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Ree
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Re: Clusters a symptom !
« Reply #25 on: Dec 29th, 2003, 12:41pm »
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remember Ester Williams well the female Gremlins have a tendancy to take after her... don't thank me... we are all genius' in our own right... my brain is just working overtime this week... I am in the process of solving the World Peace problem too.   love ree
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Re: Clusters a symptom !
« Reply #26 on: Dec 29th, 2003, 12:59pm »
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on Dec 27th, 2003, 9:39pm, Elaine wrote:
I think all but Jonny missed what I was saying.  
Could clusters be a sympton instead of a illness all by its self?

 
My personal opinion is that all diseases with pain involved, are symptoms that there's something wrong. So a clusterheadache attack signals that there is definately something going VERY seriously wrong. But that goes for a migraine as well, or a toothache. Pain is always a signal, we look at pain as useless and try to kill it off as soon as possible (me too!), but what else can your body use to signal the problem?  
 
As for my own cluster-hubby, I know he "missed" quite a LOT of signals of his own body that were definately there in the period before his cycle. But the problem with signals is, you can not always find a solution to do something about it. When you're body signals with a shadow that the balance is disturbed somewhere, you will surely be able to pick up the signal, but WHAT NEXT? What's your respons?
 
Nevertheless, it is always wise to take a close look at all the signals also the little ones and try to answer them as best as you can: stress (take vitamine B and try to cut down on stress), being tired (get your sleep!), not well sleeping (take melatonine) ...
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CJohnson
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Re: Clusters a symptom !
« Reply #27 on: Dec 29th, 2003, 4:22pm »
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 Channelopothies - Channelopathies are defined as disorders caused by pathology of ion channel function and comprise a heterogeneous group of usually hereditary disorders, which in most cases are clinically characterized by episodes of disturbed excitability of nerve or muscle cells. Such episodes are typically provoked by certain triggers.
http://www.channelopathies.org/
 
 We are almost all of us aware of the goodness of verapamil. What does it do? It blocks ion channels. Specifically calcium ion channels.
 
"Ion channels are the most basic elements of neuronal function. Proper structure, expression, localization and regulation of these channel proteins are essential for their normal activity. Abnormalities of ion channels contribute to many diseases that are now generically categorized as channelopathies. While channelopathies are broadly investigated in heart, kidney, and skeletal muscle, these disorders are seriously understudied in the central nervous system."    
   
http://www.ninds.nih.gov/news_and_events/channelopathy.htm  
   
 Here, our hero, Dr. Goadsby (among others) discusses calcium channelopathies and their possible role in trigeminovascular pain signals.
 
Br J Pharmacol. 2003 Oct;140(3):558-66. Epub 2003 Aug 26.
 
Voltage-dependent calcium channels are involved in neurogenic dural vasodilatation via a presynaptic transmitter release mechanism.
 
Akerman S, Williamson DJ, Goadsby PJ.
 
Headache Group, Institute of Neurology, Queen Square, London, UK.
 
"Amissense mutation of the CACNA1A gene that encodes the alpha1A subunit of the voltage-dependent P/Q-type calcium channel has been discovered in patients suffering from familial hemiplegic migraine. This suggested that calcium channelopathies may be involved in migraine more broadly, and established the importance of genetic mechanisms in migraine. Channelopathies share many clinical characteristics with migraine, and thus exploring calcium channel functions in the trigeminovascular system may give insights into migraine pathophysiology. It is also known that drugs blocking the P/Q- and N-type calcium channels have been successful in other animal models of trigeminovascular activation and head pain. In the present study, we used intravital microscopy to examine the effects of specific calcium channel blockers on neurogenic dural vasodilatation and calcitonin gene-related peptide (CGRP)-induced dilation. The L-type voltage-dependent calcium channel blocker calciseptine significantly attenuated (20 microg kg(-1), n=7) the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. The P/Q-type voltage-dependent calcium channel blocker omega-agatoxin-IVA (20 microg kg-1, n=7) significantly attenuated the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. The N-type voltage-dependent calcium channel blocker omega-conotoxin-GVIA (20 microg kg(-1), n=8 and 40 microg kg(-1), n=7) significantly attenuated the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. It is thought that the P/Q-, N- and L-type calcium channels all exist presynaptically on trigeminovascular neurons, and blockade of these channels prevents CGRP release, and, therefore, dural blood vessel dilation. These data suggest that the P/Q-, N- and L-type calcium channels may be involved in trigeminovascular nociception."
 
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