Acute Massive Cerebral Infarction Research Articles

Catastrophic antiphospholipid syndrome of pregnancy with acute massive cerebral infarction: A case report.

Catastrophic antiphospholipid syndrome (CAPS) is the most serious type of antiphospholipid antibody syndrome (APS) and can be easily confused with other disorders, such as hemolytic uremic syndrome, disseminated intravascular coagulation and thrombocytopenia syndromes. Timely diagnosis of CAPS poses considerable challenges due to its rarity and the fact that clinicians often lack knowledge of the disease. A 21-year-old patient was 32 weeks and 5 days pregnant when she presented to the hospital with a 7-hour history of sudden onset of left-sided limb weakness with no apparent cause. Lupus anticoagulant and/or anticardiolipin antibodies were positive. Head magnetic resonance imaging + magnetic resonance angiography + diffusion weighted imaging: right temporo-occipital insula, right basal ganglia and bilateral radial corona-hemispheric center showed multiple acute-phase cerebral infarction changes and right middle cerebral artery occlusion. Catastrophic antiphospholipid syndrome. By intracranial artery thrombectomy and anticoagulation with low-molecular heparin. The patient's left limb muscle strength recovered to grade 5. A healthy baby boy was delivered by cesarean section. Both mother and child are safe. The rarity of CAPS is such that misdiagnosis often occurs, culminating in serious complications and even death, emphasizing the need for early recognition, timely diagnosis and immediate treatment. In CAPS that improves with treatment, monitoring and prevention of recurrence is also essential.

A Rare Complication after Endoscopic Transcecal Appendectomy: Acute Massive Cerebral Infarction.

A Rare Complication after Endoscopic Transcecal Appendectomy: Acute Massive Cerebral Infarction.

Management of massive cerebral infarction as a complication of post-tonsillectomy and analysis of the risk factors: a case report

BackgroundThe majority of postoperative complications of tonsillectomy are bleeding. However, massive cerebral infarction following haemostasis is a very rare and serious complication and has rarely been reported clinically.Case presentationWe performed a left tonsillectomy on a patient with chronic tonsillitis. After that, active bleeding was found under the tonsillar fossa, so an exploratory hypopharyngeal haemostasis was performed. However, the bleeding worsened intraoperatively, so the patient was converted to a cervical angiographic embolization. The interventional procedure was completed successfully without an ectopic embolic event. After the procedure, the patient was transferred to the intensive care unit (ICU) and was diagnosed with acute massive cerebral infarction in the left cerebral hemisphere after awakening symptoms combined with cranial computed tomography angiography (CTA) results. Symptomatic treatment such as sedation and analgesia, dehydration to lower intracranial pressure, and maintenance of respiratory and circulatory stability was then administered. After treatment, the patient’s condition stabilized and he was transferred to the rehabilitation physiotherapy unit for rehabilitation.ConclusionPost-tonsillectomy haemorrhage can be augmented with a carotid arteriogram to clarify whether the tonsillar fossa is at a safe distance from the posterior internal carotid artery. Furthermore, interventional haemostasis can also be performed as early as possible to reduce the incidence of complications in cases of persistent post-tonsillectomy bleeding.

Predictive value of magnetic resonance imaging-based texture analysis for hemorrhage transformation in large cerebral infarction.

