Autonomic nervous system and gastrointestinal manifestations with an emphasis on gastric dysfunction
Abstract
Gastrointestinal (GI) symptoms are frequent in disorders that involve the autonomic nervous system (ANS) or the enteric neuromuscular apparatus. Although dysfunction may occur anywhere along the alimentary tract, gastric manifestations are often the most clinically visible 'end-organ' expression of autonomic disease because they drive nausea, vomiting, early satiety, postprandial distress, malnutrition risk, and impaired drug absorption. In this invited review, we summarize the organization of the GI neuromuscular apparatus, emphasizing how intrinsic (enteric) circuitry and extrinsic sympathetic and parasympathetic pathways cooperate to regulate gastrointestinal functions. We then link common symptom clusters (dysphagia, gastroparesis, intestinal pseudo-obstruction, constipation, diarrhea, and fecal incontinence) to likely neuroanatomic levels and review autonomic test batteries and motility studies that help characterize dysfunction. Finally, we discuss neurologic and systemic diseases in which autonomic and enteric involvement produce prominent gastric and broader GI phenotypes. These include cerebrovascular and cortical neurodegenerative disorders, Parkinson's disease, structural and inflammatory brainstem syndromes, primary autonomic failure and hereditary dysautonomia, postural orthostatic tachycardia syndrome, spinal cord disorders (including multiple sclerosis), peripheral neuropathies such as diabetes mellitus and amyloidosis, paraneoplastic and autoimmune autonomic neuropathies, and selected neuromuscular and myopathic conditions.
AI snapshot
Written from the paper’s full text.
TL;DR
This invited narrative review summarizes how the intrinsic enteric nervous system and extrinsic sympathetic/parasympathetic pathways regulate gastrointestinal function, and how neurologic and systemic diseases disrupt them, with emphasis on gastric dysfunction as the most clinically visible end-organ expression of autonomic disease. It provides a practical framework linking symptom clusters to neuroanatomic levels and to autonomic and motility testing.
Key findings
- Gastric manifestations (nausea, vomiting, early satiety, postprandial distress) are highlighted as the most clinically visible end-organ expression of autonomic disease because they also threaten nutrition and oral drug absorption; gastric motor dysfunction can impair levodopa pharmacokinetics and contribute to motor fluctuations in Parkinson disease.
- Symptom clusters map onto neuroanatomic levels: oropharyngeal dysphagia (suprabulbar, lower motor neuron, neuromuscular junction, myopathy), esophageal dysphagia/reflux (vagal dysfunction, myopathy), gastric symptoms (delayed or accelerated emptying, impaired accommodation, pyloric dysfunction), and constipation/anorectal dysfunction (slow transit vs. evacuation disorders such as pelvic floor dyssynergia).
- Disease-specific patterns are described, including prodromal GI dysmotility in Parkinson disease (with α-synuclein pathology potentially involving the ENS and vagal/brainstem nuclei early, and reduced PD risk after truncal vagotomy), area postrema syndrome with persistent nausea/vomiting in neuromyelitis optica spectrum disorder, and diabetic "autovagotomy" with loss of unmyelinated axons and interstitial cells of Cajal.
- Reported quantitative figures include: chronic neurogenic bowel dysfunction in roughly 27%–62% of individuals after spinal cord injury, with gallstones in 17%–31% and only about half developing objective signs of "acute abdomen"; in a single-center retrospective cohort of 166 MS patients, delayed gastric emptying in 16% and accelerated emptying in 22%; approximately one-third of POTS patients reporting nausea, vomiting, bloating, or constipation; and in 10 patients with lipomatosis of nerve, 3 with early-onset colonic diverticulosis.
Methods
- Design: invited narrative review, organized into sections on the GI neuromuscular apparatus and its intrinsic/extrinsic control, common GI symptom syndromes, autonomic and motility testing, and disease-specific sections (brain, brainstem, autonomic degenerations, spinal cord, peripheral neuropathy/systemic disorders, neuromuscular junction and myopathic disorders).
- Data: no primary data collection; the paper synthesizes published literature and cites references throughout, including tables (Tables 1–4) summarizing extrinsic neural wiring, GI symptoms/syndromes with investigations, and autonomic function tests for parasympathetic and sympathetic impairment.
- Main analysis: qualitative synthesis linking symptom clusters to likely neuroanatomic levels and to diagnostic tests, including cardiovagal, adrenergic, and sudomotor autonomic testing, pancreatic polypeptide response to modified sham feeding for vagal efferent integrity, and segmental motility studies (gastric emptying scintigraphy or breath testing, antroduodenal or colonic manometry, radiopaque marker/radionuclide/capsule transit testing, anorectal manometry with balloon expulsion and defecography).
Limitations
- The paper states its goal is "not to provide exhaustive disease reviews, but rather to highlight high-yield clinical patterns, relevant mechanisms, and pragmatic diagnostic and treatment considerations," indicating deliberately selective rather than comprehensive coverage.
- Evident from the text: as a narrative review without a stated systematic search strategy, inclusion of conditions and citations appears discretionary, and several cited findings rest on small or single-center studies (e.g., 12 patients in the HIV diarrhea crossover trial, 10 patients in the lipomatosis of nerve series, a single-center 166-patient MS cohort), which the paper does not appraise for quality or risk of bias.
- Evident from the text: the referenced tables (Tables 1–4) are cited as containing key wiring, symptom, and autonomic test details but their content is not reproduced in the provided text, so those specifics cannot be verified here.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
61 of 169 cited sources checked · 29 supported · 1 flagged · accuracy not yet measured
- Premisecitation
Advanced therapies can improve GI symptoms in selected patients with amyloidosis, including stem cell transplantation with cytotoxic therapy in systemic amyloidosis and liver transplantation in transthyretin amyloidosis.
“Advanced therapies can improve GI symptoms in selected patients, including stem cell transplantation with cytotoxic therapy in systemic amyloidosis and liver transplantation in transthyretin amyloidosis (Afrough et al., 2015; Wixner et al., 2015).”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites Afrough et al., 2015 source
- cites Wixner et al., 2015 source
For the liver-transplantation part attributed to Wixner et al., the Results (GI symptoms; page not specified) report that GI symptom prevalence and scores increased after transplantation. The Conclusions say gastric emptying and nutritional status were maintained, but GI symptom scores increased—not improved. The stem-cell-transplantation part is attributed to the other citation and is not judged here. (LLM, conf=0.91)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measured
- Premisecitation
Early screening and structured dysphagia management improve outcomes in acute stroke.
“Early screening and structured dysphagia management improve outcomes (Arnold et al., 2016; Martino et al., 2005), and enteral feeding strategies may be needed when aspiration risk is high (Duncan et al., 2020; Geeganage et al., 2012).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Arnold et al., 2016 source
The Discussion (page unavailable) says regular dysphagia screening by trained therapists has been shown to decrease pneumonia in acute stroke patients, supporting an improvement in one outcome. It does not establish that early screening and structured dysphagia management broadly improve clinical outcomes; the study assessed associations between dysphagia and outcomes and calls for further research on management. (LLM, conf=0.83)
Experimental — accuracy not yet measured - cites Martino et al., 2005 source
- Premisecitation
Objective measures of GI autonomic involvement have been correlated with central dopaminergic markers early in Parkinson disease.
“Objective measures of GI autonomic involvement have been correlated with central dopaminergic markers early in disease (Hinkle et al., 2018), and GI symptoms often occur prior to motor diagnosis (Cersosimo et al., 2013; Fasano et al., 2015).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Hinkle et al., 2018 source
The Results report that GI dysautonomia scores were associated with reduced caudate and putamen dopamine-transporter availability in early Parkinson disease. But the Methods describe GI involvement as measured by SCOPA-AUT questionnaire items, and the Discussion calls it a self-administered scale; the paper does not establish that the GI measures were objective. Page numbers were not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Premisecitation
The gastrointestinal tract is increasingly viewed as a therapeutic target in Parkinson disease, including approaches that aim to modulate enteric neuronal signaling.
“The gastrointestinal tract is also increasingly viewed as a therapeutic target in PD, including approaches that aim to modulate enteric neuronal signaling (Hauser et al., 2019).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Hauser et al., 2019 source
- Premisecitation
Approximately one-third of patients with POTS report nausea, vomiting, bloating, or constipation.
“Approximately one-third of patients report nausea, vomiting, bloating, or constipation (Low et al., 1994; Park et al., 2013).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Low et al., 1994 source
- cites Park et al., 2013 source
The Introduction reports that nearly 40% of adults with POTS have bloating, 25% have nausea, and smaller proportions have vomiting or constipation. It supports the claim that these symptoms occur in POTS, but does not establish that approximately one-third of patients report at least one of the listed symptoms. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Premisecitation
Structural compression of the brainstem and lower cranial nerves, including in Arnold-Chiari malformation, can cause neurogenic dysphagia.
“Structural compression of the brainstem and lower cranial nerves, including in Arnold–Chiari malformation, can also cause neurogenic dysphagia (Elta et al., 1996).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Elta et al., 1996 source
- Premisecitation
Such brainstem symptoms can occur even without elevated intracranial pressure.
“Importantly, such symptoms can occur even without elevated intracranial pressure (Mann et al., 1998).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Mann et al., 1998 source
- Premisecitation
Ganglionic acetylcholine receptor antibodies are implicated in autoimmune autonomic ganglionopathy, an acute pandysautonomia with characteristically severe gastrointestinal involvement.
“Ganglionic acetylcholine receptor (G-AChR) antibodies are implicated in autoimmune autonomic ganglionopathy, an acute pandysautonomia with characteristically severe gastrointestinal involvement.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Vernino et al., 2009 source
- Premisecitation
Autoantibodies to muscarinic M3 receptors have been reported in selective dysautonomia.
