抗抑郁治疗对卒中后抑郁及神经功能康复的影响

目的探讨氟西汀抗抑郁治疗对卒中后抑郁(PSD)患者的抑郁症状和神经功能康复的影响及其安全性。方法将91例PSD患者随机分为治疗组46例和对照组45例,两组同时应用脑血管病治疗药物,治疗组加用氟西汀治疗。采用汉密尔顿抑郁量表(HAMD)、日常生活自理能力量表(Barthel指数记分)和神经功能缺损程度评定疗效和功能改善状况。结果治疗后治疗组HAMD量表减分率与对照组比较,差异有高度显著性(P<0.01),神经功能缺损程度积分值降低与Barthel评分提高,治疗组优于对照组(P<0.05和P<0.01)。治疗组抑郁症状改善的显效率和神经功能缺损改善的总有效率均显著高于对照组(P<0.001和P<0.05)。氟西汀的主要副反应为失眠、焦虑和恶心。结论氟西汀抗抑郁治疗能明显改善PSD患者的抑郁症状和神经功能,且副反应轻。     

奥氮平联合氟西汀治疗精神分裂症阴性症状的对照研究

目的探讨奥氮平联合氟西汀治疗精神分裂症阴性症状的疗效及安全性。方法将以阴性症状为主的精神分裂症患者分为奥氮平合用氟西汀组32例和单用奥氮平组30例，两组均以PANSS量表减分情况评定疗效，TESS量表评定药物不良反应，共观察8周。结果（1）奥氮平合用氟西汀组与单用奥氮平组治疗精神分裂症的有效率为90．63％和73．33％（P〉0．05），显效率为75．00％和40．00％（P〈0．01）。（2）PANSS总分减分及PANSS阴性因子分减分在第2、4、8周末奥氮平合用氟西汀组均优于单用奥氮平组（P〈0．05或0.01）。（3）两组药物的不良反应少，奥氮平合用氟西汀组的体重增加明显低于单用奥氮平组（P〈0．05）。结论奥氮平联合氟西汀治疗能明显改善精神分裂症的阴性症状，且安全性好。     

Combination of fluoxetine and extinction treatments forms a unique synaptic protein profile that correlates with long-term fear reduction in adult mice

The antidepressant fluoxetine induces synaptic plasticity in the visual and fear networks and promotes the structural remodeling of neuronal circuits, which is critical for experience-dependent plasticity in response to an environmental stimulus. We recently demonstrated that chronic fluoxetine administration together with extinction training in adult mice reduced fear in a context-independent manner. Fear conditioning and extinction alter excitatory and inhibitory transmissions within the fear circuitry. In this study, we investigated whether fluoxetine, extinction or their combination produced distinct long-lasting changes in the synaptic protein profile in the amygdala, hippocampus and prefrontal cortex of conditioned mice. We determined that extinction induced synaptophysin expression and down-regulated the GluA1:GluA2 ratio throughout the fear network in water- and fluoxetine-treated mice, suggesting a common fluoxetine-independent mechanism for increased synaptic transmission and re-arrangement of AMPA-receptors by extinction training. In contrast to common changes, the presynaptic vesicular neurotransmitter transporters VGAT and Vglut1 were upregulated after extinction in water- and fluoxetine-treated mice, respectively. The cortical levels of the GABA transporter Gat1 were reduced in high-freezing water-drinking mice, suggesting a maladaptive increase of GABA spillover at cortical inhibitory synapses. Fear conditioning decreased, and extinction induced the expression of GABA-receptor alpha1 and alpha2 subunits in water- and fluoxetine-treated mice, respectively. Only a combination of fluoxetine with extinction enhanced GluN2A expression in the amygdala and hippocampus, emphasizing the role of this NMDA-receptor subunit in the successful erasure of fear memories. Our finding provides novel data that may become helpful in developing beneficial pharmacological fear-reducing treatment strategies.     

