title: Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury.
abstract: Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed dementia pugilistica, and more recently, chronic traumatic encephalopathy (CTE). We review 48 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 profession althletes, 1 football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum. Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular, and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. Chronic traumatic encephalopathy is a neuropathologically distinct slowly progressive tauopathy with a clear environmental etiology.
authors.affiliation: Department of Neurology, Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA. amckee@bu.edu
authors.forename: Ann C
authors.initials: AC
authors.lastname: McKee
authors.forename: Robert C
authors.initials: RC
authors.lastname: Cantu
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Nowinski
authors.forename: E Tessa
authors.initials: ET
authors.lastname: Hedley-Whyte
authors.forename: Brandon E
authors.initials: BE
authors.lastname: Gavett
authors.forename: Andrew E
authors.initials: AE
authors.lastname: Budson
authors.forename: Veronica E
authors.initials: VE
authors.lastname: Santini
authors.forename: Hyo-Soon
authors.initials: HS
authors.lastname: Lee
authors.forename: Caroline A
authors.initials: CA
authors.lastname: Kubilus
authors.forename: Robert A
authors.initials: RA
authors.lastname: Stern
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016229:Amyloid beta-Peptides / Q000032:analysis; D053327:Apolipoprotein E4 / Q000235:genetics; D001265:Athletic Injuries / Q000150:complications*; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry; D020208:Brain Injury, Chronic / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology; D016923:Cell Death; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease; D016489:Head Injuries, Closed / Q000150:complications*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000473:pathology / Q000502:physiology; D013177:Sports; D024801:Tauopathies / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology
chemical_list: D016229:Amyloid beta-Peptides; D053327:Apolipoprotein E4