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Old 07-12-2016, 12:01 PM #1
Hains Hains is offline
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Join Date: Jul 2016
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Hains Hains is offline
Junior Member
 
Join Date: Jul 2016
Posts: 58
5 yr Member
Default Calcium deposits, SPECT scans, and hyperbaric chamber oxygen therapy

Hey folks,

I'm looking for some input to supplement my self-guided research.

I've come across some information related to increased calcium concentrations to toxic levels in brain cells following concussions (Weber, 2012). Areas of the brain where this occurs can become inflammed and can experience reduced blood flow. These 'dead zones' are what manifest into disfunctions observed throughout the body and could explain why concussion/PCS victims experience a variety of different symptoms, it all depends on the brain structure that been affected by the injury (eg. the brain stem and balance disorders). My research suggests that SPECT scans can reveal areas of the brain that experience decreased blood flow and neuron activity. Inferences could be made from the results of a SPECT scan to identify the exact area(s) of the brain that are affected. If "dead zones" are identified in the SPECT scan, the recovery objective would be to direct blood flow and oxygen to that area to re-activate it, and re-establish neuron activity in the brain structure that has been affected. One suggestion that doesn't isolate individual brain structures, but rather addresses the entire brain in mild hyperbaric chamber oxygen therapy (hbot.com/hbot-spect-imaging). The idea here is to go into a controlled atmosphere of greater pressure to which decreases the size of oxygen molecules in the blood, allowing them to penetrate into the "dead zones". Then, breathing 100% oxygen saturates the blood with a large volume of smaller than normal oxygen molecules. Two resulting mechanism that I can think of are 1) increased oxygen to the brain, and 2) calcium oxidation of brain cells, or removal of calcium from brain cells. Now, there's still a lot of questions to be asked about this, such as 1) will oxygen still penetrate the "dead zones" with this treatment? Because the requirement is increased blood flow to deliver the oxygen to the "dead zones". 2) Is it possible to oxidize too much calcium of the the brain cells? How do you quantify this? 3) How do you replace the potassium that has been expelled from brain cells as a result of the initial calcium intake following the injury.

Feedback and theories are welcomed, however scientifically backed explanations are preferred.

Thanks,

Hains
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