丁苯酞联合舍曲林对缺血性脑卒中后抑郁及细胞因子的影响

目的探讨丁苯酞软胶囊联合舍曲林对缺血性脑卒中后抑郁(IPSD)及细胞因子的影响。方法 IPSD患者80例随机分为丁苯酞组、对照组各40例,均给予缺血性脑卒中基础治疗、心理治疗及口服舍曲林抗抑郁治疗,丁苯酞组在此基础上应用丁苯酞软胶囊,疗程12 w,评价丁苯酞联合舍曲林对IPSD患者抑郁症状、神经功能缺损程度及对白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α的影响。结果连续治疗4、8、12 w时两组汉密尔顿抑郁量表(HAMD)、美国国立卫生研究院卒中量表(NIHSS)评分显著降低(P<0.01),且丁苯酞组显著低于对照组(P<0.05);治疗4 w时两组神经功能损伤改善程度无统计学差异(P>0.05),治疗8、12 w时丁苯酞组效果显著优于对照组(P<0.05);连续治疗4、8、12 w时两组IL-6、TNF-α含量均显著下降(P<0.01),且丁苯酞组下降程度明显高于对照组(P<0.05)。结论丁苯酞软胶囊联合舍曲林可明显改善IPSD患者的抑郁程度、神经功能缺损及降低IL-6、TNF-α水平。     

舍曲林对慢性缺血性心衰伴抑郁患者生活质量的影响

目的:观察舍曲林对慢性缺血性心衰伴抑郁患者抑郁状态、生活质量的影响。方法:90例慢性缺血性心衰伴抑郁患者被分为常规治疗组(46例)和舍曲林组(44例,常规治疗基础上加用舍曲林,50mg/d),随访6个月。比较两组治疗前后汉密尔顿抑郁量表(HAMD)、36项简易健康调查表(SF-36)得分。结果:与常规治疗组比较,舍曲林组治疗后抗抑郁有效率(36.96%比81.82%)明显增加(P=0.001);在生活质量方面:与治疗前比较,舍曲林组SF-36量表8个维度得分均明显升高,常规治疗组除总体健康得分明显减少和情感角色限制得分明显升高(P<0.05或<0.01)外,其余无显著差异(P均>0.05);与常规治疗组比较,舍曲林组SF-36量表中生理机能[(32.21±17.16)分比(38.13±14.13)分]、生理职能[(24.53±6.71)分比(36.00±15.16)分]、总体健康[(32.91±16.73)分比(58.38±10.09)分]、活力[(31.05±12.56)分比(39.00±14.24)分]、社会功能[(44.19±21.01)分比(58.10±29.89)分]、情感职能[(42.62±19.70)分比(55.00±27.80)分]和心理健康[(44.37±19.49)分比(54.20±30.25)分]7个维度得分明显升高(P<0.05或<0.01)。结论:慢性缺血性心衰伴抑郁患者在抗心衰药物治疗基础上加用舍曲林可改善抑郁状态和生活质量。     

脑卒中后抑郁对神经功能康复的影响研究

目的 探讨脑卒中后抑郁对神经功能康复的影响.方法 选取2009-2010年医院收治的脑卒中后抑郁患者70例,将其随机分为治疗组和对照组,每组各35例,对照组给予常规治疗,治疗组患者在对照组的基础上给予氟西汀进行治疗.比较两组患者治疗前后汉密顿抑郁量表及神经功能缺损评分.结果 治疗组治疗后汉密顿抑郁量表及神经功能缺损评分均优于对照组,差异均有统计学意义(P＜0.05).治疗组患者在用药期间无明显的不良反应发生,且各项身体指标检查较对照组患者均无明显异常.结论 脑卒中后抑郁会严重影响神经功能的恢复,在进行脑卒中治疗的同时,还应重视抑郁症状的治疗.     

