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Molecular imaging of neuroinflammation in patients after mild traumatic brain injury: a longitudinal 123 I‐CLINDE single photon emission computed tomography study
Author(s) -
Ebert S. E.,
Jensen P.,
Ozenne B.,
Armand S.,
Svarer C.,
Stenbaek D. S.,
Moeller K.,
Dyssegaard A.,
Thomsen G.,
Steinmetz J.,
Forchhammer B. H.,
Knudsen G. M.,
Pinborg L. H.
Publication year - 2019
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.13971
Subject(s) - translocator protein , neuroinflammation , medicine , traumatic brain injury , rivermead post concussion symptoms questionnaire , single photon emission computed tomography , microglia , pathogenesis , magnetic resonance imaging , nuclear medicine , pathology , radiology , inflammation , psychiatry
Background and purpose Neuroinflammation has been proposed as part of the pathogenesis of post‐concussion symptoms (PCS), but the inflammatory response of the human brain to mild traumatic brain injury (mTBI) remains unknown. We hypothesized that a neuroinflammatory response is present in mTBI at 1–2 weeks post‐injury and persists in patients with PCS. Methods We scanned 14 patients with mTBI without signs of structural damage at 1–2 weeks and 3–4 months post‐injury and 22 healthy controls once using the single photon emission computed tomography tracer 123 I‐CLINDE, which visualizes translocator protein (TSPO), a protein upregulated in active immune cells. PCS was defined as three or more persisting symptoms from the Rivermead Post Concussion Symptoms Questionnaire at 3 months post‐injury. Results Across brain regions, patients had significantly higher 123 I‐CLINDE binding to TSPO than healthy controls, both at 1–2 weeks after the injury in all patients ( P = 0.011) and at 3–4 months in the seven patients with PCS ( P = 0.006) and in the six patients with good recovery ( P = 0.018). When the nine brain regions were tested separately and results were corrected for multiple comparisons, no individual region differed significantly, but all estimated parameters indicated increased 123 I‐CLINDE binding to TSPO, ranging from 2% to 19% in all patients at 1–2 weeks, 13% to 27% in patients with PCS at 3–4 months and −9% to 17% in patients with good recovery at 3–4 months. Conclusions Neuroinflammation was present in mTBI at 1–2 weeks post‐injury and persisted at 3–4 months post‐injury with a tendency to be most pronounced in patients with PCS.