“Autoantibodies to muscarinic M3 receptors have been reported in selective dysautonomia (Palma et al., 2020), and cytomegalovirus infection of the myenteric plexus can produce chronic intestinal pseudo-obstruction (Sonsino et al., 1984).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Palma et al., 2020 source
- Premisecitation
In multiple sclerosis, constipation, fecal incontinence, and evacuation disorders often co-occur with bladder dysfunction.
“Constipation, fecal incontinence, and evacuation disorders often co-occur with bladder dysfunction and can significantly impair quality of life (Almeida et al., 2019; Hinds et al., 1989; Lin et al., 2019).”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites Almeida et al., 2019 source
- cites Hinds et al., 1989
- cites Lin et al., 2019 source
The Results report frequent bladder problems, functional constipation, and faecal incontinence in the surveyed MS population, while the Introduction says bowel and bladder problems can reduce quality of life. However, the paper does not report how often those conditions co-occur in the same individuals or identify evacuation disorders as a measured condition. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Premisecitation
In multiple sclerosis, both slow transit and defecatory dyssynergia contribute to bowel symptoms.
“Objective studies using anorectal manometry, transit testing, and validated symptom instruments demonstrate that both slow transit and defecatory dyssynergia contribute to symptoms in MS, with severity often tracking neurologic disability (Almeida et al., 2019; Lin et al., 2019; Marola et al., 2016; Preziosi et al., 2014; Weber et al., 1987; Wiesel et al., 2000).”
Quote in the paperNot a substantial claim2 of 3 sources checked- cites Almeida et al., 2019 source
- cites Lin et al., 2019 source
The Introduction (page not provided) says MS-related demyelinating lesions can cause slow colonic transit. The Results > Bowel dysfunction links constipation and faecal incontinence with disability, but the paper does not identify defecatory dyssynergia or report anorectal manometry or transit testing; its Methods > Study tools describes symptom-based measures instead. (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites Marola et al., 2016 source
The Introduction (page not available) reports slower colonic transit in MS and discusses dyschezia as a contributor to constipation. It presents pelvic-floor dyssynergia as a hypothesis and says paradoxical puborectalis contraction may partly explain obstructed defecation; the claim states that contribution more definitively than the source does. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Rests on an assumption: Demyelinating lesions involving spinal long tracts and autonomic centers can disrupt colonic propulsion, anorectal sensation, and pelvic floor coordination in multiple sclerosis.
- Premisecitation
In multiple sclerosis, constipation, fecal incontinence, and evacuation disorders can significantly impair quality of life.
“Constipation, fecal incontinence, and evacuation disorders often co-occur with bladder dysfunction and can significantly impair quality of life (Almeida et al., 2019; Hinds et al., 1989; Lin et al., 2019).”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites Almeida et al., 2019 source
- cites Hinds et al., 1989
- cites Lin et al., 2019 source
The Introduction says MS-related constipation and faecal incontinence are among bowel and bladder problems that can decrease quality of life. The Results > Bowel dysfunction reports both conditions in the surveyed MS population. Our copy does not specifically address evacuation disorders or establish that these conditions often co-occur with bladder dysfunction. (LLM, conf=0.85)
Experimental — accuracy not yet measured
- Premisecitation
In a scintigraphic study, multiple sclerosis patients demonstrated delayed gastric emptying compared with controls.
“In a scintigraphic study, MS patients demonstrated delayed gastric emptying compared with controls (el-Maghraby et al., 2005).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites el-Maghraby et al., 2005 source
- Premisecitation
In a single-center retrospective cohort of 166 multiple sclerosis patients evaluated for GI motility symptoms over a 25-year interval, delayed gastric emptying was reported in 16%.
“In a single-center retrospective cohort of 166 MS patients evaluated for GI motility symptoms over a 25-year interval, delayed gastric emptying (16%) and accelerated emptying (22%) were both reported, highlighting phenotypic heterogeneity and the influence of comorbidities and medications (Khanna et al., 2022).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Khanna et al., 2022 source
- Premisecitation
In multiple sclerosis, bowel symptom severity often tracks neurologic disability.
“Objective studies using anorectal manometry, transit testing, and validated symptom instruments demonstrate that both slow transit and defecatory dyssynergia contribute to symptoms in MS, with severity often tracking neurologic disability (Almeida et al., 2019; Lin et al., 2019; Marola et al., 2016; Preziosi et al., 2014; Weber et al., 1987; Wiesel et al., 2000).”
Quote in the paperNot a substantial claim2 of 3 sources checked- cites Almeida et al., 2019 source
- cites Lin et al., 2019 source
- cites Marola et al., 2016 source
The Methods (Variables; page unavailable) say the study measured EDSS disability and bowel-symptom scores, but our copy does not report whether symptom severity tracked EDSS. The Discussion (Difference in resting anal pressure; page unavailable) instead compares EDSS with a manometric measure and finds no statistically significant difference; that does not settle the symptom-severity claim. (LLM, conf=0.72)
Experimental — accuracy not yet measured
- Rests on an assumption: Demyelinating lesions involving spinal long tracts and autonomic centers can disrupt colonic propulsion, anorectal sensation, and pelvic floor coordination in multiple sclerosis.
- Interpretationcitation
Gastric emptying abnormalities in multiple sclerosis show phenotypic heterogeneity influenced by comorbidities and medications.
“highlighting phenotypic heterogeneity and the influence of comorbidities and medications (Khanna et al., 2022).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Khanna et al., 2022 source
The Results (Gastrointestinal Transit Study; page unavailable) document both accelerated and delayed gastric emptying in patients with MS, supporting phenotypic heterogeneity. They say medications could conceivably alter gastrointestinal motility, but do not establish that medications influenced the observed gastric-emptying abnormalities; the cited passages also do not establish an influence of comorbidities. (LLM, conf=0.86)
Experimental — accuracy not yet measured
- Premisecitation
Pharmacologic augmentation of cholinergic activity with neostigmine, administered with glycopyrrolate to mitigate systemic adverse effects, has demonstrated efficacy in randomized, double-blind trials in spinal cord injury.
“Pharmacologic augmentation of cholinergic activity with neostigmine, administered with glycopyrrolate to mitigate systemic adverse effects, has demonstrated efficacy in randomized, double-blind trials (Krassioukov et al., 2010).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Krassioukov et al., 2010 source
The Pharmacological agents section (page not available in our copy) reports two good-quality randomized controlled trials supporting neostigmine, alone or with glycopyrrolate, for bowel evacuation after spinal cord injury. It does not establish that the trials were double-blind or state that glycopyrrolate was given to mitigate systemic adverse effects. (LLM, conf=0.86)
Experimental — accuracy not yet measured
- Premisecitation
Manometric studies suggest that early amyloidosis can manifest with motor incoordination consistent with neural involvement.
“Manometric studies suggest that early disease can manifest with motor incoordination consistent with neural involvement, whereas later stages may show low-amplitude contractions reflecting myopathic infiltration of smooth muscle (Battle et al., 1979; Camilleri et al., 1985; Rubinow et al., 1983).”
Quote in the paperNot a substantial claim1 of 3 sources checked - Premisecitation
In a large retrospective series, a minority of patients with systemic amyloidosis had biopsy-proven GI involvement.
“In a large retrospective series, a minority of patients with systemic amyloidosis had biopsy-proven GI involvement (Cowan et al., 2013).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Cowan et al., 2013 source
The Patients and Discussion sections describe a retrospective series of 2,334 patients with all types of amyloidosis, of whom 76 (3.3%) had biopsy-proven GI involvement. The Discussion distinguishes 60 patients with systemic amyloidosis from 16 with localized GI amyloidosis. Thus the finding supports a minority among all patients evaluated, but the paper does not give a denominator for patients with systemic amyloidosis specifically. (LLM, conf=0.85)
Experimental — accuracy not yet measured
- Premisecitation
Bowel symptoms are common across multiple sclerosis disease phenotypes.
“and bowel symptoms are common across disease phenotypes.”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites Almeida et al., 2019 source
- cites Hinds et al., 1989
- cites Lin et al., 2019 source
The Results (Bowel dysfunction; page unavailable) report constipation in 48.9% and faecal incontinence in 31.9% of respondents, supporting that bowel symptoms are common in this MS cohort. The Discussion (page unavailable) says the cohort included different disease phenotypes, but the paper does not report bowel-symptom frequency by phenotype, so it does not establish that symptoms are common across them. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Rests on an assumption: Multiple sclerosis is frequently accompanied by autonomic dysregulation.
- Premisecitation
Later stages of amyloidosis may show low-amplitude contractions reflecting myopathic infiltration of smooth muscle.
“Manometric studies suggest that early disease can manifest with motor incoordination consistent with neural involvement, whereas later stages may show low-amplitude contractions reflecting myopathic infiltration of smooth muscle (Battle et al., 1979; Camilleri et al., 1985; Rubinow et al., 1983).”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites Battle et al., 1979 source
- cites Camilleri et al., 1985 source
The Discussion (page unavailable) says neural involvement may affect the gut before muscle infiltration in primary amyloidosis and describes very low-amplitude activity as a feature of myogenic pseudoobstruction. But the authors say their patients with amyloidosis showed none of those myogenic features; they did not observe low-amplitude contractions in later-stage amyloidosis. (LLM, conf=0.85)
Experimental — accuracy not yet measured - cites Rubinow et al., 1983 source
- Premisecitation
In a single-center retrospective cohort of 166 multiple sclerosis patients evaluated for GI motility symptoms over a 25-year interval, accelerated gastric emptying was reported in 22%.
“In a single-center retrospective cohort of 166 MS patients evaluated for GI motility symptoms over a 25-year interval, delayed gastric emptying (16%) and accelerated emptying (22%) were both reported, highlighting phenotypic heterogeneity and the influence of comorbidities and medications (Khanna et al., 2022).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Khanna et al., 2022 source
- Premisecitation
Hereditary transthyretin amyloidosis can also involve small bowel motility.
