Medical Theory: Why Does Progesterone Not Work After a Traumatic Brain Injury in Humans? | Biomedgrid

Traumatic brain injury (TBI) is a great public health problem. More than 50 million head injuries occur each year worldwide. [4] In 2010, a study pointed to ECT in 89% of trauma-related deaths in low and middle-income countries. And according to the same study in the spectrum of trauma-related injuries, traumatic brain injury was considered a major cause of death and disability. [5] In the United States, traumatic brain injury is serious long-term morbidity. Between 1.6 and 3.8 million sports-related injuries are reported yearly, while an estimate of 5.3 million people lives with long-term cognitive and psychological impairment. [6] The pathophysiology of traumatic brain injury is complex and involves primary and secondary mechanisms of injury. The primary lesion induces biochemical and cellular changes leading to lesions that evolve over hours, days, months or even years with definitive neuronal damage and early death. [7] These traumatic injuries are caused by direct and indirect biomechanical forces and result in an intense neurometabolic event in the brain. [8] The main process after traumatic brain injury affecting the results is acute inflammation, involving mediators such as TNF-α, IL-6, IL-8, and IL-10. [9] After brain injury, including traumatic brain injury, GFAP expression increases in astrocytes which in turn release inflammatory cytokines and disrupt functional recovery. [10,11]