Hyperbaric oxygen therapy for cerebral blood flow and electroencephalogram in patients with acute cerebral infarction Choice for therapeutic occasion

BACKGROUND: Hyperbaric oxygen (HBO) therapy increases blood oxygen content, changes cerebral blood flow (CBF) and cerebral metabolism. Its therapeutic effects on cerebrovascular disease have been fully confirmed, but the occasion for HBO therapy is still unclear. OBJECTIVE: To observe the therapeutic effects of HBO therapy at different time on CBF and electroencephalogram (EEG) in patients with acute cerebral infarction (CI). DESIGN: Randomized controlled trial. SETTING: Department of Neurology, Shidong Hospital, Yangpu District of Shanghai. PARTICIPANTS: Ninety-six inpatients with acute CI, admitted to Department of Neurology, Shidong Hospital, Yangpu District of Shanghai from January 2001 to December 2006, were involved in this experiment. The involved participants met the diagnosis criteria of acute CI and confirmed by skull CT or MRI. They all were patients with moderate CI (16–30 points) according to neurologic deficit score formulated by Chinese Medical Association. Informed consents of detected items and therapeutic regimen were obtained from all the involved participants. They were randomized into two groups with 48 in each: early-stage treatment group and advanced-stage treatment group. Among the 48 patients in the early-stage treatment group, 21 male and 27 female, aged 53–68 years, 22 patients were found with basal ganglia infarction, 10 with brain lobe infarction, 16 with multiple infarction, 27 accompanied with hypertension and 2 accompanied with diabetes mellitus. Among the 48 patients in the advanced-stage treatment group, 23 male and 25 female, aged 52–71 years, 25 patients were found with basal ganglia infarction, 10 with brain lobe infarction, 12 with multiple infarction, 1 with brain stem infarction, 28 accompanied with hypertension and 1 accompanied with diabetes mellitus. METHODS: After admission, patients of two groups received routine drug treatment. ① Patients in the early-stage treatment group and advanced-stage treatment group began to receive HBO therapy within one week of CI and 4 weeks after CI, respectively. The total course of treatment both was 2 weeks. EEG examination was carried out before and after therapy, and CBF was determined with 133Xe inhalation. ② Assessment criteria of curative effects: Basically cured: neurologic symptoms and body signs disappeared, could work and do housework; Markedly effective: score of neurologic deficit was decreased by over 21 points, could manage himself/herself partially; Effective: score of neurologic deficit was decreased by 8 to 12 points; Non-effective: Score was increased or decreased less than 8 points, neurologic deficit was worsened, even died. Total effective rate = (number of cured+number of markedly effective+number of effective)/ number of total cases×100%. ③ t test and Chi-square test were used for comparing the difference of measurement data and enumeration data respectively, and Ridit analysis was used for comparing the difference of clinical curative effects. MAIN OUTCOME MEASURES: ① Comparison of EEG and CBF of patients from two groups before and after treatment. ② Comparison of post-treatment neurologic deficit of patients between two groups. RESULTS: All the involved 96 patients with CI participated in the final analysis. ① Clinical symptoms of patients from two groups after therapy were significantly improved as compared with those before therapy, and curative effects of early treatment group were better than those of advanced treatment group （U =1.99，P < 0.05）. ②After treatment, CBF in each region of brains, except for that in parietal lobe of patients in the advanced-stage treatment group, was significantly improved (P < 0.05–0.01); The improvement of CBF of patients in the early-stage treatment group was more obvious than that in the early-stage treatment group (P < 0.05–0.01). ③ The abnormal rate of EEF of patients from early-stage treatment group and advanced-stage treatment group before treatment was 94% and 96%, respectively. After treatment, improvement rate of EEG of patients in the early-stage treatment group was 95%, which was significantly different from that in the advanced-stage treatment group （82%，χ2 =4.32，P < 0.05） CONCLUSION: HBO therapy both at early and advanced stages of CI (within 1 week and 4 weeks after CI attack) can improve CBF and EEG of patients with early CI, especially.     

Nimodipine for treatment of perifocal edema following aspiration and drainage in patients with cerebral hemorrhage

