Claus Inga, Suttrup Judith, Muhle Paul, Suntrup-Krueger Sonja, Siemer Marie-Luise, Lenze Frank, Dziewas Rainer, Warnecke Tobias
Department of Neurology University Hospital of Münster Albert-Schweitzer-Campus 1, D- 48149, Münster Germany.
Social Brain Lab, Netherlands Institute for Neuroscience Royal Netherlands Academy of Arts and Sciences Amsterdam Netherlands.
Mov Disord Clin Pract. 2018 May 15;5(4):406-412. doi: 10.1002/mdc3.12616. eCollection 2018 Jul-Aug.
Esophageal dysfunction is a frequent phenomenon in Parkinson's disease during all disease stages, but data about esophageal involvement in atypical parkinsonian syndromes as well as possible differences between alpha-synucleinopathies and tauopathies, including causative links to the origin of the dysfunction, are lacking so far.
To describe esophageal alternation patterns in different parkinsonian syndromes and to look for differences supporting the hypothesis of alpha-synuclein aggregation being linked to gastrointestinal impairment in parkinsonian syndromes.
We performed an analysis and comparison of esophageal high-resolution manometry examination parameters in 10 patients with Parkinson's disease, 10 patients with multiple system atrophy (both alpha-synucleinopathies), 10 patients with progressive supranuclear palsy (tauopathy), and 10 age-matched controls. Additionally, pharyngeal dysphagia was evaluated by an endoscopic examination of swallowing in all three patient groups.
Statistically significant lower values for esophageal peristalsis and distal contractile integral were found for both groups of alpha-synucleinopathies (Parkinson's disease and multiple system atrophy) in comparison to the patients with tauopathy (progressive supranuclear palsy group), as well as the age-matched controls, where pathological pharyngeal findings were similar in all patient groups.
Subtle esophageal motility alterations in parkinsonian syndromes seem to be limited to alpha-synucleinopathies, but are not measurable in tauopathies, indicating a causative connection between pathological alpha-synuclein aggregation in gastrointestinal tissues and esophageal involvement.
食管功能障碍是帕金森病各疾病阶段常见的现象,但目前缺乏关于非典型帕金森综合征食管受累情况的数据,以及α-突触核蛋白病和tau蛋白病之间可能存在的差异,包括与功能障碍起源的因果关系。
描述不同帕金森综合征中的食管改变模式,并寻找支持α-突触核蛋白聚集与帕金森综合征胃肠道损害相关假说的差异。
我们对10例帕金森病患者、10例多系统萎缩患者(均为α-突触核蛋白病)、10例进行性核上性麻痹患者(tau蛋白病)以及10例年龄匹配的对照者的食管高分辨率测压检查参数进行了分析和比较。此外,通过对所有三组患者进行吞咽内镜检查来评估咽吞咽困难。
与tau蛋白病患者(进行性核上性麻痹组)以及年龄匹配的对照者相比,两组α-突触核蛋白病患者(帕金森病和多系统萎缩)的食管蠕动和远端收缩积分在统计学上显著降低,所有患者组的咽部病理表现相似。
帕金森综合征中细微的食管运动改变似乎仅限于α-突触核蛋白病,而在tau蛋白病中无法测量,这表明胃肠道组织中病理性α-突触核蛋白聚集与食管受累之间存在因果关系。