心理康复

康复心理学（rehabilitation psychology）是运用心理学理论和技术研究揭示康复中的心理活动、现象及规律的科学。心理康复的目标是帮助康复对象应对康复过程中出现的一系列心理行为障碍和问题,挖掘患者的潜能,增强康复的信心,并帮助患者接受和适应残疾,重新回归家庭和社会。卒中是突发性脑部疾病,常并发一系列精神和心理障碍,而焦虑和抑郁是最常见的心理障碍。研究表明,及时有效地对卒中后患者的焦虑和抑郁情绪进行干预,不仅有利于患者的心理康复,而且也有利于身体功能的康复。目前临床上对卒中患者的焦虑抑郁情绪多以药物治疗为主,而现代研究表明,药物治疗合并心理治疗对卒中后患者的焦虑抑郁情绪的治疗效果更佳。随着现代科技的发展,生物反馈评估与治疗技术在精神和心理康复领域中得到了很大的运用,并且在神经康复领域也得到一定的运用。各种类型的生物反馈评估与治疗技术,在卒中后心理康复领域的应用也受到相关研究者的重视。本期将聚焦卒中后患者心理治疗现状及心理康复中的生物反馈评估和治疗技术的效果开展探讨,以期与国内同行们讨论和进一步合作研究。     

连续性护理干预对减轻起搏器植入老年患者负性情绪的效果

目的：分析起搏器植入老年患者存在的负性情绪,探讨连续性护理干预的效果。方法将80例起搏器植入老年患者随机分为对照组38例和干预组42例,应用抑郁、焦虑自评量表分别在患者入院时、起搏器植入术后和出院后1 a对患者的焦虑、抑郁程度进行调查、对比分析。结果干预组患者的焦虑、抑郁情绪的改善程度明显高于对照组。结论通过对老年起搏器植入患者开展连续性护理干预,可明显减轻患者的抑郁和焦虑、抑郁情绪,促进疾病康复。     

卒中后抑郁、焦虑及干预和预后的临床研究

目的探讨脑卒中后抑郁、焦虑对患者日常生活能力和神经功能康复的影响,帕罗西汀干预急性卒中后抑郁、焦虑的效果。方法对282名脑卒中患者采用抑郁自评量表（SDS）、焦虑自评量表（SAS）进行评定,其中卒中后抑郁合并焦虑的90名随机分为干预和非干预2组,干预组接受帕罗西汀治疗;随机抽取非抑郁、焦虑患者45名为对照组,用汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）、斯堪的那维亚脑卒中量表（SSS）、Barthel指数（BI）,评定帕罗西汀的疗效和预后。结果急性脑卒中后抑郁合并焦虑发生率（68.18%）,非干预组与对照组比较6周末SSS和BI有显著性差异（P〈0.01）,干预组与对照组SSS和BI无显著性差异,干预组与非干预组HAMD、HAMA、SSS、BI有显著性差异。结论抑郁、焦虑明显降低患者神经功能康复程度和生活能力恢复,帕罗西汀可有效干预卒中后抑郁、焦虑,改善预后。     

卒中后抑郁影响因子及干预治疗研究进展

卒中后抑郁症(post-stroke depression,PSD)是卒中最常见的并发症之一[1],患者总是有表现为情绪低落,广泛性焦虑和冷漠等神经精神症状.它已成为卒中恢复的主要负面因素.抑郁有多种致病因素,最主要有生物学机制和心理因素,生物学机制包括神经递质、病变位置、炎性因子等;心理因素涉及的方面也是复杂多变,涉及环境、遗传、自身特性等[2],根据抑郁相关量表预测、诊断PSD的可靠性难以避免受主观情绪影响,本文将研究重点放在相关影响因子水平的变化上,更好的掌握卒中后抑郁等状况,保证卒中后患者康复的有利进行.对于中、重度卒中患者来说,出院后康复治疗至关重要,对于患者日后的行为能力、生活质量有很大帮助,但是近来有研究表明卒中后抑郁症与不良的预后相关,例如死亡率和残疾[3],所以对于PSD可能影响甚至致病的影响因子及相关干预治疗的研究刻不容缓.     

