脑卒中急性期患者卒中后抑郁的发生率及其危险因素

目的 探讨脑卒中急性期患者卒中后抑郁(PSD)的发生率及其危险因素.方法 连续入组的发病24 h内入院的急性脑卒中患者127例,根据入院14 d内汉密尔顿抑郁量表(17项)和蒙哥马利抑郁量表评分分为PSD组和非PSD组,分析PSD与性别、婚姻状况、年龄、文化程度、卒中类型、病灶部位、脑梗死容积、高血压、糖尿病、冠心病、吸烟、饮酒、体质量指数(BMI)、卒中家族史、卒中病史、颈动脉斑块、美国国立卫生研究院卒中量表(NIHSS)评分、Barthel指数(BI)和简易精神状态检查(MMSE)量表评分等临床因素的关系.结果 本组PSD发生率为37.0%(47例).PSD组脑梗死比率、伴高血压病比率、脑梗死容积、入院时NIHSS评分均明显高于非PSD组,BI和MMSE评分均明显低于非PSD组(P＜0.05～0.01).多因素Logistic回归分析显示脑梗死、高血压和入院时BI与PSD独立相关(OR=5.084,95%CI:1.255～20.592,P=0.023;OR=4.846,95%CI:1.447～16.225,P=0.010;OR=0.966,95%CI:0.951～0.981,P＜0.001).结论 脑卒中急性期患者PSD的发生率较高,脑梗死、高血压和入院时BI是PSD的独立危险因素.     

卒中后3个月内抑郁的累计发生率及其相关危险因素研究

目的 观察卒中（包括脑梗死和脑实质内出血）后3个月内卒中后抑郁（post-stroke depression,PSD）的发生率,探讨与PSD发生相关的人口学和临床危险因素。方法 连续收集2008年4月至2009年12月住院的卒中患者（包括脑梗死和脑实质内出血）314例。收集患者的人口学资料及相关临床指标如美国国立卫生院神经功能缺损评分（National Institute of HealthStroke Scale,NIHSS）、改良Rankin量表评分（modified Rainkin Scale,mRS）和简易精神状态检查表（minimental status examination,MMSE）评分。在发病90±7 d,使用世界卫生组织复合性国际诊断交谈3.0中文版（The World Health Organization Composite International Diagnostic Interview,WHO-CIDI 3.0）对所有患者进行访谈,按照精神疾病诊断与统计手册-IV（Diagnostic and Statistical Manual of MentalDisorders-IV,DSM-IV）的诊断标准作出抑郁的诊断。结果 PSD在卒中后3个月的累计发生率为29%（91/314）,其中重性抑郁76例（24.2%）,轻性抑郁15例（4.8%）。PSD组和non-PSD组之间性别、既往抑郁病史差异有统计学意义（P <0.01）;PSD组发病后14 d的NIHSS、mRS和发病后90 d的mRS大于non-PSD组（P <0.01）。多因素分析结果显示：性别[比值比（Odds ratio,OR）：2.178,95%可信区间（confidence interval,CI）：1.219～3.892,P <0.01]、既往抑郁病史（OR：5.762,95%CI：2.958～11.223,P <0.01）、发病后14 d的残障水平（OR：1.520,95%CI：1.212～1.907,P <0.01）是与PSD发生相关的独立危险因素。结论 卒中后3个月内,PSD的累积发生率为29%,说明PSD是卒中后的常见并发症,应该予以高度重视。女性、既往抑郁病史和发病后14 d的残障水平是卒中后3个月内发生抑郁的3个独立危险因素。     

