Use of various CT imaging methods for diagnosis of acute ischemic cerebrovascular disease

Thirty-four patients with cerebral infarction and 18 patients with transient ischemic attack were examined by multi-slice spiral CT scan, CT perfusion imaging, and CT angiography within 6 hours after onset. By CT perfusion imaging, 29 cases in the cerebral infarction group and 10 cases in the transient ischemic attack group presented with abnormal blood flow perfusion, which corresponded to the clinical symptoms. By CT angiography, various degrees of vascular stenosis could be detected in 41 patients, including 33 in the cerebral infarction group and eight in the transient ischemic attack group. The incidence of intracranial artery stenosis was higher than that of extracranial artery stenosis. The intracranial artery stenosis was located predominantly in the middle cerebral artery and carotid artery siphon, while the extracranial artery stenosis occurred mainly in the bifurcation of the common carotid artery and the opening of the vertebral artery. There were 34 cases （83%） with convict vascular stenosis and perfusion abnormalities, and five cases （45%） with perfusion abnormalities but without convict vascular stenosis. The incidence of cerebral infarction in patients with National Institutes of Health Stroke Scale scores 〉 5 points during onset was significantly higher than that in patients with National Institutes of Health Stroke Scale scores 〈 5 points. These experimental findings indicate that the combined application of various CT imaging methods allows early diagnosis of acute ischemic cerebrovascular disease, which can comprehensively analyze the pathogenesis and severity of acute ischemic cerebrovascular disease at the morphological and functional levels.

Significance of ultrasound evaluation of carotid atherosclerotic plaque for diagnosing ischemic cerebrovascular disease

BACKGROUND： Carotid artery is the main source for craniocerebral blood supply. Its intimal plaque formation and arterial stenosis degree both are the risk factors for ischemic cerebrovascular disease.Therefore, the close relationship of carotid atherosclerotic plaque and ischemic cerebrovascular disease, and ultrasound evaluation of carotid atherosclerotic plaque have become the hot spot in studying ischemic cerebrovascular disease.OBJECTIVE： This study was to detect the degree of carotid atherosclerosis of ischemic cerebrovascular disease patients by ultrasonography, and to analyze the situation of carotid atherosclerosis and its relationship with clinic.DESIGN： Clinical randomized concurrent control experiment.SETTING： Lintong Convalescent Hospital of Lanzhou Military Area Command of Chinese PLA.PARTICIPANTS： Totally 60 outpatients and inpatients with ischemic cerebrovascular disease, 42 males and 18 females, admitted to Lintong Convalescent Hospital of Lanzhou Military Area Command of Chinese PLA between January 2006 and December 2006 were involved in the patient group. They met the diagnosis criteria of ischemic cerebrovascular disease constituted by the 4th Cerebrovascular Disease Conference in 1996, and were confirmed to suffer from ischemic cerebrovascular disease by skull CT and MRI. Another 20 subjects who received healthy examination concurrently in the same hospital, 12 males and 8 females, were involved in the control group. Informed consents of detected items were obtained from involved subjects.METHODS： The plaque thickness of mid portion, distal end and crotch of common carotid artery （CCA）,internal carotid artery （ICA）, external carotid artery （ECA） and vertebral artery （VA） of involved subjects,who received health examination was separately detected with color Doppler ultrasonograph （HDI-5000）.Then, total integral of plaque was calculated. The intima-media thickness （IMT） was measured with two-dimensional ultrasonography. The inner diameter stenosis degree of subjects who had plaque was measured. Blood flow parameters were recorded, and stenosis degree and plaque area were calculated. Blood flow volume of bilateral carotid artery and VA was separately measured with ultrasound equipment software,and brain blood flow volume was calculated.MAIN OUTCOME MEASURES： Atherosclerotic degree and blood flow volume of patients of two groups.RESULTS： Sixty patients with ischemic cerebrovascular disease and twenty subjects who received health examination participated in the final analysis. ①The IMT thickness, total plaque score, and total plaque area of patient group was significantly superior to that of control group, respectively（ t=5.216 - 10.158, P 〈 0.05 ）.② There were significant differences in the stenosis degree of CCA, ICA and VA between patient group and control group （t=6.720 - 12.816, P 〈 0.05 ） . ③ The blood flow volume of CCA, ICA, VA and brain of patient group was significantly lower than that of control group, respectively （t=2.872 - 10.860, P 〈 0.05）.CONCLUSION： Ischemic cerebrovascular disease patients have different degrees of changes in atherosclerosis and arterial blood flow.

