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.     

Comparison of spontaneously recovered versus nonrecovered patients with poststroke depression

We followed 16 patients who developed depression immediately after a stroke for 6 months. By that time, six patients showed no depression (recovered group), while 10 patients were still depressed (nonrecovered group). There were no significant differences in demographic variables and social functioning between the groups, but the nonrecovered group showed less improvement in cognitive function and more physical impairments. Patients in the nonrecovered group had mainly cortical lesions, while those in the recovered group had mainly subcortical and posterior circulation strokes.     

Poststroke depression and lesion location revisited

Seventy patients with one brain infarct on magnetic resonance imaging (MRI) were studied 3 months after ischemic stroke by a standardized protocol to detail side, site, type, and extent of the brain infarct, as well as severity of white matter lesions and brain atrophy. Depression was diagnosed by DSM-III-R and DSM-IV criteria. The brain infarcts that affected structures of the frontal-subcortical circuits, (i.e., the pallidum and caudate, especially on the left side) predisposed stroke patients to depression. The size of the infarcts at these sites in the depressed patients was larger. Using a logistic regression analysis, the authors found that a brain infarct that affected pallidum was a strong independent MRI correlate for poststroke depression (odds ratio = 7.2).     

MMPI profiles in anorexia nervosa patients with and without major depression

Anorexia nervosa patients with (AN-RDC+) and without (AN-RDC-) a current episode of nonbipolar major depression (MDD) differed with respect to their Minnesota Multiphasic Personality Inventory (MMPI) profiles. Mean MMPI scores in AN-RDC+ significantly differed from AN-RDC-patients in all but two MMPI scales. AN-RDC+ patients had a significantly higher number of abnormal (T greater than 70) MMPI scales per subject and significantly more subjects with greater than or equal to 3 abnormal scales compared with AN-RDC-patients. These MMPI data suggest that the presence or absence of MDD in anorectic patients may distinguish meaningful subtypes and provide further support for the validity of the stratification of anorectic patients into those with and without nonbipolar MDD.     

Serotonin transporter gene promoter region polymorphism associated with poststroke major depression

The authors examined variations of serotonin transporter-linked promoter region (5-HTTLPR) functional polymorphism in 26 stroke patients with major depression and in 25 unrelated nondepressed stroke subjects of Caucasian descent. Findings indicate a significant association between 5-HTTLPR short variant genotype and poststroke major depression.     

Right-hemisphere deficits,lesion size and location

Abstract

Thirty-seven patients with single right-hemisphere infarcts localized on CT or isotope scans were examined on tests of constructional apraxia, neglect, visuospatial problem solving, motor praxis, and language. The patients were placed, according to the anatomical location of their lesions, into five groups: frontal, central cortical, central deep, parietal, and occipital. Mean scores for drawing, Block Design and Raven's Coloured Progressive Matrices were not significantly different across the groups, but measures of neglect and perseveration appeared significantly worse in the frontal and extensive central lesion groups. Lesion size did not correlate significantly with any of the parameters. The previously emphasized parietal locus of lesions in constructional apraxia, visuospatial difficulty, and neglect was not confirmed, suggesting a more diffusely organized right hemisphere.     

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.     

The clinical features of bipolar depression: a comparison with matched major depressive disorder patients

BACKGROUND: Despite a resurgence of interest in the treatment of bipolar depression, there have been few controlled studies of the clinical characteristics of this condition. Identification of any distinctive clinical "signatures" of bipolar depression would be helpful in determining treatment options in the clinical setting. METHOD: From a cohort of 270 inpatients and outpatients assessed in detail during a DSM-IV major depressive episode, 39 bipolar I disorder patients were identified and closely matched with 39 major depressive disorder patients for gender, age, and the presence or absence of DSM-IV melancholic subtype. Patients were compared on a broad range of parameters including the Hamilton Rating Scale for Depression (depression severity), 54 depressive symptoms, the Newcastle Endogenous Depression Diagnostic Index, 3 family history items, 2 physical health items, the CORE scale (psychomotor disturbance), and 5 history items. RESULTS: Although the bipolar patients were no more severely depressed than the major depressive disorder controls, they were more likely to demonstrate psychomotor-retarded melancholic and atypical depressive features and to have had previous episodes of psychotic depression. These findings were largely duplicated even when the population was confined to those with DSM-IV melancholia. CONCLUSION: The clinical admixture of psychomotor-retarded melancholic signs and symptoms, "atypical" features, and (less frequently) psychosis may provide a "bipolar signature" in clinical scenarios when there is uncertainty concerning the polarity of a depressive presentation.     

