帕金森病伴抑郁的研究进展

帕金森病(PD)是一种慢性进行性神经系统变性疾病,临床表现以静止性震颤、肌强直、运动迟缓、姿势反射障碍为核心症状的运动障碍性疾病.近年来,人们逐渐认识到其非运动症状对患者的生活质量影响更大,且可能是致残的主要原因[1].其中,抑郁是PD最常见的神经精神症状,伴有抑郁的PD(dPD)患者较不伴抑郁的PD患者表现出更严重的神经症状及认知功能下降[2],提示抑郁会导致PD患者更广泛的神.     

抑郁症伴躯体症状的临床特征分析

目的了解抑郁症伴躯体症状的临床特征。方法对42例抑郁症伴躯体症状和98例不伴躯体症状患者采用自编抑郁症调查问卷、汉密尔顿抑郁量表（HAMD-24项）、社会功能缺陷量表（SDSS）进行评定,并对数据进行统计分析。结果两组的疾病严重度一致。但躯体症状组平均病程显著延长,慢性病者及女性患者较多,治疗起效时间及症状改善时间显著延迟,部分社会功能缺陷较情感症状组明显。结论抑郁症伴躯体症状病程慢性化趋势明显,对治疗起效缓慢,部分社会功能缺陷明显。     

我国常用的抑郁自评量表介绍及应用

由于生活节奏的加快、生活压力的繁重,导致抑郁症发病率越来越高,但抑郁症识别率低,能够有效治疗的病例不足40%[1].有研究发现,10%~25%的轻度抑郁症患者如未能得到及时识别及治疗将在1~3年内发展为重度抑郁症[2],因此早期的识别及治疗,可以延缓患者重度抑郁症的发生.心理评定量表[3]作为一种定量及标准化工具,不但能够辅助医生对这些患者进行辨识并给予相应客观的评价,而且可以让患者意识到自身疾病的状态及程度,配合医生的治疗.因此,应重视心理量表并大力发展心理量表在临床中的应用.本文简要地概述了目前国内常用的抑郁症状评估自评量表及应用情况,旨在以后可以编制出适合我国抑郁症人群的抑郁筛查评定量表,及时发现抑郁人群,减少抑郁症的误诊、漏诊等问题.为了文章的简洁明了,在此只选择性的引用各量表的文献进行应用情况分析.     

抑郁症伴慢性疼痛的机制与药物治疗进展

抑郁症伴慢性疼痛已经成为影响公众健康的重要因素之一,流行病学研究发现66%的抑郁症患者常伴有慢性疼痛,73.3%慢性疼痛患者会诱发抑郁症.现围绕抑郁症伴慢性疼痛的神经递质、神经内分泌、神经炎症及肠道菌群失调的病理机制及药物治疗在这种共病中的作用进行综述,并对药物治疗在这些共病中未来研究的发展方向进行展望.     

91例脑卒中后抑郁症的临床分析

脑卒中后抑郁症(post-stroke depression，PSD)是脑血管疾病常见并发症之一。卒中后抑郁症影响卒中患者的神经康复和治疗，对卒中后抑郁患者进行早期诊断和治疗，有利于患者躯体功能的恢复，改善患者预后。为进一步探讨卒中后抑郁症的发生，特点及相关因素，我们对287例住院的脑卒中患者的临床资料进行研究，并将其中出现卒中后抑郁症的91例患者资料进行分析。     

抗抑郁药对血糖的影响

有关情感障碍与“应激敏感”的代谢疾病（如Ⅱ型糖尿病）的相关的研究已进行数年,但研究报道不尽一致”。例如,20世纪初期首次报道了抑郁症患者中存在葡萄糖稳态紊乱,目前的报道表明异常的葡萄糖-胰岛素稳态与抑郁严重程度的几个指标相关,它可能是抑郁症患者某些抑郁症状（如：神经认知缺损）及与躯体疾病共病（如：心血管疾病）的重要的神经激素介质。     

神经营养因子假说与抑郁症发病机制的研究进展

目前关于抑郁症发病机制的神经营养因子假说研究尚不明确,当前研究多聚焦于脑源性神经营养因子(BDNF)及其前体(proBDNF)和成熟体(mBDNF)在抑郁症中的作用。多个研究显示抑郁症患者proBDNF蛋白水平升高,而mBDNF蛋白水平降低。随着对神经营养因子假说研究的深入,有研究发现组织型纤溶酶原激活剂(tPA)可通过促使proBDNF向mBDNF转化而缓解抑郁症状,纤溶酶原激活物抑制剂-1(PAI-1)可抑制tPA的表达,PAI-1在抑郁症患者中的表达增加。本文对BDNF、proBDNF、mBDNF、tPA及PAI-1与抑郁症之间的关系进行综述,以期为抑郁症的发生机制及诊疗提供参考。     

抑郁症患者自杀行为与血清脑源性神经营养因子水平的关系

目的:探讨血清脑源性神经营养因子(BDNF)水平与抑郁症患者自杀行为之间的关系.方法:采用酶联吸附反应方法对有自杀行为的21例抑郁症患者(自杀组)、无自杀行为的52例抑郁症患者(非自杀组)以及80例正常人(对照组)血清的BDNF进行检测,应用汉密尔顿抑郁量表(HAMD)对抑郁症患者的抑郁症状进行评定. 结果:抑郁症患者...     

