重视卒中后情感障碍

卒中后可出现各种情感障碍,如抑郁、焦虑、淡漠、情感失禁和躁狂。卒中后情感障碍会加重认知功能的损害和阻碍神经功能的恢复,影响患者的预后和生活质量。虽然卒中后情感障碍发病率高,但在临床实践中其诊断率却很低,其主要原因是医师及家属一般只重视患者的躯体功能康复情况,忽视了患者情感方面的变化。1卒中后抑郁卒中后抑郁(post-stroke depression,PSD)是最常见的卒中后情感障碍之一,文献报道的PSD发病率为18%～78%,综合估计值     

卒中后焦虑和抑郁障碍的心理干预

<正>卒中(stroke)是突发性的脑部疾病,患者可因脑内动脉狭窄、闭塞甚至破裂导致脑部血液供应障碍和一过性/永久性脑功能损伤[1]。卒中后情感障碍是卒中的常见并发症之一,而焦虑和抑郁又是卒中后情感障碍最常见的类型。急性卒中常并发焦虑障碍,发生率为40%~50%[2],而有1/3卒中后患者发生卒中后抑郁(post-stroke depression,PSD)[3],国外Paolucci等[4]对卒中患者长期追踪观察发现,PSD的发生率为36%,轻度抑郁占80%。目前,     

卒中后抑郁的流行病学及临床特点

卒中后抑郁(poststroke depression,PSD)是卒中常见的并发症之一,是在有明显临床症状的卒中后出现的以情绪低落、兴趣减退、睡眠障碍等为特征的情感障碍性疾病,是继发性     

从关注卒中患者情感障碍入手,提升血管神经病学专业研究生的人文素养——浅谈卒中后抑郁教学体会

目的探讨卒中后抑郁教学对提升血管神经病学研究生人文素养的成效。方法对首都医科大学附属北京天坛医院目前在读的血管神经病学研究生开展卒中后抑郁教育及关注卒中患者情感障碍活动,评价比较教育前后研究生人文素养。结果通过卒中后抑郁教学,血管神经病学研究生对卒中患者情感障碍关注增加,沟通能力提高、临床人际关系改善。结论对血管神经病学研究生进行卒中后抑郁教学,可以很好地提升研究生人文素养。     

认知行为心理护理对脑卒中后抑郁康复的影响

脑卒中后抑郁是卒中常见的并发症之一,是在有明显的临床症状的卒中发病后出现的以情绪低落、兴趣减退、睡眠障碍为特征的情感障碍性疾病,是一种继发性抑郁,它严重影响卒中患者的生活质量,延长康复时间。     

卒中后抑郁

脑卒中是严重危害人类健康的常见病、多发病,除引起多种躯体功能障碍外,还常导致各种心理问题,抑郁则是卒中后心理障碍的常见表现之一,在脑卒中后情感障碍中居首位.卒中后抑郁障碍不仅阻碍躯体残疾的康复,增加脑卒中患者的死亡率、复发率,其本身亦严重影响患者的生活质量,是脑卒中致残的重要原因之一.随着生物医学模式向生物-心理-社会医学模式的转换,卒中后抑郁障碍引起了广泛关注[1,2].及早识别、诊断、干预卒中后抑郁障碍对于患者的躯体及心理康复具有十分重要意义.     

卒中后抑郁患者睡眠障碍的治疗

目的卒中后抑郁患者应用奥氮平治疗后症状改善情况。方法对卒中后抑郁患者86例,对照组卒中患者92例进行匹兹堡睡眠质量指数（PSQI）问卷调查,分析两组患者及组中后抑郁患者奥氮平治疗前后的睡眠情况。结果卒中后抑郁组的睡眠质量、入睡时间、睡眠时间、睡眠效率、睡眠障碍、催眠药物、日间功能等因子评分和PSQI总分均高于对照组（P〈0．05）,经奥氮平治疗后,PSQI评分明显好转（P〈0．05）。结论情感障碍可以影响患者的睡眠质量,经奥氮平治疗后睡眠障碍明显改善,显著提高了患者生活质量。     

卒中伴失语患者抑郁障碍诊断方法的研究进展

卒中后抑郁（post-stroke depression,PSD）是卒中后常见的情感障碍,严重影响患者的生活质量及预后。约有1/3的卒中患者由于失语导致交流障碍,对其是否伴有PSD及其程度无法准确评估。评价失语患者是否伴有抑郁情绪及其程度,评价工具和手段是关键。对PSD患者进行抑郁评估的手段有很多,但是尚缺乏公认的统一标准。失语患者抑郁障碍的诊断和评价工具亟待深入研究。     

卒中后抑郁促发因素研究进展

卒中后抑郁(post stroke depression,PSD)是脑血管病后常见并发症之一,它属于继发性抑郁.是指卒中发生后,以情绪低落、兴趣减退为主要表现的心境障碍或情感障碍,它不仅影响患者的生活质量,导致患者出现不良的心境体验和躯体功能障碍,同时还影响患者神经功能和肢体活动功能的康复.其发生与病灶部位、病人的年龄、性别、个性、社会、家庭、卒中后神经功能缺陷等因素有关.PSD发病机制尚不完全清楚,临床分轻、重两型,本文就卒中后抑郁的相关促发因素作一概述.     

后循环与认知障碍

传统观点认为,后循环区域不参与认知功能的形成,然而近期的研究显示后循环区域卒中也会引起不同程度的认知功能障碍:小脑可参与认知和情感的调节;脑干病变主要表现为执行功能和注意力的障碍;丘脑病变可引起广泛的神经心理学改变;枕叶卒中通常伴随大脑后动脉供血区域的病灶,在血管性痴呆的形成中起一定作用。本文就后循环区域与认知功能障碍的关系研究进展作一综述。     

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.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

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.