脑卒中后抑郁与卒中部位相关性分析

目的 探讨急性脑卒中后抑郁(PSD)与影像学上卒中部位的相关性及临床意义.方法 对412例住院及门诊脑卒中患者在卒中后1个月内采取系统的神经心理学评估及头颅MRI检查.对所有的患者进行汉密尔顿抑郁量表(HAMD)评分,并根据头颅MRI及病人症状、体征定位.结果 卒中后抑郁的发生率以左侧半球明显高于双侧及右侧,并以左侧颞...     

脑卒中后抑郁患者CT表现及其临床特征的相关研究

目的探讨脑卒中后抑郁患者的CT表现和临床特征及其相关因素。方法选择98例CT确诊脑梗死的患者,进行颅脑CT扫描确定脑部异常病变,根据抑郁自评量表(SDS)、汉密顿抑郁量表(HAMD)分值分为有无抑郁症状两组:卒中后抑郁组(PSD组,n=42)和对照组(n=56)。结果抑郁的发生率为42.8%。两组患者的年龄、性别构成、受教育程度、病程等差异无统计学意义(P>0.05)。两组患者颅脑CT比较,结果显示PSD组损害更易发生于左侧半球、皮质、额叶和小脑。PSD组内抑郁量表分值与左侧半球、双侧皮质损害容积成正相关(P<0.05)。结论脑卒中后抑郁发生率较高,CT表现和临床特征有一定特点,额叶、皮质的损害可能是PSD发生的生物学基础。     

脑卒中后抑郁症临床探讨

目的对脑卒中后并发抑郁症的临床资料进行分析,探讨脑卒中后抑郁的发生率及相关致病因素。方法对181例明确诊断为脑卒中的住院患者,采用抑郁自评量表（SDS）、汉密尔顿抑郁量表（HAMD）、改良的爱丁堡斯堪的那维亚神经功能缺损评分表（MESSS）进行评定。结果脑卒中后抑郁的发生率45.9%。抑郁的发生与性别、年龄、神经功能缺损有显著相关性,与额叶、丘脑、左侧大脑半球有关（P〈0.05）,合并高血压、糖尿病、大动脉粥样硬化的卒中患者PSD发病率明显高于无危险因素患者（P〈0.05）。结论脑卒中后抑郁发生率较高,其发生与多种因素相关。     

卒中后抑郁的相关因素分析

目的探讨卒中后抑郁(PSD)的相关因素。方法采用汉密尔顿抑郁量表(HAMD)在卒中后14 d及90 d对300例脑卒中患者进行评分,并据此分为PSD组及非PSD组,对两组间的卒中部位、美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin量表评分(mRS)及简易精神状态检查表(MMSE)评分进行比较。结果 140例(46.7%)患者发生PSD;卒中灶多发或位于左侧半球、额颞叶及基底节的患者PSD发生率明显高于卒中灶单发、位于右侧半球、顶枕叶及皮质的患者(均P<0.05);PSD组发病14 d时NIHSS评分、发病14 d及90 d时mRS评分明显高于非PSD组(P<0.05～0.01)。结论 PSD发生与多灶性卒中及卒中灶位于左侧半球、额颞叶、基底节区有关;且与卒中后神经功能缺损程度及残疾程度有关。     

脑卒中后抑郁合并认知损害的磁共振扩散张量成像研究

目的 探讨脑卒中后抑郁(PSD)合并卒中后认知功能损害(PSCI)患者的磁共振扩散张量成像(DTI)表现及脑卒中后抑郁合并认知功能损害的发病机制。方法 选取武汉大学中南医院2014年10月～2015年12月首发急性脑卒中患者52例,进行汉密尔顿抑郁量表(HAMD)、简明精神状态检查量表(MMSE)、蒙特利尔认知评估(MoCa)量表评分,分为PSD合并PSCI组13例(A组),PSD组(B组)11例,PSCI组(C组)12例,单纯脑卒中组16例(D组)。进行磁共振平扫及DTI扫描,比较各组不同部位FA值的差异。结果 A组与D组比较,双侧额叶、双侧半卵圆中心、左侧颞叶、左侧丘脑、右侧壳核FA值减低,差异有统计学意义(P<0.05)。结论 PSD合并PSCI患者可能具有相对独立的发病机制,与双侧额叶、双侧半卵圆中心、左侧颞叶、左侧丘脑及右侧壳核损害有关。     