事件相关电位P300在抑郁症中的研究进展

事件相关电位P300在抑郁症不同研究角度都有大量的研究,近几年一些新视角的研究补充了以往研究的空缺。本文从事件相关电位P300与抑郁症、P300在单双相抑郁及抑郁不同分型中的应用、P300与脑源定位技术相结合在抑郁症中的应用及P300对抑郁症严重程度和疗效评估4个角度进行综述。     

神经可塑性在抑郁障碍机制的研究进展

抑郁障碍是一种危害身心健康的精神疾病,核心症状为心境低落、精力不足、快感缺失,重度抑郁患者伴自杀倾向,抑郁症病因尚不清楚。神经可塑性受损是抑郁障碍发生的基础,其机制尚不明确。现就神经可塑性参与抑郁障碍发生的研究现状作一综述。     

Transcranial brain sonography findings related to neuropsychological impairment in multiple sclerosis

Cognitive dysfunction, fatigue and mood disorder contribute to the neuropsychological impairment that is common in multiple sclerosis (MS). The present paper reviews application of transcranial brain sonography (TCS) in MS patients and TCS findings related to neuropsychological dysfunction. TCS is a new neuroimaging method displaying tissue echogenicity of the brain through the intact skull. Whereas the cortex can not be discriminated from the subcortical white matter with TCS, subcortical brain structures such as ventricles and basal ganglia can be adequately displayed. Even though TCS proved sensitive and reliable in measuring widths of third and lateral ventricles in a number of neurodegenerative diseases, relatively few TCS studies on MS patients have been reported. Data of these studies suggest a good correlation of cognitive dysfunction and width of third ventricle which can be measured reliably with TCS. Moreover, abnormal TCS findings of basal ganglia were associated with cognitive impairment. However, TCS findings of midbrain structures, basal ganglia and ventricles did not correlate with fatigue or depression in MS patients. TCS has the advantages of low costs, short investigation times and unlimited repeatability. The use of third-ventricle and basalganglia TCS for predicting and monitoring neuropsychological impairment in MS patients, however, needs to be elucidated in further studies.     

Transcranial Sonography Findings in Depression in Association With Psychiatric and Neurologic Diseases: A Review

The transcranial sonography (TCS) finding of reduced echogenicity of brainstem raphe (hypoechogenic BR) has been associated with depressive states. Here, we review the TCS studies in subjects with depressive disorders and with depression related to degenerative brain diseases, and compare the frequency and clinical correlates of hypoechogenic BR in these reports. Summarizing the data published so far, hypoechogenic BR is present in 67% (range, 37‐95%) of depressed but only in 15% (5‐36%) of nondepressed subjects without history of neurodegenerative disease. The finding of hypoechogenic BR in these subjects is associated with a relative risk of 3.03 (95% CI, 2.44‐3.75; P < .001) of being diagnosed with depression. In patients with Parkinson's disease, hypoechogenic BR is present in 63% (35‐92%) of depressed but only in 27% (10‐62%) of nondepressed patients, resulting in a relative risk of 2.18 (95% CI, 1.80‐2.66; P < .001) of being diagnosed with depression. Hypoechogenic BR is associated with depression in a number of neurological disorders such Huntington's disease, idiopathic Rapid Eye Movement (REM) sleep behavior disorder, myotonic dystrophies, and cerebral small vessel disease. Although some studies did not show any relationship between BR echogenicity and severity of depression, others suggest an association with higher severity of depression, or even with suicidal ideation. In one study BR hypoechogenicity was found to be associated with better responsivity to serotonin reuptake inhibitors. Further studies are warranted to compare the TCS findings of BR alteration with post‐mortem histopathological findings, and with genetic variants related to cerebral serotonin metabolism.     

