Chronic neuropathologies of single and repetitive TBI: substrates of dementia?

被引:513
作者
Smith, Douglas H. [1 ,2 ]
Johnson, Victoria E. [1 ,2 ]
Stewart, William [3 ]
机构
[1] Univ Penn, Perelman Sch Med, Penn Ctr Brain Injury & Repair, Philadelphia, PA 19104 USA
[2] Univ Penn, Perelman Sch Med, Dept Neurosurg, Philadelphia, PA 19104 USA
[3] So Gen Hosp, Dept Neuropathol, Glasgow G51 4TF, Lanark, Scotland
关键词
TRAUMATIC BRAIN-INJURY; DIFFUSE AXONAL INJURY; FRONTOTEMPORAL LOBAR DEGENERATION; AMYLOID PROTEIN DEPOSITION; CAVUM SEPTI PELLUCIDI; SEVERE HEAD-INJURY; ALZHEIMERS-DISEASE; NEUROFIBRILLARY TANGLES; RISK-FACTOR; MICROGLIAL ACTIVATION;
D O I
10.1038/nrneurol.2013.29
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Traumatic brain injury (TBI) has long been recognized to be a risk factor for dementia. This association has, however, only recently gained widespread attention through the increased awareness of 'chronic traumatic encephalopathy' (CTE) in athletes exposed to repetitive head injury. Originally termed 'dementia pugilistica' and linked to a career in boxing, descriptions of the neuropathological features of CTE include brain atrophy, cavum septum pellucidum, and amyloid-beta, tau and TDP-43 pathologies, many of which might contribute to clinical syndromes of cognitive impairment. Similar chronic pathologies are also commonly found years after just a single moderate to severe TBI. However, little consensus currently exists on specific features of these post-TBI syndromes that might permit their confident clinical and/or pathological diagnosis. Moreover, the mechanisms contributing to neurodegeneration following TBI largely remain unknown. Here, we review the current literature and controversies in the study of chronic neuropathological changes after TBI. Smith, D. H. et al. Nat. Rev. Neurol. 9, 211-221 (2013); published online 5 March 2013; doi:10.1038/nrneurol.2013.29
引用
收藏
页码:211 / 221
页数:11
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