Prevalence, biomechanics, and neuro-metabolic cascade of traumatic brain injury: a focus on post-concussion syndrome

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Background. Traumatic brain injury (TBI) has been recognized as a «signature wound» of military personnel during ХХІ century conflicts. While most patients can expect to recover, those with mild TBI often report persistent somatic, cognitive, emotional, and/or behavioral issues, commonly referred to as post-concussion syndrome (PCS). Purpose – to characterize the current understanding of post-concussion syndrome, including its prevalence, biomechanics, and the neurometabolic cascade associated with mild traumatic brain injury, based on data from open sources. Materials and methods. A selection of publications was conducted using databases such as PubMed, Clinical Key Elsevier, Cochrane Library, and eBook Business Collection, focusing on current knowledge about post-concussion syndrome, its prevalence, biomechanics, and the neurometabolic cascade of mild TBI. Literature searches utilized keywords including «post-concussion syndrome», «traumatic brain injury», «neurometabolic cascade of traumatic brain injury», «biomechanics of traumatic brain injury», and «diagnosis of traumatic brain injury». Inclusion criteria for the publications subjected to content analysis included: 1) discussion of contemporary knowledge regarding mild traumatic brain injury and post-concussion syndrome; 2) adherence to the key principles of evidence-based medicine; and 3) open access to full-text articles. Results. PCS is increasingly recognized as a significant issue, with its prevalence ranging from 5 to 80% among patients with TBI. Diagnosis is based on several criteria; however, substantial differences complicate the accurate identification of symptoms. A key challenge remains determining the duration of symptoms due to the lack of consensus on this issue. Biomechanical factors, such as angular acceleration, play a crucial role in the development of brain injuries associated with mild TBI. Considering psychological and neuroimaging factors may enhance the understanding and treatment of persistent symptoms. Mild TBI initiates a complex neurometabolic cascade, leading to functional changes in the brain without obvious macroscopic injuries. Disruption of cellular homeostasis activates inflammatory processes driven by microglia and results in excessive glutamate release, contributing to neurotoxicity. Neuroprotective strategies, such as NMDA receptor modulation, may show promise in mitigating the consequences of injury. Neuroinflammation significantly contributes to symptom development and may sustain chronic disturbances. Research on inflammatory biomarkers underscores the connection between inflammatory processes and the clinical manifestations of PCS. Conclusions. PCS is a common occurrence among patients with TBI. Accurate diagnosis is complicated by the absence of unified criteria for determining the duration of symptoms. Mild TBI triggers complex neurometabolic changes and inflammatory processes that may contribute to the chronicity of the injury, making it essential to consider both biomechanical and neuroimaging aspects to improve understanding and treatment of patients with PCS.