Chronic Traumatic Encephalopathy Stage Research Articles

The spectrum of disease in chronic traumatic encephalopathy

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.

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<h3>Objective:</h3> To investigate the relationship between years of ice hockey play and risk for CTE neuropathology at autopsy. <h3>Background:</h3> Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to repetitive head impacts (RHI) including from contact sports and military service. Previous work showed a dose-response relationship between CTE risk and severity and years of American football play. A similar dose-response relationship for ice hockey has not been investigated. <h3>Design/Methods:</h3> 74 consecutive brain donors who played ice hockey from the Veterans Affairs-Boston University-Concussion Legacy Foundation and Framingham Heart Study Brain Banks [age range: 13–91; highest level of play: 7 (9%) youth, 25 (34%) high school, 22 (30%) juniors/college, 19 (26%) professional (1 unknown); 34 (46%) played an additional contact sport, including 32 (43%) who played American football] were assessed for CTE diagnosis, stage (0–IV) and cumulative neurofibrillary tangle burden across 11 brain regions commonly affected by CTE (range: 0–33). We estimated the association of duration of ice hockey play in years with each neuropathological outcome in linear models adjusted for age at death and duration of football play. <h3>Results:</h3> 40 donors were diagnosed with CTE (54%). A dose-response relationship was observed between duration of ice hockey play and each outcome. Each additional year of play corresponded to a 23% increase in odds for having CTE (95% CI: 11%–36%; p&lt;0.01), a 15% increase in odds for increasing one CTE stage (95% CI: 8%–22%; p&lt;0.01), and a 0.03 SD increase in cumulative NFT burden (95% CI: 0.01–0.05; p&lt;0.01). When limited to those who played hockey as their primary source of exposure (n=56), results remained similar. <h3>Conclusions:</h3> This is the first study to find a dose-response relationship between years of ice hockey play and CTE risk and severity. Increasing ice hockey play may pose an increasing risk for CTE in a similar manner as American football play. <b>Disclosure:</b> Bobak Abdolmohamadi has nothing to disclose. Madeline Uretsky has nothing to disclose. Mr. Nair has nothing to disclose. Nicole Saltiel has nothing to disclose. Raymond Nicks has nothing to disclose. Daniel Daneshvar has nothing to disclose. Victor E Alvarez, 5394 has nothing to disclose. Bertrand Huber has nothing to disclose. Dr. Stein has nothing to disclose. Dr. McKee has nothing to disclose. The institution of Michael Alosco, PHD has received research support from NIH. The institution of Dr. Mez has received research support from NIH, DOD.