卒中后尿失禁

尿失禁是卒中的一种常见并发症,40％～60％的卒中住院患者存在尿失禁.卒中后尿失禁是患者死亡、功能残疾和入住康复机构的强烈预测因素.尿失禁的恢复与卒中转归更好相关.文章对卒中后尿失禁的流行病学、原因和分类、对卒中转归的影响以及治疗策略进行了综述.     

经过治疗的高血压患者为什么还发生卒中?--内科医生的观点

尽管高血压病已得到广泛治疗,但卒中仍然是美国的第三大死亡原因.降压治疗预防出血性卒中要比缺血性卒中更有效.为什么降压治疗预防缺血性卒中仅有部分是成功的?要理解这一点,必须对各种卒中亚型的发病机制和治疗的差异加以分析.缺血性卒中主要有3种亚型小血管动脉病变性(腔隙性)卒中、大动脉粥样硬化血栓性卒中和心源性卒中.高血压是导致腔隙性卒中的主要原因,而在动脉粥样硬化血栓性卒中的发病机制中的作用则较小.因此,降压治疗能预防大部分腔隙性卒中,但对动脉粥样硬化血栓性卒中的发生却没有大太的影响.由于过度降压可影响大脑自动调节功能,尤其是对老年和有卒中史的高血压患者,过度降压反而会导致卒中(J型曲线).假定有效的降压治疗可预防大部分腔隙性卒中,那么未来治疗的重点就应该是动脉粥样硬化血栓性卒中和心源性栓塞的预防.在这方面,外科技术的改进、以稳定斑块为目的药物治疗方法和经食管超声心动图在心源性栓塞诊断中的应用,以及对可能发生的栓子源进行抗凝治疗均是有希望的方法.除了依从性差和治疗不充分等显而易见的原因外,对老年和卒中机制与血压无关的患者进行过度降压治疗,可以解释为什么我们在努力治疗高血压后仍有卒中发生.     

缺血性卒中患者的骨质疏松

缺血性卒中后患者多伴有骨量减少和骨质疏松,尤其是在偏瘫侧,严重影响着患者的功能预后.同时,骨质疏松也是缺血性卒中发病的独立危险因素.在众多治疗方案中,康复训练在骨质疏松的预防和治疗方面都发挥着重要的作用,近年来逐渐引起研究者的兴趣.文章对缺血性卒中与骨质疏松的关系以及骨质疏松的康复治疗进行了综述.     

卒中的基因研究进展

卒中的基因研究进展很快,新方法和新技术的应用以及致病基因的确定有助于卒中的预防、早期诊断和积极治疗.文章主要介绍了卒中基因研究方面的新进展.     

卒中治疗的组织

卒中的有效治疗与治疗组织实施的公众宣传教育、急诊科的准确诊断和早期处理、卒中病房和康复治疗密切相关。文章评价了这些策略在卒中治疗中的作用。     

欧洲卒中促进会对卒中处理的建议--2003更新版

本文是2000年Cerebravascular Diseases发表的"欧洲卒中促进会卒中处理指南"的更新版.本指南得到代表欧洲卒中委员会、欧洲神经病学会和欧洲神经科学学会联盟等3个欧洲学会的欧洲卒中促进会的认同.     

卒中治疗的组织

卒中的有效治疗与治疗组织实施的公众宣传教育、急诊科的准确诊断和早期处理、卒中病房和康复治疗密切相关。文章评价了这些策略在卒中治疗中的作用。     

抗凝药在缺血性卒中防治中的地位

抗凝是预防和治疗缺血性卒中的重要手段之一,但在降低卒中复发风险的同时有可能增加出血事件.文章通过回顾抗凝药在缺血性卒中防治中的应用以及新型抗凝药的研究,评价了抗凝药在缺血性卒中防治中的地位.     

卒中后焦虑

卒中后焦虑是卒中患者最常见和最重要的并发症之一,可严重影响卒中患者的康复以及日常生活和工作。文章就卒中后焦虑的流行病学、临床特征、危险因素和预测因素、病理生理学机制、预防和治疗进行了综述。     

卒中后尿失禁

尿失禁是卒中的一种常见并发症,40％～60％的卒中住院患者存在尿失禁。卒中后尿失禁是患者死亡、功能残疾和入住康复机构的强烈预测因素。尿失禁的恢复与卒中转归更好相关。文章对卒中后尿失禁的流行病学、原因和分类、对卒中转归的影响以及治疗策略进行了综述。     

Ischaemic colitis

The term colonic ischaemia was first coined approximately 40 years ago. Up until that point, the disease was only diagnosed in cases where the colon was completely gangrenous. In the 1960s reversible non-transmural ischaemia of the colon was described and much has been written about the disease since. Ischaemic colitis is usually a disease process that is seen in the elderly. However, the true incidence of the disease remains unknown since many cases are probably never diagnosed. We now know that the disease can occur both with occlusive and non-occlusive vascular disease, the latter being much more common. Although factors that contribute to non-occlusive disease have been identified, often the exact pathophysiology is unclear and this is an area where further research is needed. Known facts about the pathophysiology and aetiology of the disease will be discussed in this chapter. The key to diagnosis is often a high degree of clinical suspicion. Various diagnostic modalities are described, but colonoscopy remains the main instrument of accurate diagnosis. Fortunately the majority of patients will have self-limiting disease and, accordingly, they usually respond to conservative therapy. When the disease progresses to transmural infarction, surgery is required and the prognosis is guarded. Since many of the patients are elderly with other underlying diseases, it is unlikely that major treatment advances will allow us to significantly alter the prognosis in this group of patients with transmural ischaemia.     