卒中后抑郁与脑损伤部位相关性的临床研究

目的探讨不同的脑损伤部位与脑卒中后抑郁病变的关系,探讨PSD的现况以及对结局的影响。方法收集2010年09月～2011年09月期间河北联合大学附属医院神经内科脑卒中患者300例,通过颅脑CT或MRI进行卒中病灶定位,采用Hamilton抑郁量表对卒中患者在发病14±2d及90±7d进行抑郁及程度的评价。对收集患者的相关临床指标如美国国立卫生院神经功能缺损评分(NIHSS)、改良Rankin量表评分(MRS)、简易精神状态检查表(MMSE)评分等相关因素进行统计分析。结果 140例脑卒中患者合并PSD,总发生率为46.67%,其中轻中度抑郁占46.00%,重度抑郁占0.67%;多发性、左侧半球、额颞叶、基底节区脑卒中患者PSD发生率高。结论脑卒中患者神经功能缺损程度评分越高,其患抑郁的程度也就越高。PSD发生与卒中类型无关,而与卒中部位、卒中残疾程度等因素有关。     

急性脑卒中后焦虑抑郁共病状态血清单胺类递质的变化研究

目的探讨急性脑卒中后焦虑抑郁共病患者血清单胺类递质水平的关系。方法采用荧光分光光度计法测定33例急性卒中后焦虑抑郁共病患者、22例急性卒中后抑郁患者、49例卒中后非焦虑抑郁患者及37例正常人血清单胺类递质的水平。结果急性脑卒中后焦虑抑郁共病组和PSD组血清中，NE、5-HT、DA含量低于非焦虑抑郁组和对照组，共病组NE、5-HT高于抑郁组，其中5-HT差异有显著意义，而非焦虑抑郁组血清中，单胺类递质的含量亦低于对照组。而大脑左侧及前部卒中患者的血清中单胺类递质水平低于其它卒中部位患者（P〈0．05）。结论急性脑卒中后焦虑抑郁共病组和单纯PSD的发生与血清中单胺类神经递质的降低有关。     

卒中后抑郁与卒中部位的相关研究

目的 探讨卒中后抑郁（post-stroke depression PSI））与卒中病灶部位的关系。方法通过CT或MRI进行卒中病灶定位，采用Hamilton抑郁量表对200例卒中患者在发病2周和3月进行调查评分。结果急性期和恢复期大脑半球左侧、右侧、双侧卒中PSD发生率无统计学差异。2周时大脑半球前部与后部卒中病灶两PSD发生率无统计学差异（x^2=1．9546，P〉0．1）。3月时大脑半球前部与后部卒中痛灶两PSD发生率有统计学差异（x^2=6．04，P〈0．05）。结论PSD的发生无半球偏利性。急性期大脑半球前部卒中病灶与PSD无明显相关性。恢复期走脑半球前部卒中病灶与PSD存在相关性。     

缺血性脑卒中患者抑郁症状与发病部位的Logistic回归分析

目的：研究首发缺血性脑卒中偏瘫患者脑梗死部位对远期抑郁症状的预测价值,为早期干预提供依据。方法：采用临床流行病学调查方法,对103例为单侧病灶的首发缺血性脑卒中偏瘫患者进行远期（发病后20～44个月）抑郁症状与发病部位关系的现状调查,并用Logistic回归分析法进行分析。结果：103例入选病例中存在远期抑郁症状患者52例,抑郁症状发生率50．49％,其中左侧病灶24例,右侧病灶28例,差异无统计学意义（P〉0．05）。经Logistic回归分析,病灶与抑郁症状发生的相关性部位有额叶和颞叶脑梗死灶。结论：额叶和颞叶脑梗死灶是缺血性脑卒中偏瘫患者远期抑郁症状发生的独立危险因素,且颞叶梗死较额叶梗死患者抑郁症状重。     

老年期脑卒中后抑郁与病灶关系

目的：探索老年期脑卒中后抑郁症状(PSD)的发生与病灶的关系：方法：对86例老年期脑卒中后抑郁症状的发生和严重程度与病灶定位关系进行分析。结果：大脑左侧前部及皮层部病灶患者PSD发生率高，程度严重。结论：对上述部位脑卒中患者早期做好心理治疗，防止抑郁发生。     

Post-stroke affective or apathetic depression and lesion location: left frontal lobe and bilateral basal ganglia

This study was designed to examine the correlation between damage to the basal ganglia or frontal lobe and depression status (both affective and apathetic dimensions) in 243 stroke patients. We assessed the affective dimension in post-stroke depression (PSD) using the Zung Self-rating Depression Scale (SDS) and the apathetic dimension in PSD using the apathy scale (AS). We classified basal ganglia or frontal lobe damage into four groups: no damage, damage to the left side only, damage to the right side only, and damage to both sides. Affective and/or apathetic PSD was found in 126 patients (51.9%). The severity of affective depression (SDS score) was associated with left frontal lobe (but not basal ganglia) damage, and that of apathetic depression (AS score) was related to damage to the bilateral basal ganglia (but not to the frontal lobe). The anatomical correlates of PSD differ depending on the PSD dimension (affective or apathetic) and may explain interstudy differences regarding the association between lesion location and type of PSD.     

