帕金森病药物治疗的现状及进展

帕金森病是一种慢性中枢神经系统神经退行性疾病，主要以静止震颤，肌肉僵直和运动减少为临床症状，其确切病因尚不清楚，虽然目前已经提出了很多帕金森病的病因学说，但是只有多巴胺缺失学说得到大多数学者的公认。目前国内外对帕金森病的治疗均以药物治疗为主，本文对相关药物治疗的现状及进展做一简要的综述。     

帕金森病的诊断和治疗进展

帕金森病(PD)是继阿尔茨海默病之后第二大神经变性疾病,诊断需要根据患者主要的临床症状,如手足徐动、静止型震颤、肌强直或其他非运动特征,如嗅觉减退和快速眼球运动病变而决定,同时需要与原发性震颤相鉴别。帕金森病的治疗提倡从早期的体疗干预开始,当患者行动障碍影响工作和生活质量时加用药物治疗,手术的选择是在患者出现药物过敏或治疗无效时使用。目前一种新的非创伤性的治疗,磁共振引导下的聚焦超声刀(也称磁波刀)正在以有效的方式被采用,但传统的深部脑刺激手术仍然是临床上较为常用的手术。新的药物如长效左旋多巴胺类药和磁波刀这样新的技术希望能帮助患者更好地改善生活质量。     

我国科学家发现重复经颅磁刺激改善阿尔茨海默病患者认知障碍的潜在机制

正阿尔兹海默病(Alzheimer’s Disease,AD)是一种随年龄增长而大概率发生的神经退行性疾病,严重危害老年人健康,目前缺乏有效治疗药物。研究表明重复经颅磁刺激(repetitive Transcranial Magnetic Stimulation,rTMS)作为一种非侵入性脑刺激治疗方案,可缓解轻-中度AD患者认知障碍相关症状,但相关作用机制尚不清楚。     

帕金森发病机制及其最新治疗策略

帕金森病(Parkinson’s disease, PD)是一种与年龄相关的神经退行性疾病,患者大脑黑质中的多巴胺能神经细胞随着时间的推移逐渐死亡.帕金森病主要表现为静止性震颤、运动迟缓、僵硬,最终无法控制运动功能而导致严重残疾.PD的发病机制复杂且尚不清楚,治疗方案也收效甚微.从氧化应激、线粒体功能缺陷、蛋白过度表达和聚集、神经炎症以及Ca~(2+)稳态受损方面介绍帕金森病的发病机制及其最新治疗策略,为后续帕金森病的治疗提供理论基础.     

不同运动形式对参与人群认知功能改善效果的研究综述

[目的]探究外文文献中关于不同运动处方对认知功能改善效果的有效性这一问题的研究进展。[方法]采用文献资料法系统综述EBSCO Host等数据库(2008—2017年)有关运动对认知功能的有效影响文献556篇。[结果]健康的未成年通过有氧运动,抑制、工作记忆和转换的能力显著提高(P0.05),中青年及老年人群通过一定周期的有氧运动、抗阻运动和联合运动后,抑制、工作记忆、转换、注意力、记忆力、计算力和回忆能力方面都得到了一定程度的改善。随机对照试验表明有氧运动、抗阻运动和联合运动对老年群体中阿尔茨海默病的改善效果较好。[结论]体育锻炼可以改善人们日常活动的性能,对认知障碍老年人群神经精神障碍、抑郁症状、心血管和心肺功能也有一定的改善作用;运动处方的选择要结合参与者身心素质的现实状态,这样科学实施才能取得良好效果。     

帕金森病研究进展

 帕金森病（PD）是常见的神经系统变性疾病,典型的PD病理表现为脑中黑质多巴胺神经元退行性变和路易小体沉积,但这些改变不能完全解释PD产生的临床症状,目前PD的发病原因及机制尚不明确,尚未建立系统的早期诊断及保护治疗方式。随着诊断及治疗技术的提高,生物学标记物、脑网络及神经调控等有望为PD早期诊断、机制探索及个体化治疗提供基础。本文综述了PD在生物学标记物、脑网络研究及神经调控治疗领域的研究进展。     

运动病的神经通路研究进展

由失重和头部运动而引起的前庭植物神经的反应称为运动病,其症状常表现为恶心、呕吐、肠胃不适、食欲低下、头痛等．前庭一内脏神经通路活动的异常是运动病的主要诱因,揭示前庭信号影响内脏活动的神经通路是阐明运动病发生机理的基础．综述了近年来关于运动病神经基础研究的进展．     

