Pyriform sinuses retention (PSR) is one of the most common and severe signs of dysphagia. Previous studies considered that PSR could be resulted from pharyngeal swallowing delay、superior and anterior hyoid and laryngeal movement、cricopharyngeus muscle achalasia (CMA), and weak pharyngeal contraction. Corresponding regular rehabilitation techniques including tactile thermal oral stimulation、hyoid and larynx elevation training、cricopharyngeal balloon dilatation, and Mendelssohn technique. However, the researches on neural multi-factor pathomechanism of PSR and explaining the rehabilitation effect are extremely few, which limits the innovation and development of more rehabilitation methods.Our previous researches based on swallowing muscle level utilizing videofluoroscopy, fiberoptic endoscopy and electromyography discovered that multi factors resulting in PSR such as pharyngeal swallowing delay、superior and anterior hyoid and laryngeal movement、cricopharyngeus muscle achalasia (CMA), and weak pharyngeal contraction might exist independently, further finding out different focus of cerebral infarction might lead to different kinds of pathomechanism of PSR, so we established the hypothetical model of multi-factor neural pathomechanism on PSR. We add blood-oxygenation level dependent functional magnetic resonance imaging (BOLD fMRI), combined with diffusion weighted imaging(DWI) , to explore the significance of activation difference of regions of interest (ROI) among each group with different pathomechanism of PSR and normal group, and explore the significance of activation difference of ROI among each group with different pathomechanism of PSR after rehabilitation; Then we could testify if the hypothetical model of multi-factor neural pathomechanism on PSR is scientific, which let us ascertain the neural pathomechanism of PSR, and provide more empirical basis for enriching the theories of deglutition disorder, and for the research and development of more and more scientific and effective rehabilitation techniques on PSR.
梨状窝滞留是吞咽障碍最常见和最严重的体征之一。以往研究显示咽期启动迟缓、舌骨喉前上位移减少、环咽肌失弛缓,以及咽收缩减弱均可导致梨状窝滞留,常规的康复技术包括腭舌弓冰刺激、舌骨喉上抬训练、环咽肌球囊扩张术,以及门德松手法。然而有关梨状窝滞留的病理及康复机制研究甚少,制约了康复方法的创新与发展。本项目组前期采用多模式吞咽检测方法(VFSS,FEES和 EEG),发现咽期启动迟缓、舌骨喉前上位移减少、环咽肌失弛缓以及咽收缩减弱可独立存在,且不同脑病灶会导致不同成因的梨状窝滞留,故提出梨状窝滞留的中枢病理多因素的假想模型。在以往脑病灶精确定位的基础上,增加fMRI脑(区)激活的研究方法,从各病理组与正常吞咽组的感兴趣脑(区)激活差异,以及各病理组康复后脑(区)激活差异的比较两方面验证该模型的科学性,进一步探明梨状窝滞留的中枢病理机制,为丰富吞咽障碍的理论,研发更加科学有效的康复技术奠定基础。
梨状窝滞留是吞咽障碍最常见和最严重的体征之一。以往的研究显示咽期启动迟缓、舌骨喉前上位移减少、环咽肌失弛缓,以及咽收缩减弱均可能导致梨状窝滞留,常规康复技术包括腭舌弓冰刺激、舌骨喉上抬训练、环咽肌球囊扩张术及门德松技术可部分改善症状。梨状窝滞留的中枢病理及康复机制的研究甚少,制约了康复方法的创新与发展。 本项目组前期采用多模式吞咽检测方法(VFSS,FEES和 EEG),发现咽期启动迟缓、舌骨喉前上位移减少、环咽肌失弛缓,以及咽收缩减弱可独立存在,并认识到不同的脑病灶会导致不同成因的梨状窝滞留,故提出了梨状窝滞留的中枢病理多因素的假想模型。在以往脑病灶精确定位的基础上,增加BOLD-fMRI的脑(区)激活的研究方法,从各病理组与正常吞咽组的感兴趣脑(区)激活差异,以及各病理组康复后脑(区)激活差异的比较两个方面验证该模型的科学性,进一步探明梨状窝滞留的中枢病理机制,为丰富吞咽障碍的理论,研发更加科学有效的康复技术奠定基础。笨研究目前发现,与健康对照组相比,喉上抬组减少治疗前的脑干与壳核区域未观察到激活。且统计显示喉上抬减减少组治疗前比对照组的脑激活范围更广,包括大脑皮质区的左侧辅助运动区、旁扣带回、三角部额下回、皮质下区的双侧丘脑及左侧壳核。电针治疗后脑干亚区、左侧小脑半球小叶的IV、V区以及部分大脑皮质比治疗前激活增加,而左侧辅助运动区、中央旁小叶和枕叶区的脑激活减少。本研究认为控制喉上抬运动的特异性脑区为脑干与壳核。卒中后患者大脑皮质-基底节-丘脑环路的激活增强是一种代偿机制。喉上抬运动改善与小脑半球第IV、V小叶的激活增强相关,且原本卒中后辅助运动区的过度激活会随着运动功能的改善而正常化。
{{i.achievement_title}}
数据更新时间:2023-05-31
农超对接模式中利益分配问题研究
基于 Kronecker 压缩感知的宽带 MIMO 雷达高分辨三维成像
基于SSVEP 直接脑控机器人方向和速度研究
伴有轻度认知障碍的帕金森病~(18)F-FDG PET的统计参数图分析
基于细粒度词表示的命名实体识别研究
梨状皮层调控癫痫发作的脑环路机制的多模态研究
脑梗死偏瘫后针刺阳陵泉对运动相关脑网络整合调节的多模态分析研究
基于吞咽脑区MEP定位图绘制的卒中后吞咽功能重建机制研究
电针促进卒中吞咽障碍脑功能重组的fMRI研究