Massive cerebral infarction (MCI) is a devastating condition and associated with high rate of morbidity and mortality. Hemorrhagic transformation (HT) is a common complication after acute MCI, and often results in poor outcomes. Although several predictors of HT have been identified in acute ischemic stroke (AIS), the association between the predictors and HT remains controversial. Therefore, we aim to explore the value of texture analysis on magnetic resonance image (MRI) for predicting HT after acute MCI. This retrospective study included a total of 98 consecutive patients who were admitted for acute MCI between January 2019 and October 2020. Patients were divided into the HT group (n = 44) and non-HT group (n = 54) according to the follow-up computed tomography (CT) images. A total of 11 quantitative texture features derived from images of diffusion-weighted image (DWI) or T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) were extracted for each patient. Receiver operating characteristic (ROC) analysis were performed to determine the predictive performance of textural features, with HT as the outcome measurement. There was no significant difference in the baseline demographic and clinical characteristics between the two groups. The distribution of atrial fibrillation and National Institutes of Health Stroke Scale (NIHSS) were significantly higher in patients with HT than those without HT. Among the textural parameters extracted from DWI images, six parameters, f2 (contrast), f3 (correlation), f4 (sum of squares), f5 (inverse difference moment), f10 (difference variance), and f11 (difference entropy), differs significantly between the two groups (p < 0.05). Moreover, five of six parameters (f2, f3, f5, f10, and f11) have good predictive performances of HT with the area under the ROC curve (AUC) values of 0.795, 0.779, 0.791, 0.780, and 0.797, respectively. However, the texture features f2, f3, and f10 in T2/FLAIR images were the only three significant predictors of HT in patients with acute MCI, but with a relatively low AUC values of 0.652, 0.652, and 0.670, respectively. In summary, our preliminary results showed DWI-based texture analysis has a good predictive validity for HT in patients with acute MCI. Multiparametric MRI texture analysis model should be developed to improve the prediction performance of HT following acute MCI.

Application of rt-PA intravenous thrombolysis in treatment of acute massive cerebral infarction in two patients aged over 90 years old in a grass-roots hospital

Application of rt-PA intravenous thrombolysis in treatment of acute massive cerebral infarction in two patients aged over 90 years old in a grass-roots hospital

3-Mercaptopyruvate sulfurtransferase/hydrogen sulfide protects cerebral endothelial cells against oxygen-glucose deprivation/reoxygenation-induced injury via mitoprotection and inhibition of the RhoA/ROCK pathway.

3-Mercaptopyruvate sulfurtransferase (3-MST) is the major source of hydrogen sulfide (H2S) production in the brain and participates in many physiological and pathological processes. The present study was designed to investigate the role of 3-MST-derived H2S (3-MST/H2S) on oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cerebrovascular endothelial cells (ECs). Using cerebrovascular specimens from patients with acute massive cerebral infarction (MCI), we found abnormal morphology of the endothelium and mitochondria, as well as decreases in H2S and 3-MST levels. In an OGD/R model of ECs, 3-mercaptopyruvate (3-MP) and l-aspartic acid (l-Asp) were used to stimulate or inhibit the production of 3-MST/H2S. The results showed that OGD/R induced significant decreases in H2S and 3-MST levels in both ECs and mitochondria, as well as increases in oxidative stress and mitochondrial energy imbalance. Cellular oxidative stress, destruction of mitochondrial ultrastructure, accumulation of mitochondrial reactive oxygen species (ROS), reduction of mitochondrial adenosine triphosphate (ATP) synthase activity and ATP production, and decreased mitochondrial membrane potential were all significantly ameliorated by 3-MP, whereas they were exacerbated by l-Asp pretreatment. Contrary to the effects of l-Asp, the increase in RhoA activity and expression of ROCK1 and ROCK2 induced by OGD/R were markedly inhibited by 3-MP pretreatment in subcellular fractions without mitochondria and mitochondrial fractions. In addition, 3-MST-/- rat ECs displayed greater oxidative stress than 3-MST+/+ rat ECs after OGD/R injury. These findings suggest that 3-MST/H2S protects ECs against OGD/R-induced injury, which may be related to preservation of mitochondrial function and inhibition of the RhoA/ROCK pathway.