脑卒中后抑郁患者血清白细胞介素-6水平变化的研究

目的研究脑卒中后抑郁(PSD)患者血清白细胞介素-6(IL-6)水平变化,探讨PSD患者的抑郁与免疫功能变化的关系。方法采用放射免疫法检测59例PSD患者、36例非PSD患者及43例正常人的血清IL-6水平。59例PSD患者随机给予抗抑郁治疗 脑血管病恢复期方案治疗(n=29)或仅给予脑血管病恢复期方案治疗(n=30),观察患者治疗前后血清IL-6水平变化。结果治疗前,PSD组血清IL-6水平显著高于非PSD组(P<0.01)和正常对照组(P<0.01);治疗后,PSD抗抑郁治疗组与PSD未抗抑郁治疗组相比,HAMD评分(P<0.01)和IL-6水平(P<0.01)均显著降低。在PSD组治疗前、PSD抗抑郁治疗组及PSD未抗抑郁治疗组治疗后,HAMD评分与血清IL-6水平相关系数分别为0.375(P<0.01)、0.452(P<0.01)和0.397(P<0.01)呈显著性正相关。结论PSD患者血清IL-6水平明显升高并且与抑郁程度相关。     

Alprazolam in the treatment of panic attack patients with and without major depression

Sixteen patients with panic attacks were treated with alprazolam at an anxiety clinic between March 1982 and April 1983. For all patients charts were reviewed for baseline data and treatment results at 1 and 6 months. Quantitated self-rating scales and the Clinical Global Impressions scale were used to assess progress. Alprazolam appeared effective for panic, agoraphobia, and depressive symptoms in 7 of 11 patients with either panic disorder or agoraphobia with panic attacks (DSM-III-defined diagnoses); side effects occurred in 4 of the 11 patients, were limited to oversedation, and resulted in no discontinuations of drug. However, alprazolam was ineffective in controlling panic, agoraphobia, and depression in 5 patients with panic attacks and secondary major depressive episode; for this group of patients, side effects were apparently paradoxical and required drug discontinuation in 3 of these 5 patients.     

老年卒中后抑郁患者血清细胞因子的研究

目的 探讨老年卒中后抑郁患者(PSD)血清细胞因子白细胞介素-1β(II-1β)、白细胞介素-6(IL-6)以及肿瘤坏死因子(TNF-α)的水平.方法 采用酶联免疫吸附法检测PSD组(36例)及卒中后无抑郁患者(对照组;32例)的血清IL-1β、IL-6及TNF-α水平,并以汉密尔顿抑郁量表(HAMD)评分将PSD组分为轻度组(8～16分;9例)、中度组(17～23分;17例)及重度组(≥24分;10例),比较各组血清IL-1β、IL-6及TNF-α水平的差异.结果 (1)PSD组血清IL-1β[(35.2±4.2)ng/L]、IL-6[(11.3±4.3)ng/L]及TNF-α[(32.4±6.9)ng/L]水平,均高于对照组[分别为(18.1±3.3)ng/L、(6.1±1.9)ng/L及(21.6±4.8)ng/L;P＜0.01];(2)卒中后重度抑郁组血清IL-1β[(41.8±3.2)ng/L]、IL-6[(17.5±5.7)ng/L]及,TNF-α[(38.8±5.8)ng/L]水平,均高于轻度抑郁组[分别为(29.1±2.3)ng/L、(6.6 ±1.7)ng/L及(25.9 ±3.3)ng/L;P＜0.05]、中度抑郁组[分别为(34.6±2.6)ng/L、(10.2 ±3.5)ng/L及(32.1±3.6)ng/L;P＜0.05],中度抑郁组亦高于轻度抑郁组(P＜0.05);(3)血清IL-1β(r=0.637)、IL-6(r=0.698)、TNF-α(r=0.722)水平均与抑郁的严重程度显著相关(P＜0.01).结论 IL-1β、IL-6及TNF-α可能在卒中后抑郁的发生发展中起重要作用.     

