强啡肽与中枢神经系统损伤

八十年代初提出内源性阿片肽与中枢神经系统损伤有关,近年研究提示可能是强腓肽参与损伤后继发性病理生理改变,应用其拮抗剂有助于损伤后功能恢复.     

β-内啡肽与中枢神经系统损伤的研究进展

近年来研究发现急性中枢神经系统损伤后血浆、脑脊液中β-内啡肽含量明显升高。采用内源性阿片肽受体拮抗剂治疗,能有效地改善脑脊髓供血、促进神经功能恢复。并认为β-内啡肽可能与继发性中枢神经系统损伤的发病机理有关。     

持续颅内压监测下纳洛酮对重症脑外伤患者临床分析

目前认为内源性阿片肽参与了脑卒中水肿的发生发展,是加重其继发性神经系统损伤因素之一[1]。同时有效监测患者的颅内压变化,是指导患者术后治疗的有效措施,本文探讨在持续监测颅内压的情况下,使用阿片受体拮抗剂纳洛酮治疗重症脑外伤术后患者的临床疗效,现报告如下。     

纳洛酮在重型颅脑损伤救治中的应用研究

急性重度颅脑损伤后，机体释放出大量内源性阿片肽，其中β～内啡肽(β～EP)产生广泛的病理、生理效应，加重继发性脑损害，纳洛酮为阿片受体特异性拮抗剂，与阿片样受体的亲和力比与β-内啡肽等吗啡样物质大，能竞争性阻止并取代β-内啡肽类吗啡样物质的作用，达到对受损脑组织的保护作用。国内对部分学通过实验证明其对脑损伤具有良     

颅脑损伤后凝血功能障碍的机制及干预措施

正颅脑损伤伤后发生凝血功能障碍是神经外科急诊中的一种常见的并发症,发生率较高,在56%~70%[1]。颅脑损伤后的凝血功能障碍主要包括外伤后高凝状态和继发性纤溶系统亢进,使颅脑损伤后再出血和死亡的风险大大提高,严重影响病人预后。本文就颅脑损伤后凝血功能障碍的机制及干预措施进行综述。1发病机制在生理条件下,凝血功能主要通过内源性或外源性途径实现,并使凝血与纤溶系统之间保持一种平衡。颅脑损伤后出现凝血功能障碍,使正常的凝     

镁离子在治疗缺血性颅脑损伤中的研究进展

Mg2 作为一种内源性保护因子,在脑外伤后脑内神经生化及代谢的异常连锁反应导致的神经元延迟性或继发性损伤中起着重要保护作用.本文对Mg2 在缺血性颅脑损伤中的保护机制及临床应用等方面进行综述.     

重型颅脑创伤多参数脑缺血指标与预后关系的研究

创伤性脑损伤是一个非常严重的社会医学问题,美国每年有约150万的颅脑外伤患者,57％的重型颅脑创伤患者预后不良,尸检发现,颅脑外伤死亡的患者约90％都存在脑缺血,脑缺血是继发性颅脑创伤的重要原因之一[1].在颅脑创伤患者中,脑缺血是继发性损伤中最常见的病理改变.本文通过62例资料分析研究脑缺血指标与预后的关系.     

急性脑外伤后血清中泌乳素含量的变化及其临床意义

脑外伤患者除创伤的直接损害作用外,继发性脑损害更是不容忽视。这种继发性损害与原发性脑损伤后所致的多种内源性自体损害因子的释放以及机体内分泌功能紊乱有关[1,2]。我们对男性急性脑外伤患者血清中泌乳素含量的变化规律及其与损伤程度、损伤部位和预后的关系进行了探讨。1     

热量限制在颅脑创伤中的应用进展

颅脑创伤(Traumatic Brain Injury,TBI)是世界范围内年轻人和成年人致死、致残的最重要的原因之一,每年 TBI 罹患人数超过1000万[1].TBI 后脑组织的细胞死亡一部分由直接机械损伤(原发性)引起,但是更多是由损伤后一系列生化改变(继发性)引起的.这些继发性损伤包括：细胞因子释放引起的炎性反应,谷氨酸毒性,突触功能障碍,活性氧、活性氧损伤,神经元功能障碍等,这些可进一步引起线粒体功能障碍,也可使细胞死亡信号级联效应放大,最终导致神经元的死亡[2－6].对这些病理生理机制进行深入的研究可为临床的治疗提供理论依据。     

外伤性硬膜下积液治疗探讨

外伤性硬脑膜下积液是颅脑损伤的一种特殊类型,属于继发性脑损伤,发病率约5％[1],多发生于中、重型颅脑损伤后,由脑脊液的循环动力学异常而引起,传统的治疗采取钻孔引流的方法.我院2001年6月～ 2010年6月共收治118例硬膜下积液病人,依分型采取不同的治疗方案,取得良好效果,现总结如下.     

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 -