认知行为干预对脑卒中后偏瘫患者负性情绪及相关因素的影响

目的探讨认知行为干预对脑卒中后偏瘫患者负性情绪及相关因素的影响。方法 94例脑卒中后偏瘫患者随机分为观察组(47例)和对照组(47例),应用焦虑自评量表、抑郁自评量表分析患者焦虑、抑郁的现状及其影响因素。观察组实施认知行为疗法,比较2组患者负性情绪改善情况。结果 2组患者均存在明显的焦虑抑郁,与患者的年龄、经济状况、疾病知识等有关。观察组干预后负性情绪明显改善。结论认知行为干预对脑卒中后偏瘫患者负性情绪有较好的改善作用。     

冠状动脉内支架植入术治疗患者的情绪障碍及心理干预

目的　了解冠状动脉内支架植入术 (PTCA)治疗前后患者的情绪障碍和心理干预的效果。方法　在手术前后对患者进行心理干预 ,并用汉密顿焦虑量表 (HAMA)和汉密顿抑郁量表 (HAMD)在心理干预前后对患者进行测查。结果　心理干预前患者有明显的焦虑抑郁情绪 ,心理干预后患者的焦虑抑郁情绪明显改善。结论　心理干预是减轻PTCA治疗患者焦虑抑郁情绪障碍的有效方法 ,值得广泛应用     

帕罗西汀联合心理干预治疗卒中后抑郁/焦虑的前瞻性对照研究

目的　探讨卒中后抑郁/焦虑对卒中患者日常生活能力和神经功能康复的影响,以及帕罗西汀联合早期心理干预的临床疗效。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并发焦虑的81名患者随机分成3组,分别接受单用帕罗西汀治疗、帕罗西汀联合心理治疗以及不干预。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　急性脑卒中患者卒中后抑郁并焦虑患病率为29.78%,抑郁与焦虑共病率为65.85%,额叶、左侧大脑半球、基底节病灶与卒中后抑郁/焦虑的发生相关(额叶P <0.05、左侧大脑半球P <0.0001、基底节P <0.0001);治疗组I和治疗组II HAMD、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均<0.01),治疗组II HAMD、HAMA、SSS评分减少和BI评分增加较治疗组I有显著性差异(P均<0.05)。结论　卒中后抑郁/焦虑的发生与脑卒中部位相关;卒中后抑郁/焦虑障碍明显降低患者神经功能康复程度和生活能力恢复;对卒中后抑郁/焦虑患者单用药物帕罗西汀或给予帕罗西汀联合心理干预治疗均能提高患者神经功能康复程度和生活能力恢复,而且帕罗西汀联合心理干预治疗疗效更满意     

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。     

急性缺血性卒中患者住院期间照顾者焦虑抑郁的发生率及影响因素分析

目的     分析急性缺血性卒中患者的照顾者出现焦虑、抑郁情绪的影响因素,早期识别缺血性卒中照顾者的心理状态,为后续的干预措施提供参考。     

卒中后抑郁的评估进展

卒中后抑郁发病率较高,准确的评估有利于临床诊疗。目前,对卒中后抑郁的评估多依赖 量表。对于不影响语言表达的卒中患者,汉密尔顿抑郁量表、卒中后抑郁分级量表和蒙哥马利抑郁 量表应用最为广泛,且其信度和效度均较高。对于失语患者的卒中后抑郁评价量表虽然开发的比较 多,但临床应用相对较局限,其中卒中失语抑郁问卷和失语抑郁评估量表应用相对较多。目前针对卒 中后抑郁评估量表的应用人群、评估指标有所差异,在应用这些量表时,相比原发疾病,评估者更重 视抑郁情绪的问题,这可能会造成患者的不配合和排斥,从而影响量表评价的准确性,这些局限性 有待进一步研究解决。     

Neurofeedback with anxiety and affective disorders

A robust body of neurophysiologic research is reviewed on functional brain abnormalities associated with depression, anxiety, and obsessive-compulsive disorder. A review of more recent research finds that pharmacologic treatment may not be as effective as previously believed. A more recent neuroscience technology, electroencephalographic (EEG) biofeedback (neurofeedback), seems to hold promise as a methodology for retraining abnormal brain wave patterns. It has been associated with minimal side effects and is less invasive than other methods for addressing biologic brain disorders. Literature is reviewed on the use of neurofeedback with anxiety disorders, including posttraumatic stress disorder and obsessive-compulsive disorder, and with depression. Case examples are provided.     

