首发重性抑郁症患者脑结构的磁共振初步研究

目的:探讨首发重性抑郁症患者是否存在大脑结构形态学的改变。方法:对20例首发、未服药重性抑郁症患者和20例年龄、性别等相匹配对照组进行全脑MRI检查。结果:重性抑郁症患者组前额叶、左右颞叶及小脑、双侧海马及前扣带回灰质密度显著降低,左侧杏仁核灰质密度增加。结论:首发重性抑郁症患者前额叶、颞叶、小脑、前扣带回、海马杏仁核有灰质密度改变,可能是重型抑郁症患者病理性变化的脑结构基础。     

首发精神分裂症患者杏仁核静息态功能连接与情绪调节的相关性

目的:探讨首发精神分裂症患者静息状态下杏仁核的功能连接特点,及其与情绪调节的关系。方法:纳入符合ICD-10精神分裂症诊断标准的38例首发患者及年龄、性别、受教育程度匹配的45例正常对照。采用中文版精神分裂症认知功能成套测验(MCCB)中的情绪管理分测验评估被试的社会认知功能。被试均进行静息态功能磁共振成像扫描,以杏仁核为种子点进行功能连接分析,比较患者组和正常对照组之间的差异,并分析功能连接强度与情绪管理的相关性。结果:与正常对照组相比,患者组左侧杏仁核与左侧前扣带回的正性功能连接降低,与左侧枕中回和右侧颞中回正性功能连接增强,与右内侧额上回负性功能连接增强(均P 0. 005,Alpha Sim校正,体素值 25);右侧杏仁核与右侧楔前叶负性功能连接减弱(P 0. 005,Alpha Sim校正,体素值 25)。偏相关分析结果显示,患者组右侧杏仁核与右侧楔前叶的功能连接与情绪管理分测验呈负相关(r=-0. 56,P 0. 01)。结论:本研究显示静息态下首发精神分裂症患者杏仁核功能连接网络模式存在异常,其中右侧杏仁核与右侧楔前叶的负连接减弱可能与患者的情绪调节功能异常有关。     

IAPS图片诱导首发抑郁症患者的情绪偏向性

目的:探讨首发抑郁症患者情绪处理偏向性的特征。方法:应用国际情绪图片系统(IAPS)的正性、中性及负性标准化情绪图片,诱导30例首发抑郁症患者及30例匹配的健康对照者,进行情绪体验等级(ESR)评分,两组间进行病例一对照配对研究。结果:(1)所选IAPS中的正性、中性及负性情绪图片的评分与IAPS标准分之间差异无显著性(P>0.05)。(2)抑郁症患者组对正性图片的评分为(7.1±0.1)分,对照组为(7.2±0.1)分,患者组低于对照组(P<0.05);两组对中性及负性图片的评分差异无显著性(P>0.05)。结论:首发抑郁症患者存在情绪信息的负性偏向性。     

静息态下抑郁症患者脑功能与临床症状的相关性

目的: 探讨静息态下抑郁症患者脑局部一致性(regional homogeneity,ReHo)与抑郁症状群的关联.方法: 17名首发重性抑郁症患者与17名性别、年龄、教育程度相匹配的健康者参与了静息态功能磁共振(fMRI)的扫描.将患者的脑ReHo值与其抑郁症状群进行相关分析,设P<0.005,k值≥10为相关具有统计学意义.结果: 抑郁症患者以下症状群与脑区的相关具有统计学意义.焦虑与右前额中部、左脑岛ReHo值呈负相关(r=-0.85,-0.55;均P<0.001);认知障碍与左前额中部、右脑岛ReHo值负相关(r=-0.83,-0.67;P<0.01),而与右海马旁回ReHo值正相关(r=0.90;P<0.01);迟缓与左前额中部、右额下回、右尾状核ReHo值负相关(r=-0.66,-0.67,-0.55;均P<0.001),而与右前扣带回腹侧ReHo值呈正相关(r=0.80,P<0.001);睡眠障碍与左楔前叶、右脑岛ReHo值负相关(r=-0.72,-0.66;P<0.01);绝望感与左后扣带回ReHo值负相关(r=-0.84,P<0.001).结论: 本研究提示抑郁症患者的焦虑、认知障碍、迟缓、睡眠障碍及绝望感症状可能是部分特定的脑神经异常活动的表现.     

