脑损伤修复与功能重建干预策略

脑是人体的生命中枢,脑功能损害将严重影响人的生存与健康.脑损伤是造成脑功能损害的直接原因,具有发病率高,致死、致残率高的特点.无论是脑创伤、脑部缺血或出血,其共同病理特点都是神经元严重受损、缺失或死亡,造成神经功能障碍,患者出现偏瘫、失语、视力丧失、智力及意识障碍等症状,严重影响患者生活质量.在临床上,脑损伤主要包括颅脑损伤和卒中,前者因机械性损伤所致,后者因脑血管梗死或出血引起,其中缺血性卒中(缺血性脑损伤)最为多见,占80%[1].     

脑损伤修复与功能重建干预策略

脑是人体的生命中枢,脑功能损害将严重影响人的生存与健康.脑损伤是造成脑功能损害的直接原因,具有发病率高,致死、致残率高的特点.无论是脑创伤、脑部缺血或出血,其共同病理特点都是神经元严重受损、缺失或死亡,造成神经功能障碍,患者出现偏瘫、失语、视力丧失、智力及意识障碍等症状,严重影响患者生活质量.在临床上,脑损伤主要包括颅脑损伤和卒中,前者因机械性损伤所致,后者因脑血管梗死或出血引起,其中缺血性卒中(缺血性脑损伤)最为多见,占80%[1].     

血管内治疗对认知功能影响的多重性

颅内大动脉粥样硬化性狭窄不仅与缺血性卒中相关,同时还与认知功能障碍密切相关。脑低灌注是此类患者认知损害的重要病理生理学机制,这种因血流动力学改变所引起的认知损害呈可逆性,虽然颈动脉内膜切除术和支架成形术对改善脑组织灌注有效,但术中微栓塞和术后高灌注可损伤认知功能,如此造成患者术后认知功能的改善结果不尽一致。关注颅内动脉狭窄患者的认知功能预后,不断改进血管内治疗方式和围手术期管理模式,方可使患者真正受益。     

脑微出血与卒中

脑微出血作为一种具有出血倾向的脑小血管病变,随着影像学技术的发展,其检出率越来越高.目前,大量研究表明,脑微出血与缺血性卒中、脑出血和溶栓或抗栓治疗后症状性脑出血关系密切.本文旨在探讨脑微出血与上述疾病的相关性,将有利于脑微出血患者卒中防治策略的制定.     

缺血性卒中影像学研究

脑卒中是一种突然起病的脑血液循环障碍性疾病,系指脑血管病患者因各种诱发因素导致颅内动脉狭窄、闭塞或破裂所引起的急性脑血液循环障碍,亦称脑血管意外。其临床表现为短暂性或永久性神经功能障碍的症状与体征,分为出血性和缺血性卒中,其中67%～80%患者为急性缺血性卒中,神经功能的康复与脑组织存活程度密切相关。因此,应于高危因素、缺血和出血等可逆性神经功能损伤出现之前明确诊断并及时处理。近年来,CT和     

缺血性卒中与免疫反应

【摘要】 免疫和炎症反应是缺血性卒中病理过程的重要组成部分,自然免疫和适应性免疫都参与
这一过程。免疫反应不仅仅造成炎性损伤,引起外周血和免疫器官出现相应的免疫调节,还在缺血
性脑损伤后的脑组织修复和重建中发挥重要作用。抑制缺血诱导的炎症反应和进行免疫调节具有脑
保护和脑组织修复/重建作用,可能是缺血性脑损伤的一种新的治疗途径。目前关于缺血性脑损伤
的免疫治疗还存在诸多问题,需要深入了解免疫系统功能和脑缺血损伤之间的相互作用,以确保免疫
治疗的可行性、有效性和安全性。     

SDF-1/CXCR4轴与骨髓间充质干细胞修复缺氧缺血性脑损伤

缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)是一种常见的中枢神经系统损伤,其发病率高,可造成瘫痪、智力低下等后遗症,严重影响患者生活质量,给家庭和社会带来巨大负担,目前尚无理想治疗方法 .     

缺血性脑卒中后神经可塑性与运动功能恢复研究进展

卒中是导致死亡的第1位原因,也是导致成人致残的首要原因[1].在既往报道的大量缺血性脑卒中病例中,仅少数患者完全恢复,大多数患者残留有不同程度的永久性缺陷[2].然而,尽管卒中造成的功能损害很严重,但由于受损神经的重塑及相应部位的功能重组,受损功能仍能得以不断的恢复.本综述旨在介绍缺血性脑卒中后神经可塑性与运动功能的恢复的关系及其可能机制,为康复治疗提供有价值的资料.     

基因芯片技术与缺血性脑损伤的基础研究

缺血性脑损伤通常导致神经元死亡或功能障碍,从而引发脑功能障碍.细胞死亡或功能障碍往往伴随或源自特定基因表达的变化.因此,确定参与缺血性脑损伤过程及损伤后细胞修复及塑型过程的基因,对损伤机制及基于该损伤机制而采取适当的治疗措施是至关重要的.基因芯片技术是20世纪90年代发展起来的一项前沿生物技术,它从根本上改变了生理学和生物技术的观念和效率[1].其应用高密度的显微阵列进行大批量的基因筛选,只有巨大的功能信息处理能力,近年来在缺血性脑损伤的研究中得以应用,为该领域研究提供了丰富信息.     

电针刺激对脑损伤患者内源性阿片肽的影响

急性脑损伤所致的神经功能障碍除原发性因素造成脑损害之外,许多继发性因素致使其近期病情加重或出现不可逆性神经功能障碍。研究证明,原发性脑损伤后,机体产生一系列应激反应,部分体内所产生的物质会造成脑二次损伤。其中包括:凝血功能障碍;部分炎性介质释放;兴奋性氨基酸的释放增加等。尤其是部分内源性阿片肽被认为是造成脑二次损伤的因素之一。电针刺激技术用来治疗神经系统疾病康复期患者已很成熟,且证明是有效的,甚至应用于早期促醒。为     

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.