舍曲林对老年良性前列腺增生伴抑郁患者的疗效

目的考察舍曲林对老年良性前列腺增生（BPH）伴抑郁患者的疗效。方法将2011年1月至2012年5月由解放军总医院第一附属医院干部病房二科收治的118例老年BPH伴抑郁的患者随机分为治疗组（60例）和对照组（58例）。对照组采取常规前列腺增生治疗,治疗组在常规前列腺增生治疗基础上,同时给予抗抑郁药物舍曲林治疗12周。在治疗前及治疗后2,4,8,12周,使用汉密尔顿抑郁量表（HAMD-17）和汉密尔顿焦虑量表（HAMA）评定抗抑郁焦虑疗效,使用治疗不良反应量表（TESS）评定药物不良反应,治疗前后使用生活质量综合评定问卷（GQOLI-74）评定生活质量的变化。分别进行两组治疗前后对比分析,评价舍曲林对患者抑郁焦虑症状的疗效及对生活质量的影响。结果经12周治疗后,治疗组患者的抑郁、焦虑症状显著改善（P〈O．01）。生活质量的心理健康和社会功能方面明显高于治疗前,并且高于对照组,差异有统计学意义（P〈0．05,P〈0．01）。结论舍曲林对BPH伴抑郁患者的疗效显著,有利于改善患者的生活质量。     

脑卒中后抑郁与神经功能康复

目的探讨脑卒中后抑郁状态的治疗对神经功能康复的影响。方法将100例脑卒中后的抑郁患者随机分为治疗组和对照组,治疗前后行汉密尔顿抑郁量表（HAMD）神经功能缺损评分（NIHSS）评定。结果治疗组HAMD评分治疗后（3．9±2．1）较治疗前（20．12±1．5）显著下降（P〈0.01）;对照组治疗后（14．1±3．9）与治疗前（19．00±2．1）比较无统计学意义（P〉0.05）。治疗组治疗后NIHSS评分显著降低,与对照组比较有统计学意义（P〈0.01）。结论脑卒巾后抗抑郁治疗可促进脑卒中后精神神经康复。     

脑卒中后抑郁的治疗

<正>脑卒中后抑郁(post-stroke depression,PSD)是脑卒中后常见精神疾病之一,约有1/3的脑卒中患者在其后不同阶段罹患PSD[1]。PSD极大影响脑卒中患者神经功能恢复,增加致残率、病死率,降低患者生活质量,给家庭和社会带来沉重负担[2]。目前对于PSD的治疗尚无定论,较多学者认为及时合理的抗抑郁治疗不仅有助于患者精神症状的恢复,对其神经功能康复也有     

康复治疗对脑卒中后抑郁和神经功能缺损的影响

目的探讨脑卒中后康复治疗对卒中后抑郁和神经功能缺损的影响。方法收集2006-07～2009-01间122例脑卒中病人的临床资料,其中男性90例,女性32例,年龄(64±10)岁,在康复治疗前后应用汉密尔顿抑郁量表(HAMD)进行抑郁评分,用神经功能缺损评分(NIHSS)进行神经功能缺损程度评估。结果并发抑郁症者神经功能缺损更严重(P0.0001);经过康复治疗,抑郁症的患者减少,从17%减至6%;两组患者神经功能缺损经过康复治疗均能改善。结论脑卒中患者易于并发抑郁症,康复治疗有助于改善患者抑郁和神经功能缺损症状。     

抗抑郁治疗对老年脑卒中后抑郁患者神经功能康复及神经元特异性烯醇化酶的影响

目的观察抗抑郁治疗对老年脑卒中后抑郁(post-stoke depression,PSD)患者神经功能康复和神经元特异性烯醇化酶(neuron-specific enolase,NSE)的影响。方法选择2015年7月～2018年6月眉山市人民医院神经内科收治的老年脑卒中合并PSD患者119例,按照入院顺序随机双盲试验设计,分为治疗组60例和对照组59例,动态观察2组抗抑郁治疗前,治疗后2、4、8周及6个月美国国立卫生研究院卒中量表(national institute of health stroke scale,NIHSS)评分、汉密尔顿抑郁量表(Hamilton depression scale,HAMD)评分和NSE水平的差异。结果 2组治疗后2、4、8周及6个月HAMD评分和NIHSS评分较治疗前明显降低,差异有统计学意义(P0.05)。治疗组治疗后2、4、8周及6个月HAMD评分明显低于对照组,差异有统计学意义(P0.01)。治疗组治疗后4、8周及6个月NIHSS评分明显低于对照组,差异有统计学意义(P0.05,P0.01)。治疗组治疗后2、4、8周血清NSE水平明显低于对照组,差异有统计学意义[(28.70±2.38)μg/L vs (30.78±2.72)μg/L,(24.16±2.45)μg/L vs (26.12±3.02)μg/L,(13.17±2.60)μg/L vs (15.94±3.39)μg/L,P0.01]。Person相关性分析显示,治疗前血清NSE水平与NIHSS评分呈正相关(r=0.459,P0.01)。结论抗抑郁治疗可改善老年PSD患者的抑郁症状,促进神经功能恢复,早期血清NSE水平可作为神经功能康复的预测指标。     