首发重性抑郁症患者抗抑郁治疗前星形胶质源性蛋白(S100B)水平与短期疗效的关系

目的:研究重性抑郁症患者抗抑郁治疗前S100B(星形胶质源性蛋白)水平与短期疗效的关系。方法:按照入组标准和排除标准纳入首发重性抑郁症患者36例,并对抑郁症患者在入组时通过ELISA方法检测血清S100B水平。并应用汉密尔顿抑郁量表(HAMD)评估抗抑郁治疗4周的疗效(短期疗效)。结果:1短期治疗有效的患者组入组时S100B(1.64±0.77)ng/mL,与短期治疗无效的患者组(1.04±0.31)ng/mL相比有显著差异性(t=-3.276,P0.05);2重性抑郁症患者血清S100B与ΔHAMD变化值成正比(r=0.389,P0.05)。结论:首发重性抑郁症患者抗抑郁治疗前的S100B水平能够预测不同的短期疗效。     

基于区域的抑郁症默认网络内部功能连接研究

目的:探讨静息状态下首发重性抑郁症默认网络内部各节点间功能连接状况。方法:采集31例首发重性抑郁症患者、33例健康对照静息态功能磁共振数据,以后扣带回为种子点进行基于体素的时间相关分析,得到默认网络的关键节点。采用基于区域连接的方法分析默认网络内各节点间功能连接系数。结果:与正常对照组比较,抑郁症患者默认网络背内侧前额叶与后扣带回、右顶下小叶功能连接降低,左顶下小叶与右侧海马结构功能连接降低。结论:抑郁症默认网络内部各节点之间功能连接存在异常,这可能是抑郁症的核心病生理特征。     

首诊为心境恶劣障碍和抑郁症的青少年患者功能失调性态度对照研究

目的 探讨首诊为心境恶劣障碍和抑郁症的青少年患者功能失调性态度的差异性.方法 用DAS对首诊为心境恶劣障碍和抑郁症的青少年患者的功能失调性态度进行评估,对调查结果进行对照性分析.结果 两组DAS的总分和大多数因子分没有发现显著性差异,但因子D5(寻求赞许)、D6(依赖性)存在显著性差异,心境恶劣组寻求赞许因子分经统计发现高于抑郁症组,而抑郁症组依赖性因子分高于心境恶劣组.结论 首发的青少年心境恶劣障碍和抑郁症患者存在功能失调性认知一致性和不一致性,功能失调性认知可能也构成青少年心境恶劣障碍的易感素质.     

抑郁认知易感者对负性面孔的注意特征

目的:探讨抑郁认知易感者在负性情绪信息加工任务中的注意特征。方法:采用方便取样选取在校大学生1287人,获有效问卷1201份,使用认知方式问卷(CSQ)进行测查。根据最弱连接计算方法获得抑郁认知易感者(CV组)151人和非抑郁认知易感者(NCV组)192人。从两组中选取95人(CV组47人,NCV组48人)参与情绪面孔点探测任务,比较两组在任务中的正确率、反应时及偏倚分差异。结果:参加情绪点探测任务的95人中,有2人的数据(两组各1人)总正确率低于90%而被剔除。正确率与反应时的组间差异均无统计学意义(均P0.05)。CV组和NCV组在愤怒面孔注意偏倚分上差异有统计学意义,CV组的偏倚分大于NCV组(P0.05)。将偏倚分与零进行单一样本t检验显示,CV组在悲伤及愤怒面孔对上的注意偏倚分均大于零,而NCV组则在愉快面孔中的注意偏倚分大于零。结论:与非抑郁认知易感者相比,抑郁认知易感者在面对愤怒面孔时,其注意力更难从中脱离出来,且抑郁认知易感者对愉悦面孔的注意不够。对负性情绪面孔的注意偏倚是抑郁认知易感者的认知特征之一。     

