Keywords
Neuroinflammation
Psychiatry
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Abstract
Objective: To analyze the main neuroinflammatory mechanisms involved in the pathophysiology of Post-Traumatic Stress Disorder (PTSD) and their clinical implications. Literature review: Post-Traumatic Stress Disorder is a chronic psychiatric condition triggered by exposure to traumatic events and characterized by persistent alterations in the neuroendocrine, immune, and central nervous systems. Recent evidence demonstrates that neuroinflammation plays a central role in the pathophysiology of PTSD, being driven by microglial activation, increased blood-brain barrier permeability, and the release of pro-inflammatory cytokines. These processes promote dysfunction of neurotransmitter systems, including serotonin, dopamine, glutamate, gamma-aminobutyric acid (GABA), and norepinephrine, impairing synaptic plasticity, memory consolidation, and stress response regulation. Consequently, symptoms such as hypervigilance, intrusive recollections, avoidance behaviors, mood disturbances, and cognitive deficits are maintained, contributing to the chronic course of the disorder. Final considerations: Understanding the neuroinflammatory mechanisms involved provides opportunities to develop strategies capable of modulating the inflammatory response and restoring neurochemical homeostasis, thereby promoting more effective therapeutic approaches.
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