BACKGROUND: After cephalophyma removal, perifocal edema does not disappear subsequently, but progresses occasionally. Nimodipine can improve cerebral blood flow, so it maybe reduce cerebral edema area, and speed up the absorption of edematous fluid. OBJECTIVE: To observe the effect of nimodipine on perifocal edema area and neurologic function in patients with hypertensive intracerebral hemorrhage (HICH) following stereotaxic aspiration. DESIGN: Clinical controlled observation. SETTING: Department of Neurology, Third Hospital Affiliated to Liaoning Medical University. PARTICIPANTS: Totally 116 HICH inpatients admitted to the Department of Neurology, Third Hospital Affiliated to Liaoning Medical University from January 2003 to January 2005 were involved in this experiment. They all met the classification and diagnosis of cerebrovascular disease proposed in 1995 4th National Conference on Cerebrovascular Disease. The bleeding volume ≥ 35 mL was confirmed by skull CT. The involved patients, 64 male and 52 femlae, averaged 63 years old, ranging from 40 to 70 years. All the patients suffered from unilateral cerebral hemisphere hemorrhage, and muscle strength of paralyzed limb was less than degree Ⅲ. Informed consents of therapeutic items were obtained from all the patients and relatives. METHODS: ① According to different wills, the patients were assigned into treatment group (n =60) and control group (n =56). In the treatment group, the involved patients, 32 male, 28 female, averaged 63 years. They underwent operation and administration of nimodipine. In the control group, the involved patients, 30 male and 26 female, averaged 62 years old. They all underwent operation simply. Patients in the two groups all received stereotaxic aspiration, drainage, dehydration, haemostasis, antiinflammation, blood pressure controlling and other treatments. Patients in the treatment group were also intravenously injected with 0.2 g/L nimodipine(Bayer Medicine Health Care Co., Ltd., Lot No. 021127) at 10 mg/d. One course of treatment was 15 days. ② According to the clinical neurologic function deficit score of stroke proposed in the 4th National Conference on Cerebrovascular Disease (mild: 0–15 points; moderate: 16–30 points; severe: 31–45 points), neurologic function deficit score and the largest perifocal edema area of patients in two groups were recorded on the 1st, 7th and 15th days after operation. The differences in perifocal edema area and neurologic deficit score between on the 1st and 7th days and between on the 7th and 15th days were calculated. MAIN OUTCOME MEASURES: Changes in the neurologic function deficit score and the largest perifocal edema area. RESULTS: Two of treatment group and 16 of control group died. Finally, 98 patients participated in the final analysis. ①In the treatment group, the difference in the largest perifocal edema area on the postoperative 7th and 15th days and on the 1st day was (1.02±0.07) and (1.86±0.10) cm2, respectively, which changed more significantly as compared with control group, respectively [(0.02±0.04)，(0.61±0.09) cm2，P < 0.01]. ②The difference in neurologic function deficit score between on the postoperative 15th and 1st days in the treatment group was larger than that in the control group [(7.23±0.22)，(2.68±0.32) points，P < 0.01]. CONCLUSION: Nimodipine obviously reduces perifocal edema area of patients with cerebral hemorrhage following aspiration and drainage, and promotes the recovery of neurologic function.     

Fluoxetine for poststroke depression ——A randomized placebo controlled clinical trial

BACKGROUND: Studies have demonstrated that poststroke depression(PSD) may be related with the disequilibrium between noradrenaline and 5-hydroxytryptamine (5-HT) caused by cerebral injury. The injured regions involve noradrenergic and 5-hydroxytryptaminergic neurons as well as conduction pathway. The levels of noradrenaline and 5-HT would be decreased. OBJECTIVE: To observe the effect of fluoxetine on preventing against PSD and recovery of neurologic function, and analyze the relationship of fluoxetine and the 5-HT level. DESIGN: A randomized controlled clinical trial. SETTING: Department of Neurology, First Hospital Affiliated to Soochow University. PARTICIPANTS: Ninety consecutive patients, 47 female and 43 male, were recruited who admitted to hospital for recent stroke in the Department of Neurology, First Affiliated Hospital of Soochow University between September 2003 and February 2005. Subjects were aged (64±7 ) years, ranging from 47 to 79 years old. They all met the diagnosis criteria of various cerebrovascular diseases formulated in the 4th National Cerebrovascular Disease Conference and confirmed as stroke by skull CT or MRI; The time from onset to tentative administration was less than 7 days; The patients had clear consciousness, without obvious language disorder. They were randomized into treatment group (n =48) and placebo group (n =42). METHODS: ①All the patients were given routine treatment according to treatment guideline of cerebrovascular disease after admission. Patients in the treatment group and placebo group received 20 mg/d fluoxetine and placebo (component: vitamin C) for 8 weeks, respectively. ② Neurologic deficit was assessed according to 24-item Hamilton Rating Scale for Depression (HAMD) and Activity of Daily Living Scale (ADL) before and at 2,4 and 8 weeks after test, separately; Meanwhile, the levels of platelet 5-HT and plasma 5-HT were determined. Grading criteria of HAMD intergral depression: non-depression < 8 points; mild depression 8–20 points; moderate depression 21–35 points; severe depression > 35 points. ADL was assessed with Barthel index score (full mark 100 points). Higher points indicated better incidence and smaller dependence. Neurologic deficit score was made according to scoring criteria of neurologic deficit formulated in 1995 4th National Cerebrovascular Disease Conference: a score of 0–15 indicated a mild focal neurologic deficit, a score of 16–30 a moderate focal neurologic deficit, and a score of 31–45 a severe focal deficit. MAIN OUTCOME MEASURES: Scores of HAMD, ADL and neurologic deficit, and levels of plasma and platelet 5-HT of patients from 2 groups before, 2,4 and 8 weeks after test. RESULRS: Seventy-three of 90 randomized patients participated in the final analysis. In the treatment group, 11 patients dropped out due to insufficient clinical response (n =4), somatic side effects (n =2), intervening medical illness (n =1), hypomania (n =3), and other reasons (n =2). In the placebo group, 6 patients existed due to insufficient clinical response (n =2), somatic side effects (n =1) and other reasons (n =3). ① Before treatment, there were no significant differences in scores of HAMD, DAL and neurologic deficit in patients between two groups (P > 0.05). After 8 weeks of treatment, the scores of HAMD, DAL and neurologic deficit in the treatment group were significantly different from those in the placebo group (12.6±5.3 vs. 16.3 ±3.7; 8.6±6.4 vs. 11.2±6.4; 60.4±12.5 vs. 52.3±13.5, P < 0.01). ② After 8 weeks of treatment, platelet 5-HT level of patients in the treatment group was significantly lower than that in the placebo group [(325.3± 110.5) mg/L vs. (653.6±138.4) mg/L, P < 0.05], while there were no significant differences in plasma 5-HT between two groups (P > 0.05). CONCLUSION: Early fluoxetine treatment obviously retards PSD. The increase of platelet 5-HT level promotes the recovery of neurologic function.     

