Servizio di Fisiopatologia Metabolico-Nutrizionale e Nutrizione Clinica, Fondazione S Maugeri, IRCCS, Istituto Scientifico di Montescano, Montescano, Pavia, Italy.
Nutr Clin Pract. 2011 Jun;26(3):339-45. doi: 10.1177/0884533611405793.
In patients who undergo rehabilitation after ischemic stroke, nutrition strategies are adopted to provide tube-fed individuals with adequate nutrition and/or to avoid the body wasting responsible for poor functional outcome and prolonged stay in the hospital. Investigations have documented that nutrition interventions can enhance the recovery of neurocognitive function in individuals with ischemic stroke. Experimental studies have shown that protein synthesis is suppressed in the ischemic penumbra. In clinical studies on rehabilitation patients designed to study the effects of counteracting or limiting this reduction of protein synthesis by providing protein supplementation, patients receiving such supplementation had enhanced recovery of neurocognitive function. Cellular damage in cerebral ischemia is also partly caused by oxidative damage secondary to free radical formation and lipid peroxidation. Increased oxidative stress negatively affects a patient's life and functional prognosis. Some studies have documented that nutrition supplementation with B-group vitamins may mitigate oxidative damage after acute ischemic stroke. Experimental investigations have also shown that cerebral ischemia changes synaptic zinc release and that acute ischemia increases zinc release, aggravating neuronal injury. In clinical practice, patients with ischemic stroke were found to have a lower than recommended dietary intake of zinc. Patients in whom daily zinc intake was normalized had better recovery of neurological deficits than subjects given a placebo. The aim of this review is to highlight those brain metabolic alterations susceptible to nutrition correction in clinical practice. The mechanisms underlying the relationship between cerebral ischemia and nutrition metabolic conditions are discussed.
在缺血性脑卒中后接受康复治疗的患者中，采用营养策略为肠内喂养的个体提供充足的营养，或避免导致功能预后不良和住院时间延长的身体消耗。研究证明，营养干预可以增强缺血性脑卒中个体的神经认知功能恢复。实验研究表明，在缺血半影区，蛋白质合成受到抑制。在旨在研究通过提供蛋白质补充来对抗或限制这种蛋白质合成减少对康复患者的影响的临床研究中，接受这种补充的患者的神经认知功能恢复增强。脑缺血引起的细胞损伤部分也是由自由基形成和脂质过氧化引起的氧化损伤引起的。氧化应激增加会对患者的生活和功能预后产生负面影响。一些研究表明，B 族维生素的营养补充可能减轻急性缺血性脑卒中后的氧化损伤。实验研究还表明，脑缺血会改变突触锌释放，急性缺血会增加锌释放，加重神经元损伤。在临床实践中，发现缺血性脑卒中患者的锌摄入量低于推荐的膳食摄入量。与给予安慰剂的受试者相比，每日锌摄入量正常化的患者神经功能缺损恢复更好。本文综述的目的是强调那些在临床实践中易受营养纠正的大脑代谢改变。讨论了脑缺血与营养代谢状况之间关系的机制。