脑卒中后情感障碍的心理干预及帕罗西汀治疗的临床研究

目的 探讨脑卒中后情感障碍的发生率、脑卒中部位与情感障碍的关系,以及口服帕罗西汀合并早期心理干预对脑卒中后情感障碍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181例脑卒中患者进行筛查,对脑卒中后同时出现抑郁和焦虑的54例患者随机分成治疗组和对照组,在接受脑血管病常规治疗的基础上,治疗组加用帕罗西汀和心理干预.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)分别于治疗前、治疗后2周、4周及6周末进行评测.结果 181例患者中发生情感障碍81例(44.75 %),其中66.67%(54例)同时出现抑郁和焦虑,情感障碍的发生与额叶、左侧大脑半球、基底节病灶有关(P<0.05～0.001);治疗后治疗组HAMD、HAMA、SSS评分减少和BI评分增加,与对照组比较差异有统计学意义(均P<0.01),治疗后2～6周显效率显著优于对照组(P<0.05～0.01).结论 脑卒中后抑郁/焦虑的发生与脑卒中部位相关;对脑卒中后抑郁/焦虑的患者应用帕罗西汀合并心理干预治疗能显著提高患者神经功能康复程度,促进生活能力的恢复.     

Prevalence and course of depressive disorders in hospitalized stroke patients

In a sample of ninety-nine patients seen two months post-stroke, 18 percent were diagnosed as having minor depression and 14 percent major depression. At follow-up, fifteen months later, the prevalence of depressive disorder had declined substantially, to 12 percent overall. Major depression was characterized by an average duration of thirty-nine weeks, a mortality rate of 23 percent and was associated with positive family history of affective or anxiety disorder. Among patients with left hemisphere lesions, major depression was associated with cognitive impairment. Minor depression had a shorter average duration (twelve weeks) and was more common in males. These two syndromes may define distinct types of post-stroke depression with implications for treatment interventions.     

Neurofeedback and networks of depression

Recent advances in imaging technology and in the understanding of neural circuits relevant to emotion, motivation, and depression have boosted interest and experimental work in neuromodulation for affective disorders. Real-time functional magnetic resonance imaging (fMRI) can be used to train patients in the self regulation of these circuits, and thus complement existing neurofeedback technologies based on electroencephalography (EEG). EEG neurofeedback for depression has mainly been based on models of altered hemispheric asymmetry. fMRI-based neurofeedback (fMRI-NF) can utilize functional localizer scans that allow the dynamic adjustment of the target areas or networks for self-regulation training to individual patterns of emotion processing. An initial application of fMRI-NF in depression has produced promising clinical results, and further clinical trials are under way. Challenges lie in the design of appropriate control conditions for rigorous clinical trials, and in the transfer of neurofeedback protocols from the laboratory to mobile devices to enhance the sustainability of any clinical benefits.     

Modulation of subgenual anterior cingulate cortex activity with real-time neurofeedback

The advent of real-time neurofeedback techniques has allowed us to begin to map the controllability of sensory and cognitive and, more recently, affective centers in the brain. The subgenual anterior cingulate cortex (sACC) is thought to be involved in generation of affective states and has been implicated in psychopathology. In this study, we examined whether individuals could use real-time fMRI neurofeedback to modulate sACC activity. Following a localizer task used to identify an sACC region of interest, an experimental group of eight women participated in four scans: (1) a pretraining scan in which they were asked to decrease activity in the sACC without neurofeedback; (2) two training scans in which sACC neurofeedback was presented along with instructions to decrease sACC activity; and (3) a neurofeedback-free post-training scan. An additional nine women in a yoked feedback control group saw sACC activity from the participants in the experimental group. Activity in the sACC was significantly reduced during neurofeedback training in the experimental group, but not in the control group. This training effect in the experimental group, however, did not generalize to the neurofeedback-free post-training scan. A psychophysiological interaction analysis showed decreased correlation in the experimental group relative to the sham control group between activity in the sACC and the posterior cingulate cortex during neurofeedback training relative to neurofeedback-free scans. The finding that individuals can down-modulate the sACC shows that a primary emotion center in which functional abnormality has been strongly implicated in affective disorders can be controlled with the aid of neurofeedback.     

The neurobiology of the emotional adolescent: From the inside out

Adolescents are commonly portrayed as highly emotional, with their behaviors often hijacked by their emotions. Research on the neural substrates of adolescent affective behavior is beginning to paint a more nuanced picture of how neurodevelopmental changes in brain function influence affective behavior, and how these influences are modulated by external factors in the environment. Recent neurodevelopmental models suggest that the brain is designed to promote emotion regulation, learning, and affiliation across development, and that affective behavior reciprocally interacts with age-specific social demands and different social contexts. In this review, we discuss current findings on neurobiological mechanisms of adolescents’ affective behavior and highlight individual differences in and social-contextual influences on adolescents’ emotionality. Neurobiological mechanisms of affective processes related to anxiety and depression are also discussed as examples. As the field progresses, it will be critical to test new hypotheses generated from the foundational empirical and conceptual work and to focus on identifying more precisely how and when neural networks change in ways that promote or thwart adaptive affective behavior during adolescence.     