Fluoxetine for poststroke depression A randomized placebo controlled clinical trial

BACKGROUND: Studies have demonstrated that poststroke depression(PSD) may be related with the disequilibrium between noradrenaline and 5-hydroxytryptamine (5-HT) caused by cerebral injury. The injured regions involve noradrenergic and 5-hydroxytryptaminergic neurons as well as conduction pathway. The levels of noradrenaline and 5-HT would be decreased. OBJECTIVE: To observe the effect of fluoxetine on preventing against PSD and recovery of neurologic function, and analyze the relationship of fluoxetine and the 5-HT level. DESIGN: A randomized controlled clinical trial. SETTING: Department of Neurology, First Hospital Affiliated to Soochow University. PARTICIPANTS: Ninety consecutive patients, 47 female and 43 male, were recruited who admitted to hospital for recent stroke in the Department of Neurology, First Affiliated Hospital of Soochow University between September 2003 and February 2005. Subjects were aged (64±7 ) years, ranging from 47 to 79 years old. They all met the diagnosis criteria of various cerebrovascular diseases formulated in the 4th National Cerebrovascular Disease Conference and confirmed as stroke by skull CT or MRI; The time from onset to tentative administration was less than 7 days; The patients had clear consciousness, without obvious language disorder. They were randomized into treatment group (n =48) and placebo group (n =42). METHODS: ①All the patients were given routine treatment according to treatment guideline of cerebrovascular disease after admission. Patients in the treatment group and placebo group received 20 mg/d fluoxetine and placebo (component: vitamin C) for 8 weeks, respectively. ② Neurologic deficit was assessed according to 24-item Hamilton Rating Scale for Depression (HAMD) and Activity of Daily Living Scale (ADL) before and at 2,4 and 8 weeks after test, separately; Meanwhile, the levels of platelet 5-HT and plasma 5-HT were determined. Grading criteria of HAMD intergral depression: non-depression < 8 points; mild depression 8–20 points; moderate depression 21–35 points; severe depression > 35 points. ADL was assessed with Barthel index score (full mark 100 points). Higher points indicated better incidence and smaller dependence. Neurologic deficit score was made according to scoring criteria of neurologic deficit formulated in 1995 4th National Cerebrovascular Disease Conference: a score of 0–15 indicated a mild focal neurologic deficit, a score of 16–30 a moderate focal neurologic deficit, and a score of 31–45 a severe focal deficit. MAIN OUTCOME MEASURES: Scores of HAMD, ADL and neurologic deficit, and levels of plasma and platelet 5-HT of patients from 2 groups before, 2,4 and 8 weeks after test. RESULRS: Seventy-three of 90 randomized patients participated in the final analysis. In the treatment group, 11 patients dropped out due to insufficient clinical response (n =4), somatic side effects (n =2), intervening medical illness (n =1), hypomania (n =3), and other reasons (n =2). In the placebo group, 6 patients existed due to insufficient clinical response (n =2), somatic side effects (n =1) and other reasons (n =3). ① Before treatment, there were no significant differences in scores of HAMD, DAL and neurologic deficit in patients between two groups (P > 0.05). After 8 weeks of treatment, the scores of HAMD, DAL and neurologic deficit in the treatment group were significantly different from those in the placebo group (12.6±5.3 vs. 16.3±3.7; 8.6±6.4 vs. 11.2±6.4; 60.4±12.5 vs. 52.3±13.5, P < 0.01). ② After 8 weeks of treatment, platelet 5-HT level of patients in the treatment group was significantly lower than that in the placebo group [(325.3±110.5) mg/L vs. (653.6±138.4) mg/L, P < 0.05], while there were no significant differences in plasma 5-HT between two groups (P > 0.05). CONCLUSION: Early fluoxetine treatment obviously retards PSD. The increase of platelet 5-HT level promotes the recovery of neurologic function.     

Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 expression in early focal cerebral infarction following urokinase thrombolysis in rats

Activity of matrix metalloproteinase-9 increases following cerebral ischemia/reperfusion,and is associated with cerebral microvascular permeability,blood-brain barrier destruction,inflammatory cell infiltration and brain edema.Matrix metalloproteinase-9 also likely participates in thrombolysis.A rat model of middle cerebral artery infarction was established by injecting autologous blood clots into the internal carotid artery.At 3 hours following model induction,urokinase was injected into the caudal vein.Decreased neurological severity score,reduced infarct volume,and increased expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 were observed in the cerebral cortex 24 hours after urokinase thrombolysis.These results suggest that urokinase can suppress damage in the acute-early stage of cerebral infarction.     

Remodeling of motor cortex function in acute cerebral infarction patients following human urinary kallidinogenase A functional magnetic resonance imaging evaluation after 6 months

A total of 29 patients were treated within 48 hours after acute subcortical cerebral infarction with Xuesaitong or Xuesaitong plus human urinary kallidinogenase for 14 days.Neurological deficits,activity of daily living,and evaluations of distal upper limb motor functions at the 6-month follow-up showed that patients treated with Xuesaitong plus human urinary kallidinogenase recovered better than with Xuesaitong alone.In addition,functional MRI revealed that activation sites were primarily at the ipsilesional side of injury in all patients.Human urinary kallidinogenase induced hyperactivation of the ipsilesional primary sensorimotor cortex,premotor cortex,supplementary motor area,and contralesional posterior parietal cortex.Results showed that human urinary kallidinogenase improved symptoms of neurological deficiency by enhancing remodeling of long-term cortical motor function in patients with acute cerebral infarction.     

神经保护药物干预短暂性脑缺血的临床分析

Transient ischemic attack(TIA) is an acute cerebrovascular incident,and is generally considered the best opportunity for early neuroprotective treatment against cerebral ischemia.This study retrospectively analyzed 80 patients with TIA(38 males and 42 females).Among 61 patients who received neuroprotective cerebrolysin treatment within 24 hours after TIA onset,13(21.31%) patients suffered subsequent strokes.Among 19 patients who received neuroprotective cerebrolysin treatment within 24-72 hours after TIA onset,seven(36.84%) developed cerebral infarction.There was a significant difference in the proportion of subsequent strokes between patients receiving cerebrolysin treatment within 24 hours and 24-72 hours after TIA onset(P = 0.438).These findings suggest that neuroprotective drugs administrated within 24 hours after TIA onset help reduce the incidence of subsequent strokes.The results demonstrate usefulness of the ABCD2 score at TIA patients in the determination of short-term and long-term cerebrovascular risk,including the frequency of subsequent ischemic cerebral infarctions up to 12 months.     

Dynamic changes in fibrinogen levels of patients with acute cerebral infarction after taking defibrase*☆

BACKGROUND： At present, as a therapeutic drug mainly for reducing fibrinogen （FIB） levels, the dynamic influence of defibrase on the FIB levels of patients with acute cerebral infarction has not been clearly ascertained. OBJECTIVE： To observe the dynamic changes in FIB levels of patients with acute cerebral infarction at different time points after taking defibrase. DESIGN, TIME AND SETTING： Randomized controlled clinical trial. The study was conducted in the Department of Neurology, the Second Affiliated Hospital of Jinan University, from June to November 2006. PARTICIPANTS： Sixty patients with acute cerebral infarction, who had been treated by the Neurological Department of the Second Affiliated Hospital of Jinan University from June to November 2006, were selected, including 37 males and 23 females, aged 35-75 years. All cases met the diagnostic criteria formulated by the Fourth National Cerebrovascular Disease Conference within 12 hours of onset. All the patients were confirmed with definite hemiparesis and cerebral infarction without coma, and were randomly divided into two groups： a treatment group （n =40） and a control group （n =20）. Patients＇ families had the right to be informed and agree with the treatment, which had permission from the Hospital Ethics Committee. METHODS： Patients in the control group were given routine treatment with 30 mL fleabane and 0.75 g cytidine diphosphate added to 500 mL saline solution once a day for 14 consecutive days. Patients in the treatment group were given routine treatment and Haiwang defibrase injection （purchased from Changchu Guoao Bio-Pharmaceutical Co. Ltd., Approval document number H10983237） within 12 hours of infarction. Defibrase doses of 15, 12.5 and 10 U were given over 2 hours according to the patients＇ pre-treatment plasma FIB levels of ≥ 4.50 g/L, 3.50 4.49 g/L and 1.00 3.49 g/L, respectively. Plasma FIB levels in the treatment group were measured before, and once every six hours for 48 hours after administration of defib     

