Abstract：
Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological entity characterized by nonspecific symptomatology (eg, headache, visual disturbances, encephalopathy, and seizures) and classically cortical and subcortical vasogenic edema predominantly affecting the parietooccipital region. PRES etiologies are usually dichotomized into toxic PRES (eg, antineoplastic drugs, illicit drugs) and clinical condition-associated PRES (eg, acute hypertension, dysimmune disorders). Although the pathophysiology of PRES remains elusive, 2 main pathogenic hypotheses have been suggested: cerebral hyperperfusion due to acute hypertension and cerebral hypoperfusion related to endothelial dysfunction. Research into the pathogenesis of PRES has emerged through the development of animal models in the last decade. The motivation for developing a suitable PRES model is 2-fold: to fill in knowledge gaps of the pathophysiological mechanisms involved, and to open new perspectives for clinical assessment of pharmacological targets to improve therapeutic management of PRES. All current models of PRES have a hypertensive background, on which other triggers (acute hypertension, inflammatory, drug toxicity) have been added to address specific facets of PRES (eg, seizures). The initial model consisted in inducing a reduced uterine perfusion pressure that mimics preeclampsia, a leading cause of PRES. More recently, a model of stroke-prone spontaneously hypertensive rats on high-salt diet, originally developed for hypertensive small vessel disease and vascular cognitive impairment, has been studied in PRES. This review aims to discuss, depending on the research objective, the benefits and limitations of current experimental approaches and thus to define the desirable characteristics for studying the pathophysiology of PRES and developing new therapies.
摘要：
后部可逆性脑病综合征（PRES）是一种临床和放射学实体，其特征是非特异性症状（例如，头痛,视觉障碍,脑病,和癫痫发作）以及主要影响顶枕区的典型皮质和皮质下血管源性水肿。PRES病因通常分为毒性PRES(例如，抗肿瘤药物,非法药物)和临床病症相关PRES(例如，急性高血压,运动障碍）。尽管PRES的病理生理学仍然难以捉摸，已经提出了2个主要的致病假设：由于急性高血压引起的脑高灌注和与内皮功能障碍有关的脑低灌注。在过去的十年中，通过动物模型的发展，对PRES发病机理的研究已经出现。开发合适的PRES模型的动机是2倍：填补所涉及的病理生理机制的知识空白，并为药理学靶点的临床评估开辟新的视角，以改善PRES的治疗管理。目前所有的PRES模型都有高血压背景，其他触发因素(急性高血压，炎症，药物毒性)已被添加到PRES的特定方面(例如，缉获物）。最初的模型包括诱导子宫灌注压降低，模拟先兆子痫，PRES的主要原因。最近,高盐饮食下易中风自发性高血压大鼠模型，最初开发用于高血压小血管疾病和血管性认知障碍，已经在PRES中进行了研究。这篇综述旨在讨论，根据研究目标，当前实验方法的益处和局限性，从而确定研究PRES的病理生理学和开发新疗法的理想特征。
