ArticleFrontiers in physiology2012
Upper gastrointestinal dysmotility after spinal cord injury: is diminished vagal sensory processing one culprit?
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Gastrointestinal symptoms in postural tachycardia syndrome: a systematic review.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2018Pooled it
- Screening for acute hepatic porphyria in postural tachycardia syndrome.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Article
- Expert-Reviewed Nutritional Guidance for Adults with Spinal Cord Injury: A Delphi Study.Nutrients · 2025Article
- Diagnosis and Management of Cardiovascular Risk in Individuals With Spinal Cord Injury: A Narrative Review.Circulation · 2023Review
- Autogenic biofeedback training improves autonomic responses in a participant with cervical motor complete spinal cord injury- case report.Spinal cord series and cases · 2023Article
- T cell infiltration into the brain triggers pulmonary dysfunction in murine Cryptococcus-associated IRIS.Nature communications · 2023Article
- The Physiology of Neurogenic Obesity: Lessons from Spinal Cord Injury Research.Obesity facts · 2023Review
- Energy expenditure and nutrient intake after spinal cord injury: a comprehensive review and practical recommendations.The British journal of nutrition · 2022Review
- Spinal cord injury-mediated changes in electrophysiological properties of rat gastric nodose ganglion neurons.Experimental neurology · 2022Article
- Widening spinal injury research to consider all supraspinal cell types: Why we must and how we can.Experimental neurology · 2021Review
- Altered physiology of gastrointestinal vagal afferents following neurotrauma.Neural regeneration research · 2021Review
- Pathophysiology of Neurogenic Obesity After Spinal Cord Injury.Topics in spinal cord injury rehabilitation · 2021Review
- Dietetics After Spinal Cord Injury: Current Evidence and Future Perspectives.Topics in spinal cord injury rehabilitation · 2021Review
- Gastric vagal afferent neuropathy following experimental spinal cord injury.Experimental neurology · 2020Article
- Bladder and Bowel Management in Dogs With Spinal Cord Injury.Frontiers in veterinary science · 2020Review
- Gastrointestinal dysfunction after spinal cord injury.Experimental neurology · 2019Review
- Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats.Brain research · 2019Article
- Diminished gastric prokinetic response to ghrelin in a rat model of spinal cord injury.Neurogastroenterology and motility · 2018Article
- Some Autonomic Deficits of Acute or Chronic Cervical Spinal Contusion Reversed by Interim Brainstem Stimulation.Journal of neurotrauma · 2018Article
- Gastric electrical stimulation improves enteric neuronal survival.International journal of molecular medicine · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Despite the widely recognized prevalence of gastric, colonic, and anorectal dysfunction after spinal cord injury (SCI), significant knowledge gaps persist regarding the mechanisms leading to post-SCI gastrointestinal (GI) impairments. Briefly, the regulation of GI function is governed by a mix of parasympathetic, sympathetic, and enteric neurocircuitry. Unlike the intestines, the stomach is dominated by parasympathetic (vagal) control whereby gastric sensory information is transmitted via the afferent vagus nerve to neurons of the nucleus tractus solitarius (NTS). The NTS integrates this sensory information with signals from throughout the central nervous system. Glutamatergic and GABAergic NTS neurons project to other nuclei, including the preganglionic parasympathetic neurons of the dorsal motor nucleus of the vagus (DMV). Finally, axons from the DMV project to gastric myenteric neurons, again, through the efferent vagus nerve. SCI interrupts descending input to the lumbosacral spinal cord neurons that modulate colonic motility and evacuation reflexes. In contrast, vagal neurocircuitry remains anatomically intact after injury. This review presents evidence that unlike the post-SCI loss of supraspinal control which leads to colonic and anorectal dysfunction, gastric dysmotility occurs as an indirect or secondary pathology following SCI. Specifically, emerging data points toward diminished sensitivity of vagal afferents to GI neuroactive peptides, neurotransmitters and, possibly, macronutrients. The neurophysiological properties of rat vagal afferent neurons are highly plastic and can be altered by injury or energy balance. A reduction of vagal afferent signaling to NTS neurons may ultimately bias NTS output toward unregulated GABAergic transmission onto gastric-projecting DMV neurons. The resulting gastroinhibitory signal may be one mechanism leading to upper GI dysmotility following SCI.
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Registered trials
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