卒中相关睡眠障碍

<正>卒中相关睡眠障碍（stroke-related sleep disorders,SSD）是卒中后常见症状之一,SSD是指在卒中后首次出现或卒中前已有的睡眠障碍在卒中后持续存在或加重,并达到睡眠障碍诊断标准的一组临床综合征。SSD分为两种类型：卒中后睡眠障碍和卒中伴随睡眠障碍[1],主要包括失眠障碍、睡眠呼吸障碍（sleep disorderedbreathing,SDB）、昼夜节律相关睡眠-觉醒障碍（circadianrhythmsleepwakedisorders,CRSWDs）、中枢性过度睡眠、     

焦虑障碍的脑电生理研究进展

焦虑障碍临床表现复杂,目前缺乏诊断以及疗效预测相关的神经生物学指标。脑电图是 一种非侵入性的神经电生理检测工具,具有较高的时间分辨率,能锁时反映焦虑障碍认知损害的时间 进程。现对焦虑障碍的时域、频域、功能连接脑电特征的相关研究进行综述,探索焦虑障碍自上而下和 自下而上的认知加工异常,为进一步明确焦虑障碍的神经心理机制以及探索焦虑障碍预测、诊断、预后 相关的神经生物学客观指标提供参考。     

重症肌无力非神经肌肉接头处电生理改变的研究现状

重症肌无力（Myasthenia gravis，MC）是一种神经肌肉接头（NMJ）处乙酰胆碱（Ach）传递障碍的自身免疫性疾病，电生理检查表现为重复神经电刺激（RNS）及单纤维肌电图（SFEMG）等的异常。但是，近年来研究发现MG患者伴有多种中枢神经系统（CNS）损害的电生理改变，表现为脑电活动、视觉诱发电位、脑干听觉诱发电位、体感诱发电位检查等的异常。另外，Gibson等提出MG患者还存在心脏损害的电生理变化，表现为心电图的异常改变。现将电生理技术在MG非NMJ处的研究现状综述如下。     

前额叶皮层在阻塞性睡眠呼吸暂停低通气综合征 认知行为损害中作用机制的研究进展

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是一种睡眠障碍,已知的年龄（≥65岁）、男性、 肥胖、气道解剖异常等均可增加 OSAHS 的发生,但是 OSAHS 致认知行为损害的病因及发病机制尚未明 确。近年来的研究发现,前额叶皮层与 OSAHS 认知行为损害的发生密切相关,及时发现前额叶皮层中 的特异性损害可以作为早期生物标志物。OSAHS 的病理变化与前额叶皮层损伤相互作用,形成恶性循 环,促进 OSAHS 认知行为损害的进展。通过神经电生理及神经成像学技术可以发现前额叶皮层临床前 期及临床期分子水平及微细结构的改变。现综述了近年来 OSAHS 认知行为损害中前额叶皮层作用机 制和检测方法的进展,并探讨未来的研究方向。     

正常睡眠及失眠的功能神经影像研究进展

50年前发现的快速眼动相（REM）睡眠期使我们对睡眠觉醒调节基础机制的了速解向前推进了一大步,但是不论是脑电图还是多导睡眠图（polysomnography,PSG）都只能反映脑表面的电生理变化,无法涉及不同区域的大脑功能,这也限制了我们对睡眠觉醒机制的进一步探究.然而核医学与睡眠医学的结合为这一领域的深入研究开拓了一个崭新的局面.尽管进展很大,但是绝大多数研究仍处于初级阶段,主要集中在健康者的睡眠与脑功能的关系上,只有个别是针对特殊类型睡眠障碍进行的研究.以下将在描述正常睡眠过程的基础上,回顾核医学（功能神经影像）方法在睡眠与脑功能、原发性失眠和继发性失眠的应用研究.     

精神分裂症干预前后事件相关电位（P300）分析

近年来精神分裂症患者的认知功能损害问题日益受到重视，成为精神分裂症患者康复中亟待解决的问题［1］，特别是缺乏一个客观稳定的评价指标。事件相关电位（ERP ）是一种长潜伏期脑诱发电位，是受试者在注意到某个个体并对其进行认知加工时出现的电位变化，过程涉及人的注意、记忆、学习、推理、思维判断、情绪等，其中P300是最早发现的事件相关电位的内源性成分，目前已被作为评价认知功能损害的一个客观电生理指标。为此我们借助这一技术，对精神分裂症患者干预前后的事件相关电位（P300）变化进行研究，现将结果报告如下。     

发作性睡病认知障碍研究进展

睡眠对维持正常认知功能,尤其是注意力的集中和记忆的巩固至关重要。发作性睡病是一种睡眠障碍疾病,其造成的认知损害严重影响患者生活质量。目前,发作性睡病认知障碍的评估主要依靠主诉及临床观察。现有研究发现,发作性睡病患者在注意力、工作记忆、执行功能、奖励处理和决策等领域表现差,但其相关机制尚不明确。现就发作性睡病认知障碍的临床特征、发病机制以及神经心理测验、神经影像学、神经电生理等相关评估方法的研究进展进行综述,以期为探究该疾病提供新视野,为研发认知障碍筛查工具提供新思路。     

