The Effect of Traumatic Brain Injury on the Gastrointestinal System: A Comprehensive Review.
Ruhi K Shah, Justin J Lin, Tejaswi Makkapati, Arielle A Berkowitz et al.
Kernaussage
Traumatic brain injury (TBI) significantly disrupts gastrointestinal (GI) function through neuroinflammation and autonomic dysregulation, leading to a range of GI pathologies that can impede neurological recovery and are influenced by the brain-gut axis.
Abstract
Traumatic brain injury (TBI) is a significant public health concern resulting in physical, cognitive, and behavioral impairments. Emerging evidence highlights a bidirectional relationship between brain injury and gut health, known as the brain-gut axis. This paper provides a comprehensive review of current literature exploring the relationship between TBI and various gastrointestinal (GI) pathologies, examining how brain injuries contribute to GI dysfunction and how gut health influences neurorecovery. A comprehensive search of peer-reviewed articles was conducted between March and June 2025 using databases including PubMed, Scopus, and Cochrane. Studies from 2010 onwards involving human subjects were screened. Search terms included combinations of "traumatic brain injury," "TBI," and "[gastrointestinal pathology]." Data regarding study design, population, GI outcomes, and proposed mechanisms were analyzed. TBI triggers secondary injury cascades, including neuroinflammation, dysautonomia, and gut microbiome dysbiosis. The review identifies a wide spectrum of TBI-associated GI disorders, including dysphagia, esophageal disorders, gastric disorders, and intestinal disorders. Bowel dysfunction, manifesting as constipation or incontinence, is prevalent due to neurogenic factors and cognitive impairments. Additionally, metabolic dysregulation following TBI leads to malnutrition, hyperglycemia, and hypoglycemia, all of which impact morbidity. The GI system is integrally connected to TBI recovery through immune modulation and nutrient absorption. Dysfunction within the brain-gut axis, specifically altered motility, permeability, and inflammation, contributes to secondary brain injury and impedes neurological outcomes. Clinical assessment of GI dysfunction should be integrated into routine TBI care. Therapeutic strategies, including early enteral nutrition, are essential to optimize recovery and reduce systemic inflammation.
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Quelle: PubMed Central / National Library of Medicine (NLM). Apollion steht in keiner Verbindung mit NLM und wird von NLM nicht empfohlen. Evidenzgrade bewerten die methodische Studienqualität — nicht die inhaltliche Richtigkeit.
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