Gastric dysmotility in Parkinson's disease is not caused by alterations of the gastric pacemaker cells

Heimrich, Konstantin G.; Jacob, Veit Yves Pascal; Schaller, Denise; Stallmach, Andreas; Witte, Otto W.; Prell, Tino

doi:10.1038/s41531-019-0087-3

Cited by 20 publications

(18 citation statements)

References 29 publications

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“…The pathophysiology of this phenomenon is complex and likely multifactorial. The damage to, and α-synuclein deposition in the VN and ENS likely play a major role in DGE, whereas more controversial is the involvement of Cajal interstitial cells (the gastric pacemaker cells) [ 70 , 71 ]. Common medications used in PD, such as levodopa and anticholinergics, can contribute to DGE in a dose-dependent manner [ 71 , 72 ], and the interaction of some macronutrients (especially fats) with receptors in the small intestine can further inhibit gastric emptying [ 73 ].…”

Section: Pd-related Gi Disorders and The Gut-brain Axis: Practical Implicationsmentioning

confidence: 99%

The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance

2021

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Gastrointestinal disorders are one of the most significant non-motor problems affecting people with Parkinson disease (PD). Pathogenetically, the gastrointestinal tract has been proposed to be the initial site of pathological changes in PD. Intestinal inflammation and alterations in the gut microbiota may contribute to initiation and progression of pathology in PD. However, the mechanisms underlying this “gut-brain” axis in PD remain unclear. PD patients can display a large variety of gastrointestinal symptoms, leading to reduced quality of life and psychological distress. Gastrointestinal disorders can also limit patients’ response to medications, and consequently negatively impact on neurological outcomes. Despite an increasing research focus, gastrointestinal disorders in PD remain poorly understood and their clinical management often suboptimal. This review summarises our understanding of the relevance of the “gut-brain” axis to the pathogenesis of PD, discusses the impact of gastrointestinal disorders in patients with PD, and provides clinicians with practical guidance to their management.

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Section: Pd-related Gi Disorders and The Gut-brain Axis: Practical Implicationsmentioning

confidence: 99%

The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance

2021

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“…Additionally, decreased total gastric volume and decreased gastric motility was reported in patients with dyspepsia [ 89 ]. Another study used an electromagnetic capsule system to study gastric motility in PD patients and found prolonged GET compared to controls but similar frequency of gastric contractions indicating normal functioning of the intestinal cells of Cajal [ 90 ]. These methods are yet to be validated in PD but offer the possibility of repeated measurements in the same individuals without exposure to radiation.…”

Section: Objective Measures Of Gastrointestinal Dysfunctionmentioning

confidence: 99%

Gastrointestinal Dysfunction in Parkinson’s Disease

Skjærbæk

Knudsen

Horsager

et al. 2021

JCM

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Parkinson’s disease (PD) is the second most common neurodegenerative disease. Patients show deposits of pathological, aggregated α-synuclein not only in the brain but throughout almost the entire length of the digestive tract. This gives rise to non-motor symptoms particularly within the gastrointestinal tract and patients experience a wide range of frequent and burdensome symptoms such as dysphagia, bloating, and constipation. Recent evidence suggests that progressive accumulation of gastrointestinal pathology is underway several years before a clinical diagnosis of PD. Notably, constipation has been shown to increase the risk of developing PD and in contrast, truncal vagotomy seems to decrease the risk of PD. Animal models have demonstrated gut-to-brain spreading of pathological α-synuclein and it is currently being intensely studied whether PD begins in the gut of some patients. Gastrointestinal symptoms in PD have been investigated by the use of several different questionnaires. However, there is limited correspondence between subjective gastrointestinal symptoms and objective dysfunction along the gastrointestinal tract, and often the magnitude of dysfunction is underestimated by the use of questionnaires. Therefore, objective measures are important tools to clarify the degree of dysfunction in future studies of PD. Here, we summarize the types and prevalence of subjective gastrointestinal symptoms and objective dysfunction in PD. The potential importance of the gastrointestinal tract in the etiopathogenesis of PD is briefly discussed.

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“…In the smooth muscle layer, the interstitial cells of Cajal convey the signal to smooth muscle cells and are regarded as gastric pacemakers. These pacemaker cells do not seem to be altered in PD, suggesting that disturbance occurs either in the vagus nerve or in the myenteric plexus [49]. Alteration in a cholinergic anti-inflammatory pathway has also been demonstrated on an animal model of PD, which could lead to gastric muscular inflammation and muscular macrophage accumulation [50].…”

Section: Pathophysiologymentioning

confidence: 99%

Gastroparesis in Parkinson Disease: Pathophysiology, and Clinical Management

2021

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Patients with Parkinson disease (PD) experience a range of non-motor symptoms, including gastrointestinal symptoms. These symptoms can be present in the prodromal phase of the disease. Recent advances in pathophysiology reveal that α-synuclein aggregates that form Lewy bodies and neurites, the hallmark of PD, are present in the enteric nervous system and may precede motor symptoms. Gastroparesis is one of the gastrointestinal involvements of PD and is characterized by delayed gastric emptying of solid food in the absence of mechanical obstruction. Gastroparesis has been reported in nearly 45% of PD. The cardinal symptoms include early satiety, postprandial fullness, nausea, and vomiting. The diagnosis requires an appropriate test to confirm delayed gastric emptying, such as gastric scintigraphy, or breath test. Gastroparesis can lead to malnutrition and impairment of quality of life. Moreover, it might interfere with the absorption of antiparkinsonian drugs. The treatment includes dietary modifications, and pharmacologic agents both to accelerate gastric emptying and relieve symptoms. Alternative treatments have been recently developed in the management of gastroparesis, and their use in patients with PD will be reported in this review.

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Gastric dysmotility in Parkinson's disease is not caused by alterations of the gastric pacemaker cells

Cited by 20 publications

References 29 publications

The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance

The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance

Gastrointestinal Dysfunction in Parkinson’s Disease

Gastroparesis in Parkinson Disease: Pathophysiology, and Clinical Management

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