“Hereditary transthyretin amyloidosis can also involve small bowel motility (Wixner et al., 2018).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Wixner et al., 2018 source
- Premisecitation
In cohorts of patients with idiopathic, paraneoplastic, or diabetic autonomic neuropathy and in idiopathic GI dysmotility, ganglionic receptor-binding antibody titers have correlated with more severe autonomic dysfunction.
“In cohorts of patients with idiopathic, paraneoplastic, or diabetic autonomic neuropathy and in idiopathic GI dysmotility, ganglionic receptor-binding antibody titers have correlated with more severe autonomic dysfunction (Dhamija et al., 2008; Pittock et al., 2011).”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites Dhamija et al., 2008 source
The Introduction says ganglionic AChR antibodies can cause widespread autonomic dysfunction, and the Results report these antibodies in 11 patients with GI dysmotility. But the paper does not report a correlation between antibody titer and autonomic dysfunction severity, or examine the stated idiopathic, paraneoplastic, and diabetic autonomic-neuropathy cohorts (searched for titer, severity, and diabetic autonomic neuropathy). Page numbers were unavailable in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measured - cites Pittock et al., 2011 source
The Discussion (page unavailable) reports that higher ganglionic AChR antibody levels were more often accompanied by clinical evidence of an autoimmune neurological disorder, and it mentions idiopathic and paraneoplastic dysautonomia. It does not report a correlation between antibody titer and the severity of autonomic dysfunction in the listed cohorts, including diabetic neuropathy or idiopathic GI dysmotility. In this study, seropositive cases had low levels and developed no dysautonomia during follow-up. (LLM, conf=0.85)
Experimental — accuracy not yet measured
- Premisecitation
Other antibodies, including ganglionic acetylcholine receptor antibodies and CRMP-5 (CV2), have also been associated with enteric dysmotility in paraneoplastic or autoimmune contexts.
“Other antibodies, including ganglionic acetylcholine receptor antibodies and CRMP-5 (CV2), have also been associated with enteric dysmotility in paraneoplastic/autoimmune contexts (Blackburn et al., 2019; Vernino et al., 2000), and neuropathologic studies show that some patients have more extensive involvement (Sodhi et al., 1989).”
Quote in the paperNot a substantial claim1 of 2 sources checked - Premisecitation
Diarrhea may occur as an adverse effect of nelfinavir-containing antiretroviral regimens.
“Chronic diarrhea has also been attributed to autonomic mechanisms, including heightened extrinsic parasympathetic drive to the intestine (Coker et al., 1992) and/or injury to adrenergic fibers within enteric plexuses; additionally, diarrhea may occur as an adverse effect of nelfinavir-containing antiretroviral regimens (Bardsley-Elliot et al., 2000).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Bardsley-Elliot et al., 2000 source
- Premisecitation
Viral infections such as Zika and SARS-CoV-2 have been associated with neurologic syndromes that include dysautonomia and GI complaints in some patients.
“Viral infections such as Zika and SARS-CoV-2 have also been associated with neurologic syndromes that include dysautonomia and GI complaints in some patients (Counotte et al., 2019; Ghannam et al., 2020).”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites Counotte et al., 2019 source
The Results > GBS section reports a consistent association between Zika virus infection and Guillain-Barré syndrome, supporting the Zika-related neurologic-syndrome portion of the claim. Our copy does not report dysautonomia or GI complaints as features of that syndrome; searches for autonomic dysfunction and gastrointestinal symptoms did not establish those details. The separate SARS-CoV-2 citation is not assessed here. (LLM, conf=0.87)
Experimental — accuracy not yet measured - cites Ghannam et al., 2020 source
The Results (page not available) report neurological syndromes in patients with COVID-19 and say that GI symptoms preceded the syndrome in two patients. The review does not identify dysautonomia among those syndromes, and it describes GI symptoms as preceding—not forming part of—the neurological syndrome. The Zika portion has a separate citation and is not judged against this source. (LLM, conf=0.85)
Experimental — accuracy not yet measured
- Premisecitation
Juvenile dermatomyositis has been associated with novel GI tract manifestations.
“Juvenile dermatomyositis has been associated with novel GI tract manifestations (Laskin et al., 1999), and reviews of adult myositis emphasize the spectrum of esophageal and intestinal complications (Ebert, 2010).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Laskin et al., 1999 source
- Premisecitation
Esophageal dysmotility has been documented with high-resolution manometry in myasthenia gravis.
“Although myasthenia gravis (MG) is classically characterized by fatigable skeletal muscle weakness, esophageal dysmotility has been documented with high-resolution manometry in MG (Torres-Barrera et al., 2020).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Torres-Barrera et al., 2020 source
- Premisecitation
Autoantibodies directed against specific neural antigens, including ion channels and ganglionic acetylcholine receptors, have been associated with esophageal dysmotility, slow-transit constipation, and chronic intestinal pseudo-obstruction.
“Autoantibodies directed against specific neural antigens (including ion channels and ganglionic acetylcholine receptors) have been associated with esophageal dysmotility, slow-transit constipation, and chronic intestinal pseudo-obstruction.”
Quote in the paperSubstantial claim2 of 2 sources checked- cites Dhamija et al., 2008 source
- cites Pittock et al., 2011 source
The Introduction links ganglionic acetylcholine receptor antibodies to autoimmune gastrointestinal dysmotility, describes pseudo-obstruction as a prominent presentation, and reports slow GI transit in animal models. It also reports an association between a different neural antibody and achalasia. The paper does not establish the claimed association of ion-channel and ganglionic receptor antibodies with all three named conditions, particularly slow-transit constipation; its own cases and controls did not develop GI dysmotility during follow-up (Results). (LLM, conf=0.82)
Experimental — accuracy not yet measured
- Premisecitation
Adsorbent therapy with attapulgite did not demonstrate benefit compared with placebo in AIDS-associated chronic diarrhea.
“By contrast, adsorbent therapy with attapulgite did not demonstrate benefit compared with placebo (Nwachukwu et al., 2008).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Nwachukwu et al., 2008 source
- Premisecitation
Familial visceral myopathy, sometimes in association with mitochondrial myopathy, represents an important differential diagnosis for chronic intestinal pseudo-obstruction.
“Familial visceral myopathy, sometimes in association with mitochondrial myopathy, represents an important differential diagnosis for chronic intestinal pseudo-obstruction (Lowsky et al., 1993).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Lowsky et al., 1993 source
- Premisecitation
Disease-modifying strategies such as allogeneic stem cell transplantation, liver transplantation, and experimental gene therapy approaches aim to correct thymidine phosphorylase deficiency and may alter trajectory in selected patients with MNGIE.
“Case series and mechanistic studies highlight the importance of early recognition, as disease-modifying strategies such as allogeneic stem cell transplantation, liver transplantation, and experimental gene therapy approaches aim to correct thymidine phosphorylase deficiency and may alter trajectory in selected patients (D’Angelo et al., 2020; Filosto et al., 2012; Habibzadeh et al., 2020; Yadak et”
Quote in the paperNot a substantial claim1 of 3 sources checked - Premisecitation
Severe phenotypes of myotonic dystrophy include pseudo-obstruction, including in pediatric cases with smooth muscle and myenteric pathology.
“Severe phenotypes include megacolon due to degenerative neuropathy of the myenteric plexus (Yoshida et al., 1988) and pseudo-obstruction, including in pediatric cases with smooth muscle and myenteric pathology (Ho et al., 2019; Pelizzo et al., 2018).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Ho et al., 2019
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites Pelizzo et al., 2018 source
- Premisecitation
Gastrointestinal manifestations are common in myotonic dystrophy types 1 and 2, with high reported frequencies of constipation, diarrhea, abdominal pain, and dysphagia.
“Gastrointestinal manifestations are common in myotonic dystrophy types 1 and 2, with high reported frequencies of constipation, diarrhea, abdominal pain, and dysphagia (Hilbert et al., 2017).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Hilbert et al., 2017 source
The Discussion says gastrointestinal manifestations are common in both DM1 and DM2, and the Abstract reports frequent trouble swallowing in DM1 (55%) and constipation in DM2 (53%). But the baseline registry results report diarrhea in only 1.3% of patients and abdominal pain in fewer than three patients; they do not support describing those two symptoms as highly frequent. (LLM, conf=0.91)
Experimental — accuracy not yet measured
- Interpretationnone given
In dementia syndromes, GI symptoms may arise from impaired feeding behaviors, dysphagia, reduced mobility, and adverse drug effects.
“In dementia syndromes, GI symptoms may arise from impaired feeding behaviors, dysphagia, reduced mobility, and adverse drug effects.”
Quote in the paperNot a substantial claim - Premisecitation
In Alzheimer disease, large cohort data have identified increased rates of GI events.
“In Alzheimer disease, large cohort data have identified increased rates of GI events (Wu et al., 2011).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Wu et al., 2011
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Parkinson disease-associated GI manifestations span from sialorrhea to dysphagia, esophageal dysmotility, altered gastric emptying, and constipation.
“Clinically, PD-associated GI manifestations span from sialorrhea (often due to impaired spontaneous swallowing) to dysphagia, esophageal dysmotility, altered gastric emptying, and constipation (Cersosimo et al., 2013; Cersosimo et al., 2009; Edwards et al., 1993a; Edwards et al., 1991; Fasano et al., 2015; Hinkle et al., 2018; Ioannou et al., 2024; Khoshbin et al., 2021; Sakakibara et al., 2003;”
Quote in the paperNot a substantial claim0 of 3 sources checked - Premisecitation
Systematic reviews support the association between Parkinson disease and gastroparesis.
“Gastric motor dysfunction can impair levodopa pharmacokinetics and contribute to motor fluctuations (Pfeiffer et al., 2020); systematic reviews support the association between PD and gastroparesis (Heetun et al., 2012).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Heetun et al., 2012 source
- Premisecitation
Dopaminergic agents such as apomorphine can influence defecatory function in Parkinson disease.