Prognostic value of cerebral infarction coefficient in patients with massive cerebral infarction

ObjectiveWe proposed the concept of the cerebral infarction coefficient, which is cerebral infarction volume/brain volume. This study aimed to evaluate the prognostic value of the cerebral infarction coefficient in patients with massive cerebral infarction (MCI). MethodsAccording to the modified Rankin score, 71 patients with acute MCI were divided into good prognosis and poor prognosis groups. Clinical and imaging data of the two groups were collected and univariate analysis was carried out. If there were significant differences in the data between the two groups, binary logistic regression analysis was performed. ResultsThe poor prognosis group had a significantly higher cerebral infarction volume, cerebral infarction coefficient, and D-dimer levels, older age, the highest body temperature, a higher rate of a history of atrial fibrillation, and a lower rate of a history of hypertension compared with the good prognosis group (all P < 0.05). Binary logistic regression analysis showed that the cerebral infarction coefficient was an independent risk factor for a poor prognosis of patients with MCI (P < 0.05, 95 % confidence interval, 2.091, 42.562), and the odds ratio was 8.506. The area under the receiver operating characteristic curve for the cerebral infarction coefficient was 0.753. When the cut-off value was 7.8 %, the sensitivity of predicting a poor prognosis of patients with MCI was 92.5 %. ConclusionThe cerebral infarction coefficient may have predictive value in determining the prognosis of patients with MCI.

Improvement of neurological function and stress in patients with acute massive cerebral infarction by mild hypothermia: a prospective randomized controlled study

To study the effect of mild hypothermiaon neurological function and oxidative stress in patients with acute massive cerebral infarction. Sixty patients with acute massive cerebral infarction (within 12 hours of onset, the age < 70 years old) admitted to the First Hospital of Qinhuangdao from August 2017 to August 2018 were enrolled. Patients were divided into control group and observation group according to random number table method, with 30 patients in each group. The control group was given conventional treatment such as lowering intracranial pressure, anticoagulation, improving microcirculation, neurotrophy and anti-stress ulcer, while the observation group was received mild hypothermia (after 72 hours of treatment at 32-35 centigrade, it increased about 1 centigrade every 6 hours until the normal temperature). The neurological impairment (the National Institutes of Health Stroke Scale, NIHSS), motor function (Fugl-Meyer score), daily living ability (Bathel index) and coma degree (Glasgow coma scale, GCS) were observed before treatment and 72 hours after treatment. The levels of plasma malondialdehyde (MDA), superoxide dismutase (SOD) and advanced oxidative protein products (AOPP) were measured at same time. After 72 hours of treatment, the therapeutic effect was judged according to the NIHSS score. There was no significant difference in NIHSS score, Fugl-Meyer score, Bathel index and GCS scores, and the levels of plasma MDA, SOD and AOPP between two groups before treatment. Compared with before treatment, NIHSS score and plasma MDA and AOPP levels in the two groups were significantly decreased after treatment, while Fugl-Meyer score, Bathel index, GCS score and plasma SOD activity were significantly increased; and the change of observation group was more significant than those of control group [NIHSS score: 9.78±3.24 vs. 13.44±2.63, MDA (mmol/L): 8.70±2.79 vs. 10.50±3.81, AOPP (μmol/L): 51.10±17.81 vs. 72.60±18.71, Fugl-Meyer score: 55.68±8.38 vs. 46.25±3.92, Bathel index: 66.63±11.25 vs. 56.71±10.81, GCS score: 13.78±1.31 vs. 10.49±1.03, SOD (kU/L): 134.70±29.87 vs. 104.60±25.75, all P < 0.05]. The total effective rate of the observation group was significantly higher than that of the control group [93.3% (28/30) vs. 86.7% (26/30), χ2 = 6.119, P = 0.020]. Mild hypothermia was effective in treating acute massive cerebral infarction. It could significantly improve the neurological function and oxidative stress of patients, improve the quality of life, and was safe and reliable.