Neuropathological substrates and structural changes in late-life depression: the impact of vascular burden

A first episode of depression after 65 years of age has long been associated with both severe macrovascular and small microvascular pathology. Among the three more frequent forms of depression in old age, post-stroke depression has been associated with an abrupt damage of cortical circuits involved in monoamine production and mood regulation. Late-onset depression (LOD) in the absence of stroke has been related to lacunes and white matter lesions that invade both the neocortex and subcortical nuclei. Recurrent late-life depression is thought to induce neuronal loss in the hippocampal formation and white matter lesions that affect limbic pathways. Despite an impressive number of magnetic resonance imaging (MRI) studies in this field, the presence of a causal relationship between structural changes in the human brain and LOD is still controversial. The present article provides a critical overview of the contribution of neuropathology in post-stroke, late-onset, and late-life recurrent depression. Recent autopsy findings challenge the role of stroke location in the occurrence of post-stroke depression by pointing to the deleterious effect of subcortical lacunes. Despite the lines of evidences supporting the association between MRI-assessed white matter changes and mood dysregulation, lacunes, periventricular and deep white matter demyelination are all unrelated to the occurrence of LOD. In the same line, neuropathological data show that early-onset depression is not associated with an acceleration of aging-related neurodegenerative changes in the human brain. However, they also provide data in favor of the neurotoxic theory of depression by showing that neuronal loss occurs in the hippocampus of chronically depressed patients. These three paradigms are discussed in the light of the complex relationships between psychosocial determinants and biological vulnerability in affective disorders.     

Self-Rated Emotional Functioning of Patients With Neurological or Asymptomatic Form of Wilson’s Disease

Psychopathology was assessed in 50 patients with the neurological form of Wilson’s disease (WD-N) and in 17 asymptomatic patients (WD-A) compared to matched healthy controls and to rheumatoid arthritis (RA) control patients using The Hopkins Symptom Checklist. As hypothesized, WD-N patients had significantly lower interpersonal sensitivity and aggression/hostility scores than had healthy controls, but did not differ from them either in depression or anxiety levels. Retarded depression and anxiety were higher among RA patients than in WD-N patients. This nondistressed response to the chronic disabling disease was even more salient in 19WD patients with lesions in basal ganglia only. WD-A patients did not differ from their healthy peers, which suggests a tendency towards hypercompensation and denial in the former. WD-N patients’ limited awareness of their deficits (including impaired control of affective behavior) seems to result from their brain damage implicating the basal ganglia.     

The longitudinal relationship between acceptance and anxiety and depression in people who have had a stroke

ABSTRACT

Objectives: The role that acceptance may play in anxiety and depression has received little attention in stroke, unlike other chronic conditions. This study aimed to clarify whether acceptance of a stroke is related to anxiety and depression post-stroke when controlling for social support.

Design: A longitudinal design was employed with 35 participants completing measures at two time points: three-month and nine-month post-stroke.

Methods: Forty-one stroke patients, who were three-month post-stroke, were recruited from a stroke service register. Participants completed measures of anxiety, depression, social support and acceptance at two time points, six months apart.

Results: Acceptance was moderately and negatively correlated with anxiety and depression at three- and nine-month post-stroke. Acceptance showed a moderate and positive correlation with emotional and practical social support at Time 1 but not at Time 2. Acceptance at Time 1 was a stronger predictor of both anxiety and depression at Time 2 than emotional or practical social support.

Conclusions: Acceptance is an important area to consider in relation to rehabilitation and adjustment following a stroke.     

miR-137, a new target for post-stroke depression?

Expression of miR-137 is downregulated in brain tissue from patients with depression and suicidal behavior,and is also downregulated in peripheral blood from stroke patients.However,it is not yet known if miR-137 acts as a bridge between stroke and depression.To test this,we used middle cerebral artery occlusion and chronic mild stress to establish a post-stroke depression model in rats.Compared with controls,we found significantly lower miR-137 levels in the brain and peripheral blood from post-stroke depression rats.Injection of a miR-137 antagonist into the brain ventricles upregulated miR-137 levels,and improved behavioral changes in post-stroke depression rats.Luciferase assays showed miR-137 bound to the 3′UTR of Grin2A,regulating Grin2A expression in a neuronal cell line.Grin2A gene overexpression in the brain of post-stroke depression rats,noticeably suppressed the inhibitory effect of miR-137 on post-stroke depression.Overall,our results show that miR-137 suppresses Grin2A protein expression through binding to Grin2A mRNA,thereby exerting an inhibitory effect on post-stroke depression.Our results offer a new therapeutic direction for post-stroke depression.