“Randomized controlled trials have demonstrated benefit of polyethylene glycol 3350 (Zangaglia et al., 2007) and lubiprostone (Ondo et al., 2012) in PD-related constipation, and dopaminergic agents such as apomorphine can influence defecatory function (Edwards et al., 1993b).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Edwards et al., 1993b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
A robust rise in pancreatic polypeptide response to modified sham feeding above baseline supports intact vagal efferent pathways.
“More specific to abdominal vagal integrity is the pancreatic polypeptide response to modified sham feeding, where a robust rise above baseline supports intact vagal efferent pathways (Camilleri et al., 1994; Prather et al., 1997).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Camilleri et al., 1994 source
- cites Prather et al., 1997
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
GI symptoms often occur prior to motor diagnosis in Parkinson disease.
“Objective measures of GI autonomic involvement have been correlated with central dopaminergic markers early in disease (Hinkle et al., 2018), and GI symptoms often occur prior to motor diagnosis (Cersosimo et al., 2013; Fasano et al., 2015).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
Small studies suggest that transcutaneous vagal nerve stimulation may improve gastroenteric symptoms in Parkinson disease.
“Small studies also suggest that transcutaneous vagal nerve stimulation may improve gastroenteric symptoms (Kaut et al., 2019).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Kaut et al., 2019 source
- Premisecitation
Lesions and impaired circuits in the brainstem can alter gastric motor function by interrupting parasympathetic pathways, including vagal afferent fibers, neurons in the nucleus tractus solitarii, and preganglionic efferents arising from the dorsal motor nucleus of the vagus.
“Lesions and impaired circuits in the brainstem can alter gastric motor function by interrupting parasympathetic pathways, including vagal afferent fibers, neurons in the nucleus tractus solitarii (NTS), and preganglionic efferents arising from the dorsal motor nucleus of the vagus (DMV) (Travagli et al., 2006).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Travagli et al., 2006 source
- Premisecitation
Brainstem pathology may present with isolated vomiting or severe nausea due to involvement of the vomiting center in the floor of the fourth ventricle.
“Clinically, brainstem pathology may present with isolated vomiting or severe nausea due to involvement of the vomiting center in the floor of the fourth ventricle (Wood et al., 1985).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Wood et al., 1985 source
- Premisecitation
Gastrointestinal involvement (vomiting, paralytic ileus, constipation, and chronic pseudo-obstruction) has been reported in acute, subacute, and congenital forms of pandysautonomia.
“Gastrointestinal involvement (vomiting, paralytic ileus, constipation, and chronic pseudo-obstruction) has been reported in acute, subacute, and congenital forms (Camilleri, 1990; Suarez et al., 1994).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
Vomiting episodes in familial dysautonomia may be accompanied by increased circulating dopamine that likely activates dopamine receptors in the chemoreceptor trigger zone.
“Vomiting episodes may be accompanied by biochemical and autonomic signatures, including increased circulating dopamine that likely activates dopamine receptors in the chemoreceptor trigger zone (Norcliffe-Kaufmann et al., 2013b).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Norcliffe-Kaufmann et al., 2013b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Cytomegalovirus infection of the myenteric plexus can produce chronic intestinal pseudo-obstruction.
“Autoantibodies to muscarinic M3 receptors have been reported in selective dysautonomia (Palma et al., 2020), and cytomegalovirus infection of the myenteric plexus can produce chronic intestinal pseudo-obstruction (Sonsino et al., 1984).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Sonsino et al., 1984 source
- Premisecitation
Carbidopa, which reduces peripheral dopamine synthesis, has been reported to lessen the frequency and intensity of vomiting attacks in familial dysautonomia.
“Carbidopa, which reduces peripheral dopamine synthesis, has been reported to lessen the frequency and intensity of vomiting attacks (Norcliffe-Kaufmann et al., 2013a).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Norcliffe-Kaufmann et al., 2013a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Classic descriptions of Shy-Drager syndrome (now encompassed within multiple system atrophy) include constipation, gastroparesis, and, in severe cases, intestinal pseudo-obstruction.
“Classic descriptions of Shy-Drager syndrome (now encompassed within multiple system atrophy, MSA) include constipation, gastroparesis, and, in severe cases, intestinal pseudo-obstruction (Shy et al., 1960).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Shy et al., 1960 source
- Premisecitation
Dysautonomic crises in familial dysautonomia may respond to benzodiazepines as well as to α2-adrenergic agonists (e.g., clonidine or dexmedetomidine) that reduce norepinephrine release.
“These crises may respond to benzodiazepines as well as to α2-adrenergic agonists (e.g., clonidine or dexmedetomidine) that reduce norepinephrine release (Axelrod et al., 1991).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Axelrod et al., 1991 source
- Premisecitation
Several post-infectious syndromes have been described, including selective cholinergic dysautonomia with GI dysmotility after infectious mononucleosis (Epstein-Barr virus) or influenza A.
“Several post-infectious syndromes have been described, including selective cholinergic dysautonomia with GI dysmotility after infectious mononucleosis (Epstein-Barr virus) or influenza A (Lukkarinen et al., 2010; Vassallo et al., 1991).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
When aspiration or feeding failure is recurrent in familial dysautonomia, surgical strategies such as fundoplication or feeding tube placement may be required.
“When aspiration or feeding failure is recurrent, surgical strategies such as fundoplication or feeding tube placement may be required (Axelrod et al., 1991).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Axelrod et al., 1991 source
- Premisecitation
In a community cohort from Olmsted County, Minnesota, the association between constipation and type 2 diabetes was less clear.
“In a community cohort from Olmsted County, Minnesota, constipation (with or without laxative use) was more common in type 1 diabetes than in controls, whereas the association was less clear in type 2 diabetes; concomitant medications and bladder dysfunction were common contributors (Maleki et al., 2000).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Maleki et al., 2000 source
- Premisecitation
Emerging evidence suggests that macrophage phenotypes within the gut wall influence susceptibility to oxidative stress in diabetes.
“Pathologic correlates include ‘autovagotomy’ (loss of unmyelinated axons) and loss of interstitial cells of Cajal, with emerging evidence that macrophage phenotypes within the gut wall influence susceptibility to oxidative stress (Camilleri et al., 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Camilleri et al., 2018 source
- Premisecitation
GI symptoms are more frequent in diabetes mellitus than in age- and sex-matched controls.
“Population-based studies demonstrate that GI symptoms are more frequent in diabetes mellitus than in age- and sex-matched controls (Ricci et al., 2000).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Ricci et al., 2000 source
- Premisecitation
Amylin analogs and GLP-1 receptor agonists, particularly short-acting agents, can worsen gastric emptying.
“Amylin analogs and GLP-1 receptor agonists, particularly short-acting agents, can worsen gastric emptying and should be considered when symptoms arise or deteriorate (Maselli et al., 2021; Vella et al., 2002).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
In a community cohort from Olmsted County, Minnesota, concomitant medications and bladder dysfunction were common contributors to constipation in diabetes.
“In a community cohort from Olmsted County, Minnesota, constipation (with or without laxative use) was more common in type 1 diabetes than in controls, whereas the association was less clear in type 2 diabetes; concomitant medications and bladder dysfunction were common contributors (Maleki et al., 2000).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Maleki et al., 2000 source
- Premisecitation
GI dysmotility can occur as a paraneoplastic manifestation, most often in association with small cell lung carcinoma or other neuroendocrine tumors.
“Gastrointestinal dysmotility can occur as a paraneoplastic manifestation, most often in association with small cell lung carcinoma or other neuroendocrine tumors (Tannoury et al., 2021).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Tannoury et al., 2021 source
- Premisecitation
In selected patients with spinal cord injury, computerized stimulation of the sacral anterior roots may improve pelvic colonic and anorectal sphincter function, generally in conjunction with S2-S4 posterior sacral rhizotomy to reduce the risk of autonomic dysreflexia.
“In selected patients, computerized stimulation of the sacral anterior roots may improve pelvic colonic and anorectal sphincter function, generally in conjunction with S2–S4 posterior sacral rhizotomy to reduce the risk of autonomic dysreflexia (Rasmussen et al., 2015; Valles et al., 2009).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
In a community cohort from Olmsted County, Minnesota, constipation with or without laxative use was more common in type 1 diabetes than in controls.
“In a community cohort from Olmsted County, Minnesota, constipation (with or without laxative use) was more common in type 1 diabetes than in controls, whereas the association was less clear in type 2 diabetes; concomitant medications and bladder dysfunction were common contributors (Maleki et al., 2000).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Maleki et al., 2000 source
- Interpretationcitation
The pattern of reduced postprandial colonic motor activity with intact neostigmine response and normal myenteric morphology supports a mechanism consistent with extrinsic rather than intrinsic enteric denervation in lipomatosis of nerve.
“This pattern supports a mechanism consistent with extrinsic (rather than intrinsic enteric) denervation (Marek et al., 2020).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Marek et al., 2020 source
- Premisecitation
Chronic diarrhea in HIV has been attributed to autonomic mechanisms, including heightened extrinsic parasympathetic drive to the intestine and/or injury to adrenergic fibers within enteric plexuses.
“Chronic diarrhea has also been attributed to autonomic mechanisms, including heightened extrinsic parasympathetic drive to the intestine (Coker et al., 1992) and/or injury to adrenergic fibers within enteric plexuses; additionally, diarrhea may occur as an adverse effect of nelfinavir-containing antiretroviral regimens (Bardsley-Elliot et al., 2000).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Coker et al., 1992 source
- Premisecitation
Thymoma-associated immune dysregulation has been linked to severe GI syndromes such as intestinal pseudo-obstruction and chronic diarrhea.
“MG can also co-occur with autoimmune autonomic neuropathy (Vernino et al., 2001), and thymoma-associated immune dysregulation has been linked to severe GI syndromes such as intestinal pseudo-obstruction and chronic diarrhea (Anderson et al., 1996; Gupta et al., 1985).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Anderson et al., 1996 source
- cites Gupta et al., 1985
- Premisecitation
Because chest radiography may be unrevealing, chest computed tomography and/or whole-body FDG-PET can aid tumor detection and staging.
