Traumatic brain injury (TBI) produces complex and evolving metabolic disturbances that are not fully captured by structural imaging. 2-deoxy2-(18F)fluoro-d-glucose ([18F]FDG) PET provides critical insight into these changes, demonstrating an initial hypermetabolic phase followed by chronic hypometabolism associated with injury severity and clinical outcomes. Repetitive TBI results in widespread metabolic dysfunction across key brain regions. While tau and amyloid PET imaging offer mechanistic insights, their clinical utility remains limited due to inconsistent findings. [18F]FDG PET currently represents the most reliable imaging modality for assessing TBI-related metabolic abnormalities, though further standardization and longitudinal research are needed.
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Naseer et al. (2026) studied this question.
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