急性缺血性卒中后抑郁的相关危险因素分析

目的探讨急性缺血性卒中后抑郁(PSD)的发生率及其相关危险因素。方法 185例经CT或MRI证实的急性缺血性卒中患者根据精神障碍诊断和统计手册第5版(DSM-V)标准和24项Hamilton抑郁量表(HAMD)评分分为PSD组和non-PSD组;分析PSD社会人口学资料、血管危险因素、相关生化指标、NIHSS、Barthel指数(BI)、MMSE等相关因素对PSD的影响。结果本组PSD发生率为40.54%(75例),主要以轻、中度抑郁为主;与non-PSD组比较,PSD组患者糖尿病发生率高(P=0.044),神经功能缺损程度重、日常生活活动能力差(P=0.000,P=0.001),MMSE评分降低(P=0.000),而超敏C-反应蛋白(hs-CRP)和同型半胱氨酸(Hcy)水平升高(P=0.000,P=0.006);其中BI、MMSE评分与HAMD评分呈负相关(均P0.05),而NIHSS评分、hs-CRP和Hcy与HAMD评分呈正相关(均P0.05);Logistic回归分析提示,低MMSE评分、高NIHSS评分及高hs-CRP和Hcy水平可能是急性缺血性PSD的独立危险因素。结论 PSD主要以轻、中度抑郁为主;PSD与糖尿病病史、认知功能障碍、神经功能缺损程度、hs-CRP和Hcy水平密切相关。     

急性脑卒中患者营养不良、卒中后并发症及不良预后的危险因素分析

目的 探讨影响急性脑卒中患者营养不良、卒中后并发症及不良预后的危险因素.方法 收集122例急性脑卒中患者的一般资料,进行营养状况和神经功能缺损程度评估.3个月后采用改良Rankin量表(mRS)评估预后.分析各因素与急性脑卒中患者营养不良、卒中后并发症及不良预后的关系.结果 随访结束时,共91例患者纳入本次研究.年龄及NIHSS评分为入院时营养不良的危险因素(P＜ 0.05～0.001);年龄、高胆固醇血症、入院营养不良、鼻饲为7d时营养不良的危险因素(P＜0.05 ～0.001).多因素Logistic回归分析显示,入院营养不良为7d发生营养不良的独立预测因素(OR=14.15,95％CI:3.32～61.76,P＜0.001).年龄、入院NIHSS评分、入院营养不良、鼻饲、7d时NIHSS评分、7d时营养不良及营养状况恶化为发生并发症的危险因素(均P＜0.01).多因素Logistic回归分析显示,入院NIHSS评分及入院营养不良为并发症的独立预测因素(OR=1.11,95％CI:1.04 ～ 1.48,P＜0.05;OR=6.56,95％CI:1.18 ～42.72,P＜0.05).年龄、入院NIHSS评分、7d时NIHSS评分、7d时营养不良及营养状况恶化为预后不良的危险因素(P ＜0.05 ～0.01).多因素Logistic回归分析显示,7d时营养不良及7d时NIHSS评分为预后不良的独立预测因素(OR =-4.32,95％CI:1.15 ～ 18.89,P＜0.05;OR=1.81,95％CI:1.21 ～2.43,P＜0.01).结论 入院营养不良为7d发生营养不良的独立危险因素,入院NIHSS评分及营养不良为并发症的独立危险因素,7d时营养不良及NIHSS评分为预后不良的独立危险因素.     

首发脑梗死患者卒中后抑郁与卒中部位的关系

目的 研究首次发病的脑梗死患者卒中后抑郁(PSD)与卒中部位之间的关系.方法 选取340例经CT/MR确诊的脑梗死患者,其中169例抑郁自评量表指数大于或等于0.5者为PSD组,采用χ2检验和Logistic回归分析PSD与卒中部位之间的相关性.结果 脑梗死患者PSD的患病率为49.7%(169/340),其中额叶卒中患者PSD的患病率为66.7%,其他部位卒中患者PSD患病率为47.3%,两者差异有统计学意义(χ2=5.51,P=0.02).分层及回归分析显示额叶卒中是卒中6个月内PSD患病的独立危险因素,调整年龄、文化程度、梗死类型、患高血压、患心脏病、日常生活活动能力评分、认知功能后,额叶卒中患者PSD的患病风险是其他部位卒中患者的2.42倍(P=0.02,RR=2.42,95%CI:1.17-5.03).结论 脑梗死患者PSD的患病率较高,额叶卒中患者在卒中后6个月内有更高的PSD患病风险.     

