Incipient chronic traumatic encephalopathy in active American football players: neuropsychological assessment and brain perfusion measures

BACKGROUND AND AIMS: Chronic traumatic encephalopathy (CTE) is a degenerative disease caused by repetitive traumatic brain injury (TBI). Because CTE can be definitely diagnosed only post-mortem, it would be important to explore clinical and radiological correlates of CTE and TBI. The aims of this study were to assess (1) the relationship between the neuropsychological profile of active American football players and the traumatic load; (2) whether traumatic brain injury associated with American football activity has a specific cerebral perfusion pattern; and (3) whether this perfusion pattern correlates with neuropsychological performances. METHODS: In 20 American football players [median age [25th–75th percentile] 25.0 [21.6–31.2] years, all males], we evaluated history, traumatic load and symptoms using the TraQ (Trauma Questionnaire), and cognitive performances on neuropsychological tests. Brain perfusion was estimated using arterial spin labeling MRI and compared to a group of 19 male age-matched (28.0 [24.8–32.3] years) healthy subjects. RESULTS: We found different cognitive performances between American football players stratified according to field position and career length. Linemen had poorer executive, verbal, and visual performances; a career > 7 years was associated with poorer verbal fluency performances. American football players had statistically significant reduced cerebral blood flow values in sensory-motor areas in comparison with healthy controls. Poorer neuropsychological performances correlated with lower perfusion in specific brain areas. CONCLUSIONS: Our study seems to confirm that CTE in American football players is influenced by the field position and the career length, and correlates with lower cognitive performances linked to lower perfusion in specific brain areas. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10072-022-06212-7.