“Because chest radiography may be unrevealing, chest computed tomography and/or whole-body fluorodeoxyglucose positron emission tomography (FDG-PET) can aid tumor detection and staging (Koike et al., 2011).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Koike et al., 2011 source
- Premisecitation
Because presentations of MNGIE overlap with more common functional and inflammatory disorders, diagnostic pitfalls are frequent.
“Because presentations overlap with more common functional and inflammatory disorders, diagnostic pitfalls are frequent (Filosto et al., 2011).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Filosto et al., 2011 source
- Premisecitation
Patients with paraneoplastic enteric neuropathy may present with constipation, gastroparesis, intestinal pseudo-obstruction, and esophageal spasm or achalasia.
“Patients may present with constipation, gastroparesis, intestinal pseudo-obstruction, and esophageal spasm or achalasia (Chinn et al., 1988).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Chinn et al., 1988 source
- Premisecitation
In a series of 10 patients with lipomatosis of nerve involving the lumbosacral plexus and/or sciatic nerve, three individuals had early-onset colonic diverticulosis.
“In a series of 10 patients with lipomatosis of nerve involving the lumbosacral plexus and/or sciatic nerve, three individuals were noted to have early-onset colonic diverticulosis, raising the possibility of involvement of sacral pathways supplying the sigmoid colon.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Marek et al., 2020 source
- Premisecitation
Histopathology suggested enteric neuropathic mechanisms in some NF1 cases.
“Among those with motility testing, abnormalities included esophageal achalasia/spasm, delayed gastric emptying, slow-transit constipation, and pelvic floor dyssynergia; histopathology suggested enteric neuropathic mechanisms in some cases (Damianos et al., 2025).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Damianos et al., 2025 source
- Premisecitation
In a large single-center cohort study of patients with documented NF1, a subset developed clinically significant bowel obstruction or dysmotility.
“In a large single-center cohort study of patients with documented NF1, a subset developed clinically significant bowel obstruction or dysmotility.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Damianos et al., 2025 source
- Premisecitation
Circulating IgG autoantibodies such as ANNA-1 (anti-Hu), directed against neuronal nuclear antigens, support an immune attack on the enteric nervous system in paraneoplastic dysmotility.
“Circulating IgG autoantibodies such as ANNA-1 (anti-Hu), directed against neuronal nuclear antigens, support an immune attack on the enteric nervous system in paraneoplastic dysmotility (Lennon et al., 1991).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Lennon et al., 1991 source
- Premisecitation
Children with Duchenne and Becker muscular dystrophy show evolution of gastric electrical activity abnormalities and altered gastric emptying over time, consistent with progressive involvement of the gastric neuromuscular apparatus.
“Children with Duchenne and Becker muscular dystrophy show evolution of gastric electrical activity abnormalities and altered gastric emptying over time, consistent with progressive involvement of the gastric neuromuscular apparatus (Borrelli et al., 2005).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Borrelli et al., 2005 source
- Premisecitation
Myasthenia gravis can co-occur with autoimmune autonomic neuropathy.
“MG can also co-occur with autoimmune autonomic neuropathy (Vernino et al., 2001), and thymoma-associated immune dysregulation has been linked to severe GI syndromes such as intestinal pseudo-obstruction and chronic diarrhea (Anderson et al., 1996; Gupta et al., 1985).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Vernino et al., 2001 source
- Premisecitation
In that study, racecadotril also improved stool output relative to baseline.
“and racecadotril also improved stool output relative to baseline (Beaugerie et al., 1996).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Beaugerie et al., 1996
- Interpretationnone given
Neurologic and systemic diseases can disrupt gastric and pan-gut motor function through lesions of the brain, brainstem, spinal cord, autonomic nerves, enteric plexuses, pacemaker cells, and smooth muscle.
“Neurologic and systemic diseases can disrupt gastric and pan-gut motor function through lesions of the brain, brainstem, spinal cord, autonomic nerves, enteric plexuses, pacemaker cells, and smooth muscle.”
Quote in the paperNot a substantial claim - Premisecitation
Severe phenotypes of myotonic dystrophy include megacolon due to degenerative neuropathy of the myenteric plexus.
“Severe phenotypes include megacolon due to degenerative neuropathy of the myenteric plexus (Yoshida et al., 1988) and pseudo-obstruction, including in pediatric cases with smooth muscle and myenteric pathology (Ho et al., 2019; Pelizzo et al., 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Yoshida et al., 1988 source
- Interpretationreasoning
When neurogenic dysmotility is suspected, integration of targeted autonomic testing with segmental motility studies can improve diagnostic localization and clarify whether symptoms reflect predominant vagal, sympathetic, enteric, or myopathic mechanisms.
“When neurogenic dysmotility is suspected, integration of targeted autonomic testing (Tables 3 and 4) with segmental motility studies can improve diagnostic localization and clarify whether symptoms reflect predominant vagal, sympathetic, enteric, or myopathic mechanisms.”
Quote in the paperSubstantial claim
- May combine two claims. 42
- Classified as probably not a substantial claim. 21
May combine two claims.
PremisecitationCholinesterase inhibitors can contribute to nausea, vomiting, diarrhea, and weight loss, and several studies have documented increased GI adverse events with these agents.
“Cholinesterase inhibitors can contribute to nausea, vomiting, diarrhea, and weight loss, and several studies have specifically documented increased GI adverse events with these agents (Darreh-Shori et al., 2010; Farlow et al., 2011).”
Quote in the paperNot a substantial claim1 of 2 sources checkedMay combine two claims.
PremisecitationMultiple studies have characterized swallowing impairment in ALS and emphasize the importance of early recognition and multidisciplinary management.
“Multiple studies have characterized swallowing impairment in ALS and emphasize the importance of early recognition and multidisciplinary management (Chapin et al., 2020; Elbe et al., 2020; Toepfer et al., 1999; Toepfer et al., 1997).”
Quote in the paperNot a substantial claim2 of 3 sources checked- cites Chapin et al., 2020 source
- cites Elbe et al., 2020 source
- cites Toepfer et al., 1999 source
The Introduction mentions bulbar paresis, but the Discussion says participants swallowed the test meal within normal time limits; the study assesses gastric emptying rather than characterizing swallowing impairment. Searches for dysphagia, early recognition, and multidisciplinary management found no passage addressing those claims. The normal test-meal swallowing result does not contradict the broader claim about ALS. (LLM, conf=0.76)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationGI symptoms may predate motor features of Parkinson disease by years, consistent with the concept that α-synuclein pathology can involve the ENS and vagal/brainstem autonomic nuclei early in disease.
“GI symptoms may predate motor features by years, consistent with the concept that α-synuclein pathology can involve the ENS and vagal/brainstem autonomic nuclei early in disease (Rietdijk et al., 2017; Travagli et al., 2020).”
Quote in the paperSubstantial claim1 of 2 sources checked- cites Rietdijk et al., 2017 source
The “Preclinical and Clinical Evidence” section says digestive complaints can occur before motor symptoms and reports Lewy pathology in the ENS. The “Enteric Route: αSyn Spreading via Vagal Nerve” section describes pathology in the vagal nerve and dorsal motor nucleus of the vagus early in the proposed progression. The copy does not specify that GI symptoms precede motor features by years; no page numbers are available in the indexed passages. (LLM, conf=0.86)
Experimental — accuracy not yet measured - cites Travagli et al., 2020 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationEnteral feeding strategies may be needed when aspiration risk is high in acute stroke.
“Early screening and structured dysphagia management improve outcomes (Arnold et al., 2016; Martino et al., 2005), and enteral feeding strategies may be needed when aspiration risk is high (Duncan et al., 2020; Geeganage et al., 2012).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Duncan et al., 2020 source
The Discussion (page unavailable) mentions tube-feeding cessation in studies of tracheostomised acute stroke patients, and the Introduction discusses aspiration as a symptom of dysphagia. The paper does not say that high aspiration risk is an indication for enteral feeding or recommend an enteral feeding strategy. (LLM, conf=0.72)
Experimental — accuracy not yet measured - cites Geeganage et al., 2012 source
May combine two claims.
PremisecitationLarge epidemiologic studies suggest that truncal vagotomy is associated with a reduced risk of subsequent Parkinson disease, supporting a potential gut-brain contribution to pathogenesis.
“Large epidemiologic studies also suggest that truncal vagotomy is associated with a reduced risk of subsequent PD, supporting a potential gut–brain contribution to pathogenesis (Liu et al., 2017).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Liu et al., 2017 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationDistinguishing slow-transit constipation from evacuation disorders (e.g., pelvic floor dyssynergia) is a useful first step because confirmatory tests and treatment strategies differ.
“A useful first step is to distinguish slow-transit constipation from evacuation disorders (e.g., pelvic floor dyssynergia), because confirmatory tests and treatment strategies differ (Manabe et al., 2010; Metcalf et al., 1987).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Manabe et al., 2010 source
The Discussion (page unavailable) says colonic-transit measurements may guide further diagnostic tests and the choice of therapy, including prokinetics for patients with delayed transit. It does not discuss distinguishing slow-transit constipation from evacuation disorders or specify different confirmatory tests and treatments for those disorders. (LLM, conf=0.82)
Experimental — accuracy not yet measured - cites Metcalf et al., 1987 source
May combine two claims.
PremisecitationSialorrhea in Parkinson disease can be managed pharmacologically with anticholinergics such as glycopyrrolate or scopolamine, although these medications can have negative effects on other aspects of gastrointestinal function; alternatively, botulinum toxin injections can be very effective and are less likely to have negative systemic effects.