阿尔茨海默病大脑皮层的磁共振影像分析

阿尔茨海默病是一种进行性神经退化痴呆症,其特征是大脑皮层厚度萎缩和认知功能逐步下降。通过分析阿尔茨海默病患者及其早期症状轻度认知障碍患者的大脑皮层厚度变化,我们可以了解该疾病的发生发展机理,为临床早期诊断和预防提供帮助。核磁共振成像技术的出现为我们对该疾病大脑皮层变化模式的研究提供了很好的手段。本文工作是从图像处理的角度分析了阿尔茨海默病和轻度认知障碍患者大脑皮层磁共振影像结构。     

基于互信息的帕金森病脑皮层功能连接

帕金森病的早期症状是很难察觉的,目前还没有一个明确的生物标志物可以准确地检测出早期的帕金森病。本文为了探究帕金森病的潜在生物标志物,分析15名帕金森病患者和15名健康对照者闭眼状态下的溯源后的脑电信号。首先,使用互信息测量两组受试者的大脑各个区域之间的功能连接。之后,对两组受试者之间的每个连接对的互信息值进行独立样本t检验,检测两组受试者之间显著差异的连接边。最后,将具有显著差异的连接边作为特征进行分类。结果表明,帕金森病患者的大脑各个区域之间的互信息值整体小于健康对照组,并发现在额顶叶和顶枕叶之间的功能连接差异十分显著（p<0.01）。利用互信息功能连接指标对帕金森病患者和健康对照组分类时,测试准确率为76.7%,验证了基于互信息的脑功能连接对帕金森病研究的有效性。这些发现表明额顶叶和顶枕叶之间功能连接性的降低可能是帕金森病的一个潜在生物标志物。本文系首次使用互信息这一功能连接指标对帕金森病进行研究,这为帕金森病的神经机制研究提供了一个新的途径。     

神经胶质细胞与HIV相关神经认知障碍

HIV-1相关神经认知障碍(HIV-1 associated neurocognitive disorder,HAND)是艾滋病患者中枢神经系统(central nervous system,CNS)的常见并发症,其患病率高达40%~60%,是40岁以下成人痴呆的最主要原因之一;患者从确诊到死亡的平均时间约为4~6个月,且其发病机理尚待研究.已有的研究表明,HIV-1不感染神经元,但在HAND的发病机制中,神经胶质细胞的过度活化和由此而引发的神经炎症起着重要的作用.本文就神经胶质细胞在HAND的发生发展中的作用进展进行综述.     

阿尔茨海默病伴发视觉障碍研究进展

 阿尔茨海默病（AD）是老年人群常见的神经变性疾病,多以记忆力损害为首发症状,逐渐出现进行性认知功能受损和精神行为症状,对家庭和社会带来沉重的经济和照护负担。AD早期症状不明显,待诊断明确后的治疗效果差,因此,早期诊断尤为重要。研究发现,AD患者可出现视觉障碍,但尚无流行病学数据。目前AD的治疗包括非药物及药物等综合手段,AD伴发视觉障碍的治疗尚需研究。本文主要介绍AD视觉障碍的临床症状、发生机制、检测及评价手段,包括光学相干体层扫描、视觉诱发电位、视网膜微血管检查及神经影像学,以对AD患者的视觉障碍进行全面评价,寻找特异、敏感及简便的AD评估手段,为AD的早期诊断及早期干预提供依据。     

Hippocampal abnormalities in amnesic patients revealed by high-resolution magnetic resonance imaging

The identification of brain structures and connections involved in memory functions has depended largely on clinico-pathological studies of memory-impaired patients, and more recently on studies of a primate model of human amnesia. But quantitative neurobehavioural data and detailed neuropathological information are rarely available for the same patients. One case has demonstrated that selective bilateral damage to the hippocampus causes a circumscribed memory impairment in the absence of other intellectual deficits. This finding, in conjunction with evidence from humans and monkeys, indicates that the hippocampus together with adjacent and anatomically related structures is essential for the formation of long-term memory, perhaps by virtue of the extensive reciprocal connections between the hippocampal formation and putative memory storage sites in the neocortex. Although cognitive studies of amnesia provide useful information about the functional organization of normal memory, it has not usually been possible to relate memory impairment to anatomy in living patients. We have developed a high-resolution protocol for imaging the human hippocampus with magnetic resonance that permits visualization of the hippocampal formation in substantial cytoarchitectonic detail, revealing abnormalities in patients with severe and selective memory impairment.     