首发青少年抑郁症患者功能失调性态度研究

目的：探讨首发的青少年抑郁症患者功能失调性态度。方法：用DAS对先证者组，一级亲属组和对照组功能失调性态度进行评估。结果：一级亲属组除D5因子、父母亚组除D5因子与D7因子等因子外．DAS总分及其它因子与先证者组存在显著性差异，对照组所有因子及DAS总分均与先证者组存在显著性差异．而同胞亚组除D7因子外．所有闪子分及DAS总分均与先证者组相应项目不存在显著性差异。对照组与一级亲属组DAS总分及各因子分的比较结果表明，DAS总分、D1、D2、D3、D7等项目之间存在显著性差异，而D4、D5、D6、D8等项目之间差异性不显著。回归分析表明，样本性质、年龄、诊断对DAS总分的影响具有统计学意义。结论：首发的青少年抑郁症患者存在功能失调性认知，功能失调性认知可能构成青少年抑郁症患者的易感素质。     

大学生应激水平与抑郁症状:“最弱连接”因素的调节作用

目的:探讨抑郁的最弱连接因素在大学生应激水平与抑郁症状变化中的调节作用。方法:选取长沙市2所高校大学生520人,进行包括首次取样在内总共6次追踪研究。首次测试采用流调中心用抑郁量表(CES-D)、认知方式问卷(CSQ)、学生日常生活和学业应激量表(SHS)。追踪测查采用CES-D和SHS。根据最弱连接假说,借助CSQ来确定个体认知易感性的"最弱连接水平"。结果:按照Abela等的最弱连接筛选标准,共检出最弱连接抑郁认知易感者60人(男性24人,女性36人),检出率11.1%。在对高校大学生抑郁症状的预测中,首次测查CES-D得分(β=3.72,P0.001)、最弱连接(β=0.95,P0.001)、性别(β=-1.22,P0.01)、最弱连接与应激水平的交互作用(β=0.03,P0.001)对抑郁得分的变化均有主效应。结论:最弱连接水平可能在应激水平及抑郁水平关系中起到调节作用。     

Hippocampal/amygdala volumes in geriatric depression.

BACKGROUND: The hippocampus, amygdala and related functional circuits have been implicated in the regulation of emotional expression and memory processes, which are affected in major depression. Several recent investigations have reported abnormalities in these structures in adult and elderly depressives. METHODS: Elderly DSM-III-R unipolar depressives (N = 40) and normal controls (N = 46) participated in a magnetic resonance imaging study (1.0T). Brain images were obtained in the coronal plane. Using established anatomical guidelines for structure delineation, volumetric measurements of left and right hippocampus and anterior hippocampus/amygdala complex were completed under blinded conditions using a semi-automated computer mensuration system, with patients and controls in random order. RESULTS: Medial temporal volumes did not significantly distinguish either elderly depressed and age-similar normal control subjects, or late onset and early onset depressed patients (ANCOVA). Major overlap of measured volumes existed between patient and control groups. In depressives, hippocampal volumes significantly correlated with age, and cognitive and depression ratings, but not with number of prior depressive episodes or age-at-onset of first depression. CONCLUSIONS: Hippocampal volumes do not discriminate a typical clinical population of elderly depressed patients from age-similar normal control subjects. If hippocampal dysfunction contributes to a diagnosis of syndromal depression in the elderly, such dysfunction does not appear to be regularly reflected in structural abnormalities captured by volumetric measurement as conducted. On the other hand, relationships between hippocampal volumes and clinical phenomena in depressives, but not controls, suggest potentially meaningful interactions between hippocampal structure and the expression of major depression in the elderly.     

Enlarged amygdala volume and reduced hippocampal volume in young women with major depression

BACKGROUND: Evidence is increasing that amygdala and hippocampus show significant structural abnormalities in affective disorders. Two previous studies found enlarged amygdala size in subjects with recent-onset major depression. METHOD: Amygdala and hippocampal volumes were assessed in 17 young women with major depressive disorder and 17 healthy matched control subjects by use of three-dimensional structural magnetic resonance imaging. The severity of depressive symptoms was assessed using the Hamilton Depression Scale and the Beck Depression Inventory. RESULTS: Compared with control subjects, depressive subjects had significantly larger (+13 %) amygdala volumes and significantly smaller (-12%) hippocampal volumes. Amygdala and hippocampal volumes were not significantly correlated with disorder-related variables. CONCLUSIONS: Our results are consistent with previous findings of structural abnormalities of amygdala and hippocampus in subjects with recent-onset major depression. It may be suggested that the size of the amygdala is enlarged in the first years of the disorder, and may decrease with prolonged disorder duration.     

