The Role of Neuroinflammation in Neuropsychiatric Disorders Following Traumatic Brain Injury: A Systematic Review

Abstract

Background: Neuropsychiatric symptoms are common following traumatic brain injury (TBI), but their etiological onset remains unclear. Mental health research implicates neuroinflammation in the development of psychiatric disorders. The presence of neuroinflammatory responses after TBI thus prompts an investigation of their involvement in the emergence of neuropsychiatric disorders postinjury. Objective: Review the literature surrounding the role of neuroinflammation and immune response post-TBI in the development of neuropsychiatric disorders. Methods: A search of scientific databases was conducted for original, empirical studies in human subjects. Key words such as "neuroinflammation," "TBI," and "depression" were used to identify psychopathology as an outcome TBI and the relation to neuroinflammatory response. Results: Study results provide evidence of neuroinflammation mediated post-TBI neuropsychiatric disorders including anxiety, trauma/stress, and depression. Inflammatory processes and stress response dysregulation can lead to secondary cell damage, which promote the development and maintenance of neuropsychiatric disorders postinjury. Conclusion: This review identifies both theoretical and empirical support for neuroinflammatory response as feasible mechanisms underlying neuropsychiatric disorders after TBI. Further understanding of these processes in this context has significant clinical implications for guiding the development of novel treatments to reduce psychiatric symptoms postinjury. Future directions to address current limitations in the literature are discussed.

Blood glutamate scavenging as a novel glutamate-based therapeutic approach for post-traumatic brain injury anxiety and social impairment

“…A limitation to this study was that we did not study inflammation and neurodegeneration, which play an important role in the development of depression, anxiety, and other neuropsychiatric complications of TBI [ 68 ]. The pathogenesis of post-TBI neuropsychiatric disorders is complex and multifactorial [ 16 ].…”

Effect of Low Doses of Dexamethasone on Experimental Pulmonary Tuberculosis

“…TB is characterized by an excessive systemic inflammatory response [ 38 ]. Systemic inflammation produces neuroinflammation and neuronal damage caused by oxidative stress and activating microglia that impair cognitive function, including learning and memory, and can contribute to neurobehavioral changes, including the development of neuropsychiatric disorders [ 39 , 40 , 41 ]. In the absence of brain bacteria, we have shown that Mtb lung infection caused neuroinflammation and behavioral impairments [ 25 ], and similar results have been described in Mycobacterium lepraemurium [ 42 , 43 ].…”

The Putative Role of Neuroinflammation in the Interaction between Traumatic Brain Injuries, Sleep, Pain and Other Neuropsychiatric Outcomes: A State-of-the-Art Review

“…Interestingly, these frequent long-term consequences of traumatic injuries share neuroinflammation among key pathophysiological mechanisms [58,[127][128][129]. According to a recent systematic review [130], the presence of depressive and/or anxiety symptoms in TBI samples was found to be associated with higher concentrations of serum and CSF, CRP, CSF-derived markers of sVCAM-1, sICAM-1, and sFAS, and IL-10, IL-8, IL-6, and TNF-α. Acute measures of some of these biomarkers predicted the onset of depression at 6 and 12 months post-injury.…”