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1.
目的观察导尿管球囊扩张术对神经源性环咽肌失弛缓症所致吞咽障碍的疗效。方法 20例神经源性环咽肌失弛缓患者,经视频吞咽造影检查吞咽功能证实为环咽肌失弛缓。采用16号导尿管球囊扩张术、常规吞咽康复训练及低频脉冲电刺激,治疗终点为恢复经口进食或治疗已满4周。分别在治疗前、治疗终点采用才藤吞咽障碍7级评价法(吞咽评级)、视频吞咽造影检查(VFSS)进行疗效测评。结果 20例患者临床痊愈8例、显效7例、有效4例、无效1例。治疗前后吞咽评级差异有统计学意义(P〈0.05),VFSS咽通过时间治疗前(0.27±0.04)s明显高于治疗后(0.15±0.05)s(P〈0.05)。结论导尿管球囊扩张术、常规吞咽康复训练及低频脉冲电刺激治疗神经源性环咽肌失弛缓症所致吞咽障碍疗效确切。  相似文献   

2.
目的探讨不同训练方法对环咽肌失弛缓患者吞咽前食管上段括约肌(UES)压力及吞咽功能的影响。 方法共选取57例脑卒中后环咽肌失弛缓患者,按随机数字表法将其分为常规训练组、球囊扩张组、综合训练组,每组19例。3组患者均给予吞咽电刺激治疗和吞咽功能训练,常规训练组和球囊扩张组在此基础上分别增加喉上提训练和球囊扩张术治疗,综合训练组在电刺激和吞咽功能训练基础上增加喉上提训练及球囊扩张术治疗。治疗前及治疗8周后(治疗后),利用高分辨多通道胃肠功能检测仪对患者吞咽前UES压力进行测定,采用洼田饮水试验和藤岛一郎吞咽障碍分级评定患者的吞咽功能。 结果治疗前,3组患者吞咽前UES压力、吞咽障碍评级、洼田饮水试验分级及视频透视吞咽检查(VFSS)结果比较,差异均无统计学意义(P&rt;0.05)。与组内治疗前比较,球囊扩张组治疗后吞咽前UES压力[(266.4±82.7)mmHg]和综合训练组治疗后吞咽前UES压力[(269.5±83.2)mmHg]均显著提高(P<0.05),且综合训练组治疗后吞咽前UES压力高于球囊扩张组(P<0.05)。治疗后,球囊扩张组和综合训练组患者吞咽障碍分级、洼田饮水试验分级及VFSS结果均较治疗前有所好转(P<0.05),且综合训练组患者上述指标较球囊扩张组改善更为显著(P<0.05)。 结论在吞咽电刺激和功能训练基础上增加球囊扩张术和喉上提训练,可有效提高环咽肌失弛缓患者吞咽前的UES压力,降低UES张力,对其康复治疗具有重要意义。  相似文献   

3.
目的探讨球囊扩张术在环咽肌失弛缓症所致吞咽障碍中的治疗作用。 方法共选取10例经吞咽X线荧光透视检查诊断为环咽肌失弛缓症的吞咽障碍患者。利用14号导尿管球囊,采用注水方式使球囊充盈以扩张环咽肌,同时辅以低频电刺激、口颜面吞咽器官运动训练及进食指导练习等。分别于治疗前、后进行吞咽功能评估。 结果上述患者经平均19.7次球囊扩张治疗后,其扩张球囊注水量由(2.65±0.91)ml增加至(8.20±0.92)ml,环咽肌开放功能显著提高,吞咽障碍明显改善,共显效7例,有效2例,这9例患者能完全经口自主进食糊状食物,无呛咳,吞咽造影复查显示在进食糊状食物时,其咽部期残留明显减少,环咽肌正常开放,误吸现象消失,仅余下1例患者只能达治疗性进食水平,吞咽造影复查显示其吞咽肌无力,环咽肌开放不全,仍存在误吸现象;比较治疗前、后患者饮水试验分级及吞咽障碍分级,发现治疗前、后差异均有统计学意义(P<0.01)。 结论球囊扩张术能显著改善环咽肌失弛缓导致的吞咽功能障碍,值得临床推广、应用。  相似文献   

