Metabolic disorders after traumatic brain injury: a narrative review of systemic consequences.

Abstract

Traumatic brain injury (TBI) is characterized as a heterogeneous and pathological remodeling of brain physiology because of various external mechanisms, including blows, falls, and rapid acceleration and deceleration of the skull. Its pathophysiology consists of two distinct moments, beginning with a primary lesion resulting from the impact that evolves into a secondary lesion as biochemical and molecular mechanisms are activated. The severity and prognosis after TBI vary widely, depending on factors such as the site of the injury, the patient's premorbid history, and the severity of the injury, and can result in long-term sequelae impacting multiple organs and systems, with a reduction in the life expectancy of these individuals. A relevant point to be investigated is the correlation between metabolic syndrome (MS), defined as the combination of glucose intolerance, dyslipidemia, systemic arterial hypertension (SAH), and acute or chronic coronary heart disease, and the prognosis of these individuals after a TBI. Therefore, this review seeks to verify the correlation between the occurrence of MS in patients who have suffered TBI as a pre-existing comorbidity and whether it develops later, looking for evidence in studies based on animal models and cohort follow-ups of individuals who have suffered TBI in the short and long term to assess the prognosis presented.