卒中后抑郁的发生率及其相关因素的前瞻性研究

目的 前瞻性随访研究住院患者卒中后抑郁（post-stroke depression,PSD）发病率及其相关危险因素。方法 采用17项汉密尔顿抑郁量表（Hamilton Depression Scale, HAMD）对101例卒中住院患者在2周、3个月和6个月时分别进行抑郁情绪评定,调查住院患者中卒中后抑郁的发病率,同时测评患者一般资料、改良Rankin量表（modified Rankin Scales,mRS）、美国国立卫生研究院卒中量表（the NationalInstitutes of Health Stroke Scale,NIHSS）以及简明智力测验（mini-mental state examination,MMSE）,分析影响卒中后抑郁的相关临床因素。结果 （1）PSD 2周时首次发生率显著高于3个月和6个月（45.5% vs 6.4%,P <0.01;45.5% vs7.3%,P <0.01）,PSD总体发生率在2周、3个月和6个月时无统计学差异（P >0.05）,PSD患者3个月内抑郁缓解率显著高于3～6个月期间（23.9% vs 3.1%,P =0.029）,PSD患者死亡率显著高于非PSD患者（P <0.05）;（2）2周时左侧半球卒中患者PSD发生率显著高于右侧和双侧卒中患者（P =0.047）,2周、3个月和6个月时PSD患者MMSE评分显著低于非PSD患者（P均<0.01）,而mRS和NIHSS评分显著高于非PSD患者（均P <0.01）;（3）2周时PSD的发生与NIHSS（P <0.01）、mRS（P <0.01）、左侧半球卒中相关;而3个月和6个月时PSD的发生与NIHSS和mRS相关（P均<0.05）;2周、3个月和6个月时PSD的发生与MMSE无关（P >0.05）。（4）未发现PSD与性别、年龄、卒中性质、病灶数目、高血压、糖尿病、文化程度相关（P >0.05）。结论 PSD可能多发于卒中后2周内,NIHSS、mRS评分及2周大脑半球病变与PSD发生显著相关。     

急性缺血性卒中后抑郁危险因素的前瞻性队列研究

目的 在前瞻性队列研究中调查卒中单元模式下的缺血性卒中急性期卒中后抑郁（post-strokedepression,PSD）发生的独立危险因素。方法 收集发病14 d内的缺血性卒中患者,收集患者的人口学资料、既往病史、相关临床指标及影像学资料。发病后14 d进行神经功能缺损和心理量表的评定,分为PSD组和非PSD组,比较两组的人口学资料和临床资料差异,分析缺血性卒中急性期卒中后抑郁的危险因素。结果 共有268例患者入组,其中PSD组116例,非PSD组152例。PSD组女性、糖尿病史、性格急躁和内向的患者的比例高于非PSD组;PSD组发病后14 d NIHSS分值高于非PSD组,MMSE低于非PSD组;PSD组梗死病灶累及基底节的比例高于非PSD组;PSD组双侧内侧颞叶、右侧顶叶、双侧枕叶脑萎缩出现率高于非PSD组。女性（P <0.0001,OR 7.064,95%CI 3.334～14.966）、发病14 d NIHSS（P =0.0020,OR 1.158,95%CI 1.055～1.272）是PSD发生的独立危险因素;病前性格随和（P＝0.0264,OR 0.447,95%CI 0.220～0.910）是避免急性期卒中后抑郁发生的保护性因素。结论 女性、发病后14 d的神经功能缺损水平是卒中急性期发生抑郁的独立危险因素,病前性格随和是避免发生PSD的保护性因素。     

A reappraisal of poststroke depression, intra- and inter-hemispheric lesion location using meta-analysis

A recent publication based on a meta-analysis concluded that there was no association between poststroke depression (PSD) and lesion location. This study, therefore, was undertaken to reappraise the hypothesis using meta-analysis of the correlation between severity of depression following stroke and proximity of the lesion to the frontal pole, an issue that was not examined in the prior meta-analysis. Results showed there was a significant inverse correlation between severity of depression and distance of the lesion from the frontal pole among 163 patients with left hemisphere stroke but not among 106 patients with right hemisphere stroke. This study supports the hypothesis that risk of poststroke depression is related to the location of brain injury.     

