脑卒中后抑郁的相关因素及氟西汀对抑郁症状的改善作用

目的：探讨致脑卒中后抑郁与病灶部位及神经功能缺损程度的关系并观察氟西汀对抑郁症状的改善作用。方法：用汉密顿抑郁量表（Hamilton rating scale for depression，HAMD)对河南省精神病医院住院脑卒中患者110例进行评估，分为抑郁组(48例)和非抑郁组(62例)。观察抑郁与性别、脑卒中性质、病灶部位、神经功能损伤程度的关系。抑郁患者采用口服氟西汀胶囊治疗，以HAMD减分率为疗效评定标准。结果：抑郁的发生与病灶部位、神经功能缺损程度具有显著相关性（P&;lt;0．05)，氟西汀治疗前后HAMD量表评分减分率比较（治疗前后HAMD平均分分别为24．1&;#177;4．9，5.1&;#177;3．2)，差异有显著性意义(P&;lt;0．01)。结论：脑卒中后抑郁与生物因素有肯定的关系，氟西汀能明显改善抑郁症状。     

首发急性单一病灶脑卒中患者抑郁程度与认知功能的关系

目的研究脑卒中后抑郁患者的认知功能与抑郁程度的关系,以及抗抑郁治疗对认知障碍的影响. 方法选择 42例首发单一病灶的脑卒中患者作为研究对象,采用汉密尔顿抑郁量表 (HAMD), SDS抑郁自评量表、简易精神状态量表 (MMSE)进行检测,对脑卒中后抑郁患者每日给予氟西汀 20 mg治疗,连续 4周,在第 2, 4周分别进行 SDS抑郁自评量表、简易智力状态量表评定. 结果 42例首发单一病灶脑卒中患者,其中 18例于脑卒中 2周内出现抑郁表现,占 43% (18/42).脑卒中后抑郁患者的 MMSE(26.38± 2.26)分,评分显著低于非抑郁患者 (29.00± 1.91)分 (t=-3.366,P< 0.002),主要集中于时间空间、地点定向、注意计算、短程记忆、物体命名等能力的下降.且与 SDS抑郁自评量表得分显著负相关( r=-0.57,P< 0.01).氟西汀抗抑郁治疗 2周后认知损害无明显改善,治疗 4周后 MMSE评分显著升高. 结论脑卒中后抑郁患者更易出现认知功能损害,且与抑郁程度相关.随着抗抑郁治疗后抑郁症状的缓解,认知功能损害逐步好转.     

脑卒中后抑郁及其治疗对神经功能恢复的影响

背景脑卒中后抑郁(post-stroke depression,PSD)患者日常生活能力和社交活动障碍对神经功能恢复是否有影响?目的观察PSD的发生率和相关因素,探讨盐酸氟西汀(百优解)抗抑郁治疗对脑卒中后抑郁患者神经功能康复的影响.设计以诊断为依据的病例对照研究.地点和对象选自苏州大学附属第二医院2000-01/2002-03连续住院的急性脑卒中患者132例(脑梗死78例,脑出血54例),男79例,女53例,年龄48～87岁,平均(62.5±12.1)岁,受教育时间(5.2±4.5)年.方法在病程2周、1,3,6,12个月时对每一位人组患者行PSD诊断、神经功能缺损评分、日常生活能力(ADL)评分、汉密尔顿抑郁量表(HAMD)评分;同时完成Zung's抑郁自评量表(SDS)和焦虑自评量表(SAS).主要观察指标神经功能缺损,ADL,HAMD,SDS,SAS评分.结果①脑卒中患者中约44.7%出现抑郁症状.②脑卒中类型和性别与PSD发生率无相关性(P＞0.05).③PSD的发生率和严重程度与神经功能缺损和日常生活能力下降程度有关.④盐酸氟西汀能明显改善病程3,6个月时神经功能缺损,病程12个月时抑郁症状(4.63±2.37),日常生活能力(23.25±10.12),神经功能缺损(12.95±11.54)方面改善尤为显著,差异有显著性意义(t=2.016～12.174,P＜0.05).结论抗抑郁治疗能在抑郁症状明显改善的同时,促进患者日常生活能力和神经功能的恢复.     

