Original Article

You have free access to this content

Inflammation after trauma: Microglial activation and traumatic brain injury

  1. Anil F. Ramlackhansingh MRCP1,
  2. David J. Brooks MD, DSc1,
  3. Richard J. Greenwood FRCP2,
  4. Subrata K. Bose PhD3,
  5. Federico E. Turkheimer PhD1,
  6. Kirsi M. Kinnunen PhD4,
  7. Steve Gentleman PhD1,
  8. Rolf A. Heckemann PhD1,5,
  9. Karen Gunanayagam BSc1,
  10. Giorgio Gelosa MD1,
  11. David J. Sharp MRCP, PhD1,*

Article first published online: 27 JUN 2011

DOI: 10.1002/ana.22455

Issue

Annals of Neurology

Annals of Neurology

Volume 70, Issue 3, pages 374–383, September 2011

Additional Information

How to Cite

Ramlackhansingh, A. F., Brooks, D. J., Greenwood, R. J., Bose, S. K., Turkheimer, F. E., Kinnunen, K. M., Gentleman, S., Heckemann, R. A., Gunanayagam, K., Gelosa, G. and Sharp, D. J. (2011), Inflammation after trauma: Microglial activation and traumatic brain injury. Ann Neurol., 70: 374–383. doi: 10.1002/ana.22455

Author Information

  1. 1

    Centre for Neuroscience, Department of Medicine, Imperial College London, Hammersmith Hospital Campus, London, UK

  2. 2

    Institute of Neurology, University College London, London, UK

  3. 3

    MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital Campus, London, UK

  4. 4

    Goldsmiths, University of London, London, UK

  5. 5

    Neurodis Foundation, Centre for Medical Research with Positron Emission Tomography – in vivo imaging, Lyon, France

*Computational, Cognitive, and Clinical Neuroimaging Laboratory, 3rd Floor, Burlington Danes Building, Hammersmith Hospital, Du Cane Road, London, W12 0NN, United Kingdom

Publication History

  1. Issue published online: 8 SEP 2011
  2. Article first published online: 27 JUN 2011
  3. Accepted manuscript online: 18 APR 2011 08:40AM EST
  4. Manuscript Accepted: 8 APR 2011
  5. Manuscript Revised: 1 APR 2011
  6. Manuscript Received: 5 JAN 2011

SEARCH

SEARCH BY CITATION

ARTICLE TOOLS

View Full Article with Supporting Information (HTML) Get PDF (421K)

Abstract

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;

View Full Article with Supporting Information (HTML) Get PDF (421K)