Logistic regression analysis on risk factors for vascular dementia following cerebral infarction in 403 patients from Chongqing City——Hospital and family follow-up studies

BACKGROUND: Studies have demonstrated that the risk factors of vascular dementia following stroke are greatly different in region, race and other aspects. OBJECTIVE: To analyze the conditions and incidental risk factors of vascular dementia in patients with acute cerebral infarction from Chongqing City. DESIGN: Case analysis. SETTING: Department of Neurology, Daping Hospital, Third Military Medical University of Chinese PLA. PARTICIPANTS: Altogether 546 inpatients with acute ischemic stroke admitted to Department of Neurology, Daping Hospital, Third Military Medical University of Chinese PLA between May 1999 and December 2002 were involved in this study. The involved patients, including 295 males and 251 females, aged 55–94 years, dwelled in Chongqing over 5 years. They were admitted to hospital within 48 hours of attack of acute ischemic stroke, and survived for over 3 months. Informed consents were obtained from all the involved subjects. METHODS: ① Following the same standard, cognitive and social function evaluations were conducted by one physician on admission and 3 months after admission. Unified questionnaire, consisting of general characteristics, vascular risk factors, stroke characteristics, neurological physical sign, and other 28 factors of involved subjects, was used in all the patients. According to the investigation results, the patients were assigned into 2 groups: dementia group and non-dementia group. ②Ischemic stroke was diagnosed according to acute ischemic brain disorder > 24 hours and CT or MRI imageology. ③ Neurophysiological examination was conducted in all the patients at 7 to 10 days after stroke (score was two SD less than or equaled to normal level was considered as abnormal). ④Diagnosis and statistics of dementia were carried out with Mini-Mental State Examination and The Diagnostic and Statistical Manual of Mental Disorders-Ⅳ (published by American Psychiatric Association) on admission and 3 months after admission. Neurologic deficit scoring was carried out with the National Institutes of Health Stroke Scale. ⑤ Chi-square test was used for categorical variable, and t test for quantitative variable between dementia group and non-dementia group. Dementia-related factors were performed multiple-factor Logistic regression model analysis. MAIN OUTCOME MEASURES: Incidence of dementia and dementia-related risk factors of patients. RESULTS: Altogether 546 patients with stroke were involved in this study, 403 of them participated in the final analysis, and 143 dropped out. A total of 342 were followed-up in the hospital and 61 at home. At 3 months after cerebral infarction, vascular dementia occurred in 87 (21.6%) of 403 patients. The main risk factors were age (OR 1.179; 95%CI 1.130–1.230), low education level (OR 1.806; 95%CI 1.024–3.186), daily alcohol drinking (OR 3.447; 95%CI 1.591–7.468), stroke history (OR 2.531; 95%CI 1.419–4.512), atrial fibrilation(OR 3.475; 95%CI 1.712–7.057), dysphonia (OR 5.873; 95%CI 2.620–13.163) and left carotid artery infarction (OR 1.975; 95%CI 1.152–3.388). CONCLUSION: The incidence of vascular dementia is determined by synthetic action of multiple risk factors. Dysphonia is the most important influencing factor.     

Magnetic resonance diffusion tensor imaging following major ozonated autohemotherapy for treatment of acute cerebral infarction

Major ozonated autohemotherapy has been shown to promote recovery of upper limb motor function in patients with acute cerebral infarction,but whether major ozonated autohemotherapy affects remote injury remains poorly understood.Here,we assumed that major ozonated autohemotherapy contributes to recovery of clinical function,possibly by reducing remote injury after acute cerebral infarction.Sixty acute cerebral infarction patients aged 30–80 years were equally and randomly allocated to ozone treatment and control groups.Patients in the ozone treatment group received medical treatment and major ozonated autohemotherapy(47 mg/L,100 m L ozone) for 10 ± 2 days.Patients in the control group received medical treatment only.National Institutes of Health Stroke Scale score,modified Rankin scale score,and reduced degree of fractional anisotropy values of brain magnetic resonance diffusion tensor imaging were remarkably decreased,brain function improved,clinical efficiency significantly increased,and no obvious adverse reactions detected in the ozone treatment group compared with the control group.These findings suggest that major ozonated autohemotherapy promotes recovery of neurological function in acute cerebral infarction patients by reducing remote injury,and additionally,exhibits high safety.     