Etiological mechanisms of post-stroke depression: a review

Abstract

Post-stroke depression (PSD) has become a prominent negative factor of stroke recovery. Different etiological mechanisms may be involved, and there forms two major hypotheses: biological hypothesis and psychological hypothesis. Biological hypothesis included four mechanisms: lesion location mechanism, neurotransmitters mechanism, inflammatory cytokines mechanism and gene polymorphism mechanism. As for lesion location, the specific location of a lesion (e.g., basal ganglia or left frontal lobe lesions) played an important role in the etiology of PSD. For neurotransmitters, decreased serotonin and norepinephrine in the brain were associated with PSD. In inflammatory cytokines, increased cytokines [including interleukin (IL) 1β, IL-18, tumor necrosis factor α] after stroke lead to depression. For gene polymorphism, there was significant association between serotonin transporter gene-linked promoter region short variant genotype and post-stroke major depression. Psychological hypothesis suggested that social and psychological stressors associated with stroke may be the primary cause of depression. Up to now, there is no definitive evidence to support or refute either a solely biological or solely psychosocial mechanism. It appears to be a kind of biopsychosocial multifactorial mental illness.     

Depression after stroke: the importance of cerebral hemisphere asymmetries.

The pattern of brain asymmetries was visualized on computed tomography (CT) scan in patients with a single acute cerebrovascular lesion. Patients were divided into those with typical or reversed frontal and/or occipital asymmetries. Among patients with a typical occipital asymmetry, those with left frontal or left basal ganglia lesions showed a significantly higher frequency of major depression and significantly higher depression scores than patients with similar lesion location but with reversed occipital asymmetry or those with a typical asymmetry and lesions in other (left or right) brain areas. Among patients with a reversed occipital asymmetry, there was no significant association between left frontal or left basal ganglia lesions and depression. This study demonstrates that the previously reported significant association between post-stroke major depression and lesion location is restricted to patients with a typical occipital asymmetry and is not present in patients with a reversed occipital asymmetry.     

Role of the right and left hemispheres in recovery of function during treatment of intention in aphasia

Two patients with residual nonfluent aphasia after ischemic stroke received an intention treatment that was designed to shift intention and language production mechanisms from the frontal lobe of the damaged left hemisphere to the right frontal lobe. Consistent with experimental hypotheses, the first patient showed improvement on the intention treatment but not on a similar attention treatment. In addition, in keeping with experimental hypotheses, the patient showed a shift of activity to right presupplementary motor area and the right lateral frontal lobe from pre- to post-intention treatment functional magnetic resonance imaging (fMRI) of language production. In contrast, the second patient showed improvement on both the intention and attention treatments. During pre-treatment fMRI, she already showed lateralization of intention and language production mechanisms to the right hemisphere that continued into post-intention treatment imaging. From pre- to post-treatment fMRI of language production, both patients demonstrated increased activity in the posterior perisylvian cortex, although this activity was lateralized to left-hemisphere language areas in the second but not the first patient. The fact that the first patient's lesion encompassed almost all of the dominant basal ganglia and thalamus whereas the second patient's lesion spared these structures suggests that the dominant basal ganglia could play a role in spontaneous reorganization of language production functions to the right hemisphere. Implications regarding the theoretical framework for the intention treatment are discussed.     

Poststroke depression and emotional incontinence: correlation with lesion location

OBJECTIVE: To correlate the location of stroke with poststroke depression (PSD) and emotional incontinence (PSEI). METHODS: The authors prospectively studied 148 patients (94 men and 54 women, mean age 62 years) with single, unilateral stroke (126 infarcts and 22 hemorrhages) at 2 to 4 months poststroke with regard to the presence of PSD (using Diagnostic and Statistical Manual of Mental Disorders IV criteria and Beck Depression Inventory) and PSEI. The lesion location was analyzed by CT or MRI. RESULTS: Twenty-seven patients (18%) had PSD and 50 (34%) had PSEI. The presence of PSD and PSEI was not related to the nature, laterality, or size of the lesion. The frequency of PSEI, but not of PSD, was higher in women than in men and in ischemic rather than hemorrhagic stroke (p < 0. 05). Although both PSD and PSEI were related to motor dysfunction and location (anterior versus posterior cortex) of the lesion, location was a stronger determinant for PSD (p < 0.05). The prevalence of PSD/PSEI in each location was 75%/100% in frontal lobe of anterior cerebral artery territory, 50%/0 in temporal lobe, 30%/40% in frontal-middle cerebral artery territory, 13%/0 in occipital lobe, 19%/45% in lenticulocapsular area, 11%/16% in thalamus, 16%/53% in pontine base, 36%/55% in medulla, and 0/22% in cerebellum. Parietal and dorsal pontine lesions were not associated with PSD or PSEI. PSEI was more closely associated with lenticulocapsular strokes than was PSD (p < 0.01). CONCLUSION: Development of PSD and PSEI is strongly influenced by lesion location, probably associated with the chemical neuroanatomy related to the frontal/temporal lobe-basal ganglia-ventral brainstem circuitry. Although the lesion distribution is similar, PSEI is more closely related to lenticulocapsular strokes than is PSD.