心理干预合并曲唑酮治疗原发性高血压伴抑郁焦虑的疗效观察

目的　观察心理干预并曲唑酮对原发性高血压伴抑郁或焦虑情绪患者的疗效 ,寻找治疗最佳方案 .方法原发性高血压患者经汉密顿抑郁量表 17项 (HAMD)及汉密顿焦虑量表 14项 (HAMA)评分 ,其中抑郁或焦虑分分别超过 17或 14分者随机分成 3组 :A组为对照组 ,只用降压药物治疗 ;B组为降压治疗合并心理干预 ;C组降压并心理干预再加用曲唑酮治疗 .治疗 4周后用HAMD及HAMA量表评分 ,并记录血压变化 .结果　治疗后C组收缩压和舒张压降低较B组和A组明显 (p <0 .0 1,p <0 .0 0 1) .HAMD及HAMA总分C组降低较B组、A组明显 (p <0 .0 1,p <0 .0 0 1,p <0 .0 5 ) .结论　综合心理干预合并曲唑酮治疗对高血压伴心理障碍者有良好作用     

音乐放松训练对癌症放疗患者的心理干预

目的 探讨音乐放松训练对癌症患者在放射治疗期间抑郁、焦虑情绪的影响.方法 61名接受放射线治疗的癌症住院患者按照接受放射治疗的时间先后分为两组,其中一组30名患者在放疗过程中接受音乐放松训练的心理干预(干预组),另一组31名患者不予干预(对照组).且在放疗的不同时期采用汉密顿焦虑量表(HAMA)、汉密顿抑郁量表(HAMD)对患者进行心理问卷调查.结果 HAMA、HAMD评分结果显示:干预组与对照组相比,放疗开始第0周焦虑、抑郁差异不显著,无统计学意义[HAMA分(t=0.026,P=0.979);HAMD分(t=0.906,P=0.369)];放疗开始后第4周的焦虑、抑郁差异有统计学意义[HAMA分(t=2.763,P=0.008);HAMD分(t=2.134,P=0.037)];放疗开始后第8周的焦虑、抑郁差异有统计学意义[HAMA分(t=2.468,P=0.016);HAMD分(t=2.578,P=0.012)].结论 在临床上对于癌症放疗患者给予音乐放松训练进行心理干预,对缓解或减轻患者焦虑、抑郁等情绪有一定的帮助,从而增加其癌症治疗的依从性.     

心理干预对老年脑卒中患者合并抑郁焦虑的康复效果及生活质量影响

目的:探讨心理干预对改善老年脑卒中合并焦虑抑郁患者的负性心理情绪和生活质量的效果。方法:选取我院2016年1月至2017年12月于我院接受治疗的120例脑卒中合并焦虑抑郁患者的临床资料,采用随机数字表法将患者随机分为干预组和对照组,给予对照组常规药物治疗,干预组在常规药物治疗的基础上实施心理康复干预治疗,观察并比较两组患者心理干预前后焦虑(SAS)和抑郁(SDS)自评量表评分、汉密尔顿焦虑量表评分(HAMA)和汉密尔顿抑郁量表评分(HAMD)情况。结果:治疗12周后,两组患者SAS、SDS、HAMA、HAMD评分均显著低于治疗前;治疗后干预组患者SAS(t=-8.735,P0.001)、SDS(t=-8.868,P0.001)、HAMA(t=-7.615,P0.001)、HAMD(t=-4.905,P0.001)评分均显著低于对照组患者;治疗后干预组患者康复依从性与对照组比较具有显著统计学差异(χ~2=9.887,P=0.007)。结论:对脑卒中抑郁焦虑患者,实施心理康复干预能够有效改善患者抑郁焦虑症状,提高患者康复依从性。     

