RobinN
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I just received Dr Blaylock's latest newsletter. This article was in it, and I thought it might be of interest to those of you that have suffered brain injuries.
New Thinking for Brain Injuries
As a neurosurgery resident, one of my main interests was head injuries, particularly looking for the mechanism for what was termed delayed injury, which accounts for a large part of the effects of traumatic brain injury.
We know that after someone’s head is injured a gradual deterioration occurs in the brain in specific areas that can continued for days, weeks, or even years after the injury.
In my book, “Excitotoxins: The Taste That Kills, (www.blaylockwellnesscenter.com) I proposed that this delayed damage was due to a buildup of the excitotoxin glutamate within the brain.
Since then, a considerable amount of data has accumulated supporting my hypothesis. Attention to this delayed process increased tremendously
when it was realized that sports-related head injuries, especially in professional football players, could result in a similar process that can persist for decades after a series of minor concussions and can end up causing a special form of dementia called chronic traumatic encephalopathy or CTE.
Pathologically, the brains of these football players closely resembles what is seen in Alzheimer’ s disease. This has baffled neuroscientists and neurosurgeons and thus far they have no clue as to why this is so.
I have been working with a friend of mine, Dr. Joseph Maroon, to solve this puzzle. He is chief of neurosurgery at the University of Pittsburgh, and he is the team neurosurgeon for the Pittsburgh Steelers. I discussed my new hypothesis with Dr. Maroon and he was quite excited about the hypothesis and feels it is the answer.
When the brain is injured repeatedly, as seen with football players, the brain’s microglia are activated (called priming). These are the cells that control brain inflammation — they also contain large amounts of glutamate.
With the first concussion, these cells are primed for action for very long periods, even years. The second concussion and subsequent concussions cause a hyper-reaction of the microglia, causing them to secret large amounts of several excitotoxins — glutamate, aspartate, and quinolinic acid as well as powerful inflammatory cytokines and chemokines (inflammatory chemicals).
What I have shown is that these excitotoxins can produce the exact pathological findings as seen with CTE. I have named this process immunoexcitotoxicity. We plan to publish our results in a medical journal in the near future.
We are also planning to conduct a series of in- depth studies on the process as well.
There are a number of natural products that hold the promise of stopping the delayed effects of CTE, thus protecting the athlete from this devastating disorder. More on this to come.