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Traumatic brain injury (TBI) is primarily caused by external mechanical forces acting on the skull. Common causes include traffic accidents, falls from height, blunt force trauma, and sports injuries. These external forces can lead to soft tissue damage of the scalp, skull fractures, and direct or indirect damage to brain tissue. Secondary injuries arise from pathological cascade reactions triggered by the primary injury, such as cerebral edema, intracranial hematoma, neuroinflammation, and oxidative stress, which further exacerbate neuronal death and functional impairment.

Following TBI, damage to axons can disrupt traditional neural pathways, while external trauma may cause rupture or spasm of cerebral blood vessels, blocking local blood flow and resulting in ischemic and hypoxic neuronal death.

Clinical management of TBI focuses on acute-phase interventions, symptomatic treatment, and rehabilitative support. In the acute phase, treatment may include surgical evacuation of hematomas, decompressive craniectomy, or the use of hyperosmolar agents like mannitol to relieve elevated intracranial pressure. During the rehabilitation phase, neurotrophic agents and physical rehabilitation therapies are often considered.

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