Evidence for a change in neurotransmitter affecting oesophageal motility in Parkinson's disease.

Bramble, M G; Cunliffe, Jennifer M.; Dellipiani, A. W.

doi:10.1136/jnnp.41.8.709

Cited by 38 publications

(15 citation statements)

References 16 publications

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“…However, these two groups differed in the percentage of patients receiving L-dopa and disease duration. Because L-dopa therapy itself may worsen the symptoms of delayed GE [2,16], it was not clear whether the delayed GE of PD patients with motor fluctuation was affected by L-dopa therapy. There is evidence to suggest that these complications in PD patients may be attributed to peripheral, pharmacokinetic mechanisms, mainly delayed GE as a side-effect of L-dopa [5,11,14].…”

Section: Discussionmentioning

confidence: 99%

“…Djaldetti reported that delayed GE is common in PD patients and is more marked in those with response fluctuations [3]. Because L-dopa therapy itself may worsen the symptoms of delayed GE [2,16], their interpretation of the results of their study is limited. It was not clear whether the delayed GE of PD patients with response fluctuation was affected by L-dopa therapy.…”

Section: Introductionmentioning

confidence: 99%

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Is there a difference in gastric emptying between Parkinson’s disease patients under long-term l-dopa therapy with and without motor fluctuations? An analysis using the 13C-acetate breath test

et al. 2009

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The mechanism underlying the motor fluctuations that develop after long-term L-dopa therapy is not fully known. It has been speculated that malabsorption of L-dopa from the small intestine occurs. It was reported that gastric retention in Parkinson's disease (PD) patients with motor fluctuations is increased as compared with that in PD without fluctuations. Because L-dopa therapy may worsen the symptoms of delayed gastric emptying (GE), it was not clear whether the delayed GE of PD patients with motor fluctuation was affected by L-dopa therapy. We assessed GE in PD patients with and without motor fluctuations. We investigated GE in 40 patients with PD under long-term L-dopa therapy, 20 fluctuators with "delayed-on" and "noon" phenomena, 20 nonfluctuators, and 20 healthy volunteers. GE was examined by the 13C-acetate breath test ((13)CABT) [the half emptying time (HET), the peak time of the (13)C-%-dose-excess curve (T(max))], with expirations collected for 4 h after a test meal and analyzed for (13)CO(2) using an infrared (IR) spectrophotometer. The T(max) of GE as assessed using the (13)C-ABT was significantly delayed in all PD patients as compared with controls (P = 0.002). The HET was significantly delayed in all PD patients as compared with controls (P < 0.001). The T(max) and HET were not significantly delayed in PD patients with motor fluctuations as compared with PD patients without motor fluctuations. These results demonstrated that GE is commonly delayed in PD patients with long-term L-dopa therapy. Delayed GE does not differ between PD patients with and without motor fluctuations. This finding demonstrated that the motor fluctuation in PD may not be influenced by GE.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Is there a difference in gastric emptying between Parkinson’s disease patients under long-term l-dopa therapy with and without motor fluctuations? An analysis using the 13C-acetate breath test

et al. 2009

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“…In the human, disorders of esophagomotor function incident to anticholinergic drug treatment are believed to reflect mainly the peripheral parasympatholytic effects of these agents, central actions being merely hinted at [40] or surmised [41,42] by some authors. The challenge thus remains to define the role, if any, of central cholinoceptor blockade in the causation of this type of drug-induced dysphagia.…”

Section: Functional Organization Of Neurotransmitter Mechanisms Operamentioning

confidence: 99%

The brainstem esophagomotor network pattern generator: A rodent model

Bieger

1993

Dysphagia

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The evidence reviewed in this essay supports the following working model of the central function generator for esophageal peristalsis in the rat: solitarial subnucleus centralis (NTSc) neurons operate in a dual capacity as esophagomotor reflex interneurons and as command neurons programming respective outputs from nucleus ambiguus compact formation (AMBc) motoneurons during secondary and primary peristalsis. In both conditions, there is a critical requirement for cholinergic input which enables NTSc neurons to generate the timed sequence of AMBc motoneuronal activity. In primary peristalsis, the cholinergic coupling mechanism is activated centrally, probably via projections from deglutitive premotor neurons to the parvicellular reticular formation and thence to the NTS. In reflex (or secondary) peristalsis, the cholinergic input could in part be generated by cholinergic vagal viscerosensory fibers innervating the esophagus. Postulated connections between NTS deglutitive neurons and the parvicellular cholinergic neurons of the intermediate reticular formation have yet to be demonstrated. Premotor input from NTSc to AMBc is generated by somatostatinergic and excitatory aminoacidergic neurons. Coactivation of both inputs by cholinergic afferents is necessary to generate esophagomotor output from AMBc neurons. The model under study is derived from investigations into central mechanisms governing striated muscle peristaltic activity. Whether the basic operational principles revealed thus far apply to peristaltic pattern generation in species with a smooth muscle esophagus, requires further investigation.

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“…The central anti-muscarinic actions of either thymoleptics or anticholinergic (atropine-like) agents themselves would be of concern because of an expected impairment in central esophagomotor cholinergic drive. A study on parkinsonian patients with and without clinical complaints of dysphagia has revealed an enhanced sensitivity to atropine, as reflected by an increased failure rate of primary (deglutitive) esophageal peristalsis [94].…”

Section: Clinical Relevancementioning

confidence: 99%

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Bieger

1991

Dysphagia

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Pharmacologic investigations into the transmission processes underlying fictive swallowing in the rat have disclosed the potential diversity of chemical signals used in central deglutitive pathways. Monoaminergic mechanisms appear to serve as links between subcortical structures and the medullary pattern generator of swallowing (PGS), and may play a critical role in maintaining internal facilitatory drive, required by the PGS for optimal responsivity to peripheral sensory input. Cholinergic bulbar interneurons form an integral component of the PGS subnetwork controlling esophageal peristalsis. Local GABA neurons exert a tonic inhibition of the buccopharyngeal stage, may regulate buccopharyngeal-esophageal coupling, and may contribute to peristaltic rhythmic generation at both the premotoneuronal and motoneuronal level. Receptor subtypes for excitatory amino acids (glutamate, aspartate) are differentially associated with deglutitive premotoneurons for both the buccopharyngeal and esophageal stage, as well as with ambiguus motoneurons. Preliminary evidence suggests the existence of excitatory peptidergic mechanisms involving thyrotropin-releasing hormone, vasopressin, oxytocin, and somatostatin, a probable candidate for excitatory transmitter in the solitarioambigual internuncial projection to motoneurons innervating esophageal striated musculature. Further validation of this experimental model may ultimately help to establish a framework for the clinical recognition, management, and exploitation of drug actions on central deglutitive neuroeffectors.

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Evidence for a change in neurotransmitter affecting oesophageal motility in Parkinson's disease.

Cited by 38 publications

References 16 publications

Is there a difference in gastric emptying between Parkinson’s disease patients under long-term l-dopa therapy with and without motor fluctuations? An analysis using the 13C-acetate breath test

Is there a difference in gastric emptying between Parkinson’s disease patients under long-term l-dopa therapy with and without motor fluctuations? An analysis using the 13C-acetate breath test

The brainstem esophagomotor network pattern generator: A rodent model

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

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