综合心理干预对抑郁症康复的影响

目的 讨论综合心理干预对抑郁症康复的作用.方法 将62例住院患者随机分为两组.观察组采用药物治疗和综合心理干预,对照组采用单纯药物治疗,并给予简单常规介绍.采用汉密顿抑郁量表(HAMD)、汉密顿焦虑量表(HAMA)和护士用住院患者观察量表(NOSIE),对两组患者在住院期间的康复效果进行对比分析.结果 观察组和对照组在干预前HAMD、HAMA总分、NOSIE因子分无显著性差异(P＞0.05).实施干预2周时,两组间HAMD、HAMA指标,差异有显著性意义(P＜0.05);4、6周时,HAMD、HAMA指标比较均有显著差异(P＜0.01);6周后NOSIE与干预前相比有统计学意义(P＜0.01).结论 综合心理干预可以提高抑郁症患者的疗效,改变患者的抑郁症状和退缩行为,让患者正确认识自己所面临的困难,从而促进患者早日康复.     

盐酸曲唑酮治疗酒依赖稽延性戒断症状100例临床研究

目的 探讨盐酸曲唑酮治疗酒依赖稽延性戒断症状的有效性和安全性.方法 采用随机、双盲、安慰剂对照的方法把100例符合纳入和排除标准的患者分成盐酸曲唑酮组和安慰剂组.每个患者均口服盐酸曲唑酮或安慰剂每日3次,每次1片,疗程均为8周.8周内按时分别进行汉密顿焦虑量表(HAMA)、汉密顿抑郁量表(HAMD)、匹兹堡睡眠质量指数...     

伴抑郁情绪原发性高血压患者的功能失调性态度调查

目的:考察伴抑郁情绪原发性高血压患者的功能失调性态度的特征.方法:对1088例高血压患者进行医院焦虑抑郁量表(HAD)筛选,将评分阳性者再进行汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)评分,HAMD≥20分,且HAMA<14分者入选,共获得262名伴抑郁情绪高血压病患者作为研究被试.另外选择长沙的两个社区人群,共计306例作为对照组.采用功能失调性态度问卷(DAS)对其进行测查.结果:①伴抑郁情绪高血压病患者经常持有的功能失调性认知排在前三位放的依次排序为:认知哲学,寻求赞许,强制性;②受试者得分具有明显的性别差异.③除了自主性态度分量表以外,其余功能失调性态度分量表都与抑郁量表得分显著正相关(P<0.05).结论:伴抑郁情绪原发性高血压患者存在明显的功能失调性认知特征.     

帕罗西汀并心理干预治疗卒中后抑郁和焦虑共病者81例临床观察

目的：探讨脑卒中后抑郁和焦虑共病对患者生活能力和神经功能康复的影响，及帕罗西汀合并心理干预临床疗效。方法：将脑卒中伴抑郁和焦虑障碍共病者81名随机分成3组，分别接受单用帕罗西汀治疗（A组）、帕岁西汀并心理治疗（B组）以及单用脑血管药物治疗（C组）。采用斯堪的那维亚脑卒中量表、Barthel指数、汉密尔顿抑郁量表、汉密尔顿焦虑量表评估疗效。结果：脑卒中患者中，抑郁和焦虑的共病率为65．9％，A组、B组各项评分与C组比较，差异均有统计学意义。结论：卒中后抑郁和焦虑病人单用帕罗西汀或合并心理治疗均能促进患者神经功能康复和提高生活质量，且帕罗西汀并心理干预的疗效更好。     

抗抑郁药对伴焦虑抑郁症状精神分裂症的辅助治疗效应

目的 探讨抗抑郁药对伴焦虑抑郁症状的精神分裂症的辅助治疗作用及不良反应.方法 对符合CCMD-Ⅲ关于精神分裂症的诊断且伴焦虑抑郁症状的住院患者进行随机分组,研究组(64例)给予抗精神病药加抗抑郁药(西酞普兰20mg/d)治疗;对照组(67例)单给抗精神病药治疗;两组于入组时、4周末、8周末分别评定简明精神病量表(BPRS)、汉密顿抑郁量表(HAMD)和汉密顿焦虑量表(HAMA),以副反应量表(TESS)评定不良反应,然后进行比较.结果 两组的BPRS总分和HAMD、HAMA总分在治疗后均显著下降(P＜0.01);研究组4周末疗效更佳(P＜0.05～0.01);8周末疗效两组相近(P＞0.05);两组的不良反应无显著性差异(P＞0.05).结论 抗抑郁药在急性期对伴焦虑抑郁症状的精神分裂症有辅助治疗作用,不良反应轻微.     