重复经颅磁刺激治疗卒中后认知障碍的研究进展

认知障碍是卒中后常见并发症，严重影响患者康复进程及生活质量。重复经颅磁刺激 （repetitive transcranial magnetic stimulation，rTMS）作为一种新型的非侵入性神经电生理技术，通过改 变神经细胞动作电位影响脑内代谢和神经电活动，近年来逐渐被用于卒中后认知障碍的治疗。目前 rTMS在卒中后执行功能、记忆功能、语言能力及视空间能力的康复应用中均取得了较为积极的疗效， 且在指南推荐的治疗参数范围内操作基本是安全的，但仍缺乏大样本、多中心、高质量的随机对照 试验进一步明确其最佳刺激参数与治疗效果。rTMS治疗卒中后认知障碍的研究仍处于探索阶段，未 来有望进行更深入的机制研究，为rTMS治疗卒中后认知功能障碍提供更切实有力的依据。     

肠道菌群及其代谢产物与卒中后认知功能障碍相关性的研究进展

卒中后认知功能障碍（PSCI）在脑卒中患者中较为常见,影响了卒中患者的生活质量及预后,其危险因素的研究也越来越受到人们的重视。肠道菌群及其代谢产物作为近年来的研究热点之一,已被证实与中枢神经系统疾病的发生发展密切相关,尤其是脑卒中患者。有文章表明,肠道菌群及其代谢产物与早期认知功能下降及PSCI均密切相关。本文将综述肠道菌群及其代谢产物和脑卒中的相互作用机制,卒中后肠道菌群的变化,以及改变的肠道菌群和代谢产物对脑卒中及PSCI的影响,并探讨胆碱、益生菌、抗生素等在PSCI防治方面的潜在价值,为PSCI的防治提供新思路。     

炎症反应在卒中后认知功能障碍患者中的研究进展

卒中后认知功能障碍(post-stroke cognitive impairment, PSCI)是急性缺血性脑血管事件后常见的并发症之一，它不仅严重影响着卒中幸存者的生活质量，而且也增加了患者的死亡率。炎症反应(Inflammatory response)已经被证实参与急性缺血性卒中的发生和发展，它会损伤机体的神经细胞，使得机体的炎症反应更加活跃，释放出更多的炎症因子，破坏了神经环路的完整性，从而导致患者的认知功能障碍。既往的国内外研究探讨了炎症生物标志物与认知功能之间的关系，但关于两者关系的研究仍然较少，因此本文主要通过观察炎症生物标志物的水平变化来探讨炎症反应在PSCI患者中的作用。     

Mild cognitive impairment and vascular cognitive impairment in stroke patients

In 150 older stroke patients (>75) without dementia, the proportion of people meeting different criteria for early cognitive impairment varied from 17% to 23% depending upon the individual criteria used. Given this large disparity, prospective studies to clarify the utility of different criteria as a predictor of subsequent dementia are a priority.     

Diabetes and cognitive impairment

BACKGROUND: Diabetes is a risk factor for dementia,but the issue whether this concerns only vascular dementia or also Alzheimer's disease is debated. We compared the clinical diagnoses and abnormalities on brain MRI in patients with or without diabetes who received standardised, detailed diagnostic studies at a memory clinic, in order to establish whether one specific type of dementia or specific MRI abnormalities were more common in diabetes. PATIENTS AND METHODS: Patients who visited our memory clinic between January 2002 and June 2004 were divided into a group with (n = 42) or without diabetes (n = 389). The diagnoses were recorded, and MRI scans were rated for (sub)cortical atrophy, medial temporal lobe atrophy, infarctions, and white matter changes. RESULTS: The proportion of Alzheimer's disease (36% versus 28%; OR 1.1 (95% CI 0.5-2.2), adjusted for age and sex), vascular dementia (5% versus 2%; OR 2.4 (0.5-12.1)), and so called "cognitive impairment no dementia" (24% versus 17%; 1.3 (0.6-2.9)) was similar in patients with or without diabetes. On MRI lacunar and cortical infarctions were more common and cortical atrophy more pronounced among diabetic patients. By contrast, the severity of white matter changes was similar in the two groups. CONCLUSION: The relative frequency of different diagnoses among diabetic and non-diabetic patients attending a memory clinic was similar, indicating that diabetes does not predispose to one particular subtype of dementia. The imaging findings support the notion that the increased risk of cognitive decline and dementia in elderly subjects with diabetes is due to dual pathology, involving both cerebrovascular disease and cortical atrophy.     