Factors influencing ischemic cerebrovascular disease complicated by hyperhomocysteinemia

BACKGROUND： Hyperhomocysteinemia, as an important risk factor for ischemic cerebrovascular disease is receiving increasing attention. OBJECTIVE： To analyze whether differences of gender, age, cerebrovascular disease typing, and disease conditions exist when ischemic cerebrovascular disease occurs together with hyperhomocysteinemia. DESIGN： A controlled observation. SETTING： Department of Neurology, Tianjin Huanhu Hospital. PARTICIPANTS： A total of 601 acute ischemic cerebrovascular disease inpatients, comprising 386 males and 215 females, aged 33-90 years old, were admitted to the Department of Stroke, Tianjin Huanhu Hospital between August 2005 and April 2007, and were recruited for this study. All included patients consisted of 342 aged patients （≥ 60 years old） and 92 middle-aged and young patients （〈 60 years old）. Among these patients, 48 suffered from transient cerebral ischemic attack, 138 from lacunar cerebral infarction, 273 from atherosclerotic stroke, 38 from cardiogenic cerebral infarction, 44 from agnogenic ischemic stroke, and 6 from other factor-induced ischemic strokes. All included inpatients corresponded to the diagnosis criteria of acute ischemic cerebrovascular disease, formulated in the 4^th National Working Conference of Cerebrovascular Disease, and were confirmed as acute ischemic cerebral infarction by CT and/or MRI examinations. Informed consents of laboratory measurements were obtained from all subjects, and this study was approved by the Hospital＇s Ethics Committee. METHODS： Following admission, 2 mL venous blood was collected from each fasting patient on the third morning. Plasma homocysteine level was measured by an enzymatic cycling assay with a CX5 reader （Beckman, USA）. Plasma homocysteine levels ≥ 16μ mol/L were defined as hyperhomocysteinemia. Clinical neurological function deficit scoring was also performed for each ischemic stroke patient using Chinese stroke scales. Scores ranged from 0 45 （0-15： mild neurological function deficits, 16-30： moderate neurological deficits, and 31-45： severe neurological deficits）. The scores positively correlated with severity of stroke. MAIN OUTCOME MEASURES： Incidence of ischemic cerebrovascular disease patients complicated by hyperhomocysteinemia and the effects of patient age and gender; plasma homocysteine levels of each type of ischemic cerebrovascular disease; and effects of ischemic cerebrovascular disease conditions on plasma homocysteine levels. RESULTS： All 601 inpatients with acute ischemic cerebrovascular disease were included in the final analysis. The detection rate of homocysteine was significantly higher in aged patients than in middle-aged and young patients （ x^2 = 5.353 0, P 〈 0.05）. The incidence of hyperhomocysteinemia was significantly higher in male patients than in female patients （ x^2 = 9.484 4, P 〈 0.05）. There was no significant difference in the incidence of hyperhomocysteinemia among various types of ischemic cerebrovascular diseases （P 〉 0.05）. No significant difference in incidence of hyperhomocysteinemia existed between mild, moderate, and severe cerebrovascular disease patients （P 〉 0.05）. CONCLUSION： There is a greater chance of ischemic cerebrovascular disease complicated by hyperhomocysteinemia in older, male patients.

