|Year : 2019 | Volume
| Issue : 10 | Page : 1324-1327
Clinical observation in edaravone treatment for acute cerebral infarction
Z Sun1, Q Xu2, G Gao3, M Zhao4, C Sun1
1 Department of Neurology, Linzi District People's Hospital, Zibo, Shandong, China
2 Department of Neurology, Zibo Huajian Hospital, Zibo, Shandong, China
3 Linzi Zhutai Central Hospital, Zibo, Shandong, China
4 People's Hospital of Zhongmu, Zhengzhou, Henan, China
|Date of Acceptance||26-Mar-2019|
|Date of Web Publication||14-Oct-2019|
Dr. Z Sun
Department of Neurology, Linzi District People's Hospital, Zibo, Shandong
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Acute cerebral infarction threats human health and life safety. The edaravone is a new antioxidant and hydroxyl radical scavenger, which is the novel scavenger for clinical use, mainly for nervous system diseases. Objective: The purpose of this study is to observe the clinical treatment effects of edaravone on the degree of improvement of neurological impairment and functional movement impairment in patients with acute cerebral infarction. Method: A total of 130 patients admitted to our hospital because of acute cerebral infarction from December 2015 to May 2017 were selected for group analysis. These patients were divided into a control group (n = 65) and a treatment group (n = 65) with a random odd–even method. The control group accepted conventional treatment, while the treatment group received edaravone treatment on top of the conventional treatment of the control group. After treatment, the differences in functional movement, living ability score, neurological score, treatment effect, and adverse reaction of these two groups were tested and compared. Results: The total treatment efficiency of conventional treatment in the control group was significantly lower than the combination treatment in the treatment group (P < 0.05). The inter-group differences in the National Institutes of Health Stroke Scale, activities of daily living, and Fugl–Meyer assessment scores after the treatment were significant between these two groups (P < 0.05). The posttreatment effect on the treatment group was superior to that on the control group (P < 0.05). The adverse reaction rate of the treatment group did not significantly vary from that of the control group (P > 0.05). Conclusion: Edaravone can significantly improve the degree of neurological impairment during acute cerebral infarction, functional movement, and living quality with a definite effect and high safety. Thus, this drug has a good prospect in clinical treatment.
Keywords: Acute cerebral infarction, clinical treatment effect, edaravone
|How to cite this article:|
Sun Z, Xu Q, Gao G, Zhao M, Sun C. Clinical observation in edaravone treatment for acute cerebral infarction. Niger J Clin Pract 2019;22:1324-7
| Introduction|| |
Hazards of acute cerebral infarction
Acute cerebral infarction, clinically called cerebral arterial thrombosis, mainly refers to a necrotic disease caused by the anoxic and ischemic state of local brain tissues after blood circulation is disrupted., As a common and frequently occurring disease in clinical neurology, acute cerebral infarction is characterized by rapid disease progression, poor prognosis, high disability rate, and high fatality rate., It also poses serious threats to human health and life safety.
Treatments of acute cerebral infarction
Treating patients with scientific neuroprotection that corresponds to specific symptoms during an acute attack not only helps establish collateral circulation but also prevents ischemia, reperfusion injury due to ischemia, and nerve cell death., For example, edaravone is a new antioxidant and hydroxyl radical scavenger that can inhibit peroxidation in brain cells and facilitate the relief of brain tissue damage and cerebral edema caused by cerebral ischemia and anoxia., This study aimed to analyze the therapeutic effects of edaravone on acute cerebral infarction.