rt-PA 动脉溶栓联合机械取栓治疗急性脑栓塞的临床疗效研究

目的：观察 rt-PA 动脉溶栓联合机械取栓治疗急性脑栓塞的临床疗效。方法回顾性分析 rt-PA 动脉溶栓联合机械取栓治疗的10例急性脑栓塞病例,采用 NIHSS 评分评估患者治疗前及治疗24 h 后的神经功能缺损程度,3月后采用改良 Rankin 量表（mRS）评估患者预后。结果治疗24 h 后患者 NIHSS 评分显著低于治疗前（P 〈0.01）,3月后 mRS 0~2分为90%。结论rt-PA 动脉溶栓联合机械取栓是治疗急性脑栓塞的一种有效方法。     

溶栓治疗对脑梗死大鼠细胞骨架结构微管相关蛋白-2的影响

目的:观察尿激酶溶栓治疗对神经细胞骨架结构微管相关蛋白-2(MAP-2)的影响。方法:用自体血栓法制 作大鼠大脑中动脉闭塞(MCAO)模型,在MCAO后30min静脉注射尿激酶(UK)溶栓,通过神经功能评分判断溶栓的疗 效,HE染色进行病理观察,用免疫组织化学的方法研究溶栓对缺血皮层和海马MAP-2蛋白表达的影响。结果:溶栓组 神经功能评分较未溶栓组有显著提高,HE染色见病变范围明显缩小。MCAO后2h缺血区树突MAP-2表达较对照组 即有明显下降(P<0．05),随着缺血时间延长树突及胞体MAP-2降解增加,而溶栓治疗各时间点MAP-2表达较未溶栓 组显著提高(P<0．01)。结论:减少MAP-2的降解可能是溶栓治疗改善神经功能的机制之一。溶栓治疗后早期半暗带 区MAP-2表达在树突减少而在神经元胞体基本正常,这可能是缺血后神经元顿抑的形态学基础。     

尿激酶联合镁剂治疗大鼠急性脑梗死的实验研究

目的　观察尿激酶溶栓联合硫酸镁神经保护对大鼠急性脑梗死的疗效。方法　应用光化学诱导法建立大鼠大脑中动脉闭塞(MCAO)模型,分别于术后2 h、6 h和10 h 3 个时间点进行干预,每个时间点内再分为生理盐水对照组、尿激酶溶栓组、尿激酶加硫酸镁治疗组,术后24 h观察大鼠神经功能缺损评分及脑梗死体积的变化。结果　MCAO后2 h尿激酶溶栓组神经功能显著改善,梗死体积缩小(与生理盐水对照组相比,P<0.01),尿激酶加硫酸镁治疗组效果更好;MCAO后6 h、10 h尿激酶溶栓组与生理盐水对照组相比无显著性差异(P>0.05),而尿激酶加硫酸镁治疗组的神经功能缺损评分、脑梗死体积与生理盐水对照组及尿激酶溶栓组相比有显著差异(P<0.05或P<0.01)。结论　早期脑梗死特别是2 h内的超早期脑梗死应用尿激酶溶栓有效;加用镁剂进行神经保护可对尿激酶溶栓疗效产生协同作用,并可能扩大脑梗死溶栓治疗的时间窗。     

急性缺血性卒中静脉溶栓治疗的疗效及预后相关因素分析

目的::静脉溶栓治疗是急性缺血性卒中最有效的治疗方法。本研究旨在探讨在现行卒中指南的指导下,静脉溶栓治疗的早期疗效和远期预后,以期为提高静脉溶栓治疗的获益提供临床证据。方法::记录136例接受重组组织型纤溶酶原澈活剂(recombinant tissue plasminogen activator,rt-PA)静脉溶栓治疗的急性缺血性卒中患者的人口统计学特征、血管危险因素和本次卒中发生的情况。采用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)对静脉溶栓治疗的早期疗效进行评价,改良Rankin量表(modified Rankin scale,mRS)对卒中发生后3个月时的功能独立情况进行评价。采用单因素和多因素分析对静脉溶栓治疗的早期疗效和卒中发生后3个月时功能独立的相关影响因素进行分析。结果::静脉溶栓治疗后24 h时,早期有效66例(48.5%);卒中发生后3个月时,64例(47.1%)达功能独立。静脉溶栓治疗后2 h、24 h和7 d的早期疗效与卒中发生后3个月时的功能独立显著相关(P值均0.05)。静脉溶栓治疗前收缩压是静脉溶栓治疗早期疗效的独立影响因素(P0.05)。结论::降低静脉溶栓治疗前收缩压可能改善溶栓治疗的早期疗效。依据溶栓治疗的早期疗效,可能判断溶栓治疗的远期预后。     