“Sialorrhea can be managed pharmacologically with anticholinergics such as glycopyrrolate or scopolamine, although these medications can have negative effects on other aspects of gastrointestinal function; alternatively, botulinum toxin injections can be very effective and are less likely to have negative systemic effects (Seppi et al., 2011).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Seppi et al., 2011 source
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationBulbar dysfunction and dysphagia have been described in post-polio syndromes, where chronic neuromuscular weakness and impaired coordination can compromise safe swallowing and nutrition.
“Bulbar dysfunction and dysphagia have also been described in post-polio syndromes, where chronic neuromuscular weakness and impaired coordination can compromise safe swallowing and nutrition (Kay et al., 2018; Oluwasanmi et al., 2019).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Kay et al., 2018 source
- cites Oluwasanmi et al., 2019 source
The Clinical Manifestations > Dysphagia section links bulbar-muscle involvement to swallowing difficulty, aspiration risk, and nutritional problems. Management of Postpolio Syndrome also says laryngeal and esophageal muscle weakness can cause dysphagia. The copy does not specifically identify impaired coordination as a contributing mechanism; page numbers were not provided. (LLM, conf=0.86)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationFamilial dysautonomia is a hereditary sensory and autonomic neuropathy in which feeding and GI motor problems are often present from infancy.
“Familial dysautonomia is a hereditary sensory and autonomic neuropathy in which feeding and GI motor problems are often present from infancy (Rubin et al., 2017).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Rubin et al., 2017 source
The Introduction describes familial dysautonomia as a congenital sensory and autonomic neuropathy, and The FD phenotype identifies it as a hereditary sensory and autonomic neuropathy with typical swallowing difficulty and gastrointestinal dysfunction. The copy does not establish that feeding and GI motor problems are often present from infancy, or specifically characterize the GI dysfunction as a motor problem. (LLM, conf=0.86)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationIn neuromyelitis optica spectrum disorder, persistent nausea and vomiting due to area postrema involvement is a well-described 'area postrema syndrome' and should prompt neurologic evaluation in appropriate contexts.
“In neuromyelitis optica spectrum disorder, persistent nausea and vomiting due to area postrema involvement is a well-described ‘area postrema syndrome’ and should prompt neurologic evaluation in appropriate contexts (Popescu et al., 2011).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Popescu et al., 2011 source
May combine two claims.
PremisecitationPure autonomic failure is a chronic neurogenic autonomic disorder in which gastrointestinal involvement may include constipation and other manifestations of dysmotility.
“Pure autonomic failure (PAF) is a chronic neurogenic autonomic disorder in which gastrointestinal involvement may include constipation and other manifestations of dysmotility (Sakakibara et al., 2000; Thatcher et al., 1987; Yamanaka et al., 2006).”
Quote in the paperNot a substantial claim1 of 3 sources checkedMay combine two claims.
PremisecitationNeuropathologic overlap between pure autonomic failure and Lewy body disorders and multiple system atrophy has been described, supporting close longitudinal clinical surveillance.
“Neuropathologic overlap with Lewy body disorders and multiple system atrophy has been described, supporting close longitudinal clinical surveillance (Hague et al., 1997; Singer et al., 2021).”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites Hague et al., 1997 source
- cites Singer et al., 2021 source
The Discussion (page unavailable) describes Lewy body pathology in autopsy reports of patients with pure autonomic failure and calls for continued surveillance. The Results, under “Follow-up and Phenoconversion” (page unavailable), report conversion to multiple system atrophy, confirmed at autopsy in two patients, but do not establish neuropathologic overlap between pure autonomic failure and multiple system atrophy. (LLM, conf=0.84)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationPOTS may co-occur with hypermobility-type Ehlers-Danlos syndrome, fibromyalgia, chronic fatigue, interstitial cystitis, and functional GI disorders.
“POTS may co-occur with hypermobility-type Ehlers–Danlos syndrome, fibromyalgia, chronic fatigue, interstitial cystitis (DiBaise et al., 2018), and functional GI disorders (Tai et al., 2020).”
Quote in the paperNot a substantial claim1 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationNewer disease-modifying therapies, including antisense oligonucleotides and RNA interference approaches, are increasingly used for hereditary transthyretin amyloidosis.
“Newer disease-modifying therapies, including antisense oligonucleotides and RNA interference approaches, are increasingly used for hereditary transthyretin amyloidosis (Gertz et al., 2019).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Gertz et al., 2019 source
The Abstract Introduction identifies inotersen as an antisense oligonucleotide and patisiran as an RNA interference therapy. The Therapeutic landscape for ATTR section says both recently received marketing authorization for hereditary ATTR neuropathy and have demonstrated efficacy. The review does not establish that their clinical use was increasing. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationReviews of adult myositis emphasize the spectrum of esophageal and intestinal complications.
“Juvenile dermatomyositis has been associated with novel GI tract manifestations (Laskin et al., 1999), and reviews of adult myositis emphasize the spectrum of esophageal and intestinal complications (Ebert, 2010).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Ebert, 2010 source
May combine two claims.
PremisecitationExperimental immunization with neuronal nicotinic acetylcholine receptors can reproduce autonomic and GI dysfunction in animal models, supporting a pathogenic role for some antibody-mediated processes.
“Experimental immunization with neuronal nicotinic acetylcholine receptors can reproduce autonomic and GI dysfunction in animal models, supporting a pathogenic role for some antibody-mediated processes (Lennon et al., 2003).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Lennon et al., 2003 source
May combine two claims.
PremisecitationNF1 patients can develop a range of intra-abdominal tumors, including plexiform neurofibromas, malignant peripheral nerve sheath tumors, gastrointestinal stromal tumors related to interstitial cells of Cajal hyperplasia, neuroendocrine tumors, and embryonal tumors such as rhabdomyosarcoma.
“NF1 patients can develop a range of intra-abdominal tumors, including plexiform neurofibromas, malignant peripheral nerve sheath tumors, gastrointestinal stromal tumors related to interstitial cells of Cajal hyperplasia, neuroendocrine tumors, and embryonal tumors such as rhabdomyosarcoma (Dare et al., 2020; Xie et al., 2018).”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites Dare et al., 2020 source
- cites Xie et al., 2018 source
The Introduction (page unavailable) says NF1 can be associated with stromal and neuroendocrine tumors, and the case report documents rectal neuroendocrine tumors. Our copy does not identify plexiform neurofibromas, malignant peripheral nerve sheath tumors, interstitial cells of Cajal hyperplasia, or rhabdomyosarcoma as part of the claimed range. (LLM, conf=0.87)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationNeurologic immune-related adverse events from immune checkpoint inhibitors include autonomic neuropathy and can present with severe GI dysmotility.
“Neurologic immune-related adverse events from immune checkpoint inhibitors include autonomic neuropathy and can present with severe GI dysmotility (Bertrand et al., 2015).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Bertrand et al., 2015 source
The Results (‘Other irAEs’; page unavailable) describe neurologic immune-related adverse events associated with anti-CTLA-4 treatment. The References (page unavailable) include cases of ipilimumab-associated enteric neuropathy with occlusion or severe constipation, supporting the GI-dysmotility aspect. The paper does not explicitly call these cases autonomic neuropathy, and its review concerns anti-CTLA-4 antibodies rather than immune checkpoint inhibitors generally. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenGastric symptoms rarely occur in isolation; the same disease processes often affect esophageal, bowel, and anorectal function and may coexist with orthostatic intolerance, sweating abnormalities, urinary dysfunction, or neuropathic pain.
“At the same time, gastric symptoms rarely occur in isolation; the same disease processes often affect esophageal, bowel, and anorectal function and may coexist with orthostatic intolerance, sweating abnormalities, urinary dysfunction, or neuropathic pain.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationPrevertebral ganglia integrate visceral afferent information and participate in local reflex arcs, including inhibitory enteroenteric reflexes that coordinate activity across segments.
“Prevertebral ganglia integrate visceral afferent information and participate in local reflex arcs, including inhibitory enteroenteric reflexes that coordinate activity across segments (Kreulen et al., 1979; Langley et al., 1895; Szurszewski et al., 1984) (Fig. 2).”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites Kreulen et al., 1979 source
- cites Langley et al., 1895
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites Szurszewski et al., 1984
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Interpretationnone givenWhen GI circuits are disrupted by neurologic or systemic disease, symptoms commonly cluster around motor dysfunction rather than occurring as isolated sensory or secretory complaints.
“When these circuits are disrupted by neurologic or systemic disease, symptoms commonly cluster around motor dysfunction (dysphagia, impaired gastric emptying, pseudo-obstruction, constipation, or incontinence) rather than occurring as isolated sensory or secretory complaints.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationExtrinsic parasympathetic innervation reaches the upper gastrointestinal tract mainly through the vagus nerve, while sacral outflow supplies the distal colon and anorectum, generally with excitatory effects on non-sphincteric muscle and propulsion.
“Extrinsic parasympathetic innervation reaches the upper gastrointestinal tract mainly through the vagus nerve, while sacral outflow supplies the distal colon and anorectum, generally with excitatory effects on non-sphincteric muscle and propulsion.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Camilleri, 1997
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S4 (based).
Interpretationnone givenGastric manifestations are often the most clinically visible end-organ expression of autonomic disease because they drive nausea, vomiting, early satiety, postprandial distress, malnutrition risk, and impaired drug absorption.
“Although dysfunction may occur anywhere along the alimentary tract, gastric manifestations are often the most clinically visible ‘end-organ’ expression of autonomic disease because they drive nausea, vomiting, early satiety, postprandial distress, malnutrition risk, and impaired drug absorption.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationSympathetic control arises from thoracolumbar segments via prevertebral ganglia; in most regions it inhibits propulsive smooth muscle activity and enhances sphincter tone, acting as a functional 'brake' on transit.
