• Douglas H Smith, Victoria E Johnson, and William Stewart.
• Penn Center for Brain Injury and Repair and Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania, 105 Hayden Hall, 3320 Smith Walk, Philadelphia, PA 19104, USA.
• Nat Rev Neurol. 2013 Apr 1; 9 (4): 211-21.

AbstractTraumatic 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-β, 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.

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