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1.
阿立哌唑合并氟西汀治疗难治性抑郁症   总被引:9,自引:0,他引:9  
目的:探讨阿立哌唑合并氟西汀治疗难治性抑郁症的效果。方法:将56例难治性抑郁症患者随机分成两组,分别给予阿立哌唑合并氟西汀(合用组)与单用氟西汀(单用组)治疗12周,以汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)评定临床疗效,以治疗中出现的症状量表(TESS)和相关检查评定不良反应。结果:治疗结束时两组HAMD和HAMA的评分均显着降低,以合用组疗效显著较好而快。结论:阿立哌唑合并氟西汀治疗难治性抑郁症的疗效优于单用氟西汀,且耐受性好。  相似文献
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Abstract:  Clinical trials indicate that over 50% of depressed patients show an inadequate response to antidepressant therapy, and that incomplete recovery from major depressive disorder (MDD) increases the risk of chronicity and recurrence. Recovery, complete remission of symptoms, and a return to baseline psychosocial function, should be the goal of therapy. Poor response to adequate antidepressant treatment has been termed treatment resistant depression (TRD). Issues such as adherence, missed diagnosis of psychotic depression, bipolar disorder, or comorbid anxiety must be investigated as reasons why patients have not responded to initial therapeutic strategies. Beyond ensuring optimal use of the index antidepressant, treatment strategies for TRD include switching to another antidepressant, and augmentation or combination with two or more agents. Since little comparative data exist it is important to consider side-effect burden, partial response, and previous medication history when deciding between strategies. In patients with TRD, adding or augmenting with lithium, tri-iodothyronine or atypical antipsychotics have demonstrated benefits. Augmentation with atypical antipsychotics, including risperidone, olanzapine, ziprasidone, and quetiapine, show promising results in terms of improving remission rates. Other interventions, including non-pharmacologic strategies and investigational physical treatments, have demonstrated some benefits, but availability and patient preference should also be considered. With today's therapeutic alternatives, full remission of depression is an attainable goal. For some patients, combination and augmentation strategies earlier in treatment may increase the likelihood of remission.  相似文献
4.
Previous studies in unipolar depression have shown that early decreases in prefrontal values of the QEEG cordance measure identified responders to pharmacotherapy. These studies have all examined individuals who were drug-free prior to the first physiologic assessment, yet in the clinical management of treatment resistant depression (TRD), many patients undergo changes in treatment without a drug-free interval between treatments. Here, we investigated whether cordance decreases were associated with response in Stage I TRD subjects without wash-out between treatment trials. Awake EEGs were recorded from 12 adults with unipolar depression. Subjects were receiving naturalistic treatment, had failed SSRI monotherapy, and were starting a new treatment prescribed by their treating psychiatrists. EEG data were recorded before starting the new treatment and after approximately 1 week. Six of the 12 subjects responded to treatment after 8--10 weeks. Five of the six responders showed an early cordance decreases, compared with two of the six nonresponders (accurate characterization in 75% of the cases). Consistent with previous treatment trials, decreases in prefrontal cordance differentiated responders from nonresponders in this setting as well. These findings suggest that cordance biomarkers may be a useful tool in effectiveness trials that parallel clinical practices in SSRI nonresponders, and may not require a wash-out period between treatments.  相似文献
5.
Background: Major depressive disorder is a condition associated with dysregulated cytokine levels; among these, IL6. Furthermore, genetic variations within cytokine genes have been proposed to predict antidepressant treatment outcome.

Objectives: This study aims to evaluate the role of IL6-174G?>?C and IL6R D358A A?>?C functional polymorphisms in antidepressant treatment phenotypes, specifically remission, relapse, and treatment resistant depression (TRD).

Methods: The referred polymorphisms were genotyped in 80 MDD patients followed at Hospital Magalhães Lemos, Portugal, within a period of 27 months.

Results: It was found that patients carrying IL6-174 GC genotype present a protection towards the development of TRD (OR?=?0.242; 95% CI?=?0.068–0.869; p?=?.038), when compared with GG genotype. Additionally, carriers of IL6-174?CC genotype remit earlier than patients with IL6-174 GG/GC genotypes, with a median time to remission of 6 weeks for CC carriers and 15 weeks for GG or GC carriers (p?=?.030, Log-rank test). No association was found between IL6R D358A genetic polymorphism and any of the treatment phenotypes evaluated.

Conclusions: The IL6-174G?>?C polymorphism influences antidepressant treatment outcome in this sub-set of MDD patients, providing a putative mechanistic link for the dysregulated IL-6 levels described in the literature in patients with TRD.  相似文献