认知、隐喻和语义

认知语言学认为,和其他认知领域一样,语义结构反映了人们在与现实接触的经验中形成的心理范畴,来源于语言使用者的认知思维.隐喻作为一种重要的认知手段,对语言的更新和发展起着十分重要的作用.把隐喻性的认知机制运用到语言学习之中,可提高理解和使用语言的能力.     

认知潜意识:潜意识研究的新动向

认知潜意识是根据认知的信息加工理论提出来的,它包括所有不能觉知的认知过程。认知心理学家进行了许多实验研究,用以证实认知潜意识的存在及其在个体心理机能中的重要影响。认知潜意识的提出,扩大了潜意识的研究领域,为我们提供了认识潜意识现象的新视野。认知潜意识的研究以实验为取向,有助于我们更为客观地认识潜意识现象。     

MRS study on lentiform nucleus in idiopathic Parkinson‘s disease with unilateral symptoms

OBJECTIVE: To investigate changes in magnetic resonance spectroscopy (MRS) of lentiform nucleus during the early stage of Parkinson's disease. METHODS: Twenty-five patients with idiopathic Parkinson disease with unilateral symptoms (IPDUS) and 25 healthy volunteers were enrolled in this study. MRS of the lentiform nucleus in each patient was taken and then concentrations of N-acetylaspartate (NAA), Creatine (Cr) and Choline (Cho) were calculated. RESULTS: Compared to that in the control, NAA/ (Cho+Cr) was significantly lower in the lentiform nucleus contralateral to symptoms and even that in the ipsilateral side in IPDUS patients (all P<0.05); while there was no difference between the two sides in the healthy volunteer (P>0.05). The ratio of NAA/(Cho+Cr) ipsilateral to the sympatomatic side of the patient was also lower than that of the control (P<0.05). CONCLUSIONS: There might be some changes with MRS on the lentiform nucleus during the early stage of idiopathic Parkinson's disease with unilateral symptom. MRS may be one of the reliable methods for early or even sub-clinical diagnosis.     

The corticomotoneurone connection is normal in Parkinson's disease

Voluntary movements in Parkinson's disease are initiated and executed slowly. It is assumed that the motor cortex and its output pathway are intact and that bradykinesia is due to abnormal motor commands delivered to a normal corticospinal system. We have tested this assumption using electrical stimulation of the motor cortex through the scalp in three patients with severe Parkinson's disease, studied during fluctuations from relatively normal mobility when receiving drugs (ON) to severe bradykinesia when not receiving drugs (OFF). Thresholds and latencies for motor cortex stimulation to excite thumb flexor muscles and the resulting fast mechanical responses were the same in both ON and OFF conditions, even though the patients were unable to execute fast thumb flexion movements voluntarily when OFF. We conclude that the excitability and conduction velocity of the corticospinal motor pathways are normal in Parkinson's disease.     

Melanized dopaminergic neurons are differentially susceptible to degeneration in Parkinson's disease

In idiopathic Parkinson's disease massive cell death occurs in the dopamine-containing substantia nigra. A link between the vulnerability of nigral neurons and the prominent pigmentation of the substantia nigra, though long suspected, has not been proved. This possibility is supported by evidence that N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolite MPP+, the latter of which causes destruction of nigral neurons, bind to neuromelanin. We have directly tested this hypothesis by a quantitative analysis of neuromelanin-pigmented neurons in control and parkinsonian midbrains. The findings demonstrate first that the dopamine-containing cell groups of the normal human midbrain differ markedly from each other in the percentage of neuromelanin-pigmented neurons they contain. Second, the estimated cell loss in these cell groups in Parkinson's disease is directly correlated (r = 0.97, P = 0.0057) with the percentage of neuromelanin-pigmented neurons normally present in them. Third, within each cell group in the Parkinson's brains, there is greater relative sparing of non-pigmented than of neuromelanin-pigmented neurons. This evidence suggests a selective vulnerability of the neuromelanin-pigmented subpopulation of dopamine-containing mesencephalic neurons in Parkinson's disease.