Brain glucose hypometabolism is associated with neuropsychiatric impairment following traumatic brain injury

Title : Brain glucose hypometabolism is associated with neuropsychiatric impairment following traumatic brain injury

Abstract:

Background: The neurological and psychiatric sequelae of Traumatic Brain Injury (TBI) have become an increasing concern. However, the long-term effects of TBI on brain glucose metabolism, particularly in individuals more than a decade after injury, remain poorly understood. This study aimed to characterize alterations in brain glucose metabolism in patients with chronic TBI and to examine the relationship between regional metabolic abnormalities and neuropsychiatric impairment.
Methods: Twenty-one patients with TBI (mean ± SD: 47.7 ± 12.8 years), including 10 patients with single severe TBI (ssTBI) and 11 patients with repetitive mild TBI (rmTBI), and 15 healthy controls (42.2 ± 14.8 years) were included. The mean interval between the head injury and assessment was 16.7 ± 14.3 years in the ssTBI group, and the mean interval since the first head injury was 30.9 ± 11.3 years in the rmTBI group. Brain glucose metabolism of the patients was assessed using ¹⁸F-fluorodeoxyglucose (FDG) PET and MRI scans. Regions of Interest (ROIs) were defined in multiple areas in the neocortical gray matter (GM), white matter (WM), and subcortical regions for each T1-weighted image. TBI patients also underwent several clinical evaluations including a diagnosis of the modified criteria for traumatic encephalopathy syndrome (TES), and assessments of cognitive impairments using neuropsychological tests.
Results: TBI patients exhibited significantly lower ¹⁸F-FDG standardized uptake value ratios (SUVRs) in the GM areas than age-matched HC subjects, particularly in the frontal GM, cerebellar GM, and the thalamus. Among TBI patients, whole GM ¹⁸F-FDG SUVRs negatively correlated with BPRS scores, but positively correlated with scores for MMSE, ROCFT immediate recall, and ROCFT delayed recall. Furthermore, exploratory univariate analysis suggested lower ¹⁸F-FDG SUVRs in the ssTBI group than in the rmTBI group in several regions. No significant difference in whole GM ¹⁸F-FDG SUVRs were observed between the TES and non-TES groups.
Discussion: ¹⁸F-FDG PET demonstrated reduced brain glucose metabolism in the chronic stages of TBI, indicating that metabolic abnormalities may persist for more than a decade after injury. Reduced brain glucose metabolism was associated with psychiatric symptoms and cognitive impairment but not with the clinical diagnosis of TES. These findings suggest that the effects of TBI on brain function may persist over the long term and are predominantly linked to neuropsychiatric symptoms and cognitive dysfunction.

Biography:

Linna Sato is a student researcher from Hiroo Gakuen Senior High School, with a strong passion for neuroscience, psychology, and philosophy. Through her experience as a soccer player, she has developed an interest in concussions and the consequences it may bring. Outside of her research as a trainee at the National Institutes of Quantum Science and Technology (QST), she also spreads her passion for neuroscience through her activities as the executive community manager at IYNA Japan.