Meta-analysis of 5, 10-methylenetetrahydrofolate reductase gene polymorphism as a risk factor for ischemic cerebrovascular disease in a Chinese Han population

OBJECTIVE： To assess whether 5, 10-methylenetetrahydrofolate reductase （MTHFR） gene polymorphism （TT genotype or T allele） is a risk factor for ischemic cerebrovascular disease （ICVD）. DATA SOURCES： MEDLINE and PubMed databases from September 1997 to December 2009 were searched for case-control studies that examined MTHFR genotype in human ICVD using ＂MTHFR, gene, polymorphism, and ischemic cerebrovascular disease＂ as search key words. STUDY SELECTION： Eighteen associated studies were identified. The methods used to collect relevant information factors were similar between case and control groups, and diagnosis of ischemic cerebrovascular disease was in accordance with Trial of ORG 10172 in Acute Stroke Treatment criteria classification, with some referring to European Stroke Diagnostic Criteria. Quality of all included studies was evaluated, and meta-analysis was conducted using RevMan4.2 software （Cochrane Collaboration, http：//www.cochrane-handbook.org） following strict screening. MAIN OUTCOME MEASURES： The correlation between MTHFR gene TT genotype or T allele and ICVD was determined. RESULTS： Eighteen studies involving 4 295 patients with ICVD and 6 169 control subjects were included for this meta-analysis. There was a significant difference in MTHFR gene TT genotype or T allele frequency （x^2 = 15.737, 9.186, P 〈 0.01） between ICVD cases and controls. In addition, six Chinese Han population studies were specially reviewed by meta-analysis. Results showed no significant difference between ICVD and control groups with regard to frequency of MTHFR gene TT genotype and T allele （x^2 = 1.076, 2.434, P 〉 0.05） in the Chinese Han population. CONCLUSION： Results from the present meta-analysis suggested that the MTHFR gene TT genotype or T allele is a risk factor for ICVD. However, the TT genotype or T allele is not a risk factor for ICVD in the Chinese Han population.

Genetic relationship between serum pregnancy-associated plasma protein-A gene polymorphism and ischemic cerebrovascular disease in a Northern Han Chinese population

The present study recruited 193 patients with ischemic cerebrovascular disease from Inpatient and Outpatient Departments at the Affiliated Hospital of Qingdao University Medical College, China from August 2008 to May 2010, as well as 120 healthy volunteers from the Medical Examination Center at the Affiliated Hospital of Qingdao University Medical College, China, who served as controls for this study. Patients and control subjects were from the Han population in northern China. Enzyme- linked immunosorbent assay analysis revealed increased levels of serum pregnancy-associated plasma protein-A （PAPP-A） in ischemic cerebrovascular disease patients compared with healthy controls. In addition, the patients exhibited greater frequency of genotype CC and C alleles in a missense A/C （Tyr/Ser） polymorphism （dbSNP： rs7020782） of exon 14 in the PAPP-A gene. Multiple-factor logistic regression analysis on correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and ischemic stroke family history showed that the risk for ischemic cerebrovascular disease in the population without the A allele at the A/C genetic locus in exon 14 of the PAPP-A was 2-folds greater than the population expressing the A allele. These experimental findings suggested that ischemic cerebrovascular disease correlated with the C allele in exon 14 of PAPP-A. In addition, the A allele is likely a protective gene; individuals carrying the A allele were less prone to ischemic cerebrovascular disease compared with individuals without the A allele.

Effects of hypoxia-inducible factor 1 on ischemic cerebrovascular disease

Hypoxia-inducible factor 1, a nuclear transcription factor, is induced by hypoxia. Hypoxia-inducible factor 1, a heterodimeric DNA-binding protein, is composed of hypoxia-inducible factor 1α and hypoxia-inducible factor 1βsubunits, which are family members of the basic helix-loop-helix-PER, ARNT, SIM （PAS） protein. O2 concentration regulates hypoxia-inducible factor 1 activity via this subunit. Hypoxia-inducible factor 1α plays a major role in response to hypoxia and transcriptional activation, as well as in the target gene specificity of the DNA enhancer. Hypoxia-inducible factor 1β cannot be induced by hypoxia. This effect may be due to hypoxia-inducible factor 1 stability and activated conformation due to dimerization. Previous studies have shown that hypoxia-inducible factor 1 mRNA expression increases in the penumbra following ischemia/hypoxia. Hypoxia-inducible factor 1 plays an important role in brain tissue injury after ischemia by affecting a series of target genes, elevating tolerance to hypoxia, and ensuring survival of neural cells. This article summarizes the structure, function, expression, regulatory mechanisms, biological effects, and significance of hypoxia-inducible factor 1 in patients with ischemic cerebrovascular disease. As a transcriptional activator, hypoxia- inducible factor 1 plays a key role in hypoxic responses by stabilizing the internal environment. It also has been shown to regulate the expression of several genes. The regulatory effects of hypoxia-inducible factor 1 in patients with ischemic cerebrovascular disease have been described. The present review re-examined the concept of brain protection at the level of gene regulation.

