脑干病变后吞咽障碍患者咽肌及上食管括约肌运动协调性的特征研究

关键词：脑干病变  吞咽障碍  咽肌  上食管括约肌  咽腔测压

Keywords:brainstem lesions  dysphagia  pharyngeal muscle  upper esophagus sphincters  pharyngeal manometry

摘要：

      摘要 目的：观察不同病程脑干病变后吞咽障碍患者咽肌及上食管括约肌运动协调性紊乱的特点，为制定咽期吞咽障碍的康复治疗提供依据。 方法：回顾性分析2012年7月至2019年1月的脑干病变后吞咽障碍患者的高分辨率咽腔测压检查结果，纳入脑干病变后确诊为吞咽障碍的患者117例，包括脑干卒中、脑干或四脑室肿瘤术后但未经放疗者、视神经脊髓炎、脑干脑炎患者。按照病程分为3组，其中A组病程3个月以内（50.4±12.3d），共44例；B组病程3—8个月（170.3±34.5d），共41例；C组病程8个月以上（281.6±23.4d），共32例。分析各压力峰值参数：腭咽、下咽的收缩压力峰值、上食道括约肌（UES）静息压和UES残余压；以及时间学参数：腭咽收缩与UES松弛的时间间隔和腭咽与下咽部的时间间隔，并分析咽部收缩曲线的斜率，以明确咽部收缩与UES的协调性以及咽部收缩运动的时序性变化。 结果：脑干病变后吞咽障碍患者的UES静息压均较正常对照组降低（P<0.05），残余压升高（P<0.05），组间比较发现B组患者UES残余压增高最明显（82.5±60.3mmHg），3组患者出现UES残余压过高的比例分别为22.7%、58.5%、21.9%；3组患者腭咽收缩峰与UES松弛的时间差较正常对照组无差异（P>0.05），但延长的比例分别为：25%、9.7%、15.6%；3组患者的腭咽和下咽收缩压峰值均较正常对照组下降（P<0.05），而B组患者腭咽收缩压峰值较A和C组高（P<0.05），上下咽部收缩压力峰值的时间差缩小的比例分别为43.2%、36.6%、40.6%，组间比较提示差异无显著性意义（P>0.05）。咽部收缩压力峰值的曲线的斜率比较也表明，3组患者的斜率均较正常对照组升高（P<0.05），3组间的差异无显著性意义（P>0.05）。 结论：脑干病变后吞咽障碍患者UES残余压明显升高主要出现在发病3—8个月以后的脑干病变患者中，而UES延迟松弛的比例在发病3个月以内较高。脑干病变患者常见上下咽部收缩时序的不协调，可能与脑干及小脑病变导致的运动计划受损有关，与病程无关。

Abstract:

      Abstract Objective: To explore the coordinative characteristics of upper and lower pharyngeal muscle as well as pharyngo-upper esophagus sphincters (UES) in patients with dysphagia following brainstem lesions. Method: Retrospective analysis of high-resolution pharyngeal manometry in patients with dysphagia after brainstem lesions from July 2012 to January 2019 was conducted. One hundred and seventeen patients including brain stem stroke， brainstem or quadrant ventricle tumor after surgery but without radiotherapy， optic neuromyelitis located in medullary，brainstem encephalitis were enrolled in this study. According to the onset time of disease， they were divided into 3 groups， of which 44 cases within 3 months (50.4±12.3d) was involved in group A; 41 cases with duration of 3 to 8 months (170.3±34.5d) in group B; and 32 cases with more than 8 months (281.6±23.4d) in group C. Analysis of various pressure peak parameters: systolic blood pressure of the pharynx， hypopharynx， upper esophageal sphincter (UES) resting pressure and UES residual pressure; as well as time data: time lag 1 between pharyngeal constricting and UES relaxation and time lag 2 between velopharyngeal and hypopharyngeal level. The slope of the pharyngeal contraction curve was also analyzed to clarify the temporal coordination of pharyngeal motion. Result: The silent pressure of UES in patients with dysphagia after brainstem lesions was significantly lower than that in the normal group (P<0.05)， and the residual pressures during relaxation significantly increased (P<0.05)， and among them， group B was the most significant increase (82.5±60.3mmHg).The time lag 1 in the three groups was not different from the normal control group (P>0.05)， the prolonged proportions were: 25%， 9.7%， 15.6%. The peak pressures of the velopharyngeal and hypopharyngeal area significantly decreased， compared to control group (P<0.05)， but pressures of velopharyngeal muscle in group B was obviously higher than that in group A and group C(P<0.05). The time lags between peaks of the velopharyngeal and hypopharyngeal pressure in three case groups were shorter than those in normal group (P<0.05). The rate of shorter time lags between the upper and lower pressure peaks was 43.2%， 36.6%， and 40.6% in three groups，respectively. There was no statistically significant difference between the case groups (P>0.05). Moreover， the slopes of the peak curves of the pharyngeal contraction pressure in three groups were higher than those of normal control group (P<0.05)， but the difference between the three groups was not statistically significant (P>0.05). Conclusion: The UES residual pressures in patients with dysphagia after brainstem lesions was significantly increased in patients after 3 to 8 months duration from onset，while the proportion of delayed relaxation of UES within less than 3 months was higher than other groups. The incoordination of the upper and lower pharyngeal muscle contraction in patients with brainstem lesions has nothing to do with the course of the disease. It was speculated that the incoordination may result from the damage of motor planning controlled by brain stem and cerebellar.