O2 Muu
Neuroinflammation following traumatic brain injury: A positron emission tomography study

Julkaisun tekijät: Mehrbod Mohammadian, Jouni Tuisku, Jussi Hirvonen, Riitta Parkkola, Pekka Jokinen, Eero Rissanen, Olli Tenovuo
Julkaisuvuosi: 2017
Journal: Brain Injury
Volyymi: 31
Julkaisunumero: 6-7
Sivujen määrä: 1
ISSN: 0269-9052
eISSN: 1362-301X


Objective: To study microglial activation as a biomarker for neuroinflammation in patients with traumatic brain injury (TBI) compared to healthy controls, using positron emission tomography (PET).

Methods: In this study, 20 patients with TBI (age 44 ± 15) and 8 healthy controls (age 50 ± 8) underwent dynamic PET scan with translocator protein ligand [11C]-PK11195. For TBI patients the PET imaging was performed using GE Advance PET scanner (General Electric Medical Systems, Milwaukee, WI, USA) 507 days post injury on average and High-Resolution Research Tomograph (HRRT) PET scanner was used for the healthy controls. Correspondingly the brain MR imaging was performed using 3T Achieva (Philips Medical Systems, The Netherlands) for TBI patients and with Philips Gyroscan Intera 1.5 T Nova Dual scanner (Philips, Best, the Netherlands) for healthy controls. Regions of interest were extracted using Freesurfer (v5.3.0). Image analysis was then done using MATLAB (R2011a) and PMOD (version 3.4, 2013 PMOD Technologies Ltd, Zurich, Switzerland) software. From the PET images, distribution volume ratio (DVR) and binding potential (BPnd) of [11C]-PK11195 ligand were calculated for evaluation of microglial activation by using supervised clustering method to find a reference region with no specific binding. DVR was estimated using Logan’s method within time interval 20–60 minutes and BPnd was estimated with simplified reference tissue model (SRTM). Statistical analysis was performed using SPSS (versoin 23, SPSS IBM, New York, NY) and 95% confidence interval was considered as statistically significant for the results.

Results: We observed that patients with TBI had statistically significantly higher TSPO binding than controls in almost all regions of the brain studied. Patients showed higher binding potentials in the amygdala (p = 0.002), brain stem (p < 0.0001), caudate (p < 0.001), cerebellum (p < 0.0001), hippocampus (p = 0.001), left cerebral white matter (p = 0.008), lateral temporal cortex (p < 0.001), medial temporal lobe (p < 0.0001), occipital cortex (p = 0.003), pallidum (p = 0.001), posterior cingulate cortex (p = 0.021), putamen (p = 0.026), thalamus (p < 0.0001) and diencephalon (p < 0.001).

We also observed that in most patients the thalamus and brain stem had the highest binding potentials.

Conclusions: Our results indicate that patients with TBI have higher level of microglial activation compared to healthy controls in most of the brain regions studied. Thalamus and brain stem showed the highest binding potential in most subjects. This suggests that patients with TBI may have chronic neuroinflammation.

Last updated on 2019-21-08 at 22:46