Gastrointestinal dysfunction after brain injury: Mechanisms and the role of the brain-gut axis

Brain injury (BI) encompasses traumatic BI and stroke, and is a leading cause of mortality and morbidity worldwide. In addition to primary brain damage, BI can cause a series of sequelae, of which gastrointestinal (GI) dysfunction is one of the most important affecting patient outcomes. GI dysfunction, including delayed gastric emptying, increased intestinal permeability, and gut dysbiosis, is common among patients with BI. GI dysfunction not only impairs nutrient absorption and increases the risk for infection, but also enhances secondary BI by aggravating the systemic inflammatory response. The brain-gut axis refers to the bidirectional communication network between the central nervous system and enteric nervous system. This article provides an overview of the mechanisms underlying GI dysfunction after BI and the close relationship with the brain-gut axis. Furthermore, the potential mechanisms underlying brain-gut modulation by probiotics, fecal microbiota transplantation, and vagus nerve stimulation are discussed, which may provide new insights into the treatment of GI dysfunction in patients with BI. An in-depth understanding of the interaction between the brain and GI system is essential to develop more effective therapeutic strategies to alleviate patient suffering and improve survival and quality of life.