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Inflammation after trauma: Microglial activation and traumatic brain injury
Author(s) -
Ramlackhansingh Anil F.,
Brooks David J.,
Greenwood Richard J.,
Bose Subrata K.,
Turkheimer Federico E.,
Kinnunen Kirsi M.,
Gentleman Steve,
Heckemann Rolf A.,
Gunanayagam Karen,
Gelosa Giorgio,
Sharp David J.
Publication year - 2011
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.22455
Subject(s) - traumatic brain injury , medicine , microglia , neuroscience , magnetic resonance imaging , chronic traumatic encephalopathy , neuroinflammation , putamen , inflammation , diffusion mri , functional magnetic resonance imaging , brain damage , neuropsychology , pathology , concussion , psychology , cognition , poison control , radiology , psychiatry , injury prevention , environmental health
Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function. Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered. Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage. Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed. ANN NEUROL 2011;