骨折后负性情绪调查及心理干预对患者的影响

目的:调查骨折后患者负性情绪状态及原因,分析心理干预对骨折患者负性情绪、心理韧性、并发症发生率的影响。方法:选取2017年1月-2018年12月某院收治的118例骨折住院患者为研究对象,采用汉密顿焦虑量表(HAMA)、汉密顿抑郁量表(HAMD)调查患者焦虑、抑郁情况;按照住院顺序奇偶数法将患者分为观察组59例和对照组59例,对照组进行骨科常规干预,观察组在常规干预基础上给予心理干预,比较两组干预前、干预后4周HAMA、HAMD评分及阳性检出率,采用心理韧性量表(CD-RISC)评价患者干预前后心理韧性,并比较两组术后6个月内并发症发生情况。结果:118例骨折住院患者,HAMA得分(15.61±5.62)分,焦虑阳性检出率为30.51%,HAMD得分(19.10±7.22)分,抑郁阳性检出率为34.75%;承受较大躯体痛苦(72.88%)、抱怨生活无法自理(70.34%)、担心影响身体功能(60.17%)是导致骨折住院患者负性情绪最常见原因;干预后,观察组HAMA、HAMD评分均显著低于对照组(t=-4.685,-4.998;P0.05);观察组抑郁阳性检出率3.39%,显著低于对照组的13.56%(χ~2=3.933,P0.05);观察组CD-RISC评分显著高于对照组(t=4.935,P0.05);观察组术后6个月内并发症总发生率为6.78%,显著低于对照组的20.34%(χ~2=4.628,P0.05)。结论:骨折后患者焦虑、抑郁负性情绪水平较高,积极进行心理干预可缓解患者焦虑、抑郁情绪,提高患者心理韧性,有利于降低患者术后并发症发生率。     

不同性别的慢性胃炎影响因素及临床特征分析

目的探讨不同性别的慢性胃炎患者影响因素及临床特征。方法收集女性患者52例(A组)、男性患者48例(B组),对其一般人口学资料、汉密顿抑郁量表(HAMD)、汉密顿焦虑量表(HAMA)、应激评定量表、艾森克人格问卷、血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)进行测定和对照。结果 1A组平均年龄较B组高(t=2.83,P0.01),高中及高中以上文化程度人数较B组少(χ2=4.83,P0.05),A、B两组在婚姻等方面比较差异无显著性(χ2=0.00,P0.05);2A组HAMA分值、神经质性人格者、应激量表中社会习惯应激、焦虑因子分、血清IL-6、TNF-α浓度高于B组(P0.05);3B组HAMD分值、应激量表中社会交往、生活事件、抑郁因子分高于A组(P0.05)。结论了解不同性别的慢性胃炎患者的临床特点,有助于患者早期、有效的治疗。     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

即早基因c-fos与脑血管病及学习记忆

即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.     

自主创新学习与问题探究教学改革的探索与实践

<正>人体解剖学与组织学胚胎学是高职护理及助产专业的学生接触最早而又重要的医学基础核心课程。鉴于目前高职护理及助产专业的教学内容多,课时少等难题,教与学的矛盾日益突出。因此,如何在有限的时间内既保证教学体系的完整性,又能解决时间与内容冲突的矛盾,从而使医学生对所学内容真正达到"必须、够用",是授课教师面临的严峻挑战。同时,顺应医学终身教育发展的需求,提高医学生自主学习的能力,