帕金森病中的胃动力障碍并非由胃起搏细胞的改变所致。
Gastric dysmotility in Parkinson's disease is not caused by alterations of the gastric pacemaker cells.
作者信息
Heimrich Konstantin G, Jacob Veit Y P, Schaller Denise, Stallmach Andreas, Witte Otto W, Prell Tino
机构信息
1Department of Gastroenterology, Jena University Hospital, Jena, Germany.
2Department of Neurology, Jena University Hospital, Jena, Germany.
出版信息
NPJ Parkinsons Dis. 2019 Jul 26;5:15. doi: 10.1038/s41531-019-0087-3. eCollection 2019.
The enteric nervous system is involved in the pathology of Parkinson´s disease and patients frequently have symptoms related to delayed gastric emptying. However, the pathophysiology of gastric dysmotility is yet not well understood. The objective of this study was to assess interdigestive gastric motility in Parkinson´s disease. Using an electromagnetic capsule system, the dominant gastric contraction frequency (primary outcome measure) and the gastric transit time were assessed in 16 patients with Parkinson´s disease and 15 young healthy controls after a fasting period of 8 h. Motor and non-motor symptoms were assessed using the Movement Disorder Society Unified Parkinson´s Disease Rating Scale III (MDS-UPDRS III), the Non-Motor Symptoms Questionnaire (NMS-Quest), and Hoehn & Yahr staging. The Gastroparesis Cardinal Symptom Index was used to record symptoms related to delayed gastric emptying. In healthy controls and patients with Parkinson's disease, the dominant contraction frequency was 3.0 cpm indicating normal function of interstitial cells of Cajal. In patients with Parkinson's disease, the gastric transit time was longer than in younger controls (56 vs. 21 min). The dominant contraction frequency and gastric transit time did not correlate with age, disease duration, Hoehn & Yahr stage, levodopa equivalent daily dose, MDS-UPDRS III, NMS-Quest, and Gastroparesis Cardinal Symptom Index. Changes of gastric motility in Parkinson´s disease are not caused by functional deficits of the gastric pacemaker cells, the interstitial cells of Cajal. Therefore, gastroparesis in Parkinson's disease can be attributed to disturbances in neurohumoral signals via the vagus nerve and myenteric plexus.
肠道神经系统参与帕金森病的病理过程,患者常出现与胃排空延迟相关的症状。然而,胃动力障碍的病理生理学尚未完全明确。本研究的目的是评估帕金森病患者消化间期的胃动力。采用电磁胶囊系统,在16例帕金森病患者和15名年轻健康对照者禁食8小时后,评估其胃主导收缩频率(主要观察指标)和胃排空时间。使用运动障碍协会统一帕金森病评定量表Ⅲ(MDS-UPDRSⅢ)、非运动症状问卷(NMS-Quest)和Hoehn&Yahr分期评估运动和非运动症状。采用胃轻瘫主要症状指数记录与胃排空延迟相关的症状。在健康对照者和帕金森病患者中,主导收缩频率为3.0次/分钟,表明 Cajal间质细胞功能正常。帕金森病患者的胃排空时间比年轻对照者长(56分钟对21分钟)。主导收缩频率和胃排空时间与年龄、病程、Hoehn&Yahr分期、左旋多巴等效日剂量、MDS-UPDRSⅢ、NMS-Quest和胃轻瘫主要症状指数均无相关性。帕金森病患者胃动力的改变并非由胃起搏细胞即Cajal间质细胞的功能缺陷引起。因此,帕金森病中的胃轻瘫可归因于通过迷走神经和肌间神经丛的神经体液信号紊乱。
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本文引用的文献
J Parkinsons Dis. 2018
Parkinsonism Relat Disord. 2018-6-6
J Parkinsons Dis. 2017
Int Rev Neurobiol. 2017
Parkinsonism Relat Disord. 2015-12
Lancet Neurol. 2015-6
J Smooth Muscle Res. 2013
Curr Opin Clin Nutr Metab Care. 2013-1
J Smooth Muscle Res. 2011