Ischaemic mitral insufficiency

Ischaemic mitral insufficiency (IMI) due to regurgitation of an anatomically normal valve, due to dysfunction directly related to myocardial ischaemia, is observed in over 20% of post-infarction patients and is associated with a doubling of the risk of death. The responsibility of ventricular remodelling with displacement of the papillary muscles in the genesis of IMI has been demonstrated experimentally. 3-D echocardiography has improved our understanding of the central role of geometrical changes of the subvalvular apparatus. The inconsistent results of surgery using an undersized mitral annulus have led to the search for alternative techniques. The correction of mitral insufficiency at coronary bypass surgery is a current topic of research. The application of new techniques of mitral valvuloplasty seems more effective and should provide an answer to this problem.     

缺血性脑水肿

缺血性脑水肿似乎涉及截然不同的两个过程,其相对促成作用和时间过程取决于缺血的持续时间、严重程度以及是否再灌注.第一个过程涉及组织中Na+和水含量的增加,同时伴胞饮作用增强和跨内皮细胞Na+,K+-ATP酶活性增高,这在梗死早期和出现明显的结构损伤之前非常明显,再灌注可加剧这一现象.第二个过程是脑实质和血管系统本身梗死引起的更加广泛的迟发性血脑屏障(BBB)受损所致.在第二阶段,虽然组织Na+水平似乎仍然是水肿形成的主要渗透力量,但血清蛋白酶的渗出是另一潜在的有害因素.尽管蛋白酶作用的相对重要性还不清楚,但细胞外基质的降解确实可导致BBB的进一步破坏和组织软化,这一阶段的特征以脑肿胀最为明显.许多因素可参与和调节缺血性脑水肿的形成,但目前的大部分信息来自于实验模型,仍缺乏来自微观水平的临床资料.有临床意义的脑水肿通常在大面积半球卒中后以迟发性方式出现,是病死率高的一个原因.在检测和评价卒中后水肿引起的继发性损伤方面,神经体征的重要性至少与直接颅内压(ICP)测量和神经影像学检查相当.然而,卒中的神经影像学特征,尤其是早期发现大脑中动脉区域受累超过1/2对随后数小时和数天严重脑水肿的形成具有很高的预测价值.尚无有效的内科治疗能够确实消除脑水肿和ICP升高,在大多数情况下,这些治疗充其量只是在勉强应付而已.半侧颅骨切除术似乎是能够使患者避免死于脑受压的最有希望的一种方法,但手术的最佳时机和选择患者的方式目前还在研究之中.所有治疗广泛性缺血性脑肿胀的方法都笼罩在患者虽然存活但功能转归可能很差的阴影之下.通过控制血压,给予选择性液体控制血清渗透压以及控制其他加重脑水肿的全身性因素是可能的.因此,在这里也给出了宽泛的治疗卒中后脑水肿的指南.     

Ischaemic penumbra: highlights

The ischaemic penumbra was described for the first time in the late 1970s as a ring of hypoperfused zone surrounding the region of complete infarction. The penumbral zone is a functionally silent tissue which is able to regain its function if promptly reperfused. This implies that the ischaemic penumbra is not a static but a "dynamic" and "time-dependent" concept. In this paper we describe the role of neuroimmaging tecniques such as single photon emission tomography (SPET), positron emission tomography (PET), and diffusion-weighted and perfusion-weighted magnetic resonance imaging (DWI and PWI) in the study of ischaemic penumbra. These functional imaging techniques have the advantage of giving "in vivo" quantitative estimate of cerebral blood flow (CBF) as well as information on how the ischaemic tissue metabolic changes develop. It follows that, as therapeutic options for treating acute stroke evolve, neuroimaging strategies are assuming an increasingly important role in the initial evaluation and management of the acute ischaemic patient. In this regard, a wide range of therapeutic approaches have been investigated for either ameliorating the perfusion, or interfering with the pathobiochemical cascade leading to ischaemic neuronal damage, or improving endogenous neuroprotection pathways. The "time windows" required for these treatments to be effective varies being rather short for reperfusion and longer for neuroprotection. Salvaging more penumbra would enhance recovery and thereby allow the most appropriate candidate for therapeutic trials to be selected.