Serotonin transporter gene status predicts caudate nucleus but not amygdala or hippocampal volumes in older persons with major depression

BACKGROUND: Although the short allele of the serotonin transporter promoter polymorphism (5-HTT) has been linked to increased risk of major depression in early adult life, its relationships with late-life depression and to changes in subcortical nuclei remain unclear. METHODS: 5-HTT genotypes (SS, SL, LL) were determined for 45 older persons with major depression (mean age=52.0, sd=12.8) and 16 healthy controls (mean age=55.8, sd=10.3). MRI-derived volumes of the amygdala, hippocampus, caudate and putamen were determined by reliable tracing techniques. RESULTS: In those with depression, the short allele of 5-HTT was associated with smaller caudate nucleus volumes. Although hippocampal and amygdala volumes were smaller in those with depression as compared with control subjects, 5-HTT gene status did not predict this reduction in size. LIMITATIONS: The findings are limited by the number of clinical and control participants. CONCLUSIONS: Reduced caudate nucleus volume in older patients with major depression was associated with the short allele of the 5-HTT gene. This regional brain change may be a consequence of early developmental expression as well as later vascular or degenerative effects of this genotype.     

Increased amygdala volumes in female and depressed humans. A quantitative magnetic resonance imaging study

The amygdala are thought to play an important role in emotional information processing. First studies indicate a link between amygdala atrophy, fear and aggression and between amygdala hypertrophy and depression. To investigate a possible relationship between amygdala volumes, aggression and depression, we measured the amygdala of 62 patients with temporal lobe epilepsy (TLE) with and without aggressive behavior or depression and 20 healthy volunteers using quantitative magnetic resonance imaging (MRI). Amygdala volumes of female patients (n=26) were significantly larger than those of males (n=36) (left side: P=0.001; right side P=0.05). Depressed patients displayed significant enlargement of both amygdala (left side: P=0.008; right side: P=0.001) There was no significant finding relating to the factor aggression neither was there any significant interaction between aggression, dysthymia and gender.     

Quantitative MRI of the hippocampus and amygdala in severe depression

BACKGROUND: There is little evidence to support possible structural changes in the amygdala and hippocampus of patients with severe depression. METHODS: Quantitative MRI of the amygdala and hippocampus, as well as proton spectroscopy (MRS) of mesial temporal structures were studied in 34 drug-resistant in-patients with major depression and compared with 17 age-matched controls. Volumetric MRI data were normalized for brain size. RESULTS: The volume of the left hippocampus was significantly smaller in the patients compared with the controls. Both groups exhibited similar significant hippocampal asymmetry (left smaller than right). The patients, but not the controls, had significant asymmetry of the amygdalar volumes (right smaller than left). No differences were observed between the patients and controls in the T2 relaxation times for the hippocampus and amygdala. Mesial temporal lobe MRS revealed a significantly elevated choline/creatine ratio in the patients compared with the controls. CONCLUSIONS: This quantitative MRI study provides support for a possible association between structural and biochemical substrates and severe drug-resistant major depression.     

Amygdala hyperactivation and prefrontal hypoactivation in subjects with cognitive vulnerability to depression

The hopelessness theory (HT) of depression is a diathesis-stress theory which construes cognitive vulnerability (CV) to depression. Neuroimaging studies examining depression have implicated the amygdala as an important potential locus of dysfunction in the processing of salient threatening stimuli. However, little is known about neural activation in the brain of subjects with CV to depression. Medication-free major depressive disorder (MDD) subjects (N=29), never depressed subjects with CV (N=26), and demographically matched never depressed healthy control (HC) subjects (N=31) were scanned using functional magnetic resonance imaging (fMRI) while performing an emotional matching task. The MDD subjects showed elevated left amygdala responses and reduced left dorsolateral prefrontal cortex (dlPFC) activation levels relative to HC subjects. Similarly, CV subjects had greater activity in the amygdala bilaterally and lesser activation in the dlPFC bilaterally, relative to HC subjects. The present findings raise the possibility that cognitive vulnerability to depression might be characterized by hypoactivation of the prefrontal cortex and hyperactivation of the amygdala in response to emotional stimuli; our observations might provide a potential interpretation to explain the abnormalities in neural networks mediating cognitive modulation of emotions in individuals with cognitive vulnerability to depression.     