舍曲林联合高压氧治疗脑卒中后抑郁的日常生活能力的临床观察

目的明确舍曲林联合高压氧治疗脑卒中后抑郁（PSD）的日常生活能力的临床疗效。 方法选取苏州瑞盛康复医院神经康复科自2016年10月至2018年10月收治的80例PSD患者为研究对象,采用随机数字法将其分为观察组与对照组,每组40例。2组均给予舍曲林治疗,观察组在服用舍曲林的基础上给予高压氧治疗,比较2组患者治疗前后日常生活能力量表（ADL）评分、功能独立程度评定量表（FIM）评分。 结果治疗前2组患者ADL、FIM评分比较差异无统计学意义（P>0.05）,治疗后观察组ADL、FIM评分优于对照组,差异具有统计学意义（P<0.05）。治疗后观察组总有效率（90%）高于对照组（73%）,差异具有统计学意义（P<0.05）。 结论在PSD患者的临床治疗中,应用舍曲林联合高压氧治疗方案,可显著改善患者抑郁等不良情绪,提高日常生活能力及生活质量,值得临床推广。     

Patterns of change in depression after stroke

OBJECTIVES: To provide estimates of change in depressive symptoms and determine how changes in depressive symptom influence recovery of functional status. DESIGN: Prospective cohort study. SETTING: Eleven inpatient medical rehabilitation facilities located across the United States. PARTICIPANTS: Five hundred forty‐four persons with a first‐time stroke. MEASUREMENTS: General linear regression model estimates assessed associations between depressive symptom change and functional status 3 and 12 months after discharge. RESULTS: The majority of persons with stroke were aged 75 and older, white, female, and married. The most prevalent stroke type was ischemic. For participants without depression at discharge, those who reported fewer depressive symptoms 12 months after stroke than before had an adjusted functional status score of 108.2, whereas those with more symptoms had an adjusted functional status score of 104.6. For participants who were depressed at discharge, those who reported fewer depressive symptoms 12 months after stroke than before had an adjusted functional status score of 100.3, whereas those with more symptoms had an adjusted functional status score of 88.0. CONCLUSION: Tracking depressive symptom change in the hospital and after discharge is clinically relevant and is an important component of patient care and recovery of functional status.     

Anxiety and depression are related to autonomic nervous system function in women with irritable bowel syndrome

This study compared women with irritable bowel syndrome who had a history of an anxiety or depressive disorder to those without symptoms of either disorder on indicators of cardiac parasympathetic activity, autonomic nervous system balance, and general autonomic activity. The Diagnostic Interview Schedule was used to determine anxiety or depressive disorders, and a Holter monitor was used to record R-R intervals over 24 hr. A similar comparison was done with healthy controls. Among women with irritable bowel syndrome, those with a positive history had lower parasympathetic and general activity throughout the 24-hr period than did women without a diagnosis. Indicators of autonomic balance were slightly higher in women with a positive history compared to those without a history. Similar differences were seen in controls. Thus, a history of anxiety and depressive disorders is associated with lower parasympathetic activity, both in women with IBS and healthy controls. Further exploration is needed to understand if lower parasympathetic activity influences the pain and stool pattern changes seen in persons with irritable bowel syndrome.     

舍曲林合并生物反馈疗法对冠心病患者焦虑抑郁及心肌酶的影响

目的探讨舍曲林合并脑电生物反馈疗法对冠心病患者焦虑抑郁及心肌酶的影响。方法将80例伴有焦虑抑郁的冠心病患者随机分为研究组和对照组各40例,均给予舍曲林100~200 mg/d治疗,研究组同时接受生物反馈治疗,疗程8周。治疗前后检测心肌酶水平,同时采用汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)评定患者焦虑抑郁状态。结果 (1)有效率比较:治疗8周后,研究组和对照组有效率分别为95.0%和77.5%,差异有统计学意义(P0.05)。(2)焦虑抑郁比较:治疗2、4、8周后2组HAMA、HAMD量表评分均较治疗前降低(P0.05),治疗后第4、8周研究组HAMA、HAMD量表评分均与对照组有统计学差异(P0.05)。(3)心肌酶比较:治疗8周后2组心肌酶5项指标均较治疗前改善(P0.05),研究组CK-MB水平与对照组差异有统计学意义(P0.05)。2组不良反应比较无统计学差异(P0.05)。结论生物反馈疗法合并舍曲林能明显改善冠心病患者的焦虑抑郁状态及心肌酶水平,值得临床推广应用。     

