血管性抑郁

血管性抑郁作为抑郁的一种亚型,在临床表现、影像学特征和治疗转归等方面均有特殊性。文章就血管性抑郁的定义、分类、发病机制、临床表现、诊断、治疗和转归进行了综述,着重介绍了近年来支持血管性抑郁假说的临床证据,并对血管性抑郁与血管危险因素、脑血管病和痴呆的关系进行了讨论。     

血管性抑郁

血管性抑郁为抑郁症的一种亚型,在临床特征、影像学表现和治疗转归等方面均有其特殊性.文章综述了对血管性抑郁的危险因素、发病机制、诊断、临床特征、治疗和转归等方面的研究进展,特别是血管性抑郁的血管危险因素、神经血管单元稳态变化、免疫细胞因子激活、脑白质损害的影像学特征、重复经颅磁刺激治疗及其与痴呆和心脑血管病的相互关系.     

老年期抑郁中的血管性抑郁

文章系统回顾了近10年来对血管性抑郁的临床表现、病理生理学、神经影像学、生物化学和分子生物学等方面的认识和研究，探讨了血管性抑郁诊断标准的建立。     

老年期抑郁中的血管性抑郁

文章系统回顾了近10年来对血管性抑郁的临床表现、病理生理学、神经影像学、生物化学和分子生物学等方面的认识和研究,探讨了血管性抑郁诊断标准的建立。     

预防卒中后抑郁的治疗

情绪异常是一种重要的卒中后遗症，可能会对恢复和转归产生影响。然而，抑郁和焦虑通常被忽视或不单独进行治疗。其中部分的原因是对卒中发病后早期抗抑郁治疗能否预防抑郁和改善转归还存在疑虑。     

部队离退休人员血管性抑郁与社会心理因素的关系

目的了解老年血管性抑郁的发生情况及其相关的社会心理因素。方法采用汉密尔顿抑郁量表、艾森克个性问卷和社会支持评定量表,对107例脑血管病患者进行评估,并对各相关因素进行比较分析。结果血管性抑郁发生率为45.8%。与非抑郁组相比,血管性抑郁患者患有高血压的比例更高,个性特征以内倾性、神经质为主,主观社会支持度较低。结论社会心理因素在老年血管性抑郁的发生中具有重要作用。     

血管性痴呆伴发抑郁症状评估方法的适用性

目的了解血管性痴呆伴发抑郁症状的发生率及评估方法的适用性。方法用单盲交叉设计,由不同职称的临床医生分别采用Hamilton抑郁量表(HAMD)和老年抑郁量表(GDS)对36例符合《精神与行为障碍分类》(ICD-10)血管性痴呆患者的抑郁症状进行评估。结果 HAMD评分为(18.0±11.13)分。抑郁症状发生率为41.7%;GDS评分为(12.60±5.96)分,抑郁症状发生率为36.1%。HAMD条目中较常见的有能力减退26例(72%)、精神性焦虑23例(64%)、有罪感19例(53%)、抑郁17例(47%)、睡眠障碍17例(47%)。逐步多元回归分析表明,影响抑郁症状评定的因素有病情严重程度、患者受教育程度和GDS。结论血管性痴呆伴发抑郁症状较常见,评估时应注意患者的病情、教育程度。HAMD适用于血管性痴呆病人抑郁症状的评估。     

血管性抑郁与冠心病的关系

随着对血管性抑郁的深入研究发现,血管性疾病和抑郁性疾病之间是双向联系的：抑郁状态既是血管性疾病的危险因子,又可成为血管性疾病导致的后果之一。抑郁患者常常具有一种或多种不良生活方式及心血管疾病的危险因素,导致该类人群的冠心病高发。而冠心病患者的病情越严重,患抑郁症的可能性也越大。治疗方面,应对存在血管性抑郁或/和冠心病的患者进行相关因素的分析,以便更好的对相应的危险因素、生活方式进行干预,并同时注意患者用药的安全性、合理性。     

氟西汀治疗冠心病抑郁状态及对预后的影响

目的 探讨氟西汀治疗冠心病抑郁状态及对疾病预后的影响。方法 采用HAMD对162例冠心病患者进行评定，以评分≥20分者为抑郁组共63例，（8分为无抑郁组共52例，将抑郁组随机分为试验组31例，对照组32例，试验组加服氟西汀，对照组服用安慰剂。共治疗6w。结果 冠心病抑郁发病率为38．9％，试验组经氟西汀治疗后HAMD分值减低，抑郁状态缓解，心律失常、再梗死的发生率明显低于对照组，ST-T段恢复情况优于对照组（P〈0．05）。结论 氟西汀对冠心病抑郁状态有显著的疗效，对冠心病心肌缺血的临床转归有明显协同治疗作用。     

心律失常患者伴发焦虑抑郁症状的鉴别及治疗研究

房性早搏（房早）、室性早搏（室早）是临床上较常见的心律失常，其中有相当一部分患者除心律失常外无其他器质性心脏病，预后良好。目前，应用抗心律失常药物并不能改善房早、室早患者的预后，致使这类心律失常药物治疗面临很大困难。研究表明焦虑抑郁本身可引起明显胸闷、心悸等症状，这可能与房早、室早引起的症状相混淆而不被认识。本组从心理学角度对有房早、室早引起的心律失常患者进行焦虑抑郁状态的评估，同时对伴有一定程度焦虑抑郁的心律失常患者，用抗抑郁焦虑药进行治疗，探讨心理障碍对房早、室早患者临床症状的影响及治疗转归。     