早期应用氟西汀改善脑卒中患者神经功能缺损及预防脑卒中抑郁的近期效果

目的探讨早期应用氟西汀改善急性脑卒中患者神经功能缺损和预防脑卒中后抑郁的疗效和安全性. 方法采取随机对照的方法选择住院的急性脑卒中患者,治疗组 33例,入院后在进行急性脑卒中常规药物治疗的同时,给予氟西汀胶囊 20 mg, 1次 /d口服.对照组 34例,仅进行常规药物治疗, 4周后对照研究. 结果治疗组总有效率为 88%( 29/33),对照组为 59%( 20/34),两组比较差异有显著性意义(χ 2=7.17, P< 0.01) ,治疗组 4周后神经功能缺损评分较对照组有明显改善 (t=-2.68, P< 0.01),治疗组 4周后汉密尔顿抑郁量表( Hamiltion depression scale, HAMD)≥ 17分者为 2例 ,抑郁发生率为 6%( 2/33),对照组 4周后 HAMD≥ 17分者 8例 ,抑郁发生率为 24%( 8/34),差异亦有显著性意义 (χ 2=40.24, P< 0.01).治疗组未发现明显不良反应. 结论早期应用氟西汀能改善急性脑卒中患者的神经功能缺损和减少脑卒中后抑郁急性期的发生率.     

氟西汀治疗脑卒中后抑郁76例

为探讨氟西汀(商品名百优解)治疗脑卒中后抑郁(PSD)的疗效。将76例脑卒中后抑郁(post—stroke depression，PSD)患者随机分为两组，分别应用常规治疗和加用氟西汀治疗4周，治疗前后应用汉密尔顿抑郁量表(HAMD)、简易精神状态检查表(MMSE)、自评抑郁量表(SDS)进行疗效评定。氟西汀组HAMD，MMSE，SDS评分的减分率明显优于对照组(P&;lt;0．01)。提示氟西汀治疗PSD有明确疗效。     

氟西汀对脑梗塞恢复早期抑郁障碍的治疗作用

目的探讨氟西汀对脑梗塞恢复早期抑郁障碍的治疗作用.方法在神经康复门诊应用Zung抑郁自评量表对145例新近出院的初发脑梗塞恢复早期患者进行神经心理评定,把其中有抑郁障碍的63例(43.4%)随机分为氟西汀治疗组32例,对照组31例.氟西汀治疗前、治疗4周和8周后除分别进行Zung抑郁自评量表评定外,还进行神经功能缺损和ADL能力评定.结果在氟西汀治疗组治疗4周和8周后,抑郁评分与治疗前相比均明显下降(P<0.05和P<0.01),而对照组下降不明显,两组间相比差异显著(P<0.05);神经功能缺损评分也分别明显下降(P<0.05和P<0.01),ADL能力评分则分别明显上升(P<0.05和P<0.01),两者恢复速度均比对照组加快,两组间同比差异显著(P<0.05);上述三项最后一次评分基本接近无抑郁障碍组水平(P>0.05).结论脑梗塞恢复早期抑郁障碍发生率并不比急性期低,氟西汀能有效地改善其抑郁障碍,同时也加速患者神经功能与ADL能力的康复.     

氟西汀对脑梗死后抑郁患者神经功能缺损及日常生活能力的影响

目的 观察氟西汀对脑梗死后抑郁患者神经功能缺损及日常生活能力的影响.方法 临床选取急性脑梗死后抑郁患者80例,随机将患者分为治疗组(氟西汀)和对照组各40例,治疗前后分别用改良爱丁堡-斯堪的那维亚脑卒中评分量表(MESSS)、汉密顿抑郁量表(HAMD)和改良巴氏指数量表(MBI)进行评分,评定氟西汀的治疗作用.结果 治疗前两组间HAMD、MESSS和MBI无显著性差异( P＞0.05),治疗后6周两组间HAMD、MESSS和MBI均有显著性差异( P＜0.01).结论 氟西汀能缓解急性脑梗死患者的抑郁症状,促进急性脑梗死患者的神经功能恢复,提高患者的日常生活能力.     

