“Sharing symptoms with PTSD, patients who died with CTE have been described to present with poor concentration and memory, irritability, depression, and suicidality.” THERE, I SAID IT – CTE!
Chronic Traumatic Encephalopathy – It seems that it was/is much easier to identify these injuries in football and hockey players, and boxers and MMA fighters…..Why? There are more than 250,000 cases of Mild TBI in the military from OEF and OIF, and many of these are multiple and repetitive injuries. Maybe we should take a closer look, and just like the NFL, NHL, and other professional contact sports.
Believe me, the VA and the military does not like this term, nor do they want to address it!
Yet, I believe the brain heals. It continues to repair itself after injury unless other factors become involved. One of those factors is repeated or aggravated injury, and which then may lead to other problems. If you have repetitive or multiple Mild TBIs, (concussions with loss of consciousness), and which is many guys within the Special Operations community then you should understand the risks. May also explain if things seem to be getting worse and not better….This is from the 2013 Report to Congress on Traumatic Brain Injury (Link Below)
Risk of Neurodegenerative Disease Following TBI
Epidemiologic evidence indicates that synergy exists between TBI and permanent neurodegeneration. Longitudinal MRI-based studies have demonstrated brain atrophy occurring in the months to years after TBI (Ross, 2011). Contradictory findings regarding the relationship between TBI and Alzheimer’s disease exist (Van Den Heuvel et al. 2007). Evidence suggests that risk for dementia is increased two to four fold after moderate or severe TBI, but risk following mild TBI is unclear (Shively, Scher, Perl, and Diaz-Arrastia, 2012).
Additionally, evidence indicates that repetitive TBI can cause a unique neurodegenerative disorder first reported in boxers and called dementia pugilistica (Martland, 1928). Now termed chronic traumatic encephalopathy (CTE), this disorder is characterized by the aggregation of the microtubule-associated protein called tau in nerve cells. This is the same protein that aggregates inside dying neurons in Alzheimer’s disease and in the brains of persons with a tau gene variant that causes fronto-temporal dementia. Some studies demonstrate that tau aggregation, once started, has the ability to spread from one nerve cell to another; this could explain how an initial focal injury could lead to widespread damage over time (de Calignon et al. 2012). The genetic variant apolipoprotein E4, a known risk factor for Alzheimer’s disease, has been associated with poorer outcomes after head injury (Nathoo et al., 2003) and in some studies with increased risk for the later development of Alzheimer’s disease (Graham et al., 2002; Luukinen et al., 2005; Rabadi and Jordan, 2001; Jordan et al., 1997). However, this association has not been found in all studies (Jellinger, 2004). More recently, CTE has been described in athletes who participated in contact sports and in 21 veterans (86% of whom were also athletes) (Goldstein et al.2012; McKee et al., 2009). Sharing symptoms with PTSD, patients who died with CTE have been described to present with poor concentration and memory, irritability, depression, and suicidality. The extent of the burden of CTE in service members exposed to TBI is unknown.
Again, It seems that it was/is much easier to identify these injuries in football and hockey players, and boxers and MMA fighters…..Why?