“Sympathetic control arises from thoracolumbar segments via prevertebral ganglia; in most regions it inhibits propulsive smooth muscle activity and enhances sphincter tone, acting as a functional ‘brake’ on transit.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Camilleri, 1997
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenChronic intestinal pseudo-obstruction occupies an important middle ground between focal and diffuse neuromuscular disease: patients appear obstructed clinically and radiographically, but mechanical causes are absent and the underlying mechanism may be neuropathic, myopathic, or mixed.
“Chronic intestinal pseudo-obstruction occupies an important middle ground between focal and diffuse neuromuscular disease: patients appear obstructed clinically and radiographically, but mechanical causes are absent and the underlying mechanism may be neuropathic, myopathic, or mixed.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningA system-based autonomic testing approach allows for assessment of distribution and severity of autonomic failure, can help localize dysfunction to preganglionic versus postganglionic pathways, and can support broader diagnostic evaluation when autonomic impairment is widespread.
“This system-based approach allows for the assessment of distribution and severity of autonomic failure, can help localize dysfunction to preganglionic versus postganglionic pathways, and can support broader diagnostic evaluation when autonomic impairment is widespread.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationMore widespread autonomic dysfunction is common in dementia with Lewy bodies, adding another cause for GI symptoms akin to those in Parkinson's disease.
“More widespread autonomic dysfunction is common in dementia with Lewy bodies adding another cause for GI symptoms akin to those discussed in more detail in the following section on Parkinson’s disease, another synucleinopathy (Thaisetthawatkul et al., 2004).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Thaisetthawatkul et al., 2004 source
Probably not a substantial claim: may not pass S4 (based).
Interpretationnone givenIntegrating segmental motility measurements with autonomic testing can clarify whether symptoms reflect isolated enteric disease, extrinsic autonomic denervation, or combined neuromuscular pathology.
“In clinical practice, integrating segmental motility measurements with autonomic testing can clarify whether symptoms reflect isolated enteric disease, extrinsic autonomic denervation, or combined neuromuscular pathology.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
InterpretationreasoningDisruption of vagal circuits, enteric inhibitory pathways, or pyloric control can present with similar symptoms despite distinct mechanisms.
“Disruption of vagal circuits, enteric inhibitory pathways, or pyloric control can therefore present with similar symptoms despite distinct mechanisms.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenEsophageal dysphagia and reflux symptoms may reflect vagal dysfunction, esophageal myopathy, or primary esophageal motor disorders and warrant endoscopic and high-resolution manometric evaluation.
“Esophageal dysphagia and reflux symptoms may reflect vagal dysfunction, esophageal myopathy, or primary esophageal motor disorders and warrant endoscopic and high-resolution manometric evaluation.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationRandomized controlled trials have demonstrated benefit of polyethylene glycol 3350 and lubiprostone in Parkinson disease-related constipation.
“Randomized controlled trials have demonstrated benefit of polyethylene glycol 3350 (Zangaglia et al., 2007) and lubiprostone (Ondo et al., 2012) in PD-related constipation, and dopaminergic agents such as apomorphine can influence defecatory function (Edwards et al., 1993b).”
Quote in the paperNot a substantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenGastric symptoms such as early satiety, postprandial fullness, nausea, and vomiting may reflect delayed emptying (gastroparesis), impaired accommodation, pyloric dysfunction, or, less commonly, accelerated gastric emptying.
“Gastric symptoms such as early satiety, postprandial fullness, nausea, and vomiting may reflect delayed emptying (gastroparesis), impaired accommodation, pyloric dysfunction, or, less commonly, accelerated gastric emptying.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationConstipation after stroke is common and is driven by a combination of reduced mobility, impaired cortical control of defecatory reflexes, medication effects, and autonomic imbalance.
“Constipation after stroke is common and is driven by a combination of reduced mobility, impaired cortical control of defecatory reflexes, medication effects, and autonomic imbalance (Cheng et al., 2020; Li et al., 2017; Yi et al., 2011).”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites Cheng et al., 2020 source
- cites Li et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites Yi et al., 2011
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationAcute colonic pseudo-obstruction has been described in the setting of stroke.
“Acute colonic pseudo-obstruction has also been described in the setting of stroke (Reynolds et al., 1977).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Reynolds et al., 1977 source
Probably not a substantial claim: may not pass S3 (load-bearing).
InterpretationreasoningLoss or dysfunction of pacemaker/intermediary cells, together with enteric neuropathy or myopathy, can produce gastric dysrhythmias, impaired accommodation, pyloric dysfunction, and delayed or rapid emptying.
“Loss or dysfunction of these cells, together with enteric neuropathy or myopathy, can produce gastric dysrhythmias, impaired accommodation, pyloric dysfunction, and delayed or rapid emptying.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationGastric motor dysfunction can impair levodopa pharmacokinetics and contribute to motor fluctuations in Parkinson disease.
“Gastric motor dysfunction can impair levodopa pharmacokinetics and contribute to motor fluctuations (Pfeiffer et al., 2020); systematic reviews support the association between PD and gastroparesis (Heetun et al., 2012).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Pfeiffer et al., 2020 source
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Interpretationnone givenOropharyngeal dysphagia is a high-stakes symptom because it increases aspiration risk and can limit nutrition and hydration.
“Oropharyngeal dysphagia is a high-stakes symptom because it increases aspiration risk and can limit nutrition and hydration.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationIn acute spinal cord injury, "acute abdomen" may present atypically: patients may exhibit vague or poorly localized abdominal pain, vomiting, or agitation, and only about half develop objective signs such as focal tenderness, fever, or leukocytosis.
“Importantly, “acute abdomen” in this population may present atypically: instead of guarding or absent bowel sounds, patients may exhibit vague or poorly localized abdominal pain, vomiting, or agitation, and only about half develop objective signs such as focal tenderness, fever, or leukocytosis (Ebert, 2012).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Ebert, 2012
May combine two claims.
PremisecitationPersistent upper gastrointestinal motility problems are relatively uncommon in the chronic phase of spinal cord injury, whereas colonic and anorectal dysfunction predominate, reflecting loss of supraspinal modulation of sacral parasympathetic outflow and impaired postprandial colonic motor responses.
“Persistent upper gastrointestinal motility problems are relatively uncommon in the chronic phase, whereas colonic and anorectal dysfunction predominate, reflecting loss of supraspinal modulation of sacral parasympathetic outflow and impaired postprandial colonic motor responses (Bruninga et al., 1997).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Bruninga et al., 1997
May combine two claims.
PremisecitationCommon features of familial dysautonomia include oropharyngeal incoordination, poor suck, excessive drooling, gastroesophageal reflux, and episodic vomiting that is often triggered by physical or emotional stress.
“Common features include oropharyngeal incoordination, poor suck, excessive drooling, gastroesophageal reflux, and episodic vomiting that is often triggered by physical or emotional stress (Krausz et al., 1994).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Krausz et al., 1994 source
May combine two claims.
PremisecitationStructural and functional abnormalities in familial dysautonomia include reduced neuronal density in the myenteric plexus and severe esophageal dysmotility with dilatation and fluid stasis in some patients.
“Structural and functional abnormalities include reduced neuronal density in the myenteric plexus (Bar-Shai et al., 2004) and severe esophageal dysmotility with dilatation and fluid stasis in some patients (Palma et al., 2018).”
Quote in the paperNot a substantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPOTS is characterized by an exaggerated heart rate rise with upright posture in the absence of orthostatic hypotension.
“It is characterized by an exaggerated heart rate rise with upright posture in the absence of orthostatic hypotension (Schondorf et al., 1993).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Schondorf et al., 1993 source
May combine two claims.
PremisecitationEsophageal and gastric transit may be delayed in familial dysautonomia, which can contribute to recurrent aspiration pneumonia.
“Esophageal and gastric transit may be delayed, which can contribute to recurrent aspiration pneumonia (Krausz et al., 1994).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Krausz et al., 1994 source
Probably not a substantial claim: may not pass S4 (based).
Interpretationnone givenWhen brainstem symptoms are accompanied by more widespread autonomic deficits, particularly combined vagal and preganglionic sympathetic involvement suggested by anhidrosis on thermoregulatory sweat testing with preserved postganglionic responses on QSART, neuroimaging and broader evaluation for central nervous system lesions are warranted.
“When brainstem symptoms are accompanied by more widespread autonomic deficits, particularly combined vagal and preganglionic sympathetic involvement suggested by anhidrosis on thermoregulatory sweat testing with preserved postganglionic responses on quantitative sudomotor axon reflex testing (QSART), neuroimaging and broader evaluation for central nervous system lesions are warranted (Tables 3 and”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationChronic neurogenic bowel dysfunction is common, reported in roughly 27%-62% of individuals following spinal cord injury, and most often manifests as constipation, bloating, abdominal discomfort, rectal bleeding, hemorrhoids, fecal incontinence, and episodes of autonomic hyperreflexia; gallstones are also frequent (17%-31%).
“By contrast, chronic neurogenic bowel dysfunction is common, reported in roughly 27%–62% of individuals following spinal cord injury, and most often manifests as constipation, bloating, abdominal discomfort, rectal bleeding, hemorrhoids, fecal incontinence, and episodes of autonomic hyperreflexia; gallstones are also frequent (17%–31%) (Ebert, 2012).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Ebert, 2012
May combine two claims.
Interpretationnone givenGastric emptying abnormalities are not central features in ALS, but reduced mobility, respiratory compromise, and medication effects can contribute to constipation and feeding difficulties.
“Gastric emptying abnormalities are not central features, but reduced mobility, respiratory compromise, and medication effects can contribute to constipation and feeding difficulties.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationAcute spinal cord injury can be accompanied by transient disturbances of upper gastrointestinal motility, including dysphagia; ileus and acalculous cholecystitis have also been described, particularly after acute cervical injury.
“Acute spinal cord injury can be accompanied by transient disturbances of upper gastrointestinal motility, including dysphagia; ileus and acalculous cholecystitis have also been described, particularly after acute cervical injury (Wolf et al., 2003).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Wolf et al., 2003 source
May combine two claims.
