Chronic Traumatic Encephalopathy and Suicide: A Systematic Review

Departments of Psychiatry and Neurology, University of Colorado School of Medicine, Denver, CO 80045, USA.
BioMed research international 11/2013; 2013(134, article 134ra60):424280. DOI: 10.1155/2013/424280
Source: PubMed


Traumatic brain injury (TBI) is a global health concern, and the recent literature reports that a single mild TBI can result in chronic traumatic encephalopathy (CTE). It has been suggested that CTE may lead to death by suicide, raising important prevention, treatment, and policy implications. Thus, we conducted a systematic review of the medical literature to answer the key question:
What is the existing evidence in support of a relationship between CTE and suicide?
Systematic searches of CTE and suicide yielded 85 unique abstracts. Seven articles were identified for full text review. Only two case series met inclusion criteria and included autopsies from 17 unique cases, 5 of whom died by suicide. Neither studies used blinding, control cases, or systematic data collection regarding TBI exposure and/or medical/neuropsychiatric history. The identified CTE literature revealed divergent opinions regarding neuropathological elements of CTE and heterogeneity regarding clinical manifestations. Overall quality of evidence regarding a relationship between CTE and suicide was rated as very low using Grading of Recommendations Assessment, Development and Evaluation Working Group (GRADE) criteria. Further studies of higher quality and methodological rigor are needed to determine the existence and nature of any relationship between CTE and suicide.

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Available from: Lisa Anne Brenner, Jul 26, 2014
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    ABSTRACT: Suicide among athletes and military personnel diagnosed with chronic traumatic encephalopathy (CTE) was an international concern (Korngold, Farrell, & Fozdar, 2013; Wortzel, Shura, & Brenner, 2013; Kristof, 2012; Meterko, et al., 2012; Omalu, et al., 2011). Omalu (2013) and Tanner (2010) observed a correlation between brain injury and perceived social alienation resulting in injuries. It is suggested that, due to the unique social bonds created within each group, athletes and military personnel formed individual identities based on the dynamics of the group. Current psychotherapeutic approaches had limited effectiveness dealing with suicidal tendencies. Utilizing Seeman's (1959, 1967, 1971, 1975, and 1983) five alienation factors as redefined under a Christian Neo-Thomistic Personalist approach (Schmidt, 2011, 2012) could provide insight into why CTE-related suicide occurred and thereby initiate discussion regarding adjustments to social and cultural aspects of faith in treatment programs.
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    ABSTRACT: Accumulation of phosphorylated tau (p-tau) is accepted by many as a long-term consequence of repetitive mild neurotrauma based largely on brain findings in boxers (dementia pugilistica) and, more recently, former professional athletes, military service members, and others exposed to repetitive head trauma. The pathogenic construct is also largely accepted and suggests that repetitive head trauma (typically concussions or subconcussive forces) acts on brain parenchyma to produce a deleterious neuroinflammatory cascade, encompassing p-tau templating, transsynaptic neurotoxicity, progressive neurodegenerative disease, and associated clinical features. Some caution before accepting these concepts and assumptions is warranted, however. The association between the history of concussion and findings of p-tau at autopsy is unclear. Concussions and subconcussive head trauma exposure are poorly defined in available cases, and the clinical features reported in chronic traumatic encephalopathy are not at present distinguishable from other disorders. Because control groups are limited, the idea that p-tau drives the disease process via protein templating or some other mechanism is preliminary. Much additional research in chronic traumatic encephalopathy is needed to determine if it has unique neuropathology and clinical features, the extent to which the neuropathologic alterations cause the clinical features, and whether it can be identified accurately in a living person.
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