Relevant research of autophagy and carotid plaque of ischemic cerebrovascular disease

Objective To analyze the correlation of autophagylevel and carotid plaque of ischemic cerebrovascular disease,so as to provide data evidence to its pathomechanism.Methods 127 patients with ischemic cerebrovascular disease were divided into 3 groups according to carotid plague scores.The count and degree of cranial artery stenosis were observed with digital subtraction angiogra-

Ischemic stroke susceptibility gene in a Northern Han Chinese population

Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, we recruited 291 patients with ischemic cerebrovascular disease from the Affiliated Hospital of Qingdao University Medical College, China, and 226 healthy controls. Both patients and controls were from the Han population in northern China. Immunoresonance scattering assays detected increased serum amyloid A protein, C-reactive protein, and interleukin-18 levels in ischemic cerebrovascular disease patients compared with healthy controls. Analysis of the –607C/A （rs1946518） polymorphism in the interleukin-18 gene promoter showed ischemic cerebrovascular disease patients exhibited increased frequencies of the CC genotype and C alleles than healthy controls. Genotype and allele frequencies of the interleukin-18 –137G/C （rs187238） polymorphism and the –13T/C （rs11024595） polymorphism in the 5＇-flanking region of serum amyloid A, showed no significant difference between the two groups. Multivariate logistic regression analysis on the interleukin-18 promoter A/C genetic locus, for correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and an ischemic stroke family history, showed ischemic cerebrovascular disease risk in individuals without the A allele （C homozygotes） was 2.2-fold greater than in A allele carriers. Overall, our findings suggest that the –13T/C （rs11024595） polymorphism in the 5′-flanking region of serum amyloid A has no correlation with ischemic cerebrovascular disease, but the C allele of the –607C/A （rs1946518） polymorphism in the interleukin-18 promoter is a high-risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely a protective gene for ischemic cerebrovascular disease.

Changes in HIF-1α, VEGF, NGF and BDNF Levels in Cerebrospinal Fluid and TheirRelationship with Cognitive Impairment in Patients with Cerebral Infarction

Summary： This study was carried out to investigate the role of intrinsic neuroprotective mechanisms in the occurrence and development of vascular cognitive impairment （VCI） with the goal of providing a target for the treatment and prevention of VCI. Inpatients with proven cerebral infarction on cranial computed tomography （CT） were recruited as the ischemic cerebrovascular diseases （ICVD） group, and the patients with mixed stroke were excluded. In ICVD group, 12 patients were diagnosed as having VCI and served as VCI group. Inpatients undergoing surgical operation in our hospital were enrolled as control group. Double-antibody sandwich enzyme-linked immunosorbent assay （ELISA） was employed to detect the levels of hypoxia-inducible factor 1-alpha （HIF-1α）, vascular endothelial growth factor （VEGF）, nerve growth factor （NGF） and brain-derived neurotrophic factor （BDNF） in the cerebrospinal fluid of patients with ICVD. Associations between the levels of these factors and the Mini-Mental State Examination （MMSE） score were evaluated. In ICVD and VCI groups, the levels of HIF-1α and NGF in the cerebrospinal fluid were markedly lower than those in control group （P=-0.037 and P=0.000; P=0.023 and P=-0.005）. In ICVD and VCI groups, the MMSE score was negatively related to VEGF level in the cerebrospinal fluid （r=-0.327, P=0.021; r=-0.585, P=0.046）. In VCI group, HIF-1α level was correlated with NGF level （r=0.589, P=0.044）. HIF-1α and NGF are involved in ischemic and hy- poxic cerebral injury. The HIF signaling pathway plays an important role in intrinsic neuroprotection. Upregulation and maintenance of HIF-1α and NGF expression may attenuate VCI. Changes in VEGF levels are related to the occurrence and development of cognitive impairment.