PremisecitationPathologic correlates of diabetic GI dysfunction include autovagotomy, loss of unmyelinated axons, and loss of interstitial cells of Cajal.
“Pathologic correlates include ‘autovagotomy’ (loss of unmyelinated axons) and loss of interstitial cells of Cajal, with emerging evidence that macrophage phenotypes within the gut wall influence susceptibility to oxidative stress (Camilleri et al., 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Camilleri et al., 2018 source
May combine two claims.
PremisecitationDiabetes can affect motility along the entire gut, producing gastroparesis often with antral hypomotility and pyloric dysfunction, rapid gastric emptying, impaired gastric accommodation, diarrhea, constipation, and fecal incontinence.
“Diabetes can affect motility along the entire gut, producing gastroparesis (often with antral hypomotility and pyloric dysfunction), rapid gastric emptying, impaired gastric accommodation, diarrhea, constipation, and fecal incontinence (Camilleri et al., 2018; Chedid et al., 2019).”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationAmong NF1 patients with motility testing, abnormalities included esophageal achalasia or spasm, delayed gastric emptying, slow-transit constipation, and pelvic floor dyssynergia.
“Among those with motility testing, abnormalities included esophageal achalasia/spasm, delayed gastric emptying, slow-transit constipation, and pelvic floor dyssynergia; histopathology suggested enteric neuropathic mechanisms in some cases (Damianos et al., 2025).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Damianos et al., 2025 source
May combine two claims.
PremisecitationIn one case of lipomatosis of nerve, postprandial colonic motor activity was reduced, while pharmacologic stimulation with intravenous neostigmine remained intact; myenteric neuronal morphology was reported to be normal.
“In one case, postprandial colonic motor activity was reduced, while pharmacologic stimulation with intravenous neostigmine remained intact; myenteric neuronal morphology was reported to be normal.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Marek et al., 2020 source
May combine two claims.
PremisecitationConstipation is frequent in children with neurofibromatosis type 1 and can be associated with increased rectal diameter and prolonged colonic transit.
“Constipation is frequent in children with neurofibromatosis type 1 (NF1) and can be associated with increased rectal diameter and prolonged colonic transit (Pedersen et al., 2013).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Pedersen et al., 2013 source
May combine two claims.
PremisecitationIn acute intermittent porphyria, neurovisceral attacks may mimic surgical abdomen and can be accompanied by ileus or pseudo-obstruction, reflecting autonomic neuropathy and visceral motor dysfunction.
“In acute intermittent porphyria, neurovisceral attacks may mimic surgical abdomen and can be accompanied by ileus or pseudo-obstruction, reflecting autonomic neuropathy and visceral motor dysfunction (Berlin et al., 1950; Stein et al., 1970; Stolzel et al., 2019).”
Quote in the paperNot a substantial claim0 of 3 sources checked- Rests on an assumption: Acute hepatic porphyrias can present with severe abdominal pain, nausea, constipation, and autonomic instability.
May combine two claims.
PremisecitationGuillain-Barré syndrome can feature prominent dysautonomia, and there are reports of associations with gastrointestinal infections such as Helicobacter pylori.
“Guillain–Barré syndrome can feature prominent dysautonomia, and there are reports of associations with gastrointestinal infections such as Helicobacter pylori (Dardiotis et al., 2020).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Dardiotis et al., 2020 source
May combine two claims.
InterpretationreasoningDisease-specific patterns, such as prodromal dysmotility in Parkinson disease, area postrema syndromes, diabetic autovagotomy, and antibody-mediated enteric neuropathy, provide additional diagnostic clues and may guide treatment.
“Disease-specific patterns, such as prodromal dysmotility in Parkinson disease, area postrema syndromes, diabetic ‘autovagotomy,’ and antibody-mediated enteric neuropathy, provide additional diagnostic clues and may guide treatment.”
Quote in the paperSubstantial claim
The paper relies on this without support.
Gastrointestinal symptoms are frequent in disorders that involve the autonomic nervous system or the enteric neuromuscular apparatus.
“Gastrointestinal (GI) symptoms are frequent in disorders that involve the autonomic nervous system (ANS) or the enteric neuromuscular apparatus.”
The paper relies on this without support.
The enteric nervous system can generate patterned behaviors such as peristalsis and the migrating motor complex with a high degree of autonomy, largely independent of extrinsic neural control.
“Through sensory neurons, interneurons, and motor/secretomotor neurons, the ENS can generate patterned behaviors such as peristalsis and the migrating motor complex with a high degree of autonomy. Thus, such patterns of motor function are largely independent of extrinsic neural control.”
The paper relies on this without support.
Constipation and anorectal dysfunction are among the most frequent gastrointestinal manifestations of neurologic disease.
“Constipation and anorectal dysfunction are among the most frequent GI manifestations of neurologic disease.”
The paper relies on this without support.
Gastrointestinal complaints are common in the general population and most often arise from primary GI disorders rather than neurologic disease.
“GI complaints are common in the general population and most often arise from primary GI disorders rather than neurologic disease.”
The paper relies on this without support.
Swallowing impairment is a well-recognized complication of acute stroke and contributes to aspiration pneumonia and poor nutritional status.
“Swallowing impairment is a well-recognized complication of acute stroke and contributes to aspiration pneumonia and poor nutritional status.”
The paper relies on this without support.
Parkinson disease is a prototypical neurologic disorder in which autonomic and enteric pathology contributes substantially to morbidity.
“Parkinson disease (PD) is a prototypical neurologic disorder in which autonomic and enteric pathology contributes substantially to morbidity.”
The paper relies on this without support.
The brainstem contains key integrative circuits for autonomic regulation of the stomach and upper gut.
“The brainstem contains key integrative circuits for autonomic regulation of the stomach and upper gut.”
The paper relies on this without support.
POTS is a form of orthostatic intolerance that is particularly common in younger women.
“Postural orthostatic tachycardia syndrome (POTS) is a form of orthostatic intolerance that is particularly common in younger women.”
The paper relies on this without support.
Delayed recognition of an intra-abdominal emergency in spinal cord injury can contribute to excess mortality.
“Delayed recognition of an intra-abdominal emergency in this setting can contribute to excess mortality.”
The paper relies on this without support.
Disruption of coordinated pelvic floor and anal sphincter function contributes to defecatory disorders and incontinence in spinal cord injury.
“Disruption of coordinated pelvic floor and anal sphincter function further contributes to defecatory disorders and incontinence.”
The paper relies on this without support.
Multiple sclerosis is frequently accompanied by autonomic dysregulation.
“Multiple sclerosis (MS) is frequently accompanied by autonomic dysregulation, and bowel symptoms are common across disease phenotypes.”
The paper relies on this without support.
Demyelinating lesions involving spinal long tracts and autonomic centers can disrupt colonic propulsion, anorectal sensation, and pelvic floor coordination in multiple sclerosis.
“Physiologically, demyelinating lesions involving spinal long tracts and autonomic centers can disrupt colonic propulsion, anorectal sensation, and pelvic floor coordination.”
The paper relies on this without support.
Gastrointestinal dysfunction in amyloidosis may result from mucosal infiltration, neuromuscular infiltration, and/or extrinsic autonomic neuropathy.
“Gastrointestinal dysfunction in amyloidosis may result from mucosal infiltration, neuromuscular infiltration, and/or extrinsic autonomic neuropathy.”
The paper relies on this without support.
Amyloid neuropathy may cause dysphagia, constipation, diarrhea, and steatorrhea, besides sensorimotor and cardiovascular autonomic deficits.
“Clinically, amyloid neuropathy, besides sensorimotor and cardiovascular autonomic deficits, may cause dysphagia, constipation, diarrhea, and steatorrhea.”
The paper relies on this without support.
Acute hepatic porphyrias can present with severe abdominal pain, nausea, constipation, and autonomic instability.
“Acute hepatic porphyrias can present with severe abdominal pain, nausea, constipation, and autonomic instability.”
The paper relies on this without support.
Chronic peripheral neuropathy is the most prevalent neurologic substrate for GI motor dysfunction.
“Chronic peripheral neuropathy is the most prevalent neurologic substrate for GI motor dysfunction.”
The paper relies on this without support.
GI symptoms are common and nonspecific.
“Because GI symptoms are common and nonspecific, identifying a neurogenic mechanism requires careful pattern recognition and attention to accompanying autonomic and neurologic features.”
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Self-citationDysphagia in acute stroke: incidence, burden and impact on clinical outcome
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- Authors
- Shouman, K., Camilleri, M., & Singer, W.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Singer, Wolfgang
- Venue
- Autonomic Neuroscience
- Publisher
- Elsevier BV
- Published
- 2026-12
- Volume
- 268
- Pages
- 103474
- ISSN
- 1566-0702 (ISSN-L)
- PMC
- PMC13618994
- OpenAlex
- W7204518322
- Semantic Scholar
- 45d37d22739fc178c5f4f3d917cfeae223352673
- Cited by
- 0
- References
- 155
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 276 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Autonomic Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Michael J Fox Foundation for Parkinson's Research
- US Food and Drug Administration (R01 FD07290)
- NIH (R01NS92625, R01NS126406, R01DK135540)
- Mayo Foundation for Medical Education and Research
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Surgery › Cardiovascular Syncope and Autonomic Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Keywords
- autonomic nervous system, gastrointestinal dysfunction, gastric dysfunction, enteric nervous system, gastrointestinal motility, gastroparesis, intestinal pseudo-obstruction, dysphagia, constipation, diarrhea, fecal incontinence, autonomic function testing, Parkinson's disease, primary autonomic failure, postural orthostatic tachycardia syndrome, multiple sclerosis, diabetic neuropathy, amyloidosis, neuromuscular disorders, cerebrovascular disease, neurodegenerative diseases, brainstem syndrome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-22.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-22.
Cited sources are checked by gpt-6-sol.
Statistics and arithmetic are recomputed, not judged.
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