首发与复发抑郁症患者重复性神经心理测查系统的比较研究

目的探讨首发组和复发组抑郁症患者认知功能损害的特点。方法以166例首发组抑郁症患者和94例复发组抑郁症患者为研究对象。采用汉密尔顿抑郁量表(HAM D-17)评估抑郁严重程度,采用重复性神经心理测查系统(RBAN S)测定认知功能。结果首发组与复发组的抑郁总分(t=-3.476,P<0.05)、迟缓(t=-3.079,P<0.05)和睡眠障碍(t=-3.514,P<0.05)存在显著差异;在RBAN S测查中,首发组与复发组在注意维度(t=2.016,P<0.05)存在显著差异,图形临摹(t=2.278,P<0.05)、线条定位(t=2.133,P<0.05)、图画命名(t=2.031,P<0.05)、编码测验(t=4.123,P<0.05)和图形回忆(t=2.952,P<0.05)分测验结果存在显著差异。结论复发组抑郁症患者认知功能损害较首发组患者严重。     

Severe life events predict specific patterns of change in cognitive biases in major depression

BACKGROUND: A long-standing debate concerns whether dysfunctional cognitive processes and content play a causal role in the etiology of depression or more simply represent correlates of the disorder. There has been insufficient appreciation in this debate of specific predictions afforded by cognitive theory in relation to major life stress and changes in cognition over time. In this paper we present a novel perspective for investigating the etiological relevance of cognitive factors in depression. We hypothesize that individuals who experienced a severe life event prior to the onset of major depression will exhibit greater changes in dysfunctional attitudes over the course of the episode than will individuals without a severe life event. METHOD: Fifty-three participants diagnosed with major depression were assessed longitudinally, approximately 1 year apart, with state-of-the-art measures of life stress and dysfunctional attitudes. RESULTS: Depressed individuals with a severe life event prior to episode onset exhibited greater changes in cognitive biases over time than did depressed individuals without a prior severe event. These results were especially pronounced for individuals who no longer met diagnostic criteria for major depression at the second assessment. CONCLUSIONS: Specific patterns of change in cognitive biases over the course of depression as a function of major life stress support the etiological relevance of cognition in major depression.     

Medial temporal lobe abnormalities in pediatric unipolar depression

In vivo anatomical magnetic resonance imaging (MRI) studies in adults with major depressive disorder (MDD) have implicated neurocircuitries involved in mood regulation in the pathophysiology of mood disorders. Specifically, abnormalities in the medial temporal lobe structures have been reported. This study examined a sample of children and adolescents with major depressive disorder to investigate anatomical abnormalities in these key medial temporal brain regions. Nineteen children and adolescents with DSM-IV major depression (mean age +/- S.D.=13.0 +/- 2.4 years; 10 unmedicated) and 24 healthy comparison subjects (mean age +/- S.D.=13.9 +/- 2.9 years) were studied using a 1.5T Philips MRI scanner. We measured hippocampus and amygdala gray matter volumes. MRI structural volumes were compared using analysis of covariance with age and total brain volumes as covariates. Pediatric depressed patients had significantly smaller left hippocampal gray matter volumes compared to healthy controls (1.89 +/- 0.16 cm(3) versus 1.99 +/- 0.18 cm(3), respectively; F=5.0, d.f.=1/39, p=0.03; effect size: eta2(p) =0.11). Unmedicated depressed patients showed a trend towards smaller left hippocampal volumes compared to medicated patients and healthy subjects (F=2.8, d.f.=2/38, p=0.07; effect size: eta2(p) =0.13). There were no statistically significant differences in mean volumes for left or right amygdala. Smaller left hippocampal volumes in children and adolescents with MDD are in agreement with findings from adult studies and suggest that such abnormalities are present early in the course of the illness. Amygdala volumes are not abnormal in this age group. Smaller hippocampal volumes may be related to an abnormal developmental process or HPA axis dysfunction.