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。     

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。     

缺血性脑卒中NIHSS评分与卒中抑郁的相关性分析

目的探讨缺血性脑卒中患者美国国立卫生研究院卒中量表(NIHSS)评分与卒中后抑郁(PSD)的相关性。方法选择2017-10—2018-10期间在湖南省脑科医院就诊的缺血性脑卒中患者150例,收集病史资料及NIHSS评分,并跟踪观察1个月,以中国精神障碍诊断和分类标准第3版(CCMD-3)的抑郁诊断标准诊断PSD,采用汉密尔顿抑郁量表(HAMD,17项版本)评估抑郁症状的严重程度。将研究对象分为非PSD组(HAMD评分≤6分)和PSD组(HAMD评分7分),再将PSD组进一步分为轻度抑郁亚组(HAMD评分7分且≤16分)、中-重度抑郁症亚组(HAMD评分≥17分)。计算PSD患病率,并分析影响PSD患病率的相关因素(性别、高血压、糖尿病、高血脂、房颤、吸烟、饮酒、既往有无脑卒中史),以及抑郁症状的严重程度(HAMD评分)与NIHSS评分的相关性。结果缺血性脑卒中后1个月内PSD的患病率为34.0%(51例),其中轻度抑郁症状患者占64.7%(33例)。PSD组既往脑卒中史的构成比(83.3%)显著高于非PSD组(30.3%;P0.05)。PSD组NIHSS评分与HAMD评分具有相关性(OR=5.231,95%CI=1.204～10.154,P=0.01)。结论 PSD以轻度抑郁症状为主,既往有脑卒中病史者患病率高,且NIHSS评分与抑郁症状的严重程度具有相关性,NIHSS评分越高,PSD患病几率越大。     

青年人群卒中后抑郁与阿替普酶静脉溶栓相关性的临床研究

目的 探讨阿替普酶静脉溶栓是否可以降低青年缺血性脑卒中患者卒中后抑郁(PSD)的发生率以及青年卒中患者PSD的影响因素。方法 回顾性分析210例青年缺血性脑卒中患者临床资料,根据是否使用阿替普酶静脉溶栓分为溶栓组（110例）和非溶栓组（100例）。比较2组患者在发病14 d及发病3个月时PSD的发生率。采用单因素分析及Logistic回归分析青年卒中患者PSD的影响因素。结果 发病14 d时溶栓组和非溶栓组青年卒中患者PSD发生率差异有统计学意义(χ²=3.988,P<0.05);发病3个月时2组PSD发生率差异无统计学意义(χ²=1.432,P>0.05)。Logistic回归分析显示NIHSS评分、是否静脉溶栓为发病14 d时发生PSD的影响因素;NIHSS评分、社会支持为发病3个月时发生PSD的影响因素。结论 青年卒中患者PSD发生率较高;阿替普酶静脉溶栓可以降低青年卒中患者PSD的发生率。     

卒中后抑郁与患者神经功能及再发卒中风险的关系

目的探讨卒中后抑郁与卒中患者神经功能以及卒中复发的关系。方法回顾性分析2017年3月至2018年3月于我科就诊并完成1年随访的脑卒中患者,以卒中后抑郁(PSD)患者108例为PSD组,并选取112例同期治疗的不伴有PSD患者作为无PSD组,分析PSD与患者远期功能恢复和1年内再发风险的关系。结果中、重度PSD患者的NIHSS评分、1年内卒中复发率、mRS评分均高于无PSD和轻度PSD患者(P0.05),Pearson相关模型显示SDS评分与NIHSS评分呈正相关(r=0.628,P0.001);多因素Logistic回归分析显示,收缩压、PSD、卒中后2周NIHSS评分、卒中后2周mRS评分均为1年内卒中再发的危险因素。结论 PSD与患者远期功能恢复以及1年内再发卒中风险呈显著相关性,PSD患者远期功能恢复较差,加强早期对PSD的发现与干预。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.     

Summary of Legislation of 1933 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -