Posted by Miguel (188.8.131.52) on February 06, 2000 at 16:06:13:
In Reply to: Cause of Clusters? - please read! posted by Carl D on February 06, 2000 at 14:51:29:
Carl, that post was extremely well written, as well as bing quite insigful and thought provoking(sp?). It is something to consider since I do suffer from insomnia, which becomes more agravated after episodes of CH. I guess I am pretty much on my way to becoming chronic?! UGH!!! i.e.: my last episode has been in remission for the last 8 to nine days (tough to get a handle on time without much sleep). I think that I have been able to get about 8 hours of sleep all together, with a couple of hours here and there, over the last 4 days. Last night...well...another all-nighter in NC. However, the positive side of it - I am getting to be a self taught Visual Basic guru of sorts (BTW, NEVER even consider byuing "Sams Teach Yourself Visual Basic 6 in 24 Hours"...it ain't worth a sh*t!).
Anyway, my point is: How about if it was totally the other way around. What I mean by this is not vasodilation but vasoconstriction, perhaps nearing the point of localized smal arterioles and capillary collapse. This perhaps triggered by some cascading-mediated-path, influenced by localized receptor malfunction either at the cerebral, nerve, ganglial, or vasculal level. For instance, consider what happens when...lets say your leg, arm or any part of your body "goes to sleep", as is idiomatically named. It is right down painful. However, the pain is distributed over a rather large area, thus less focused and severe pain is expressed locally, while that tingling sensation, along the "needling" feeling of the affected area quickly alert you to change posture. If that is the case in a very small section of the brain, changing posture of one's right hemisphere is perhaps impossible, as compared to moving a leg and hoping up and down to get circulation back in there. The mechanism of such "gone to sleep" phenomena is well understood. It seems that circulation to a certain area may be diminished by posture, as with a leg or butt, or arm, etc. This in turn deprives the nerve running along the vessel from much needed O2. Susequently triggering the physical responses that we feel when that conditon happens. We get up, move the affected area, get flow back....(get O2 back to the affected area - The Key)...and the problems is resolved in a few seconds. Mind you, such condition is posturaly created (or inflicted, if you will). The condition in the brain may not be caused by exactly the same reasons, but it may hold some parallelisms with that of other areas of the body when affected in a similar way. Lets say the Hypo, or heart are the ones creating that "magic" agent. That would give reason to not finding a solution as simple as violently shaking one's head to move the brain around, and get O2 back into the afflicted area. It is not like we can say - OK Hypo, or Heart stop producing that #@$%@# agent. The causing organ listens and stops and one is back to normal within a few secs. We may likely have some receptor dynamics involved with whatever substance is aflicting that specific area, be it vascularly-, or CNS-born, thus it takes time to recover from each attack. It would then be reasonable to think that if we have dinished blood flow to one small sector of our brain, for whatever unknow biological reason such regional specificity might be, it would make sense that the therapeutic use of O2 would aleviate the problem quite well. That is because if we have a localized blod flow restricition, perhaps enriching the blood with O2 allows for higher tissue supply of that O2 even when faced with diminished blood flow because of the higher plasma O2 saturation reached through the therapeutical use of O2. It would be interesting to perform a localized blood flow and PO2 analysis in healthy v. CH-afflicted individuals right in the middle of a sever CH attack. This perhaps somewhat impossible because of the nature of the region where the samples need to be extrated from. Perhaps with improvement of fiber-optic-derived PO2 measuring devices, i.e.: as in a Blood-Gas probe small enough to be able to fit in a very small brain arteriole or capillary, coupled with a blood-flow probe of the same size, while both having the unbelibable hability to allow for its user to manouver it to specific, secluded and obscure regions of the brain vascualture, we might be able to start gaining some practical knowledge to dispell so many theories (as mine, for instance, ROFL). Also, micro-sampling of localized vasculature for further agent/substance analysis would be extremely helpfull once the probe gets in there...just wishful thinking at this point, but who knows. I feel sometimes that the progress of science is so amazing, while other times I feel like I am watching an elephant being asked to get up from its behind by way of poking it with a fountain pen.
Thank you again for the post.
May the Beast die a death conmesurate with the life it has given us...
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