Neuroinflammation in Traumatic Brain Injury-Related Delirium: Mechanisms and Clinical Significance

Junjie Li; Zhigang Wang

doi:10.54097/5hkpmb84

Authors

Junjie Li
Zhigang Wang

DOI:

https://doi.org/10.54097/5hkpmb84

Keywords:

Neuroinflammation, Traumatic Brain Injury, Delirium, Inflammatory Mediators, Immune Response, Neuropsychiatric Complications

Abstract

Traumatic brain injury (TBI) is one of the leading causes of neurological dysfunction and mortality, often accompanied by various neuropsychiatric complications. Among these, delirium occurs with a notably high incidence and significantly impairs rehabilitation and quality of life. Recent studies have identified neuroinflammation as a central pathological mechanism underlying the onset and progression of post-TBI delirium. This process is characterized by excessive release of inflammatory mediators, abnormal activation of glial cells, infiltration of peripheral immune cells, and activation of the complement system, ultimately leading to neurotransmitter imbalance and disruption of brain network function. Pro-inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), together with chemokines, play pivotal roles in amplifying inflammatory responses, while microglial polarization and blood–brain barrier disruption represent key events in central immune dysregulation. Despite growing evidence, the molecular signaling pathways and multicellular interactions mediating neuroinflammation-induced delirium remain incompletely understood. This review summarizes the mechanistic role of neuroinflammation in post-TBI delirium, aiming to provide a theoretical reference for its prevention and management.

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