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The neuroinflammatory response in humans after traumatic brain injury
Author(s) -
Smith C.,
Gentleman S. M.,
Leclercq P. D.,
Murray L. S.,
Griffin W. S. T.,
Graham D. I.,
Nicoll J. A. R.
Publication year - 2013
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12008
Subject(s) - traumatic brain injury , diffuse axonal injury , neuroinflammation , medicine , chronic traumatic encephalopathy , head injury , microglia , closed head injury , traumatic injury , white matter , pathology , poison control , disease , surgery , magnetic resonance imaging , inflammation , injury prevention , concussion , psychiatry , radiology , environmental health
Aims Traumatic brain injury is a significant cause of morbidity and mortality worldwide. An epidemiological association between head injury and long‐term cognitive decline has been described for many years and recent clinical studies have highlighted functional impairment within 12 months of a mild head injury. In addition chronic traumatic encephalopathy is a recently described condition in cases of repetitive head injury. There are shared mechanisms between traumatic brain injury and A lzheimer's disease, and it has been hypothesized that neuroinflammation, in the form of microglial activation, may be a mechanism underlying chronic neurodegenerative processes after traumatic brain injury. Methods This study assessed the microglial reaction after head injury in a range of ages and survival periods, from <24‐h survival through to 47‐year survival. Immunohistochemistry for reactive microglia ( CD 68 and CR 3/43) was performed on human autopsy brain tissue and assessed ‘blind’ by quantitative image analysis. Head injury cases were compared with age matched controls, and within the traumatic brain injury group cases with diffuse traumatic axonal injury were compared with cases without diffuse traumatic axonal injury. Results A major finding was a neuroinflammatory response that develops within the first week and persists for several months after traumatic brain injury, but has returned to control levels after several years. In cases with diffuse traumatic axonal injury the microglial reaction is particularly pronounced in the white matter. Conclusions These results demonstrate that prolonged microglial activation is a feature of traumatic brain injury, but that the neuroinflammatory response returns to control levels after several years.