NEUROINFLAMMATION AS A BIOMARKER FOR TBI

I’m not a doctor at all and in my whole life I’ve always and only gone to see a doctor if something was bothering me with the precise expectation to have the doctor fully and finally take care of my reason to be seeing him.

What I write and post here is simply my understanding of what I learn in my never-ending internet research on TBI and possible solutions, excluding its prevention (obviously).

Traumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuro-protective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglial response despite these inflammatory cells’ detrimental effects on the brain. A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Inflammatory mechanisms that accompany TBI in an effort to increase the understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.

This concept of neuron-inflammation is what drove the successful use of Etanercept, or Enbrel to reduce such inflammation, when injected in the spine so it can pass the brain barriers and give the anti-inflammatory effect to the neurons that work under the stress of being overloaded by the absence of the ones that are dead.

A prescription developed only for the treatment of rheumatoid arthritis has been casually found to decrease the inflammation of neurons following a TBI giving back to the brain its plasticity, that’s always working as long as we live.

The doctor who very casually discovered such property of this medicament named Etanercept by the German Pfizer has patented with the US registration office its use for TBI and Alzheimer conditions, and is being referred by medical publications as “A new ground-breaking study that provides clinical evidence, for the first time, that chronic neurological dysfunction from stroke or traumatic brain injury can rapidly improve following a single dose of this drug that targets brain inflammation, even years after the stroke or traumatic event.”

Since – as I’ve been saying for years – the guess-science of medicine doesn’t ever give any certainty on anything for anyone, I’ve been fighting against those who are supposed to love me and say they want the best for me, to be given the freedom to give to this new and still unproven (they say) therapy at least one chance to improve my disabilities.

I guess that I can say that only God knows how this battle will end, but the loss once again of Michele’s support makes the hole in my heart even bigger, deeper and more painful.

1. http://www.cnn.com/2011/HEALTH/05/05/brain.plasticity.giffords/
2. http://www.huffingtonpost.com/edward-taub-phd/the-plasticity-of-the-bra_b_6031376.html
3. http://journal.frontiersin.org/researchtopic/2781/mechanisms-of-neuroinflammation-and-inflammatory-neurodegeneration-in-acute-brain-injury
4. https://www.ncbi.nlm.nih.gov/books/NBK326735/
5. http://jonlieffmd.com/blog/update-on-traumatic-brain-injury-and-inflammation
6. https://en.wikipedia.org/wiki/Neuroinflammation