Central neuroendocrine dysregulation in ischaemic stroke sequelae: pathophysiological mechanisms-a narrative review.

Traumatic brain injury (TBI) is still a leading cause of death and disability worldwide, as well as one of the main causes of trauma-related death and long-term neurological morbidity. In addition to its immediate lethality, TBI also causes severe physical, cognitive, behavioral, and emotional impairment in patients, families, and health systems. Among the intracranial lesions after TBI, traumatic parenchymal mass lesions are of greatest clinical significance, occurring in up to 8.2% of all TBI cases and in 13%–35% of severe injuries, and accounting for a significant proportion of surgically treated intracranial lesions. Cerebral contusions are among the most clinically significant traumatic parenchymal lesions and are focal areas of cortical tissue injury with varying levels of hemorrhage, edema, and necrosis, mainly involving the frontal and temporal lobes because of the impact on the irregular skull. Their frequency is important, as well as their association with neurological deterioration, persistent neurocognitive deficits, and poor functional outcome. A defining feature of cerebral contusions is that they tend to enlarge after the initial injury. Most progression occurs within 24 hours, but the enlargement may continue over the following days in some patients. This process is known as hemorrhagic progression of contusion or contusion blossoming and is important in clinical practice because increasing lesion size can cause worsening mass effect, neurological decline, a greater need for surgical intervention, and higher mortality.