Depression in Parkinson’s disease: brainstem midline alteration on transcranial sonography and magnetic resonance imaging

Recent studies using transcranial sonography (TCS) have provided evidence of alterations in the mesencephalic midline structures in patients with unipolar depression and depression in Parkinson’s disease (PD), suggesting an involvement of the basal limbic system in primary and secondary mood disorders. This study tested the hypothesis of brainstem midline abnormality in depression and investigated 31 PD patients by magnetic resonance imaging (MRI) and TCS. Signal intensity of the pontine and mesencephalic brainstem midline was rated on T2-weighted images and measured by relaxometry. In addition, two blinded investigators assessed the echogenicity of the brainstem midline by TCS. The severity of motor symptoms and depression were graded independently using standard research scales. Rating of signal intensity and T2 relaxometry of the pontomesencephalic midline structures revealed significant difference between depressed and nondepressed PD patients (P < 0.05). This corresponded to a significant reduction in mesencephalic midline echogenicity of depressed PD patients on TCS images. No correlation was found between raphe signal intensity, T2 relaxation times, or TCS echogenicity and the severity of motor symptoms or depression. This study is the first to show changes in signal intensity and T2 relaxation time of the pontomesencephalic midline structures on MRI in depressed PD patients confirming previous TCS findings. As these midline structures comprise fiber tracts and nuclei of the basal limbic system, the findings may support the hypothesis of an alteration in the basal limbic system in mood disorders. Received: 14 May 1999 Received in revised form: 28 July 1999 Accepted: 29 August 1999     

Late-life depression: a neuropsychiatric approach

Late-life depression refers to depressive syndromes defined in the American Psychiatric Association's Diagnostic and Statistical Manual and in the International Classification of Diseases that arise in adults older than 65 years of age. Late life depressive syndromes often arise in the context of medical and neurologic disorders. There is a high prevalence of depression in various neurodegenerative disorders such as Alzheimer's disease, Lewy body disease, Parkinson's disease, cerebrovascular disease and frontotemporal dementias. It has been well recognized that late life depression may itself be the presenting symptom of a latent neurodegenerative disorder. Therefore, an accurate diagnosis of late-onset depression may serve to identify a high-risk group that would benefit from initiation of therapies with the goal of delaying or possibly even preventing the onset of dementia.     

The role of zinc in neurodegenerative inflammatory pathways in depression

According to new hypothesis, depression is characterized by decreased neurogenesis and enhanced neurodegeneration which, in part, may be caused by inflammatory processes. There is much evidence indicating that depression, age-related changes often associated with impaired brain function and cognitive performances or neurodegenerative processes could be related to dysfunctions affecting the zinc ion availability. Clinical studies revealed that depression is accompanied by serum hypozincemia, which can be normalized by successful antidepressant treatment. In patients with major depression, a low zinc serum level was correlated with an increase in the activation of markers of the immune system, suggesting that this effect may result in part from a depression-related alteration in the immune-inflammatory system. Moreover, a preliminary clinical study demonstrated the benefit of zinc supplementation in antidepressant therapy in both treatment non-resistant and resistant patients. In the preclinical study, the antidepressant activity of zinc was observed in the majority of rodent tests and models of depression and revealed a causative role for zinc deficiency in the induction of depressive-like symptoms, the reduction of neurogenesis and neuronal survival or impaired learning and memory ability. This paper provides an overview of the clinical and experimental evidence that implicates the role of zinc in the pathophysiology and therapy of depression within the context of the inflammatory and neurodegenerative hypothesis of this disease.     

Platelet activating factors in depression and coronary artery disease: A potential biomarker related to inflammatory mechanisms and neurodegeneration

The persistence of a depressive episode in coronary artery disease (CAD) patients not only heightens the risk of acute ischemic events, but it is also associated with accelerated cognitive decline. Antidepressant interventions for depression in CAD have only modest effects and novel approaches are limited by a poor understanding of etiological mechanisms. This review proposes that the platelet activating factor (PAF) family of lipids might be associated with the persistence of a depressive episode and related neurodegenerative pathology in CAD due to their association with leading etiological mechanisms for depression in CAD such as inflammation, oxidative and nitrosative stress, vascular endothelial dysfunction, and platelet reactivity. The evidence implicating PAFs in CAD, vascular pathology, and neurodegenerative processes is also presented. We also propose future directions for the investigation of PAFs as mediators of persistent depression. In summary, PAFs are implicated in leading mechanisms associated with depression in CAD. PAFs may therefore be associated with the persistence of depression in CAD and related to neurodegenerative and cognitive sequelae.     