脑梗死患者早期应用氟西汀对卒中后康复影响的观察

目的评价氟西汀早期应用脑梗死患者对患者康复的影响。方法随机将符合诊断标准的40例脑梗死的患者分为治疗组和对照组各20例进行治疗观察。治疗组早期给予氟西汀,2组其他常规治疗药物相同。结果治疗4周后治疗组在神经功能缺损评分及日常生活活动能力Barthel指数均优于对照组,差异有统计学意义(P<0.05和P<0.01)。结论早期预防性应用氟西汀可使脑梗死患者卒中后抑郁发生及相关症状明显缓解,更利于调整患者的情绪,使患者积极参与康复训练以利康复。     

系统性红斑狼疮合并抑郁症的临床干预

目的研究系统性红斑狼疮(SLE)患者中抑郁症的发病情况,评价配合其治疗方案进行临床干预的效果。方法选择本院2005年1月-2008年12月的SLE住院患者46例,用汉密尔顿抑郁量表(HAMD)进行问卷调查,并对确诊患者给予口服盐酸氟西汀及心理治疗。结果69%SLE患者具有抑郁症的临床表现,病程越长,抑郁症的发生率越高(P<0.05),抗抑郁药物及心理行为干预治疗有效(P<0.05)。结论在SLE中存在一定程度的抑郁症状,治疗疾病的过程中要关注患者的心理健康。     

尼莫地平联合氟西汀治疗脑卒中后抑郁的临床研究

目的探讨尼莫地平联合氟西汀对脑卒中后患者抑郁状态的影响。方法将我院68例脑卒中后抑郁患者随机分为观察组36例和对照组32例，观察组患者给予尼莫地平＋氟西汀，对照组患者单纯给予氟西汀，在治疗前和治疗后8周分别用汉密尔顿抑郁量表（Hamiltondepression，HAMD）、简易精神状态检查量表（Mini Mental State Examination，MMSE）、临床神经功能缺顿量表（Chinese stroke scale，CSS）、Barthel指数（Modified Barthel index，MBI）评价两组患者的疗效。结果两组患者疗效间差异有显著性意义（P〈0．05），观察组患者治疗前、后厦两组患者治疗后HAMD、MMSE、CSS、MBI评分间差异有显著性意义（P〈0．05）；对照组患者治疗前、后HAMD、MMSE评分间差异有显著性意义（P〈0．05）。结论尼莫地平联合氟西汀对脑卒中后抑郁有较好疗效，而且能够明显改善患者认知能力和神经功能，提高日常生活活动能力。     

电针配合中药治疗卒中后抑郁临床研究

目的：观察中药联合电针治疗卒中后抑郁症的临床疗效。方法：将60例卒中后抑郁患者随机分为治疗组和对照组。两组在一般治疗的基础上,治疗组30例给予电针配合柴胡疏肝散口服治疗,对照组30例单用氟西汀胶囊治疗,28 d为1个疗程。观察患者治疗前后临床症状、神经功能缺损评分、汉密尔顿抑郁量表评分。结果：治疗组有效率96.67%,对照组有效率80.00%,两组比较,差异有统计学意义（ P<0.05）。治疗组神经功能缺损评分、汉密尔顿抑郁量表改善程度显著优于对照组（P<0.05）。结论：电针配合中药治疗卒中后抑郁疗效确切。     

Gray colored glasses: Is major depression partially a sensory perceptual disorder?

Background

Major depression is a neuropsychiatric disorder that can involve profound dysregulation of mood. While depression is associated with additional abnormalities besides reduced mood, such as cognitive dysfunction, it is not well established that sensory perception is also altered in this disorder (aside from in psychotic depression). Recent studies have shown that visual processing, in as early a stage as the retina, is impaired in depression. This paper examines the hypothesis that major depression can involve alterations in sensory perception.