Inhibitory effect of icariin on expression of myelin inhibitory factors in the central nervous system of rats with focal cerebral ischemia

Icariin, the major active component of Chinese medicinal herb epimedium brevicornum maxim, is used widely in traditional Chinese medicine for the treatment of neurological diseases. However, the effects of icariin on myelin inhibitory factors are as yet unclear. In the present study, administration of icariin at 20 mg/kg showed a marked reduction in neurological deficit of middle cerebral artery occlusion rats. Icariin exhibited better inhibitory effects on myelin inhibitory factors： Nogo-A, myelin-associated glycoprotein and oligodendrocyte myelin glycoprotein in ischemia regions of middle cerebral artery occlusion rats compared with monosialotetrahexosylganglioside. These results indicate that icariin exhibits potent inhibitory effects on expression of myelin inhibitors after middle cerebral artery occlusion-induced focal cerebral ischemia in vivo. This effect may be mediated, at least in part, by the inhibition of both Nogo-A, myelin-associated glycopretein and oligodendrocyte myelin glycoprotein activation, followed by the enhancement of axonal sprouting and regeneration, resulting in neurological functional recovery.

Buyanghuanwu decoction promotes angiogenesis after cerebral ischemia/reperfusion injury：mechanisms of brain tissue repair

Buyanghuanwu decoction has been shown to protect against cerebral ischemia/reperfusion injury,but the underlying mechanisms remain unclear.In this study,rats were intragastrically given Buyanghuanwu decoction,15 m L/kg,for 3 days.A rat model of cerebral ischemia/reperfusion injury was established by middle cerebral artery occlusion.In rats administered Buyanghuanwu decoction,infarct volume was reduced,serum vascular endothelial growth factor and integrin αvβ3 levels were increased,and brain tissue vascular endothelial growth factor and CD34 expression levels were increased compared with untreated animals.These effects of Buyanghuanwu decoction were partially suppressed by an angiogenesis inhibitor（administered through the lateral ventricle for 7 consecutive days）.These data suggest that Buyanghuanwu decoction promotes angiogenesis,improves cerebral circulation,and enhances brain tissue repair after cerebral ischemia/reperfusion injury.

Neuroprotective effects of tetrandrine against vascular dementia

Tetrandrine is one of the major active ingredients in Menispermaceae Stephania tetrandra S.Moore,and has specific therapeutic effects in ischemic cerebrovascular disease.Its use in vascular dementia has not been studied fully.Here,we investigated whether tetrandrine would improve behavioral and cellular impairments in a two-vessel occlusion rat model of chronic vascular dementia.Eight weeks after model establishment,rats were injected intraperitoneally with 10 or 30 mg/kg tetrandrine every other day for 4 weeks.Behavioral assessment in the Morris water maze showed that model rats had longer escape latencies in training trials,and spent less time swimming in the target quadrant in probe trials,than sham-operated rats.However,rats that had received tetrandrine showed shorter escape latencies and longer target quadrant swimming time than untreated model rats.Hematoxylin-eosin and Nissl staining revealed less neuronal necrosis and pathological damage,and more living cells,in the hippocampus of rats treated with tetrandrine than in untreated model rats.Western blot assay showed that interleukin-1β expression,and phosphorylation of the N-methyl-D-aspartate 2B receptor at tyrosine 1472,were lower in model rats that received tetrandrine than in those that did not.The present findings suggest that tetrandrine may be neuroprotective in chronic vascular dementia by reducing interleukin-1β expression,N-methyl-D-aspartate receptor 2B phosphorylation at tyrosine 1472,and neuronal necrosis.