| Materials and Methods|| |
A total of 130 patients admitted to our hospital because of acute cerebral infarction from December 2015 to May 2017 were selected for group analysis. All of the selected patients conformed to the relevant diagnostic criteria for cerebral infarction formulated by the academic conference on cerebrovascular disease. They were diagnosed with cerebral infarction through MRI or CT examination, and those with concurrent serious complications, such as cerebral hemorrhage, coma, drug allergy, mental disorder, and other severe organic lesions in the brain, were excluded. The patients were then divided into a control group (n = 65) and a treatment group (n = 65) according to a random odd − even method. The control group comprised of 40 males and 25 females. Their age ranged from 47 years to 65 years, with an average age of 51.3 ± 4.2 years. Of these patients, the following cases were observed: 17 with brainstem infarction, 15 with lobe infarction, 25 with infarction in the basal ganglia region, and 8 with multiple infarctions. The treatment group also included 37 males and 28 females. Their age varied from 46 years to 67 years, with an average age of 52.4 ± 4.1 years. Of these patients, the following cases were noted: 15 with brainstem infarction, 18 with lobe infarction, 20 with infarction in the basal ganglia region, and 12 with multiple infarctions. The obtained data were processed using statistical software with the corresponding version. Inter-group comparison did not show any significant difference (P > 0.05). As such, data could be compared.
Conventional treatment method was used for the control group: 80 mg of ligustrazine injection (SFDA approval number: H20043160; drug specification: chemical medicine; 2 mL: 40 mg; Beijing Yanjing Pharmaceuticals Co., Ltd., China) +250 mL of 0.9% sodium chloride solution was intravenously injected once per day. Afterward, 100 mg of aspirin enteric-coated tablets (SFDA approval number: J20080078; drug specification: chemical medicine; 100 mg; Bayer Healthcare Co., Ltd., Hong Kong) was administered orally before sleep. Basic treatment procedures, including dehydration and intracranial pressure drop, blood pressure and glucose regulation, and water–electrolyte imbalance correction, were performed according to the disease severity of the patients. Edaravone (SFDA approval number: H20120042; drug specification: chemical medicine; 20 ml: 30 mg; Xi'an Lijun Pharmaceuticals Co., Ltd., Xi'an, China) was given to the treatment group based on the treatment for the control group. In particular, 30 mg of edaravone added to 100 ml of 0.9% sodium chloride solution was intravenously injected twice per day, and this procedure was completed within half an hour. Both treatments were given for 2 weeks, and treatment methods, such as solution expansion, anticoagulation, thrombolysis, or use of other drugs, which might influence the therapeutic effect, were prohibited during the treatment.
Adverse reactions: During drug treatment, possible adverse drug reactions were observed and recorded, and hepatic and renal function analyses and routine blood and urine examinations were carried out after the treatment period.
Daily living ability and movement function: After 2 weeks, the Barthel scale of activities of daily living (ADL) was used to evaluate the patients' living qualities. A high score corresponded to enhanced living quality. Fugl–ugl score corresponded to enhanced living quality. Fuglvaluate the patients' living qualities.orde A low score indicated poor movement function.
Neurologic impairment degree: The National Institutes of Health Stroke Scale (NIHSS) was used to evaluate the neurological impairment of patients before the treatment, in the first week of the treatment, and in the second week of the treatment. A high NIHSS score implied a serious neurological impairment.
Efficacy of edaravone was evaluated according to the clinical symptoms and manifestations of the patients and their NIHSS scores. The score of neurological deficit degree was assessed using the criteria defined by the fourth section of the Cerebrovascular Congress. Recovery criteria: clinical symptoms disappeared, the NIHSS score reduced to within 91−100%, and invalidism degree with grade 0; excellent efficient: clinical symptoms evidently improved, the NIHSS score reduced to within 46–90%, and invalidism degree within grades 1−3; partially efficient treatment: clinical symptoms slightly relieved, the NIHSS score reduced to within 18−45%, and patients basically recovered their self-care ability of daily living; ineffective treatment: clinical symptoms were not improved at all and even aggravated, and the NIHSS score reduced to not greater than 17%. The total treatment efficiency was calculated as follows: edaravone efficacy = recovery percentage + excellence efficient + partially efficient.