晚发型抑郁障碍与轻度认知功能损害患者的认知功能差异研究

目的 探讨晚发型抑郁障碍患者与轻度认知功能损害患者的认知功能损害的差异.方法 研究对象为2012年7月～2013年8月上海市精神卫生中心老年科住院与门诊就诊符合DSM—Ⅳ诊断标准且起病年龄≥60岁的抑郁障碍患者,共26例为晚发型抑郁障碍组（LOD组）,另选择26例轻度认知功能损害的患者（MCI组）与26例正常老年人（NC组）.认知功能评估采用简明精神状态量表（MMSE）、蒙特利尔量表（MoCA）.结果 MMSE总分、MMSE分测验中计算力与注意力及MoCA总分、MoCA分测验中连线、注意、持续注意、计算、复述、延迟回忆在LOD组与MCI组差比较异无统计学意义（P＞0.05）,两组与NC组比较差异有统计学意义（P＜0.05）.三组在MMSE分测验的时间定向、延迟回忆、三步指令、书写书面指令及MoCA分测验的复制图、画钟、命名比较,MCI组均值最低,与NC组比较差异有统计学意义（P＜0.05）,与LOD组比较差异无统计学意义（P＞0.05）.结论 LOD组认知功能在注意力、延迟回忆、连线测验方面与MCI组损害程度相当.MCI组认知功能受损范围较LOD组广泛.     

Vascular cognitive impairment

Cognitive impairment commonly accompanies clinical syndromes associated with vascular disease of the brain. Because of evolving definitional criteria, however, the frequency of cognitive impairment attributable to cerebrovascular disease is difficult to determine. Dementia occurs in up to one-third of elderly patients with stroke, a subset of whom have Alzheimer's disease (AD) rather than a pure vascular dementia syndrome. In fact, pure vascular dementia has been shown to be uncommon in most large autopsy series. A mixed etiology of AD and cerebrovascular disease is thought to become more common with increasing age, although no clinical criteria for the diagnosis of AD with cerebrovascular disease are currently available. Epidemiological studies have implicated subcortical small-vessel disease as a risk factor for cognitive impairment and dementia, but the cognitive expression and clinical significance of MRI white matter changes in individual patients is difficult to establish. The frequency of specific neuropathologic features of vascular cognitive impairment depends largely on study inclusion criteria. Cerebral meningocortical microangiopathies with distinctive clinicopathological profiles are associated with dementia in both sporadic cases and familial syndromes. In patients with AD, the contribution of amyloid-beta protein to the degree of cognitive impairment has not been clearly defined.     

Mild cognitive impairment

Great interest is now devoted to elderly people with memory or other cognitive complaints who are not demented. The determination of this impairment from normality is difficult, because memory performance may decline slowly along the lifetime of the individual. On the other hand, the identification of dementia depends on the criteria used for dementia (DSM-IV or ICD-10). Furthermore, cognitive deterioration of the elderly appears to be heterogenous and may forerun not only Alzheimer’s disease but also other forms of dementia. By applying a set of criteria for frontotemporal mild cognitive impairment, it was possible to identify, retrospectively, a series of patients with behavioral, affective, or speech symptoms suggestive of frontotemporal dysfunction and deficits in frontal lobe-dependent neuropsychological tests, but who have maintained activities of daily living and are not demented. These patients appear to have a high probability of progressing subsequently to dementia of the frontotemporal type. Several potential neuroprotective compounds are now being subjected to clinical trials. Should they be effective in delaying the progression to dementia, the need to detect and treat elderly people with cognitive impairment will become very important.     

Mild cognitive impairment

Mild cognitive impairment is an emerging term that encompasses the clinical state between elderly normal cognition and dementia. Controversy surrounds its characterization, implementation, and definition. Mild cognitive impairment is now the focus of natural history studies, biomarker studies, along with Alzheimer's disease prevention studies. The mild cognitive impairment stage may be the optimum stage at which to intervene with preventive therapies. Depending on the cohort source and definition, between 19 and 50% of mild cognitive impairment individuals progress to dementia (usually Alzheimer's disease) over 3 years. Despite controversy, progress has been achieved in defining risk factors for progression from mild cognitive impairment to dementia. New treatments to prevent development of Alzheimer's disease are targeting mild cognitive impairment as a treatment group and neurologists will increasingly be called upon to make this diagnosis.     

Vascular cognitive impairment

Cerebrovascular disease is the second most common cause of acquired cognitive impairment and dementia and contributes to cognitive decline in the neurodegenerative dementias. The current narrow definitions of vascular dementia should be broadened to recognise the important part cerebrovascular disease plays in several cognitive disorders, including the hereditary vascular dementias, multi-infarct dementia, post-stroke dementia, subcortical ischaemic vascular disease and dementia, mild cognitive impairment, and degenerative dementias (including Alzheimer's disease, frontotemporal dementia, and dementia with Lewy bodies). Here we review the current state of scientific knowledge on the subject of vascular brain burden. Important non-cognitive features include depression, apathy, and psychosis. We propose use of the term vascular cognitive impairment, which is characterised by a specific cognitive profile involving preserved memory with impairments in attentional and executive functioning. Diagnostic criteria have been proposed for some subtypes of vascular cognitive impairment, and there is a pressing need to validate and further refine these. Clinical trials in vascular cognitive impairment are in their infancy but support the value of therapeutic interventions for symptomatic treatment.