静脉溶栓后丁苯肽序贯治疗急性脑梗死的疗效观察

目的评价静脉溶栓后丁苯肽序贯治疗急性脑梗死的疗效。方法选取我院神经内科于2012-06-2016-12确诊的48例急性脑梗死患者为研究对象,随机分为常规治疗组和序贯治疗组。常规治疗组采取rt-PA溶栓+常规进行治疗(活血化瘀、改善循环、抗血小板聚集、改善脑代谢、清除自由基等),序贯治疗组在溶栓+常规治疗的基础上加用丁苯肽氯化钠注射液,14d后改为丁苯肽软胶囊治疗。疗程结束后,评价2组疗效和神经功能缺陷评分。结果与治疗前相比,常规治疗组和序贯治疗组治疗后NIHSS评分均显著降低,序贯治疗组降低更为明显(P0.05);序贯治疗组mRS评分和有效率均显著优于常规治疗组(P0.05)。结论静脉溶栓后丁苯肽序贯治疗能更有效治疗急性脑梗死。     

Neurologic worsening during the acute phase of ischemic stroke

BACKGROUND: Although capacities for intensive monitoring of patients with stroke are still limited, patients at risk for early neurologic worsening are poorly defined. OBJECTIVE: To identify patients at risk for neurologic worsening. DESIGN: An inception cohort was assessed using the National Institutes of Health Stroke Scale (NIH-SS) at hospital admission and again 48 to 72 hours later. SETTING: Eleven neurologic departments with acute stroke units. PATIENTS: A total of 1964 consecutive patients admitted within 4 hours of the onset of acute cerebral ischemic symptoms. MAIN OUTCOME MEASURES: Underlying reasons for and possible predictors of neurologic worsening. RESULTS: A total of 256 patients (13.0%) had an increased score of 1 point or more on the NIH-SS after 48 to 72 hours. Neurologic worsening was attributed to progressive stroke in 33.6% of patients, increased intracranial pressure in 27.3%, recurrent cerebral ischemia in 11.3%, and secondary parenchymal hemorrhage in 10.5%. A multivariate logistic regression analysis identified internal carotid artery occlusion, medial cerebral artery (M1) occlusion, territorial infarction, brainstem infarction, and diabetes mellitus as independent predictors of neurologic worsening on the NIH-SS. Worsening of key neurologic functions (consciousness, gaze, arm or leg motor function, and speech) occurred in 223 patients (11.4%), and worsening of 4 points or more on the NIH-SS total score occurred in 148 patients (7.5%). CONCLUSION: Besides initial stroke severity and comorbid conditions, ultrasound and imaging can provide valuable information about the risk of worsening of stroke symptoms in the acute phase and thus can identify patients who could benefit most from intensive monitoring.     

Solitaire AB支架取栓治疗静脉溶栓禁忌的急性缺血性脑卒中

目的探讨应用Solitaire AB支架机械取栓治疗静脉溶栓禁忌的急性缺血性脑卒中的疗效和安全性。方法回顾性分析2015年1月~2016年8月在吉林大学第二医院接受Solitaire AB支架机械取栓治疗的19例静脉溶栓禁忌的急性缺血性脑卒中患者的临床资料。男性13例,女性6例,年龄30~82岁,静脉溶栓禁忌的因素为超过最佳溶栓时间窗(6 h)和(或)NIHSS评分较高(>22)。采用t检验比较患者术前和术后脑梗死溶栓分级(TICI分级)、术前和术后1 w的NIHSS评分的变化评价疗效,采用术后90 d改良的Rankin量表(mRS)评估预后。结果 19例患者中的18例责任血管均成功获得再通,再通率94.7%。从发病到血管再通时间:颈内动脉系统为(6.8±1.5)h,椎动脉系统为(10.0±2.9)h,其中从穿刺到再通时间为(83.3±39.9)min。术前NIHSS评分为(27.3±9.0)分,术后7 d时NIHSS评分为(9.71±7.98)分,较术前有明显改善(P<0.01)。术后90 d随访,预后良好者11例(mRS 0~2),预后良好率为57.89%,死亡3例,死亡率为15.79%。结论 Solitaire AB支架取栓治疗静脉溶栓禁忌的急性缺血性脑卒中安全有效,血管再通率高,可明显改善临床预后。     

