# The Effect of Traumatic Brain Injury on the Gastrointestinal System: A Comprehensive Review

**Authors:** Ruhi K. Shah, Justin J. Lin, Tejaswi Makkapati, Arielle A. Berkowitz, Brian D. Greenwald

PMC · DOI: 10.3390/brainsci16030254 · Brain Sciences · 2026-02-25

## TL;DR

Traumatic brain injury can cause widespread gastrointestinal problems, and addressing these issues early may improve recovery outcomes.

## Contribution

This paper comprehensively reviews the bidirectional relationship between TBI and GI dysfunction, emphasizing the importance of early GI assessment in TBI care.

## Key findings

- TBI leads to GI dysfunction through disruptions in the brain–gut axis, including dysmotility, dysbiosis, and metabolic disturbances.
- Common GI disturbances in TBI patients include dysphagia, gastroparesis, and bowel dysfunction like constipation or incontinence.
- Early enteral nutrition and GI assessment are promising strategies to improve neurorecovery and reduce systemic inflammation.

## Abstract

What are the main findings?
Traumatic brain injury can lead to widespread gastrointestinal dysfunction through disruptions of the brain–gut axis, dysmotility, dysbiosis, malnutrition, and metabolic disturbances.Patients with TBI may experience GI disturbances, including dysphagia, gastroparesis, and sialorrhea, among many others.

Traumatic brain injury can lead to widespread gastrointestinal dysfunction through disruptions of the brain–gut axis, dysmotility, dysbiosis, malnutrition, and metabolic disturbances.

Patients with TBI may experience GI disturbances, including dysphagia, gastroparesis, and sialorrhea, among many others.

What are the implications of the main findings?
Routine assessment and early management of gastrointestinal dysfunction should be integrated into standard TBI care to optimize recovery.Targeted interventions, such as early enteral nutrition, represent promising strategies to improve neurorecovery.

Routine assessment and early management of gastrointestinal dysfunction should be integrated into standard TBI care to optimize recovery.

Targeted interventions, such as early enteral nutrition, represent promising strategies to improve neurorecovery.

Background/Objectives: 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. Methods: 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. Results: 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. Conclusions: 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.

## Linked entities

- **Diseases:** Traumatic brain injury (MONDO:0858950), gastroparesis (MONDO:0006769), constipation (MONDO:0002203)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** Gastroparesis (MESH:D018589), urinary tract infection (MESH:D014552), chest pain (MESH:D002637), laryngitis (MESH:D007827), organ failure (MESH:D009102), Peptic Ulcer Disease (MESH:D010437), HSV infection (MESH:D006561), autoimmune diseases (MESH:D001327), Oral Ulcers (MESH:D019226), gain (MESH:D015430), dehydration (MESH:D003681), diabetic ketoacidosis (MESH:D016883), arousal disturbances (MESH:D020921), sepsis (MESH:D018805), Damage to the frontal lobe (MESH:D001927), Sialorrhea (MESH:D012798), Duodenitis (MESH:D004382), confusion (MESH:D003221), neurological injury (MESH:D020196), sores (MESH:D063806), ) pathologies (MESH:D005598), hyperphagia (MESH:D006963), toxic megacolon (MESH:D008532), oral herpes (MESH:D013283), rectal bleeding (MESH:D012002), weight loss (MESH:D015431), Gastric Disorders (MESH:D013272), polyuria (MESH:D011141), Mesenteric ischemia (MESH:D065666), loss of appetite (MESH:D001068), Bowel Obstruction (MESH:D012778), fever (MESH:D005334), diarrhea (MESH:D003967), mucosal damage (MESH:D052016), duodenal obstruction (MESH:D004380), Hyperglycemia (MESH:D006943), calcium (MESH:D002128), neurological deficits (MESH:D009461), metabolic disturbances (MESH:D024821), regurgitation (MESH:D008944), rectum (MESH:D012004), melena (MESH:D008551), cough (MESH:D003371), neuronal cell loss (MESH:D002292), fatigue (MESH:D005221), H. pylori infection (MESH:D016481), Hyper- (MESH:D007589), necrotic (MESH:D009336), gut microbiome (MESH:C536735), glutamate (MESH:C537425), Coma (MESH:D003128), paralytic ileus (MESH:D007418), ischemic injury (MESH:D017202), TBI (MESH:D000070642), disorders of consciousness (MESH:D003244), olfactory nerve injury (MESH:D061219), Memory impairments (MESH:D008569), Mesenteric Artery Syndrome (MESH:D013478), gingival inflammation (MESH:D007249), seizures (MESH:D012640)
- **Chemicals:** ciprofloxacin (MESH:D002939), metronidazole (MESH:D008795), T3 (MESH:D014284), 5-ASA (MESH:D019804), vancomycin (MESH:D014640), omega-3 fatty acids (MESH:D015525), linaclotide (MESH:C523483), blood glucose (MESH:D001786), rifaximin (MESH:D000078262), bile acid (MESH:D001647), polyethylene glycol (MESH:D011092), fluconazole (MESH:D015725), steroids (MESH:D013256), famciclovir (MESH:D000077595), valacyclovir (MESH:D000077483), foscarnet (MESH:D017245), nitrogen (MESH:D009584), glucose (MESH:D005947), cortisol (MESH:D006854), nystatin (MESH:D009761), bisacodyl (MESH:D001726), acyclovir (MESH:D000212), sucralfate (MESH:D013392), curcumin (MESH:D003474), T4 (MESH:D013974), glycopyrrolate (MESH:D006024), fidaxomicin (MESH:D000077732), D-lactate (-), lubiprostone (MESH:D000068238), cidofovir (MESH:D000077404), scopolamine (MESH:D012601), metoclopramide (MESH:D008787), testosterone (MESH:D013739), alcohol (MESH:D000438), amoxicillin-clavulanate (MESH:D019980), glycerol (MESH:D005990), clotrimazole (MESH:D003022)
- **Species:** Candida [taxon 1535326], Helicobacter pylori (species) [taxon 210], gut metagenome (species) [taxon 749906], Clostridioides difficile (species) [taxon 1496], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13023969/full.md

## References

148 references — full list in the complete paper: https://tomesphere.com/paper/PMC13023969/full.md

---
Source: https://tomesphere.com/paper/PMC13023969