The modern concept of neuroprotective therapy in the acute period of ischemic stroke

Abstract

In recent years, significant successes have been achieved in the treatment of acute ischemic stroke. Given the trend towards an increase in the proportion of patients undergoing intravenous thrombolysis and / or mechanical thrombectomy, the question justifies: is there place for neuroprotective therapy (NT) in the era of active introduction of reperfusion treatment? The review discusses the main mechanisms of brain damage in ischemia / reperfusion and the leading neuroprotective strategies studied in clinical trials. Neuroprotective approaches to suppress excitotoxicity, oxidative and nitrosative stress are presented. The clinical efficacy of magnesium sulfate, uric acid, and edaravone is discussed. Non-pharmacological methods of neuroprotection have been characterized, including remote ischemic conditioning, therapeutic hypothermia and neurostimulation. NT in a situation of impossibility of cerebral reperfusion is discussed. The results of randomized clinical trials and meta-analyzes on citicoline (ceraxon) are analyzed. A clinical case is presented illustrating the management of a patient for whom reperfusion therapy was not feasible due to the course of the disease. In the era of the active development of reperfusion methods for the treatment of ischemic stroke, the goal-setting of NT has changed: it is intended to expand the possibilities of application and increase the effectiveness of intravenous thrombolysis and/or mechanical thrombectome, as well as neutralize their negative reperfusion effects. The main targets for NT remain excitotoxicity, oxidative and nitrosative stress. On the other hand, the real clinical situation associated with the low frequency of reperfusion technology in our country necessitates the use of neuroprotectors effective in this category of patients. In this regard, the administration of ceraxon increases the chances of achieving functional independence. The most effective use of the drug from the first day of the disease at a dose of 2000 mg per day intravenously for at least 4-6 weeks with further long-term oral administration at a dose of 1000 mg per day.