Hot spots and future directions of research on the neuroprotective effects of nimodipine

Calcium antagonists are widely used in the clinical treatment of ischemic cerebrovascular disease because of their vascular and neuroprotective effects. Nimodipine, a typical calcium antagonist, can cross the blood-brain barrier and act selectively at neurons and blood vessels of target tis-sues, thus exerting neuroprotective effects. The aim of the present study was to explore the hot spots and future trends of research on the neuroprotective effects of nimodipine. We retrieved 425 articles on the neuroprotective effects of nimodipine that were indexed in the Web of the Science database between 2000 and 2014. The retrieved articles were analyzed using document analysis reporting and the derived information function in the Web of Science, and the infor-mation visualization software CiteSpace III. The reference co-citation network was plotted, and the high frequency key words in these publications were used to analyze the research fronts and development trends for nimodipine neuroprotection. According to these co-citation clusters, the research front of nimodipine neuroprotection is the use of randomized controlled trials to study nimodipine intervention of subarachnoid hemorrhage. Using time zone view analysis on hot spots labeled with a key word, the areas of interest in the ifeld of nimodipine neuroprotection are nimodipine pharmacology and therapeutics, blood-brain barrier, trials, and anti-angiospasm.

High frequency electrical field-ultrashort wave therapy for treatment of cerebral ischemia/reperfusion injury in rats Histopathological evaluation

BACKGROUND： Ultrashortwave （USW） therapy may be a new method for treatment of ischemic cerebrovascular diseases. It is necessary to study its treatment time window. OBJECTIVE： To observe the effect of USW on reperfusion injury after occlusion of the middle cerebral artery （MCAO） in rats and discuss its acting mechanisms and best occasion. DESIGN： Randomized controlled observation, animal experiment. SETTING： Laboratory of Department of Rehabilitation Medicine, First Hospital Affiliated to China Medical University. MATERIALS： Sixty-six healthy Wistar rats of either gender and of clean grade, aged 18–20 weeks, weighing from 250 to 300 g, were provided by the Experimental Animal Center of China Medical University. An USW device （Shanghai Electrical Device Company） with the frequency of 40.68 MHz and the maximum output power of 40 W, and the first channel power controlled at about 11 W was used in this study. Output power was determined by photometry. METHODS： Sixty-six rats were randomly divided into 3 groups： Sham-operation group （n =6）： The suture was inserted only 1.0 depth during operation, which did not cause MACO; Model group （n =12）： The USW treatment procedure was performed with the power off on the model rats; USW treatment group （n =48）： The 48 rats were randomly divided into modeling 0, 6, 12 and 18 hours 4 subgroups. USW therapy without heat was used on the head of rats for 10 minutes at each time point. Twelve rats in USW treatment group were decapitated following treatment at each time point, and then their brain tissues were harvested. The rat brain tissues in other groups were harvested by decapitation at 24 hours after modeling. When the rats were awake, the neurologic deficit was scored by Zea-Longa five-point scale （a score of 0 indicated no neurologic deficit, a score of 1 indicated failure to extend left paw fully, a score of 2 indicated circling to the left, and a score of 3 indicated falling to the left, and rats with a score of 4 did not walk spontaneously and has a depressed level of consciousness.） Rats which still survived at 24 hours and was scored 1 and 2 on the neurologic scoring were involved in the analysis. ① Determination of cerebral water content： Cerebral water contents of healthy and injured hemisphere were determined by wet/dry weighing method. Cerebral water content （100%） =（1–dry/wet weight）×100%.②Infarction volume： The brain tissue was sliced into 2 mm sections and each section was stained with 20 g/L 2,3,5-triphenyltetrazolium chloride （TTC） by TTC staining technique for 30 minutes in a water bath at 37 ℃.Then, the section was fixed in 100 g/L formaldehyde for 10 minutes .The infarction volume was analyzed by using an imaging analyzer.③ Preparation of light microscopic sample： The rat brain tissue fixed by 100 g/L neutral formaldehyde and stained with TTC, were gradiently dehydrated with alcoholic, embedded with paraffin, sliced and stained by HE, finally, the sections were observed under the light microscope. MAIN OUTCOME MEASURES： Cerebral water content, cerebral infarction volume and cerebral histomorphology of rats in each group. RESULTS： Sixty-six rats were involved in the final analysis. ①Cerebral water content： There were no significant differences of cerebral water content in healthy hemisphere among groups （P 〉 0.05）. Cerebral water content of injured hemisphere in the model group and at modeling 0, 6, 12 and 18 hours in the USW treatment group was （81.50±0.74） %, （81.02±0.83） %, （79.78±0.70） %, （79.74±0.84） %, （79.39± 1.06） %, respectively, which was significantly higher than that in the sham-operation group [（78.09±0.52） %, P 〈 0.05]. At modeling 0, 6 and 12 hours, the cerebral water content in the injured hemisphere in the USW treatment group was significantly lower than that in the model group, respectively （P 〈 0.05）. It indicatedthat USW treatment given at 6, 12 and 18 hours after ischemia/reperfusion can lessen brain edema. ② Cerebral infarction volume： At modeling 18 hours, cerebral infarction volume in the injured hemisphere of USW treatment group was smaller than that in the model group [（191.62±121.45）,（362.03±142.01）mm3, t =2.23,P 〈 0.05]. ③ Cerebral histomorphological observation： No swelling was found in the brain tissue section of rats in the sham-operation group. In the model group, the size of infarction hemisphere was obviously increased, gyrus became flattened, cortical sulci was shallow, the color at infarct focus obviously became light, and the tissue was fragile and brittle. In the sham-operation group, it was found under the microscope that mesenchyma was highly swelled, neuronal peripheral interspace was obviously broadened, neurons presented triangle, nucleoli were reduced, condensed even disappeared, and neutrophils in the vascular cavity were obviously increased. In the USW treatment group, pathological injury was not obviously lessened at 0 hour, moderate or mild edema could be found in the injured hemisphere of USW treatment group at modeling 6,12 and 18 hours, and at this time, neutrophils in vascular cavity were increased slightly, and pathological injuries were lessened. CONCLUSION： USW may play a protective effect on cerebral ischemia/reperfusion injury by decreasing brain edema and/or cerebral infarction volume. The treatment action of USW may start at 6 hours after reperfusion, and the best occasion of application may be at 18 hours after reperfusion.