阿替普酶静脉溶栓治疗急性脑梗死的疗效及安全性

目的研究重组组织型纤溶酶原激活物(rt-PA)静脉给药溶栓治疗急性脑梗死的临床效果。方法回顾性分析发病在4.5h内,具有溶栓指征的急性脑梗死患者105例,其中对照组56例仅给予抗血小板聚集、调脂稳定斑块等常规治疗方案,观察组49例给予rt-PA静脉溶栓治疗,24h后若无明显出血,开始给予脑梗死常规治疗。比较2组治疗后90d美国国立卫生院卒中量表(NIHSS)评分、Barthel指数(BI)评分及改良Rankin量表(mRS)评分改善情况,以评价rt-PA治疗急性脑梗死临床疗效。结果 2组治疗前NIHSS评分差异无统计学意义(P0.05),观察组溶栓后2h、24h、7d时NIHSS评分显著低于对照组(P0.05);观察组90d时mRS评分显示预后良好的患者较对照组明显增多,2组比较差异有统计学意义(P0.05);与对照组比较,观察组90d时Barthel指数评分明显升高(P0.05)。虽然观察组总体出血事件较对照组增高(P0.05);但2组症状性脑出血比较差异无统计学意义(P0.05)。结论发病4.5h以内,静脉给予rt-PA溶栓治疗急性脑梗死具有显著的临床疗效,且安全性较高,值得临床推广应用。     

Predictors of clinical improvement, angiographic recanalization, and intracranial hemorrhage after intra-arterial thrombolysis for acute ischemic stroke.

BACKGROUND AND PURPOSE: We sought to evaluate predictors of clinical outcome, angiographic success, and adverse effects after intra-arterial administration of urokinase for acute ischemic stroke. METHODS: We designed a Brain Attack program at University Hospitals of Cleveland for diagnosis and treatment of patients presenting within 6 hours of onset of neurological deficit. Patients with ischemia referable to the carotid circulation were treated with intra-arterial urokinase. Angiographic recanalization was assessed at the end of medication infusion. Intracerebral hemorrhage was investigated immediately after and 24 hours after treatment. Stroke severity was determined, followed by long-term outcome. RESULTS: Fifty-four patients were treated. There was improvement of >/=4 points on the National Institutes of Health Stroke Scale from presentation to 24 hours after onset in 43% of the treated patients, and this was related to the severity of the initial deficit. Forty-eight percent of patients had a Barthel Index score of 95 to 100 at 90 days, and total mortality was 24%. Cranial CT scans revealed intracerebral hemorrhage in 17% of patients in the first 24 hours, and these patients had more severe deficits at presentation. Eighty-seven percent of patients received intravenous heparin after thrombolysis, and 9% of them developed a hemorrhage into infarction. Angiographic recanalization was the rule in complete occlusions of the horizontal portion of the middle cerebral artery, but distal carotid occlusions responded less well to thrombolysis. CONCLUSIONS: The intra-arterial route for thrombolysis allows for greater diagnostic precision and achievement of a higher concentration of the thrombolytic agent in the vicinity of the clot. Disadvantages of this therapy lie in the cost and delay. Severity of stroke and site of angiographic occlusion may be important predictors of successful treatment.     

血清L-Arg,ADMA水平与急性脑梗死患者静脉溶栓疗效的相关性分析

目的 探究血清L-精氨酸(L-Arg)、非对称性二甲基精氨酸(ADMA)水平与急性脑梗死患者行重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓疗效的相关性。方法 选取2017年10月-2019年10月在本院神经内科接受rt-PA静脉溶栓治疗的急性脑梗死患者80例为研究对象,随访90 d,根据随访的mRS评分分为预后良好(mRS评分≤2分)组53例和预后不良(mRS评分>2分)组27例; 采用酶联免疫吸附(ELISA)法检测各研究对象rt-PA静脉溶栓后24h内血清中L-Arg,ADMA的水平; 在患者rt-PA静脉溶栓后24 h内及治疗5天后行美国国立卫生研究院卒中量表(NIHSS)测评,比较患者2个时间点NIHSS评分差(△NIHSS分); Pearson法分析L-Arg与ADMA水平、△NIHSS水平的相关性; 采用COX法分析影响急性脑梗死患者静脉溶栓后预后不良的危险因素。结果 与预后良好组比较,预后不良组患者血清L-Arg水平、△NIHSS评分较低(P<0.05),血清ADMA水平较高(P<0.05); Pearson分析显示,L-Arg与ADMA水平呈负相关(r=-0.758,P<0.05); 与△NIHSS正相关(r=0.668,P<0.05),ADMA水平与△NIHSS呈负相关(r=-0.674,P<0.05); 多因素COX分析显示,低水平L-Arg、高水平ADMA、低△NIHSS评分是影响急性脑梗死患者rt-PA静脉溶栓后预后不良的独立危险因素(P<0.05)。结论 急性脑梗死患者静脉溶栓的疗效可能与血清L-Arg,ADMA水平相关,L-Arg水平降低、ADMA水平升高可能提示急性脑梗死患者静脉溶栓后预后不良的发生。