西酞普兰治疗急性卒中后抑郁的疗效及其对卒中康复的影响

目的观察西酞普兰治疗急性卒中后抑郁的疗效及其对卒中康复的影响。方法105例急性卒中后抑郁患者随机分为西酞普兰组(52例)和对照组(53例),2组均接受常规药物治疗,治疗组同时加用西酞普兰治疗。治疗前后应用Hamilton抑郁量表(HRSD)评价抑郁状况,治疗前、治疗后4周和12周采用简易智能状态量表(MMSE)、中国卒中量表(CSS)和Barthel指数(BI)评价患者的认知和神经功能状况。结果治疗组1例死亡,1例失访;对照组2例死亡,2例失访。治疗后12周时西酞普兰组治愈率和总有效率分别为64%和96%,显著高于对照组的16·33%和57·44%(P<0·05)。治疗后4周和12周时西酞普兰组MMSE评分较对照组显著增加(P<0·01)。治疗后4周时,两组CSS和BI评分均有改善,但无显著性差异;治疗12周后西酞普兰组CSS和BI评分均优于对照组(P<0·01)。西酞普兰的主要不良反应为中枢神经系统和消化系统反应,但症状轻微。结论西酞普兰治疗卒中后抑郁安全有效,且能改善12周时的认知功能、神经功能和转归。     

抑郁症患者甲状腺功能与植物神经功能的关系

目的研究抑郁症患者甲状腺功能和植物神经功能的变化。方法研究我院门诊患者单相抑郁症38例,双相抑郁症组42例,正常对照组30例。用汉密顿量表(17项版本)进行精神测评。用化学发光法测定血清FT3、FT4、TSH的水平,用植物神经平衡指数来评定植物功能。结果与对照组比较,单相抑郁症患者血清FT3水平下降,FT4水平上升,TSH水平无变化,双相抑郁症患者血清FT3水平下降、FT4水平上升更显著(P<0.01)。单相抑郁和双相抑郁患者植物神经功能评定均提示交感神经活性增强。与轻度抑郁症相比,重度抑郁症患者血清FT3水平下降、FT4水平上升和植物神经平衡指数上升更显著(P<0.01)。结论抑郁症患者交感神经活性增强,其血清FT3水平下降、FT4水平上升。     

老年卒中后抑郁与急性期神经功能缺损程度的相关研究

目的探讨老年脑卒中后抑郁（PSD）发生率以及与急性期神经功能缺损程度的关系。方法对292例住院诊断为脑卒中的老年患者，用改良的爱丁堡斯堪的那维亚神经功能缺损评分表（SSS）对卒中急性期进行评分，根据急性期神经功能缺损情况分为三组。用汉密尔顿抑郁量表进行随访调查抑郁评分。结果老年PSD的发生率在随访1年期间中随着时间的延长逐渐增加；老年PSD的发病率和重度PSD的发生率随神经功能缺损程度的加重而增加；老年PSD的程度随着神经功能缺损程度增加而加重。结论PSD是老年脑卒中后的常见并发症，卒中后1年中发病逐渐增加，其严重程度与卒中急性期的神经功能缺损程度一致。     

早期康复治疗对老年卒中患者预后的影响

目的探索早期康复治疗对老年脑卒中患者预后的影响。方法入选2008年1月至2010年11月收治的急性脑卒中患者150例,其中康复组80例,对照组70例,对所有患者在入院24h内及入院后21d、35d采用神经功能缺损评分(NIHSS)评定其肢体运动功能状态;于治疗后35d采用Barthel指数(BI)评定其日常生活活动能力,同时统计其并发症及住院费用。结果康复组的肢体功能缺损评分在治疗后明显低于对照组(P<0.05),BI评分明显高于对照组(P<0.05),而其并发症及住院费用明显低于对照组(P<0.05)。结论早期康复治疗可以明显促进卒中患者肢体功能的恢复,增强患者的自理能力,减少并发症的产生,减轻患者负担,对老年患者是有效和安全的。     