Sleep quality and immune functions in rheumatoid arthritis patients with and without major depression

The purpose of this study was to determine the discriminative factors between rheumatoid arthritis (RA) patients with and without major depression (MD). We assessed subjective sleep quality, pain, and cell-mediated immune functions in RA patients with (n = 20) and without (n = 20) MD by using Pittsburgh Sleep Quality Index (PSQI), visual analogue scale (VAS), and fluorescein isothiocyanat (FITC) labeled CD3, CD4, CD8, CDI9, CD45, CD56, and HLADR T monoclonal antibodies by flow cytometry. We found that the RA patients with MD had significantly higher pain level, poorer sleep equality, higher HDRS points, and higher HLADR T cell level than those without MD; and that these variables are discriminant factors between patient groups. These findings suggest that the RA patients with MD may be differentiated from those without MD by using VAS, PSQI, and HLADR levels; that these variables correctly classify the depressed and non depressed groups up to an accuracy level of 96.8%.     

Prevention and treatment of poststroke depression with mirtazapine in patients with acute stroke

BACKGROUND AND OBJECTIVE: Poststroke depression is one of the most frequent complications of stroke, affecting approximately 20% to 40% of all patients. In spite of the importance of this neuropsychiatric disorder, little attention has been given to the prevention of poststroke depression. The purpose of this study was to examine whether prophylactic treatment with the antidepressant mirtazapine in patients with acute stroke given from day 1 after the incidence prevents poststroke depression. METHOD: Patients with ischemic stroke received either 30 mg mirtazapine or no antidepressant medication from day 1 after the stroke in an open, randomized study design. Data were collected from August 2001 to December 2002. Seventy patients were enrolled in the study and were reexamined on days 7, 44, 90, 180, 270, and 360 using neurologic, functional, and depression rating scales. Those poststroke patients who developed depression (DSM-IV criteria) but had been randomly assigned to the nontreatment group were given the antidepressant mirtazapine after the diagnosis of depression had been established. RESULTS: Forty percent (14/35) of the nontreated patients and only 5.7% (2/35) of the patients who were treated with mirtazapine developed poststroke depression. Altogether, 16 patients developed poststroke depression, 15 of whom remitted after initiation of treatment with mirtazapine. CONCLUSION: Mirtazapine significantly reduced the rate of poststroke depression in patients with acute stroke. The study also demonstrated that this antidepressant was highly effective in treating poststroke depression.     

帕罗西汀治疗脑卒中后抑郁症疗效研究

目的探讨帕罗西汀对卒中后抑郁、焦虑患者日常生活能力和神经功能康复的影响。方法采用抑郁自评量表（SDS）、焦虑自评量表（SAS）对272例脑卒中患者进行抑郁、焦虑状态评定,其中患有卒中后抑郁合并焦虑的81例患者分别接受帕罗西汀治疗、帕罗西汀联合心理干预治疗以及不干预。采用斯堪的那维亚脑卒中量表（SSS）、Barthel指数（BI）、汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）评测治疗前后的疗效。结果急性脑卒中病人卒中后抑郁并焦虑患病率为2978%,抑郁与焦虑共病率为65.85%;治疗组I和治疗组ⅡHAMD、HAMA、SSS评分减少和BI评分增加与对照组比较均有显著性差异（P〈0.01）。结论卒中后抑郁、焦虑病人给予帕罗西汀治疗能提高患者神经功能康复程度和生活能力恢复。     

Comparison of pramipexole, fluoxetine, and placebo in patients with major depression

Pramipexole, a dopamine D2 receptor agonist, was tested in 174 patients with major depression, with or without melancholia and without psychotic features. Three daily dose levels (0.375 mg, 1.0 mg, and 5.0 mg) were compared to fluoxetine (Prozac) at 20 mg and placebo in a randomized, double-blind, parallel-group study. After a 1 week placebo run-in period, patients were treated for 8 weeks, had a post-study follow-up (week 9), and were evaluated primarily with the Hamilton Psychiatric Rating Scale for Depression (HAM-D), the Montgomery-Asberg Depression Rating Scale (MADRS), and the Clinician's Global Impressions-Severity of Illness scale (CGI-SI). All patients who received one dose of study medication were included in the observed-case analysis (no missing data were replaced). Results indicated that by endpoint (week 8), patients receiving pramipexole at the 1.0 mg per day dose had significant improvement over baseline compared to the placebo group by measure of the HAM-D, MADRS, and CGI-SI. Significant improvement in this dose group was seen at other timepoints as well. The most obvious improvement was seen in the pramipexole 5.0 mg group, although a substantial dropout rate for this group precluded statistical tests vs. placebo late in the study. Patients taking fluoxetine also showed significant improvements at endpoint on the MADRS and earlier in the study on the HAM-D. No new or unusual safety concerns were generated during this study. Pramipexole helped safely alleviate the symptoms of depression at 1.0 mg per day and especially in those patients who could tolerate the escalation to 5 mg per day.