Trans-cranial Doppler predicts early neurologic deterioration in anterior circulation ischemic stroke after successful endovascular treatment

Background:Early neurologic deterioration(END)may occur in patients with anterior circulation ischemic stroke(ACIS)after receiving endovascular treatment(EVT).Hemodynamic insufficiency,re-occlusion,and post-re-canalization hyper-perfusion are likely to play a critical role in END.We hypothesized that hemodynamic changes can predict END in patients with ACIS postsuccessful EVT using trans-cranial Doppler(TCD).Methods:We utilized a prospectively maintained database of ACIS patients treated with EVT between September 2016 and June 2018 in the Xuanwu Hospital,Capital Medical University.TCD parameters including peak systolic velocity(PSV),bilateral mean flow velocity(MFV),and pulse index(PI)were determined via the middle cerebral arteries within 72 h post-EVT.A logistic regression model was applied to detect independent predictors for END.Results:Totally,112 EVT patients were included in this study and 80/112 patients experienced successful re-canalization with<50%residual stenosis,while 17/80(21.3%)patients suffered END,for which vasogenic cerebral edema(11/17)was considered as a leading role and followed by symptomatic intra-cranial hemorrhage(4/17)and ischemia progression(2/17).For the 80 patients,the PSV(median:127 cm/s vs.116 cm/s,P=0.039),the ratio of ipsilateral-MFV/contra-lateral-MFV(iMFV/cMFV)(median:1.29 vs.1.02,P=0.036)and iMFV/mean blood pressure(MBP)(median:0.97 vs.0.79,P=0.008)in END patients were higher than those of non-END.Using the receiver-operating characteristic curve to obtain cut-off values for PSV,PI,iMFV/cMFV,and iMFV/MBP for END,we found that PI≥0.85(odds ratio:11.03,95%confidence interval:1.92–63.46,P=0.007)and iMFV/MBP≥0.84(odds ratio:9.20,95%confidence interval:2.07–40.84,P=0.004)were independent predictors of END in a multivariate logistic regression model,with a sensitivity of 82.4%and 76.5%and a specificity of 42.9%and 66.7%,respectively,and had the positive predictive values of 29.0%and 38.2%,and negative predictive values of 90.0%and 91.3%,with an area under the receiveroperating characteristic curve of 0.57 and 0.71,respectively.Conclusion:TCD examination of EVT patients may be used as a real-time tool to detect END predictors,such as the higher PI and iMFV/MBP,allowing for better post-thrombectomy management in ACIS patients.