Christian LoBue1,2, Jeff Schaffert1, C Munro Cullum1,2,3. 1. Department of Psychiatry. 2. Department of Neurological Surgery. 3. Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Abstract
PURPOSE OF REVIEW: Chronic traumatic encephalopathy (CTE) is hypothesized to be a progressive neurodegenerative disease leading to dementia after repetitive head impacts. This review summarizes the recent evidence on CTE to highlight the facts currently known and the areas that remain poorly understood. RECENT FINDINGS: Increasing evidence suggests that many of the prior assertions about CTE in relation to repetitive head trauma are premature. First, CTE lesions have been observed in individuals with no history of head trauma/impacts. In addition, attempts to characterize possible clinical markers of CTE have had several shortcomings, notably an absence of detailed clinical assessments during life, vague/nonspecific symptom reports, and crude methodology. Moreover, recent studies demonstrate that current CTE pathological criteria have limitations and are in need of refinement/validation. SUMMARY: CTE is still in the early stages of research as a neuropathological condition and no specific clinical criteria exist. Claims about CTE being a progressive disease entity and caused exclusively by head trauma/impacts are not well supported at present. Such assertions may have impeded our understanding of the frequency and significance of this disorder. Refining diagnostic criteria to reduce ambiguity in classifying cases will be essential before risk factors and/or possible clinical markers may be identified.
PURPOSE OF REVIEW: Chronic traumatic encephalopathy (CTE) is hypothesized to be a progressive neurodegenerative disease leading to dementia after repetitive head impacts. This review summarizes the recent evidence on CTE to highlight the facts currently known and the areas that remain poorly understood. RECENT FINDINGS: Increasing evidence suggests that many of the prior assertions about CTE in relation to repetitive head trauma are premature. First, CTE lesions have been observed in individuals with no history of head trauma/impacts. In addition, attempts to characterize possible clinical markers of CTE have had several shortcomings, notably an absence of detailed clinical assessments during life, vague/nonspecific symptom reports, and crude methodology. Moreover, recent studies demonstrate that current CTE pathological criteria have limitations and are in need of refinement/validation. SUMMARY:CTE is still in the early stages of research as a neuropathological condition and no specific clinical criteria exist. Claims about CTE being a progressive disease entity and caused exclusively by head trauma/impacts are not well supported at present. Such assertions may have impeded our understanding of the frequency and significance of this disorder. Refining diagnostic criteria to reduce ambiguity in classifying cases will be essential before risk factors and/or possible clinical markers may be identified.