脳梗塞後の回復に対する栄養

脳梗塞後の回復に対する栄養に関するレビュー論文を紹介します。

Aquilani R, Sessarego P, Iadarola P, Barbieri A, Boschi F. Nutrition for brain recovery after ischemic stroke: an added value to rehabilitation. Nutr Clin Pract. 2011 Jun;26(3):339-45.

エビデンスとしてはまだ不十分ですが、蛋白質投与が認知機能回復に有効、ビタミンB群が急性期脳梗塞後の酸化ストレスを緩和、亜鉛が機能回復に有効という報告もあります。今後さらに質の高いエビデンスが出てくれば、ビタミンB群や亜鉛を急性期脳卒中で積極的に使用することになるかもしれません。現状では、ビタミンB群と亜鉛の不足に留意して、欠乏時には補給するというスタンスでよいと思います。

現状では脳梗塞後に回復期や維持期でサルコペニアを合併することが少なくないので、栄養に関連したサルコペニア（飢餓）を避ける栄養管理を行うことが大切です。PEGにしたのに1日エネルギー必要量を投与していないために、体重減少が続くという方も中にはいます。非麻痺側のレジスタンストレーニングを行うまえに、栄養評価が必要です。

Abstract
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.