand the mechanisms involved in CH's.
so many of you seem to get teh medical side of this. please point out what's right/wrong with my thinking...
for episodic sufferers,
CH's are caused by sudden cerebral vasodilation, triggered from within the hypothalamus by some sort of circadian rhythm change. this stimulus causes something to happen to the trigeminal nerve, which results in the pain being located where it typically is.
what role, if any, is serotonin thought to play in this whole process?

thanks in advance for clarification/information.
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MJ
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Re: pathophysiology of CH's?
Reply #1 - Jun 29th, 2008 at 3:05am
 
One large school of thought says that we are subject to a serotonin storm of sorts causing or preceding an attack.

I really dont understand it hardly at all but heres my take anyways.

The hypothalmus is thought to regulate serotonin as well as the many other neurologically important chemicals in our bodies and mind.
The hypothalmus is also thought to regulate our body clocks or circadian rythms.

At times with surprising rythmicity the clock gets skewered and an attempt is made to cause a correction. A larger release of serotonin is played out and boom ouch. It may be an unseen glitch in the program of our makers

This in turn causes the sudden vasodilation talked about.

There are I think 14 different types (unknown how many of each) of serotonin receptors involved. Called 5HT receptors.

Imitrex acts in a few of these 5HT receptors but not all to block the uptake of serotonin wich throws us CHers into pain. It was developed for this reason as a stab in the dark. Eventually I think trex will be thought of as we think of trepanning now.

Cluster buster meds act in many more ways to possibly better regulate the flow of serotonin or block many more receptors. Or even possibly reset the hypothalumic clock.

Many of these meds deviate only slightly in their molecular structure from serotonin but just enough to either neutralyze, change or block the reuptake of serotonin. This is possibly the reason why so many have had success eliminating CH with some certain medications like CBs

Meds like verapamil et al. treat a few of the resulting vascular issues but not the cause.

My belief is that serotonin overproduction is the causative issue with CH and and therefore should be the issue of primary treatment.

Just my thoughts with room for error.
There are many here with a much greater understanding.
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« Last Edit: Jun 29th, 2008 at 3:13am by MJ »  

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MJ
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Re: pathophysiology of CH's?
Reply #2 - Jun 29th, 2008 at 3:11am
 
Didnt mean that post to be a clusterbuster add but the two serotonin and CBs go hand in hand in helping my understanding.
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kika
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Re: pathophysiology of CH's?
Reply #3 - Jun 29th, 2008 at 8:17am
 
hi MJ

thanks for your perspective. this term, " serotonin storm" is a new one to me, is it a CH term?
i have heard of " thyroid storm" and wonder if it is a similar phenomenon.
my interest in the serotonin role come from my understanding that i am serotonin DEFICIENT, hence being on an SSRI. to think that i may have too much of the stuff, or, anually not be able to re uptake it properly, strikes me as odd. i know it's just a theory, but seems to me like this particluar neurotransmitter is implicated in more and more things/problems everyday.
again, pardon my ignorance, but don't LSD and mushrooms promote serotonin production or release? if this is the case, wouldn't they make teh symptoms worse?

also, on another note, has there been discussion of a potential pyscholigical basis for the onset of CH's. i know it's a stretch and cannot fathom that this degree of suffering could possibly be caused by an emotionally upsetting event. the timing of mine are strange, which is why i ask.
thanks for the insight.
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Bob Johnson
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Re: pathophysiology of CH's?
Reply #4 - Jun 29th, 2008 at 8:45am
 
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]
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Bob Johnson
 
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