4.
导尿管球囊扩张治疗环咽肌失弛缓症2例报告   总被引:2,自引:0,他引:2       下载免费PDF全文
目的 探讨导尿管球囊扩张治疗环咽肌失弛缓症的可行性,客观评价其治疗效果。方法 放射性脑病、脑干梗死伴吞咽障碍患者各1例,经吞咽X线荧光透视检查和光纤内窥镜吞咽检查,拟诊环咽肌失弛缓症。利用14号导尿管球囊,采用注水方式使球囊充盈,牵拉导尿管,自下而上缓慢移动球囊,使球囊反复多次通过狭窄的食道入口,逐渐扩张环咽肌。同时在颈部结合Vitalstim神经肌肉低频电刺激,进食指导训练。结果 分别给予4次及15次扩张治疗后,2例患者均可独立自主进食糊状食物,无呛咳。吞咽造影复查显示在食团通过时,环咽肌正常开放,误吸消失。结论 导尿管球囊扩张术能有效缓解环咽肌失弛缓,操作简单,安全可靠。吞咽动态造影是明确诊断及疗效评价必不可少的检查方法。  相似文献   

5.
目的探讨导管球囊扩张术联合精细化管理模式对脑卒中后环咽肌失弛缓症的疗效。方法选取2017年5月—2019年8月在本科行康复训练的40例脑卒中后环咽肌失弛缓症患者作为研究对象,采用随机数字表法分为试验组和对照组,各20例,对照组予以导管球囊扩张术,试验组予以导管球囊扩张术联合精细化管理模式。使用洼田饮水实验、吞咽障碍评分(VGF)、标准吞咽功能评定(SSA评分)进行疗效评价。结果两组患者的各项指标在治疗完成后均有不同程度的改善(P0.05),试验组患者在洼田饮水实验、吞咽障碍评分(VGF)、SSA评分上的改善优于对照组(P均0.05)。结论对脑卒中后环咽肌失弛缓症患者应用导管球囊扩张联合精细化管理模式能显著改善部分吞咽功能,有助于让患者获得更好的康复治疗效果。  相似文献   

6.
目的:探讨导脑卒中后环咽肌失弛缓症的必要性及治疗方法。客观评价其治疗效果。选择脑干梗死伴咽期吞咽障碍患者2例,经吞咽X线荧光透视检查检查。拟诊环咽肌失弛缓症。病例1单纯采用神经肌肉电刺激治疗,而病例2在神经肌肉电刺激的基础上加用球囊扩张术。结果:经治疗后,2例患者均可独立自主进食糊状食物,无呛咳。吞咽造影复查显示在食团通过时,环咽肌正常开放。结论:球囊扩张术对于脑卒中引起的环咽肌失弛缓症并非必要。可通过咽喉肌肉神经运动功能,促进环咽肌的开放。  相似文献   

7.
目的探讨改良双腔球囊导管治疗环咽肌失弛缓症患者的可行性及安全性。方法将环咽肌失弛缓症患者50例随机分为试验组和对照组,每组各25例。两组均接受常规治疗,包括药物治疗、吞咽功能训练、摄食训练及辅以VitalStim神经肌肉低频电刺激治疗。试验组采用改良双腔球囊导管进行环咽肌扩张治疗,对照组采用14号普通导尿管进行环咽肌扩张治疗。采用洼田氏饮水试验和吞咽X线电视透视检查(VFSS)对治疗效果进行评估,评估患者黏膜水肿、出血和疼痛等并发症情况。结果治疗后两组洼田氏饮水试验和VFSS评分均明显高于治疗前(P0.05),两组间差异无统计学意义(P0.05)。对照组并发症的发生率明显高于试验组(P0.05)。结论两组治疗均可有效缓解环咽肌失弛缓症,应用改良双腔球囊导管可明显减少并发症的发生。  相似文献   

8.
目的探讨导尿管球囊扩张术在脑卒中后环咽肌失弛缓症所致吞咽障碍中的治疗作用及随访情况。方法共选取28例经电视透视下吞咽功能检查(VFSS)诊断为脑卒中后环咽肌失弛缓症的吞咽障碍患者,应用14号导尿管球囊,采用注水方式使球囊充盈以扩张环咽肌,同时辅以神经肌肉电刺激、常规吞咽康复训练。治疗终点为恢复经口进食或治疗已满6周。分别于治疗前、治疗终点时进行吞咽功能评估及吞咽造影检查,1年后随访。结果在导尿管球囊扩张治疗终点,28例患者中有22例恢复经口进食普通饮食,包括固体食物、流质物及水,24例可进食糊状食物,与治疗前比较有显著性差异(P<0.01)。吞咽造影中,治疗后咽通过时间缩短(P<0.05);VFSS吞咽障碍程度评分明显高于治疗前(P<0.01)。治疗终点时VFSS疗效评价显示总有效率达89.28%。1年后随访发现,23例(82.14%)患者均能从口进食普通食物;12例患者咽通过时间、吞咽障碍程度评分已接近正常。结论导尿管球囊扩张术能显著改善脑卒中后环咽肌失弛缓导致的吞咽功能障碍,且具有远期疗效。  相似文献   