Optogenetic neuronal stimulation promotes functional recovery after stroke

Clinical and research efforts have focused on promoting functional recovery after stroke. Brain stimulation strategies are particularly promising because they allow direct manipulation of the target area’s excitability. However, elucidating the cell type and mechanisms mediating recovery has been difficult because existing stimulation techniques nonspecifically target all cell types near the stimulated site. To circumvent these barriers, we used optogenetics to selectively activate neurons that express channelrhodopsin 2 and demonstrated that selective neuronal stimulations in the ipsilesional primary motor cortex (iM1) can promote functional recovery. Stroke mice that received repeated neuronal stimulations exhibited significant improvement in cerebral blood flow and the neurovascular coupling response, as well as increased expression of activity-dependent neurotrophins in the contralesional cortex, including brain-derived neurotrophic factor, nerve growth factor, and neurotrophin 3. Western analysis also indicated that stimulated mice exhibited a significant increase in the expression of a plasticity marker growth-associated protein 43. Moreover, iM1 neuronal stimulations promoted functional recovery, as stimulated stroke mice showed faster weight gain and performed significantly better in sensory-motor behavior tests. Interestingly, stimulations in normal nonstroke mice did not alter motor behavior or neurotrophin expression, suggesting that the prorecovery effect of selective neuronal stimulations is dependent on the poststroke environment. These results demonstrate that stimulation of neurons in the stroke hemisphere is sufficient to promote recovery.Stroke is a major acute neurological insult that disrupts brain function and causes neuron death. Functional recovery after stroke has been observed and is currently attributed to both brain remodeling and plasticity (1–4). Structural and functional remodeling of areas next to an infarct or remote regions can alter signaling within bilateral neuronal networks and thus contribute to functional recovery (3–7). Rewiring of neural connections is mediated by electrical activity, which can activate a number of plasticity mechanisms, including the release of activity-dependent neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) (8–10). Both BDNF and NGF have been shown to improve recovery by enhancing axonal and dendritic sprouting (10–12).Tremendous effort has been focused on promoting recovery after stroke, including pharmacological treatment, rehabilitation (e.g., constraint-induced therapy), stem cell transplantation, and brain stimulation (1, 4, 13). Brain stimulation is a promising area of research because it allows direct activation and manipulation of the target area’s excitability (14–16). The primary motor cortex (M1) is a commonly stimulated area as it directly innervates the corticospinal tract to initiate movement (1, 7). Although electrical stimulation and transcranial magnetic stimulation show promise in promoting recovery (17, 18), these techniques are limited by imprecision and indiscriminate activation or inhibition of all cell types near the stimulated site; thus, they can produce undesired effects such as psychiatric and motor/speech problems (19–21). In addition, it has been difficult to elucidate the cell type and mechanisms driving recovery, as multiple cell types such as neurons, astrocytes, and oligodendrocytes have been shown to contribute to remodeling and recovery processes after stroke (5, 22–27).To elucidate whether activation of neurons alone can promote recovery, we used optogenetics to selectively manipulate the excitability of specific cell groups with millisecond-scale temporal precision in a manner more similar to endogenous neuronal firing patterns (21, 28, 29). This technique uses light-activated microbial proteins such as Channelrhodopsin 2 (ChR2), which depolarizes neurons when illuminated with blue light, or Halorhodopsin (NpHR), which hyperpolarizes neurons (21, 28, 29). Optogenetic approaches have been used in rodents to probe neuronal circuits for several neurological/neurodegenerative diseases, including Parkinson disease (30) and epilepsy (31). Recent studies have also used optogenetics to map functional organization after stroke (32–35). The safety and efficacy of using optogenetics in nonhuman primates has also been characterized (29, 36).In this study, we used optogenetics to selectively stimulate neurons in layer V of the ipsilesional primary motor cortex (iM1) and examine the effects of repeated neuronal stimulations in normal and stroke mice. Sensory-motor behavior tests were used to evaluate functional recovery after stroke, and plasticity-associated mechanisms, such as cerebral blood flow (CBF)/neurovascular coupling responses and activity-dependent neurotrophin expression, were investigated.