Abstract PR167

Background & Objectives: Excitotoxicity caused by the excess overshoot of the glutamat is like a starter of the neuronal death at the acute brain injury (ABI). Exitotoxicity can be neutralized by the blockade of NMDA-receptors. Amantadin sulphate being non-competitive antagonist of NMDA-receptors decreases the flow of Ca2+ into the cell, inhibits the violation of the neurons and does neuroprotective action. The goal of study: learning the efficiency of amantadin sulphate as neuroprotector in patients with ABI. Materials & Methods: 32 patients with ABI were observed (26 men and 6 female), the average age 43±5,3 years. The cause of ABI were: severe head injury - 18 patients, subarachnoidal hemorrhage 14 patients. The level of consciousness on the Glasgo’s coma scale (GCS) at the admission consisted 6,2±2,1 points. The following investigations were done: dynamics of the consciousness’ level, the duration of carrying out of the artificial pulmonary ventilation (APV), clinical outcome by the Glasgo’s outcomes scale (GOS). Results: The patients were prescribed the traditional therapy at the ABI. All the patients were divided into two groups. The 1st one (n=15) were the patients got the traditional intensive therapy, the second one (n=17) were the patients whom the traditional intensive therapy was completed by 400 mg\day of amantadin sulphate intravenously dropwise. The positive clinical effect of amantadin sulphate has been revealed from the first day of the treatment. The level of consciousness increased for 14,3% and to the 3rd day it was got the reliable difference (p≤0.001) in compare with the 1st group. In the 1st one the results were worse. The duration of APV in the main group was also shorten for 15,9%. It is connected with the rapid recovery of consciousness of the patients and the early transference to the self-breathing. The clinical outcome by the Glasgo’s outcomes scale was also better in the 1st group Conclusion: 1. The usage of indirect antagonist of NMDA-receptors of amantadin sulphate in the therapy of the patients with ABI improves the neurological status, the early recovering from coma. 2. Using of the medication allows to shorten the duration of APV of the patients. Disclosure of Interest: None declared

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