After an extensive review of the literature and personal experience in war and sports injuries, Russell Blaylock and Joe Maroon have developed a hypothesis for the development of Chronic Traumatic Encephalopathy extending from concussion to the damage seen after multiple injuries to the brain. This replica watches concept is based on a primed inflammatory response in the CNS that continues longer with repeated injury leading to neuronal death. It can explain not only the Chronic Traumatic Encephalopathy of fighters (“dementia pugilistica”) and football players, but can be extended to the development of Parkinson’s syndrome, Alzheimer’s disease, and even depression. The paper is written primarily for basic scientists, so it is not an easy read, becoming more molecular the further you read. The name Russell has given to the pathogenesis of the events is Immunoexcitotoxicity, with the involvement of the microglia, the repeated and chronic release of toxic messenger substances, the excessive amounts of glutamate, the major transmitter in the CNS, all of which lead to the toxic death and destruction of neurons. (Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis) So that most readers can understand the hypothesis, I had both authors summarize the basic concepts in the paper with two short summaries that appear after the abstract. The authors will have other papers in the future on this concept. SNI already published a summary of a paper supporting their hypothesis (From Bench to Bedside) and others have been recently presented. (JAMA August 2, 2011-Traumatic Brain Injury…Medical News). This concept will change the understanding of many CNS diseases.
