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Sarah Marrinan MBBS MRCP Anton V. Emmanuel MD FRCP David J. Burn MD FRCP 《Movement disorders》2014,29(1):23-32
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. © 2013 International Parkinson and Movement Disorder Society 相似文献
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Christos Ganos MD Panagiotis Kassavetis MD Roberto Erro MD Mark J. Edwards MD John Rothwell PhD Kailash P. Bhatia MD FRCP 《Movement disorders》2014,29(4):437-443
The putative involvement of the cerebellum in the pathogenesis of cortical myoclonic syndromes has been long hypothesized, as neuropathological changes in patients with cortical myoclonus have most commonly been found in the cerebellum rather than in the suspected culprit, the primary somatosensory cortex. A model of increased cortical excitability due to loss of cerebellar inhibitory control via cerebello‐thalamo‐cortical connections has been proposed, but evidence remains equivocal. Here, we explore this hypothesis by examining syndromes that present with cortical myoclonus and ataxia. We first describe common clinical characteristics and underlying neuropathology. We critically view information on cerebellar physiology with regard to motorcortical output and compare findings between hypothesized and reported neurophysiological changes in conditions with cortical myoclonus and ataxia. We synthesize knowledge and focus on neurochemical changes in these conditions. Finally, we propose that the combination of alterations in inhibitory neurotransmission and the presence of cerebellar pathology are important elements in the pathogenesis of cortical myoclonus. © 2014 Movement Disorder Society 相似文献
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Naomi Holman PhD Peter Knighton MPhys Jackie OʼKeefe MSc Sarah H. Wild PhD Sarah Brewster MRCP Hermione Price FRCP Kiran Patel PhD Wasim Hanif MD Vinod Patel MD Edward W. Gregg PhD Richard I. G. Holt PhD Roger Gadsby MB Kamlesh Khunti MD Jonathan Valabhji MD Bob Young MD Naveed Sattar MD 《Diabetes, obesity & metabolism》2021,23(12):2728-2740
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Christopher Sainsbury MD Jingya Wang PhD Krishna Gokhale MSc Dionisio Acosta-Mena PhD Samir Dhalla MRPharmS Nathan Byne Joht Singh Chandan PhD Astha Anand BMBCh Jennifer Cooper MBBCh Kelvin Okoth MPH Anuradhaa Subramanian MSc Mansoor N. Bangash PhD Thomas Taverner PhD Wasim Hanif PhD Sandip Ghosh FRCP Parth Narendran PhD Kar K. Cheng PhD Tom Marshall PhD Georgios Gkoutos PhD Konstantinos Toulis PhD Neil Thomas PhD Abd Tahrani PhD Nicola J. Adderley PhD Shamil Haroon PhD Krishnarajah Nirantharakumar MD 《Diabetes, obesity & metabolism》2021,23(1):263-269