Bakheit A M O
Peninsula Medical School, Universities of Exeter & Plymouth, Mount Gould Hospital, Plymouth PL4 7QD, UK.
Expert Rev Neurother. 2004 Mar;4(2):211-7. doi: 10.1586/14737175.4.2.211.
Impairment of language function (aphasia) is one of the most common neurological symptoms after stroke. Approximately one in every three patients who have an acute stroke will suffer from aphasia. The estimated incidence and prevalence of stroke in Western Europe is 140 and 800 per 100,000 of the population. Aphasia often results in significant disability and handicap. It is a major obstacle for patients to live independently in the community. When recovery from aphasia occurs, it is usually incomplete and patients are rarely able to return to full employment and other social activities. Currently, the main treatment for aphasia is conventional speech and language therapy. However, the effectiveness of this intervention has not been conclusively demonstrated and empirical observations suggest that spontaneous biological recovery may explain most of the improvement in language function that occurs in aphasics. The generally poor prognosis of the severe forms of poststroke language impairment (Broca, Wernicke and global aphasia), coupled with the limited effectiveness of conventional speech and language therapy has stimulated the search for other treatments that may be used in conjunction with speech and language therapy, including the use of various drugs. Dopamine agonists, piracetam (Nootropil), amphetamines, and more recently donepezil (Aricept), have been used in the treatment of aphasia in both the acute and chronic phase. The justification for the use of drugs in the treatment of aphasia is based on two types of evidence. Some drugs, such as dextroamphetamine (Dexedrine), improve attention span and enhance learning and memory. Learning is an essential mechanism for the acquisition of new motor and cognitive skills, and hence, for recovery from aphasia. Second, laboratory and clinical data suggest that drug treatment may partially restore the metabolic function in the ischemic zone that surrounds the brain lesion and also has a neuroprotective effect following acute brain damage. An example of this is the nootropic agent piracetam. Extensive animal studies have demonstrated the beneficial effects of this and other drugs on neural plasticity, but data on humans are still sparse. This review provides a critical analysis of the current evidence of the effectiveness of these drugs in the treatment of acute and chronic aphasia.
语言功能障碍(失语症)是中风后最常见的神经症状之一。每三名急性中风患者中约有一人会患失语症。西欧中风的估计发病率和患病率分别为每10万人140例和800例。失语症常导致严重的残疾和障碍。这是患者在社区独立生活的主要障碍。当失语症出现恢复时,通常是不完全的,患者很少能够恢复到全职工作和参与其他社会活动。目前,失语症的主要治疗方法是传统的言语和语言治疗。然而,这种干预的有效性尚未得到确凿证明,实证观察表明,自发的生物学恢复可能解释了失语症患者语言功能改善的大部分情况。中风后严重形式的语言障碍(布罗卡失语、韦尼克失语和完全性失语)总体预后较差,再加上传统言语和语言治疗效果有限,促使人们寻找可与言语和语言治疗联合使用的其他治疗方法,包括使用各种药物。多巴胺激动剂、吡拉西坦(脑复康)、苯丙胺,以及最近的多奈哌齐(安理申),已被用于急性和慢性期失语症的治疗。使用药物治疗失语症的依据基于两类证据。一些药物,如右旋苯丙胺(右旋安非他明),可改善注意力持续时间并增强学习和记忆。学习是获得新的运动和认知技能的重要机制,因此也是从失语症中恢复的重要机制。其次,实验室和临床数据表明,药物治疗可能部分恢复脑损伤周围缺血区的代谢功能,并且在急性脑损伤后具有神经保护作用。益智药吡拉西坦就是一个例子。广泛的动物研究已经证明了这种药物和其他药物对神经可塑性的有益作用,但关于人类的数据仍然很少。本综述对这些药物治疗急性和慢性失语症有效性的现有证据进行了批判性分析。