9.
目的观察创新性球囊扩张术对脑干病变后环咽肌失弛缓症所致吞咽障碍的治疗作用。 方法30例脑干病变后吞咽障碍患者,经吞咽造影诊断为环咽肌失弛缓症,分为治疗组与对照组。治疗组给予球囊扩张术及常规吞咽康复训练,对照组仅给予常规吞咽康复训练,治疗终点为恢复经口进食或治疗已满4周。分别在治疗前、治疗终点采用视频吞咽造影检查、进食功能评价进行测评。 结果治疗组患者经球囊扩张术治疗10~24次后,15例患者中有12例进食功能改善,对照组仅7例进食功能有改善,2组差异有统计学意义(P<0.05)。治疗前、后视频吞咽造影检查分析发现,治疗组12例环咽肌开放情况改善,而对照组中仅7例有所改善,2组差异有统计学意义(P<0.05);视频吞咽造影检查中咽通过时间比较,治疗组中治疗前平均0.23 s,治疗后为0.15 s,差异有统计学意义(P<0.05)。 结论球囊扩张术对脑干病变后环咽肌失弛缓症所致吞咽障碍疗效显著,可明显改善咽期及食管期症状。  相似文献   

10.
目的探讨导尿管球囊扩张治疗环咽肌失弛缓症的可行性。方法报道1例因脑梗死致环咽肌失弛缓症利用导尿管球囊扩张治疗的临床经过。结果经38次扩张治疗后,患者可独立自主进食,无呛咳。吞咽造影复查显示在食团通过时,环咽肌正常开放,误吸消失。结论导尿管球囊扩张术能有效缓解环咽肌失弛缓,操作简单,安全可靠。  相似文献   

11.
It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.  相似文献   

12.
本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。  相似文献   

13.
目的:探讨腹膜后纤维化(RPF)导致肾积水的原因及诊治经验。方法:回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果:(1)RPF患者常见首发症状为腰背痛或腹痛(69.2%);(2)红细胞沉降率(ESR)增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影(IVP)和CT尿路成像(CTU)表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例(37.5%),优于超声检查;(3)输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;(4)特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论:影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。  相似文献   

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15.
Fibrinogen and fibrin structure and functions   总被引:12,自引:0,他引:12  
Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.  相似文献   

16.
Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.  相似文献   

17.
Designing interprofessional primary care teams composed of physicians and nurse practitioners (NPs) is a national priority. We assessed how profession and gender affect teamwork and job satisfaction among primary care physicians and NPs by using survey data from 186 physicians and 398 NPs practicing in New York State. Our regression models show profession (NP vs physician) moderates the associations of gender with teamwork and job satisfaction. Among NPs, men had higher job satisfaction than women. Among physicians, women had higher job satisfaction than men. Our results can benefit interprofessional primary care teams to optimize their professional and gender mix.  相似文献   

18.
目的探讨儿童慢性顽固性咳嗽与肺炎支原体(MP)感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点:在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58%(32/55)的病例无肺部体征;②外周血:85%(47/55)的病例外周血变化不大,WBC(4—10)×10 9/L之间,嗜酸性粒细胞增多;③特别检查:47.27%(26/55)肺炎支原体IgM(MP—IgM)抗体阳性,83.64%(46/55)PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体(MP)感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。  相似文献   

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目的探讨妊娠合并血小板减少症伴随重要脏器的损伤情况。方法前瞻性研究我院及北华大学附属医院2004年10月至2005年5月妊娠合并血小板减少症的临床资料,对41例妊娠合并血小板减少症者尿素氮(BUN)、肌酐(CREA)、谷丙转氨酶(ALT)、乳酸脱氢酶(LDH)的测定及妊娠期高血压疾病与血小板计数(PLT),血小板平均体积(MPV)和血小板体积分布宽度(PDW)参数的测定进行对比分析。结果妊娠合并血小板减少症患者心、肝、肾等重要脏器均有不同程度的改变,且随着血小板计数降低,损害程度加剧,差异具有显著性(P〈0.01)。妊娠期高血压疾病,随着疾病程度的加重,血小板计数较正常孕妇明显减少,MPV、PDW明显升高,有显著性差异(P〈0.01)。结论血小板参数是判断疾病的重要参考指标,肝、肾、心脏器损伤程度与血小板计数具有相关性。  相似文献   

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