Sonographic basal ganglia alterations are related to non-motor symptoms in multiple sclerosis

The anatomical basis of cognitive dysfunction and other non-motor symptoms in multiple sclerosis (MS) is poorly understood. In MS patients, transcranial sonography (TCS) shows neurodegenerative disease-like lesions of the substantia nigra (SN) and basal ganglia, thought to reflect iron accumulation. The present study deals with the question of whether sonographic changes of SN, brainstem raphe, lenticular nucleus (LN) or caudate nucleus are related to non-motor symptoms of MS. We used TCS to investigate 54 MS patients and 54 age- and sex-matched healthy subjects. Degree of cognitive (executive) dysfunction, fatigue, depression, and urinary urge incontinence in MS patients was assessed using the Paced Auditory Serial Addition Test, the Faces Symbol Test, the Modified Fatigue Impact Scale, the Beck Depression Inventory, and the Urinary Distress Inventory. Abnormal TCS findings of SN, brainstem raphe, LN, and caudate nucleus were found in 13, 7, 11, and 6% of the healthy subjects, but in 54, 43, 62, and 41% (each, p < 0.001) of the MS patients, with similar frequency in relapsing-remitting and primary or secondary progressive MS patients. Sonographic alteration of the LN correlated with cognitive dysfunction. Combined alteration of both, LN and SN, was clearly associated with cognitive dysfunction and cognitive fatigue. The combined sonographic alteration of SN and brainstem raphe indicated severe urinary urge incontinence irrespective of the presence of spinal MS lesions. No relation was found between depression and any of the TCS findings. These findings suggest that neurodegenerative processes affecting deep brain structures contribute to cognitive and autonomic dysfunction in MS.     

Late life depression

Depression has an overall prevalence of 5-8%. The prevalence of late life depression is estimated among people 65 years of age to be 15%. There is a great under-diagnosis and under-treatment of late life depression with the most serious consequence being premature death. Depression is also an important and independent risk factor for mortality following myocardial infarction, while patients with stroke associated with depression also have a higher death rate. The suicide rate is increased in elderly especially elderly men with depression. The aetiology of depression is more heterogeneous than depression in younger adults. Obviously age-related changes in the brain increase the risk for depression. Patients with neurodegenerative disorders also run a higher risk for being depressed. In Alzheimer's disease the frequency is around 50%. Deficiency of essential nutrients like folic acid and vitamin B12 is an obvious risk factor for both disorders with cognitive impairment and depression. Treatment of depression in the elderly follows the same lines as treatment of depression in younger patients. Many different drugs may be prescribed; however, the risk of adverse events is greater in the elderly. The drugs of choice are the selective serotonin re-uptake inhibitors (SSRIs), which have a response rate of around 65%. Of interest is that emotional disturbances like irritability, aggressiveness and anxiety also respond to treatment with SSRIs. A comprehensive treatment of late life depression, which includes social and psychological support, has a response rate of 80-90%.     

Discontinuation of interferon beta therapy in multiple sclerosis patients with high pre-treatment disease activity leads to prompt return to previous disease activity

Recently, several studies using transcranial sonography (TCS) have resulted in the alteration of the mesencephalic midline in patients with depression. We aimed to investigate and compare sonographic abnormalities in the brainstem raphe (BR) in patients with Parkinson's disease (PD) and controls, according to presence of depression. Study participants totaled 61 patients with PD (29 PD without depression, 32 PD with depression) and 41 controls. Results indicated that decreased BR echogenicity was much higher in PD patients with depression (PD+D) than in those without depression (PD-D). Of the 61 PD patients, 32 (52.4%) had depression as diagnosed by psychiatric assessment, and 13 (17.6%) were excluded, due to insufficient temporal windows. Based on these results, the use of TCS with respect to the mesencephalic midline may be useful in detecting depression, a risk factor for the development of PD.     

Organic bases of late-life depression: a critical update

Late-life depression (LLD) is frequently associated with cognitive impairment and increases the risk of subsequent dementia. Cerebrovascular disease, deep white matter lesions, Alzheimer disease (AD) and dementia with Lewy bodies (DLB) have all been hypothesized to contribute to this increased risk, and a host of studies have looked at the interplay between cerebrovascular disease and LLD. This has resulted in new concepts of LLD, such as “vascular depression”, but despite multiple magnetic resonance imaging (MRI) studies in this field, the relationship between structural changes in human brain and LLD is still controversial. While pathological findings of suicide in some elderly persons revealed multiple lacunes, small vessel cerebrovascular disease, AD-related lesions or multiple neurodegenerative pathologies, recent autopsy data challenged the role of subcortical lacunes and white matter lesions as major morphological substrates of depressive symptoms as well as poorer executive function and memory. Several neuropathological studies, including a personal clinico-pathological study in a small cohort of elderly persons with LLD and age-matched controls confirmed that lacunes, periventricular and deep white matter demyelination as well as AD-related lesions are usually unrelated to the occurrence of LLD. In the same line, neuropathological data show that early-onset depression is not associated with an acceleration of age-related neurodegenerative changes. Very recent data on the critical role of glia-modulating neuronal dysfunction and degeneration in depression are discussed.