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: 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.
    04/2015; 74(6). DOI:10.1097/NEN.0000000000000193
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    ABSTRACT: Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder attributed to repetitive mild traumatic brain injury. The diagnosis in a living individual can be challenging and can be made definitively only at autopsy. The symptoms are often nonspecific and overlap with neurodegenerative disorders such as Alzheimer's disease (AD) and frontotemporal dementia (FTD). Higher exposure to repetitive head trauma increases the risk of CTE. Genetic risk factors such as presence of an apolipoprotein E ε4 allele may be important. Individuals have varying degrees of cognitive, behavioral, and motor decline. Limitations in the manner in which data have been obtained over the years have led to different clinical descriptions of CTE. At present, there are no biomarkers to assist in the diagnosis. Standard neuroimaging may show nonspecific atrophic changes; however, newer imaging modalities such as positron emission tomography (PET) and diffusion tensor imaging (DTI) show promise. Neuropsychological testing may be helpful in determining the pattern of cognitive or behavioral decline.
    Current Neurology and Neuroscience Reports 05/2015; 15(5):541. DOI:10.1007/s11910-015-0541-5 · 3.06 Impact Factor
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    ABSTRACT: Chronic traumatic encephalopathy (CTE) was initially termed dementia pugilistica, and described among approximately 15 % of professional boxers. In the context of recent high-profile athlete suicides, a surge of scientific literature regarding CTE has focused on football players, other contact sportspersons, and combat Veterans. The aim of this review is to analyze the current literature on CTE, to juxtapose CTE literature with the more abundant research on mild traumatic brain injury (mTBI), and to offer recommendations for clinicians working with at-risk patients. Recent CTE research is presented, and mTBI-related epidemiology, neuroimaging, and prognosis research is considered. Differing CTE definitions and methodological limitations of CTE research preclude definitive suppositions about CTE. Additional research will be needed before CTE can be reliably diagnosed in clinical settings. In the meantime, clinical formulations surrounding diagnosis and prognosis might best be informed by the better-developed medical literature on mTBI.
    06/2015; 3(2). DOI:10.1007/s40141-015-0089-y
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