Methods

A Pubmed literature search investigated several lines of evidence: innervation of sensory cortex by serotonin and norepinephrine; antidepressant drugs and depression itself affecting processing of facial expressions of emotion; electroencephalography (EEG) studies of depressed persons and antidepressant drugs; involvement of the serotonergic 5HT2A receptor in both depression and hallucinogenic drug action; psychotic depression involving sensory distortions; dopamine possibly playing a role in depression; and the antidepressant effect of blocking the NMDA receptor with ketamine.

Results

Data from each of these lines of evidence support the hypothesis that major depression can involve sensory perceptual alterations.

Conclusions

Loss of interest in one's daily activities and inability to experience pleasure, also known as anhedonia, in major depression may in part be mediated by sensory abnormalities, whereby normal sensory perceptions are no longer present to activate reward circuitry.

Limitations

The data supporting the hypothesis tend to be associative, so further confirmation of the hypothesis awaits additional controlled experiments.     

奥氮平联合氟西汀治疗伴自杀意念抑郁症患者的效果

目的:观察奥氮平联合氟西汀治疗伴自杀意念抑郁症患者的效果。方法:选取80例伴自杀意念抑郁症住院患者为研究对象,采用随机数字表法分为研究组和对照组各40例。对照组采用氟西汀治疗,研究组在对照组基础上联合奥氮平治疗。比较两组的抑郁量表(HAMD-17)评分、自杀意念(BSSI量表)评分、认识功能(MoCA量表)评分、治疗效果及不良反应发生情况。结果:治疗2周、4周、8周后,两组HAMD-17评分和BSSI评分均低于治疗前,且研究组均低于对照组,差异有统计学意义(P<0.05);治疗8周后,两组MoCA总分均高于治疗前,且研究组高于对照组,差异有统计学意义(P<0.05);研究组治疗总有效率为90.00%,明显高于对照组的67.50%,差异有统计学意义(P<0.05);研究组不良反应发生率为55.00%,与对照组的42.50%比较,差异无统计学意义(P>0.05)。结论:奥氮平联合氟西汀治疗伴自杀意念抑郁症患者,可降低抑郁评分和自杀意念评分,提高认识功能和治疗总有效率,效果优于单纯氟西汀治疗效果。     

氟西汀对癫痫合并抑郁大鼠海马GFAP、NeuN表达的影响

目的探讨氟西汀对癫痫合并抑郁大鼠海马齿状回胶质纤维酸性蛋白(GFAP)、神经元核抗原(NeuN)表达的影响。方法SPF级SD大鼠60只,随机分为对照组、模型组、氟西汀低、中、高剂量组各12只。模型组和对照组给予等剂量生理盐水,1次/d,腹腔注射;氟西汀低、中、高剂量组给予氟西汀(5.0、7.5、10.0 mg/kg),1次/d,腹腔注射。治疗28 d,采用强迫游泳实验和旷场实验测试大鼠行为学表现,采用免疫组化、RT-PCR检测海马GFAP、NeuN表达。结果造模后,与对照组相比,模型组、氟西汀低、中、高剂量组不动时间延长,垂直运动次数、水平运动次数明显下降(P<0.05)。干预后,模型组不动时间明显长于对照组,垂直运动次数、水平运动次数明显低于对照组(P<0.01);与模型组相比,氟西汀低、中、高剂量组不动时间缩短,垂直运动次数、水平运动次数明显增加(P<0.05);尤其是氟西汀高剂量组,较氟西汀低、中剂量组相比有统计学意义(P<0.05)。免疫组化、RT-PCR显示,与对照组相比,模型组GFAP表达明显增加、NeuN表达明显下降(P<0.05);与模型组相比,氟西汀低、中、高剂量组GFAP表达明显下降、NeuN表达明显增加(P<0.05);尤其是氟西汀高剂量组,较氟西汀低、中剂量组相比有统计学意义(P<0.05)。结论氟西汀可能通过改变海马区GFAP、NeuN表达,并呈剂量依赖性,发挥神经保护作用,改善癫痫合并抑郁大鼠抑郁症状。