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Traumatic Brain Injury (TBI), Dave Duerson suicide

Posted: Mon Feb 21, 2011 8:50 pm
by brian
Feb 22, 2011: In a sad continuation of our threads on Today news came out that former Chicago Bears safety Dave Duerson killed himself last week and asked that his brain be studied. If researchers find evidence of a chronic condition, it'll be up to the NFL to take immediate action on head injuries.
See the full article Dave Duerson's suicide could be a turning point for NFL

Re: Traumatic Brain Injury (TBI), Dave Duerson suicide

Posted: Fri Jun 08, 2012 1:06 pm
by MSI
June 8, 2012: NY Times Head Injury Lawsuits Against N.F.L. Consolidated
Scores of lawsuits involving thousands of former players touched by concussions and brain injuries have been consolidated into one master complaint, setting up a huge case for the N.F.L. Lawyers for the players filed the complaint in Philadelphia, accusing the N.F.L. of hiding information that linked football-related head trauma to permanent brain injuries. Among the illnesses cited were dementia and Alzheimer’s disease.

Re: Traumatic Brain Injury (TBI), Dave Duerson suicide

Posted: Mon Dec 03, 2012 4:33 pm
by MSI
Dec 3, 2012: Over the weekend another professional football player committed suicide: Another study of Traumatic Brain Injury was also released and reported in the NYTimes:
  • From the article:
    • The growing evidence of a link between head trauma and long-term, degenerative brain disease was amplified in an extensive study of athletes, military veterans and others who absorbed repeated hits to the head, according to new findings published in the scientific journal Brain: The spectrum of disease in chronic traumatic encephalopathy
    From the report Summary:
    • Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behaviour. Eighteen age- and gender-matched individuals without a history of repetitive mild traumatic brain injury served as control subjects. In chronic traumatic encephalopathy, the spectrum of hyperphosphorylated tau pathology ranged in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions, including the medial temporal lobe, thereby allowing a progressive staging of pathology from stages I–IV. Multifocal axonal varicosities and axonal loss were found in deep cortex and subcortical white matter at all stages of chronic traumatic encephalopathy. TAR DNA-binding protein 43 immunoreactive inclusions and neurites were also found in 85% of cases, ranging from focal pathology in stages I–III to widespread inclusions and neurites in stage IV. Symptoms in stage I chronic traumatic encephalopathy included headache and loss of attention and concentration. Additional symptoms in stage II included depression, explosivity and short-term memory loss. In stage III, executive dysfunction and cognitive impairment were found, and in stage IV, dementia, word-finding difficulty and aggression were characteristic. Data on athletic exposure were available for 34 American football players; the stage of chronic traumatic encephalopathy correlated with increased duration of football play, survival after football and age at death. Chronic traumatic encephalopathy was the sole diagnosis in 43 cases (63%); eight were also diagnosed with motor neuron disease (12%), seven with Alzheimer’s disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lobar degeneration (6%). There is an ordered and predictable progression of hyperphosphorylated tau abnormalities through the nervous system in chronic traumatic encephalopathy that occurs in conjunction with widespread axonal disruption and loss. The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein.
See the NY Times article on the study: Study Bolsters Link Between Routine Hits and Brain Disease
And the study The spectrum of disease in chronic traumatic encephalopathy