Is there delayed gastric emptying in patients with multiple system atrophy? An analysis using the 13C-acetate breath test

Tanaka, Yuji; Kato, Tomohiro; Nishida, Hiroshi; Yamada, Megumi; Koumura, Akihiro; Sakurai, Takeo; Hayashi, Yuichi; Kimura, Akio; Hozumi, Isao; Araki, Hiroshi; Murase, Masahiko; Nagaki, Masahito; Moriwaki, Hisataka; Ishii, Takashi

doi:10.1007/s00415-011-6372-7

Cited by 20 publications

(11 citation statements)

References 27 publications

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“…Delayed GE is one of the autonomic failures and may be a clinical marker of MSA. [68] Symptoms relating to disturbed gastric motility in MSA are uncommon, although some patients have gastric fullness postmeal that may be troublesome. Drugs such as anticholinergic and dopaminergic agents are often used to treat motor disorder and may impair motility.…”

Section: Multiple System Atrophymentioning

confidence: 99%

Gastrointestinal dysfunction in idiopathic Parkinsonism: A narrative review

2016

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Currently, gastrointestinal (GI) dysfunctions in Parkinson's disease (PD) are well-recognized problems and are known to be the initial symptoms in the pathological process that eventually results in PD. Many types of PD-associated GI dysfunctions have been identified, including weight loss, nausea, hypersalivation, dysphagia, dyspepsia, abdominal pain, intestinal pseudo-obstruction, constipation, defecatory dysfunction, and small intestinal bacterial overgrowth. These symptoms can influence on other PD symptoms and are the second most significant predictor of the quality of life of these patients. Recognition of GI symptoms requires vigilance on the part of clinicians. Health-care providers should routinely ask direct questions about GI symptoms during office visits so that efforts can be directed at appropriate management of these distressing manifestations. Multiple system atrophy (MSA) and progressive supranuclear palsy are two forms of neurodegenerative Parkinsonism. Symptoms of autonomic dysfunctions such as GI dysfunction are common in patients with parkinsonian disorders. Despite recent progress in the recognition of GI dysfunctions, there are a few reviews on the management of GI dysfunction and GI symptoms in idiopathic Parkinsonism. In this review, the clinical presentation, pathophysiology, and treatment of each GI symptom in PD, MSA, and prostate-specific antigen will be discussed.

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Section: Multiple System Atrophymentioning

confidence: 99%

Gastrointestinal dysfunction in idiopathic Parkinsonism: A narrative review

2016

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“…The roles of the vagal system and the ENS in control of gastric emptying have been outlined and as both are early sites of alpha‐synuclein deposition, it is postulated that resultant neural damage and dysfunction contributes to impaired gastric motility. Indirect evidence supporting the hypothesis that abnormal alpha‐synuclein accumulation underlies impaired gastric motility in PD comes from studies demonstrating delayed gastric emptying in multiple system atrophy, another synucleinopathy . To the best of our knowledge, no evaluations of gastric emptying in the context of dementia with Lewy bodies have been published.…”

Section: Delayed Gastric Emptying In Pdmentioning

confidence: 99%

Delayed gastric emptying in Parkinson's disease

2013

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Gastrointestinal symptoms are evident in all stages of Parkinson's disease (PD). Most of the gastrointestinal abnormalities associated with PD are attributable to impaired motility. At the level of the stomach, this results in delayed gastric emptying. The etiology of delayed gastric emptying in PD is probably multifactorial but is at least partly related to Lewy pathology in the enteric nervous system and discrete brainstem nuclei. Delayed gastric emptying occurs in both early and advanced PD but is underdetected in routine clinical practice. Recognition of delayed gastric emptying is important because it can cause an array of upper gastrointestinal symptoms, but additionally it has important implications for the absorption and action of levodopa. Delayed gastric emptying contributes significantly to response fluctuations seen in people on long-term l-dopa therapy. Neurohormonal aspects of the brain-gut axis are pertinent to discussions regarding the pathophysiology of delayed gastric emptying in PD and are also hypothesized to contribute to the pathogenesis of PD itself. Ghrelin is a gastric-derived hormone with potential as a therapeutic agent for delayed gastric emptying and also as a novel neuroprotective agent in PD. Recent findings relating to ghrelin in the context of PD and gastric emptying are considered. This article highlights the pathological abnormalities that may account for delayed gastric emptying in PD. It also considers the wider relevance of abnormal gastric pathology to our current understanding of the etiology of PD.

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“…Previous studies have shown that patients with MSA frequently exhibit delayed gastric emptying [1] and slow colonic transit [2]. Accumulating evidence suggests that active ghrelin facilitates motility of the gastric antrum [4,5] and colorectum [21], and unacylated ghrelin may SCOPA-AUT gastrointestinal score Active ghrelin ratio (%) Fig.…”

Section: Discussionmentioning

confidence: 93%

Abnormal ghrelin secretion contributes to gastrointestinal symptoms in multiple system atrophy patients

Ozawa

Tokunaga

Arakawa

et al. 2013

Autonomic Neuroscience

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Patients with multiple system atrophy (MSA) often have evidence of compromised gastrointestinal motility. Ghrelin is a gut hormone that influences gastrointestinal motility in humans. The aim of this study was to determine whether ghrelin secretion is affected in MSA patients, and to investigate the relation between ghrelin secretion and gastrointestinal symptoms. Plasma levels of active ghrelin and unacylated ghrelin were measured in patients with MSA (n = 30), other atypical parkinsonian disorders including progressive supranuclear palsy-Richardson syndrome and corticobasal syndrome (n = 24), and control subjects (n = 24) using enzyme-linked immunosorbent assays. Gastrointestinal symptoms were quantified in all subjects using a self-report questionnaire. The ratio of active ghrelin to total ghrelin in the plasma (active ghrelin ratio) was lower in patients with MSA (mean: 8.0 %) than in patients with other atypical parkinsonian disorders (mean: 13.7 %, P = 0.001) and control subjects (mean: 13.9 %, P = 0.001). The active ghrelin ratio was correlated with the severity of gastrointestinal symptoms in MSA (r = -0.5, P = 0.004). Our observations indicate that ghrelin secretion is affected in patients with MSA. The low active ghrelin ratio may contribute to gastrointestinal symptoms in MSA.

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Is there delayed gastric emptying in patients with multiple system atrophy? An analysis using the 13C-acetate breath test

Cited by 20 publications

References 27 publications

Gastrointestinal dysfunction in idiopathic Parkinsonism: A narrative review

Gastrointestinal dysfunction in idiopathic Parkinsonism: A narrative review

Delayed gastric emptying in Parkinson's disease

Abnormal ghrelin secretion contributes to gastrointestinal symptoms in multiple system atrophy patients

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