Occurrence of anterior ST depression in inferior myocardial infarction and relation to clinical outcome

In 229 patients admitted to the coronary care unit (CCU) at Sahlgren's Hospital developing inferior myocardial infarction, and with no previous myocardial infarction, the clinical outcome was related to the presence of ST-segment depression in 16 anterior chest leads. In all, 64% had anterior ST-segment depression. These patients differed from those not having ST depression in several aspects. They had larger infarcts, as assessed by serum enzyme activity and ECG recording. They were more prone to congestive heart failure and required more treatment for this complication. Their intensity and duration of pain during the first 4 days appeared to be more substantial. During a 5-year follow-up, patients with anterior ST depression tended to have a higher mortality. We conclude that among patients with inferior myocardial infarction and no previous infarction, those with anterior ST-segment depression form a subgroup with a more severe clinical course.     

Parmacologic treatment of depression in patients with myocardial infarction

Depression is a common medical problem and is more prevalent among patients with coronary artery disease.Whether early detection and treatment of depression will enhance cardiovascular outcome is uncertain.Obviously,the safety and efficacy of the anti-depression drugs is an important link.This article reviews the pathophysiologic and behavioural links between depression and cardiovascular disease progression,the treatment of depression,and the potential benefits of anti-depressants in patients with coronary disease.     

Pharmacologic treatment of depression in patients with myocardial infarction

Depression is a common medical problem and is more prevalent among patients with coronary artery disease. Whether early detection and treatment of depression will enhance cardiovascular outcome is uncertain. Obviously, the safety and efficacy of the anti-depression drugs is an important link. This article reviews the patho-physiologic and behavioural links between depression and cardiovascular disease progression, the treatment of depression, and the potential benefits of anti-depressants in patients with coronary disease.     

Clinician Burden and Depression Treatment: Disentangling Patient- and Clinician-Level Effects of Medical Comorbidity

Background  Efforts to improve primary care depression treatment have assessed strategies across heterogeneous groups of patients, but few have examined clinician-level influences on depression treatment. Objective  To examine clinician characteristics that affect depression treatment in primary care settings, using multilevel ordinal regression modeling to disentangle patient- from clinician-level effects. Design  Secondary analysis from the Quality Improvement in Depression Study dataset. Participants  The participants were 1,023 primary care patients with depression who reported on treatment in the 6-month follow-up and whose clinicians (n = 158) had at least 4 patients in the study. Measurements  Primary outcome variable was depression treatment intensity, derived from assessment of concordance with AHCPR depression treatment guidelines based on patient-reported data on their treatment. Primary independent variable was clinical practice burden for treating depression, derived from patient- and clinician-reported composite measures tested for significant association with clinician-reported practice burden. Results  Clinicians who treat patients with more chronic medical comorbidities perceive less burden from treating depressed patients in their practice (Spearman’s rho = −.30, p < .05). Clinicians who treat patients with more chronic medical comorbidities also provide greater intensity of depression treatment (adjusted OR = 1.44, p = .02), even after adjusting for the effects of patient-level chronic medical comorbidities (adjusted OR = 0.95, p = .45). Conclusions  Clinicians who provide more chronic care also provide greater depression treatment intensity, suggesting that clinicians who care for complex patients can integrate depression care into their practice. Targeting interventions to these clinicians to enhance their ability to provide guideline-concordant depression care is a worthwhile endeavor and deserves further investigation. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Diabetic Peripheral Neuropathy and Depression: Dancing with Wolves? - Mini-Review and Commentary on Alghafri et al. “Screening for depressive symptoms amongst patients with diabetic peripheral neuropathy”

The co-existence of diabetic peripheral neuropathy (DPN) and depression in subjects with diabetes is being increasingly recognized. The interaction of these two serious comorbidities may increase morbidity and mortality. An emerging thought is that persisting depression, along with stroke and cognitive dysfunction, may represent a cluster of potential microvascular injuries affecting the brain, which shares a common risk factor with DPN. Current evidence highlights metabolic and clinical covariates, which may interact in subjects with DPN and depression. However, there is a lack of rigorous enquiry into the confounding effect of cognitive dysfunction and vascular brain disease. Furthermore, high-quality longitudinal studies exploring the direct impact of these comorbidities on diabetes course and on the progression of the comorbidities themselves are lacking. Improved insights into comorbid DPN and depression may help to improve screening for and treatment of both these conditions.     

Depression in COPD �C management and quality of life considerations

Depression is common in COPD patients. Around 40% are affected by severe depressive symptoms or clinical depression. It is not easy to diagnose depression in COPD patients because of overlapping symptoms between COPD and depression. However, the six-item Hamilton Depression Subscale appears to be a useful screening tool. Quality of life is strongly impaired in COPD patients and patients’ quality of life emerges to be more correlated with the presence of depressive symptoms than with the severity of COPD. Nortriptyline and imipramine are effective in the treatment of depression, but little is known about the usefulness of newer antidepressants. In patients with milder depression, pulmonary rehabilitation as well as cognitive-behavioral therapy are effective. Little is known about the long-term outcome in COPD patients with co-morbid depression. Preliminary data suggest that co-morbid depression may be an independent protector for mortality.