6.
目的 探讨难治性抑郁症(TRD)患者血清血管内皮生长因子(VEGF)水平在改良电抽搐治疗(MECT)治疗前后的变化情况.方法 采用酶联免疫吸附法检测26例TRD患者MECT治疗前后及27例正常对照者的血清VEGF浓度;采用汉密尔顿抑郁量表17项(HAMD-17)评估TRD患者的临床症状.组间血清VEGF浓度比较采用Wilcoxon符号秩和检验,治疗前后血清VEGF浓度变化与HAMD总评分的相关性分析使用Speaman秩相关.结果 TRD患者MECT治疗后24例(92.3%)达到治疗有效标准.TRD组MECT治疗前血清VEGF水平与对照组差异无统计学意义(P >0.05);MECT治疗后血清VEGF水平有升高趋势,但差异无统计学意义(P>0.05).治疗前后血清VEGF浓度与HAMD总评分变化的相关性有统计学意义(r=-0.663,P<0.01).结论 血清VEGF水平变化可能对临床疗效的评估有一定参考价值.  相似文献
7.
目的 探讨难治性抑郁症患者的下丘脑-垂体-肾上腺轴、细胞免疫调节功能及REM睡眠结构.方法 选择符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)单相抑郁发作诊断标准的难治性抑郁症患者和非难治性抑郁症患者各30例.采用汉密尔顿焦虑(HAMA)、汉密尔顿抑郁量表(HAMD-17)分别评定焦虑、抑郁症状.测定白细胞介素6(IL-6)和肿瘤坏死因子-α(TNF-α),皮质醇,采用多导睡眠记录仪监测整夜睡眠.结果 ①难治性抑郁症共病焦虑、重度抑郁组血清皮质醇、IL-6、TNF-α高于非难治性抑郁症组,差异有统计学意义(P<0.05或0.01).②IL-6浓度与HAMD总评分、认识障碍因子分、HAMA总评分、躯体性焦虑因子分呈正相关(r=0.395~0.635,P<0.05或0.01),TNF-α浓度与HAMA总评分、躯体性焦虑因子分呈正相关(r=0.522、0.563,P<0.01).③难治性抑郁症组REM睡眠密度增加,持续时间、周期缩短(P<0.05或0.01),与抑郁严重程度呈正相关(r=0.492,P<0.01).结论 下丘脑-垂体-肾上腺轴功能异常和细胞免疫调节紊乱可能参与难治性抑郁症的发病机制.REM睡眠密度可能提示难治性抑郁症的严重程度和预后.  相似文献
8.
目的探讨齐拉西酮联合文拉法新治疗难治性抑郁症的疗效和安全性。方法将84例难治性抑郁症患者随机分为2组,研究组应用齐拉西酮联合文拉法新,对照组单用文拉法新,观察8周。第2、4、8周末采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)评定疗效,副反应量表(TESS)评定不良反应。结果 2组在第2周末HAMD和HA-MA评分较治疗前均显著下降(P〈0.05),研究组更为明显(P〈0.01)。至第8周末研究组有效率88.10%,对照组66.67%,研究组明显高于对照组(P〈0.05)。不良反应两组间无明显差异(P〉0.05)。结论齐拉西酮联合文拉法新治疗难治性抑郁症,疗效明显优于单一应用文拉法新治疗起效快,不良反应轻,安全性好。  相似文献
9.
Objective: The nerves and axons of the retinal nerve fibre layer (RNFL) are similar to those in the brain and therefore retina is considered as the extension of the brain. We aimed to evaluate the RNFL thickness in the treatment-resistant major depressive patients before and after repetitive transcranial magnetic stimulation (rTMS) treatment and at least 6 months later after rTMS treatment using optical coherence tomography (OCT).

Methods: Thirty patients with treatment resistant major depression and 24 healthy controls were included in the study. rTMS was applied to the left dorsolateral prefrontal cortex (DLPFC) of the patients.

Results: rTMS was initiated in 28 patients. OCT assessments were performed in 24 patients at baseline and after rTMS treatment and in 19 patients at least sixth months after the rTMS treatment. We found significant increase in RNFL thickness compared with controls at the baseline and further increase in RNFL thickness after rTMS treatment. Although there was a decreasing trend in RNFL thickness 6 months after rTMS treatment, 6 months later RNFL thickness was still higher compared with controls.

Conclusions: RNFL thickness is increased in treatment resistant major depression and rTMS over the left DLPFC further increases RNFL thickness in treatment resistant major depressive patients.  相似文献

10.

Background

Repetitive transcranial magnetic stimulation (rTMS) is an effective treatment for depression, but only some individuals respond. Predicting response could reduce patient and clinical burden. Neural activity related to working memory (WM) has been related to mood improvements, so may represent a biomarker for response prediction.

Primary hypotheses

We expected higher theta and alpha activity in responders compared to non-responders to rTMS.

Methods

Fifty patients with treatment resistant depression and twenty controls performed a WM task while electroencephalography (EEG) was recorded. Patients underwent 5–8 weeks of rTMS treatment, repeating the EEG at week 1 (W1). Of the 39 participants with valid WM-related EEG data from baseline and W1, 10 were responders. Comparisons between responders and non-responders were made at baseline and W1 for measures of theta (4–8 Hz), upper alpha (10–12.5 Hz), and gamma (30–45 Hz) power, connectivity, and theta-gamma coupling. The control group's measures were compared to the depression group's baseline measures separately.

Results

Responders showed higher levels of WM-related fronto-midline theta power and theta connectivity compared to non-responders at baseline and W1. Responder's fronto-midline theta power and connectivity was similar to controls. Responders also showed an increase in gamma connectivity from baseline to W1, with a concurrent improvement in mood and WM reaction times. An unbiased combination of all measures provided mean sensitivity of 0.90 at predicting responders and specificity of 0.92 in a predictive machine learning algorithm.

Conclusion

Baseline and W1 fronto-midline theta power and theta connectivity show good potential for predicting response to rTMS treatment for depression.  相似文献
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