针灸与药物治疗脑卒中后抑郁的疗效比较

应用汉密尔顿抑郁(HAMD)量表及脑卒中患者临床神经功能缺损程度评分标准(MSSS)量表评估脑卒中患者,筛选出脑卒中后抑郁(post-strokedepression,PSD)患者,并应用针灸及氟西汀治疗。结果显示针灸及氟西汀治疗PSD患者均有效,但针灸较氟西汀显效快,副作用少。     

针灸与药物治疗脑卒中后抑郁的疗效比较

应用汉密尔顿抑郁(HAMD)量表及脑卒中患临床神经功能缺损程度评分标准(MSSS)量表评估脑卒中患，筛选出脑卒中后抑郁(post-stroke depression，PSD)患，并应用针灸及氟西汀治疗。结果显示针灸及氟西汀治疗PSD患均有效，但针灸较氟西汀显效快，副作用少。     

急性脑卒中后抑郁的临床观察

目的观察急性脑卒中后抑郁与病损部位、神经功能缺损程度的关系 ,以及百忧解治疗此症的疗效。方法对 86例急性脑卒中患者进行Zung氏抑郁自评量表 (self ratingdepressionscale,SDS)检测 ,SDS≥ 50分为急性脑卒中后抑郁 ,观察抑郁症状与病损部位、神经功能缺损程度的关系 ,对有抑郁症状的患者给予百忧解治疗。结果符合入选条件的有 34例 (其中轻度 2 7例、中度、重度 7例 ) ,抑郁症状与疾病严重程度呈正相关 (P <0 .0 5) ,且皮质下卒中患者抑郁的发生率高于大脑皮质及小脑卒中患者 (P<0 .0 1 ) ;氟西汀 (百忧解 )治疗有效。结论急性脑卒中后抑郁与疾病严重程度呈正相关 ,氟西汀对急性脑卒中后抑郁有显著疗效     

Diagnosis of depression

The importance of the identification of depressions in clinical practice is emphasised. The author suggests the use of modern operationalized diagnostic criteria. In atypical depressions and depressions with comorbid psychiatric disorders the diagnosis is sometimes missed. Occasionally, it is impossible to decide if a depression is present or not. In such cases it is in general indicated to try antidepressive treatment.     

Biology of depression

Research over the past three decades has led to a greater understanding of the biologic basis of depression. Observations that certain medications could improve or worsen mood led to the development of hypotheses describing the possible role of specific neurotransmitters in the brain in depression. Modifications of these original hypotheses focused on altered receptor function, failures in the regulation of neurotransmitter systems, and interactions of the monoamines with cholinergic systems. Strategies using endocrinologic measurements in the evaluation of the depressed patient have provided researchers with new clues regarding disordered neuroendocrine function in depression and clinicians with new tests to aid in diagnosis and management. Moreover, the development of standardized sleep EEG methodology has proven useful for the identification of characteristic sleep abnormalities in depression. Although there are many methodologic and clinical problems still to be resolved, the use of biological markers in the assessment of the depressed patient is increasing, and is likely to be of significant importance in the future. Finally, recent advances in molecular genetics hold promise for further advances in our understanding of the inheritance and biochemistry of depression.     

Pathophysiology of depression

Neurobiological findings of depression are reviewed in this paper. Modern neurobiological methods have revealed pathophysiological mechanism associated with depression. Monoamine hypothesis, which was advocated in the 1950's, emphasizes that the deficiency of monoamine neurotransmitters bring about depressive symptoms. This theory played an important role in promoting the development of new antidepressants, but some inconsistent findings were pointed out concerning this theory. Neuroendocrine studies have revealed the hypothalamic-pituitary-adrenal (HPA) axis dysfunctions in depressive patients, and increased activity of HPA axis are considered as state marker of depression. Morphological changes of hippocampus, polymorphism of serotonin transporter gene, and down regulation of neurotrophin are also discussed in this review.     

Classification of depression

The results of recent research indicate that the traditional subdivision of depressive disorders into a "biological" ("endogenous") and a "psychosocial" ("neurotic") type cannot be upheld in this simple categorical form today. This is demonstrated by referring to such new developments as the construction of international compromise classification systems, the formulation of operational research diagnosis criteria, attempts at validating diagnostic formulations by external variables (such as biological markers) and the introduction of multiaxial diagnostic systems. The use of a "polydiagnostic" approach to psychiatric research is recommended, i.e. to use several diagnostic formulations for subtyping depression simultaneously in psychiatric research. It is anticipated that by applying the "polydiagnostic" approach the growing uncertainty and confusion in the subclassification of depression can be reduced.     

Psychotherapy of depression

Patients with depressive disorder are often guilty of their dysfunction and desperate of their future. In acute stage, it is most important to give patients the insight into their illness and to give them such reassurance that they will recover with treatment. Clinicians should advise the patients to take a rest. To encourage and motivate the patients to do work or other activities is often harmful. In the recovery stage, it is useful for the patients to reflect on their premorbid personality and behavioral traits that facilitate the development of depressive disorder, which may lead to their changing way of life and prevent recurrence of the illness.