Lidocaine is a widely used amide local anesthetic, which is used clinically for anesthesia and treatment of arrhythmia. Experimental studies have shown that lidocaine has a protective effect on ischemic and hypoxic brain injury. In our department, 36 patients with ischemic stroke were treated with small doses (5 mg?kg-1, d-1) of lidocaine and observed with the control group for control treatment to explore the efficacy and safety of lidocaine in the treatment of ischemic stroke. Xu Shanheng, Department of Neurology, Lujiang County People’s Hospital
Clinical information
I. General information
The 72 patients were all patients with acute ischemic cerebrovascular disease hospitalized in the Department of Neurology of the hospital, including 52 males and 20 females.
Their ages ranged from 41 to 75 years old, with an average of 58±9 years old. The diagnosis was in accordance with the diagnostic criteria for ischemic stroke established by the 4th National Academic Conference on Cerebrovascular Diseases in 1995, and all of them were excluded from hemorrhagic disease by cranial CT examination. Anyone with significant cardiac, hepatic or renal insufficiency or those who could not take care of themselves before the onset of stroke were excluded from this group. 72 patients were randomly divided into the control lidocaine group, and there were no significant differences in age, sex, stroke involvement hemisphere, time of starting treatment and mean base score of Modified Edinburgh + Scandinavia Study Group Score (MESSS) between the groups at the time of admission.
II. Treatment methods
The control group was treated with conventional therapy using low right, mannitol and chuangozanide; the lidocaine group was treated with conventional therapy with the addition of lidocaine 5 mg/kg dissolved in 5% GS 500 ml, intravenous drip, 30 drops/min, once/d, for 7 d. The conventional therapy was continued thereafter. efficacy score was performed at 12 weeks and compared with the score at admission.
III. Efficacy evaluation
The Barthel Index was used for the recovery of self-care ability; the MESSS was used for the recovery of neurological function; and the MMSE was used for the recovery of cognitive ability.
The X2 test was used for statistics, and P<0,05 was used for significant differences.
IV. Results
1. degree of recovery of self-care ability: Barthel>60 was considered effective (out of 100) according to the efficacy score at the 12th week.
Lidocaine was effective in 27 cases and ineffective in 9 cases, while the control group was effective in 14 cases and ineffective in 22 cases. The efficiency of the lidocaine group was 79%, and the efficiency of the control group was 38,8%, by statistical treatment, X2=9,57, P<0,005, the two groups had highly significant amazement, and the lidocaine group was better than the control group.
2, the degree of neurological recovery: according to the score of patients with basic recovery of neurological function at week 12, MESSS score (out of 45) > 20 is the basic recovery of neurological function, the lidocaine group was effective in 12 cases, ineffective in 14 cases, the control group was effective in 5 cases, ineffective in 31 cases, the efficiency of the control group was 13, 8%, the efficiency of the lidocaine group was 58, 3%, by statistical processing, X2=4 There was a significant difference between the two groups, and the lidocaine group was better than the control group.
3, the degree of cognitive ability recovery: according to the 12th week MMES>25 score assessment, MMSE score (out of 30) >25 is better recovery, the results show that the lidocaine group effective 21 cases, ineffective 15 cases, the control group effective 12 cases, ineffective 24 cases, the control group effective 33, 3%, lidocaine group effective 58, 3%, by statistical processing, X2 = 4, 53, P<0, 05, the two groups compared significantly different, the lidocaine group is better than the control group. P<0,05, there is a significant difference between the two groups, and the lidocaine group is better than the control group.
4. Side effects: In 36 patients in the lidocaine treatment group, ECG tracings were performed before, during and after treatment, and no significant changes were found. No side effects such as drowsiness, nausea, vomiting and irritability were also found.
Discussion
Lidocaine is an amide-type local anesthetic. Studies have confirmed that lidocaine has a neurocytoprotective effect on ischemic and hypoxic brain injury, and its mechanism of action is as follows: (1) it increases cerebral blood flow; (2) it can significantly reduce infarct volume and neuronal loss; (3) it can block cell membrane K+ and Ca2+ ion channels and delay secondary damage after cerebral ischemia and hypoxia; (4) it can reduce the free radical chain of value-added reactions excited during blood reperfusion (5) reduce the release of excitatory amino acids such as aminobutyric acid, glycin and other acidic amino acids.
The pathophysiological changes of ischemic stroke are extremely complex and closely related to a variety of factors. Finding effective cerebral cytoprotective agents in terms of reperfusion, anti-inflammation and neuronal protection is one of the keys to successful treatment of ischemic brain injury. The cerebroprotective effect of barbiturates is difficult to be applied clinically because of its inhibitory effect on the conscious good circulatory system. Based on the results of the quantitative-effect relationship study of lidocaine, that is, small doses of lidocaine can significantly reduce the volume of cerebral infarction, while this effect is lost at high doses, we used small doses of early administration, 5 mg?kg-1, d-1 for 7 d as a course of treatment. No change in QT interval, no arrhythmia or cardiac ischemia was observed in the ECG, indicating that lidocaine had no significant effect on the cardiovascular system. No lidocaine toxicity, allergic reactions, and suppression of respiratory function and hematopoietic system were found in this group. As assessed by Barthel index, MESSS, and MMSE, lidocaine had significant efficacy compared with the control group.
Zang Donglian et al. treated 80 patients with cerebral infarction with different doses of lidocaine, 10 mg?kg?d in the high-dose group and 5 mg?kg?d in the low-dose group for 14 d. The clinical efficacy and infarct volume before and after treatment of the two groups were better in the low-dose group than in the high-dose group, and there was a significant difference. This group was treated with low-dose lidocaine, which supports the conclusion that low-dose lidocaine is effective in the treatment of ischemic stroke.