Data were statistically analyzed using SPSS22.0. x˒ ± s was used to express the measurement data (ADL score, FMA score, and NIHSS score), and t-test was conducted for intergroup comparison. Percentage (%) was used to present numerical data (total effective rate of treatment and adverse reaction rate), and χ2 test was performed for intergroup comparison. P < 0.05 is regarded as there is a significant difference between groups.
| Results|| |
Comparison of the daily living ability and movement function scores of the two groups before and after treatment
After edaravone combined treatment, the ADL and FMA scores of the control and treatment groups were both increased, which mean the living ability and the functional movement were greatly improved. The P values of ADL and FMA scores of treatment groups were 0.0001 and 0.0000, respectively, which are lower than the P values in control groups. These results indicated the improvement of daily living ability and functional movement is more significant after edaravone combined treatment. Their intergroup differences were significant (P < 0.05; [Table 1]).
|Table 1: Comparison of the daily living ability and functional movement scores of the two groups before and after treatment (X̄ ± s, score)|
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Comparison of the NIHSS scores of the two groups before and after treatment
After edaravone combined treatment, the degree of neurological impairment was significantly reduced, and the difference was statistically significant. The NIHSS scores in both groups at 1 week and 2 weeks after different treatment were reduced, but the edaravone combined treatment showed a significantly stronger protective effect on neurological impairment than control treatment (P < 0.05), which mean that the edaravone combined treatment effect is better than the conventional treatment. These results significantly varied between the two groups (P < 0.05; [Table 2]).
|Table 2: Comparison of the NIHSS scores of the two groups before and after treatment (X̄ ± s, score)|
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Comparison of the adverse reaction rates of the two groups
The adverse reaction rates of the control group and the edaravone combined treatment group was 9.23% and 6.15%, respectively, There was no significant difference in the adverse reaction rates between the two groups. (P > 0.05; [Table 3]).
|Table 3: Comparison of the adverse reaction rate of the two groups [n (%)]|
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Comparison between the two groups in total treatment efficiency
The total effective rates of the control group and the treatment group were 81.54% and 95.38%, respectively, and these values were significantly different (P < 0.05; [Table 4]).
|Table 4: Comparison of edaravone efficacy between the two groups [n (%)]|
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| Discussion|| |
As aging worsens, the incidence of acute cerebral infarction continues to increase; acute cerebral infarction has the character of high morbidity and fatality rates. Brain damage will induce the production of oxygen radicals, which can damage the cytomembrane of brain cells and finally damage the nervous system and cause cerebral injury as well as the cerebral edema. The traditional treatments can improve the clinical symptoms of patients in some extents. However, it lacks strong prognostic reliability.
Edaravone is an antioxidant and oxygen radical scavenger that can inhibit lipid peroxidation during the scavenging of oxygen free radicals. Edaravone has a low molecular weight, so it can penetrate the blood–brain barrier easily., There are lipophilic groups in the molecular structure of edaravone, which is beneficial for it to scavenge a large amount of oxygen free radicals formed in the ischemic penumbra in brain tissues during ischemic–reperfusion process and can stimulate prostaglandins. It can inhibit the activation of hypoxanthine oxidase and xanthine oxidase, thereby reducing the accumulation of inflammatory mediators, such as leukotrienes., Besides, it can also elicit antiinflammatory protective effects for nerve cells, increase cerebral blood flow volume, prevent the aggravation of cerebral hypoperfusion toward necrosis, significantly reduce nerve damage, and effectively improve neurological functions and prognosis.
| Conclusion|| |
In this study, the adverse reaction rates of the two groups did not significantly differ (P > 0.05), but the ALD, FMA, NIHSS scores and total treatment efficiency are significantly improved (P < 0.05). These findings indicated that edaravone can significantly alleviate the degree of neurological impairment caused by acute cerebral infarction and enhance the movement function and living quality of patients definitely and safely. Moreover, edaravone has high safety and few adverse reactions, which are worthy of clinical promotion.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4]
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