Procalcitonin as a Biomarker for Malignant Cerebral Edema in Massive Cerebral Infarction

The objective of this study is to explore whether procalcitonin (PCT) can serve as an early biomarker of malignant cerebral edema in patients with massive cerebral infarction (MCI). Ninety-three patients with acute MCI were divided into death or survival groups based on whether they died or survived within 1 week of cerebral herniation. Differences in laboratory parameters between these two groups were analyzed by univariate analysis, followed by multivariate logistic regression analyses if the influencing factors were significantly different. Compared with the survival group, the patients in the death group had a larger cerebral infarct area, higher body temperature, neutrophil counts, PCT level, and neuron-specific enolase (NSE) level within 48 h of onset. Multivariate logistic regression analyses revealed an odds ratio (OR) of 1.830 or 1.235 for PCT and neutrophil counts respectively, suggesting that PCT and neutrophil counts are two independent risk factors for death in MCI. The area under receiver operating characteristic (ROC) curve was 0.754 for PCT, larger than that for neutrophil counts. Thus, both serum PCT levels and neutrophil counts can be used as biomarkers to predict malignant cerebral edema at the early stages after MCI, but PCT levels are superior predictors of malignant cerebral edema.

The optimal time window for the use and dosage of nimodipine for acute massive cerebral infarction: study protocol for a randomized controlled trial

Background: A neuroprotective effect of nimodipine on acute cerebral infarction has been confirmed, but there are few reports regarding the therapeutic effect of nimodipine on acute massive cerebral infarction. There is also no consensus on the optimal time window for the use and dosage of nimodipine. This trial is planned to answer these questions using a double-blind randomized controlled design. Methods/Design: This is a double-blind randomized controlled trial. The experiments will be conducted in the Department of Neurology, Central Hospital Affiliated to Shenyang Medical College of China. One hundred patients with acute massive cerebral infarction will be randomly assigned to a control group and a treatment group. Patients in the control and treatment groups will receive intravenous infusion of citicoline and intravenous infusion of nimodipine (10 mg/d) respectively, for 7 consecutive days. Simultaneously, to determine the appropriate time window for treatment with nimodipine, patients in the treatment group will be divided into four subgroups according to the time of nimodipine administration: 24 hours. The main outcome measures are: the National Institutes of Health Stroke Scale and the Rankin scale will be used to assess the severity and recovery of neurological impairment, respectively. Cranial computed tomography and magnetic resonance imaging will be used to evaluate brain lesions and the Barthel index will be used to assess the activities of daily living. Secondary outcome measures are heart rate and blood pressure. Discussion: It is hoped that the experimental results can determine the best application time window and dosage of nimodipine for acute massive cerebral infarction. Trial registration: ClinicalTrials.gov identifier: NCT02248233; registered on 22 September 2014.

Propofol in combination with mild hypothermia for cerebral infarction in large area

Objective To explore the curative effect of propofol in combination with mild hypothermia for cerebral infarction in large area and provide some references for its clinical treatment.Methods 42 patients with cerebral infarction in large area were randomly divided into a treatment group (22 cases) and a control groups (20 cases).The control group received conventional treatment and mild hypothermia.In addition,the treatment group were treated with propofol.The clinical efficacies of both groups was compared.Results 5 datys after the treatment,the effective rate of neurologic deficits was 39.9％ in treatment group and was 20.0％ in the control group; the mortality rate was 9.1％ in the treatment group and was 20.0％ in the control group; with statistical differences (P＜0.05).The state of consciousness was improved more in the treatment group than in the control group.Conclusions Propofol can recover the neurological function of the patients with acute massive cerebral infarction and reduce the mortality. Key words: Propofol; Mild hypothermia; Cerebral infarction

Study on risk factors of hemorrhagic transformation in acute massive cerebral infarction

Objective To investigate the factors that influence the occurrence of hemorrhagic transformation (HT) in patients with acute massive cerebral infarction,and to provide references for clinical treatment.Methods The clinical data of 60 patients with acute ischemic stroke were retrospectively analyzed.All the 60 patients were divided into HT group and non-hemorrhagic transformation (NHT) group.Risk factors associated with cerebrovascular disease,such as general data (gender,age,histories of drink and smoke),history of past illness (hypertension,diabetes,coronary disease,atrial fibrillation and cerebral stroke) and clinical data (infarction location,therapeutic methods,blood pressure,blood glucose,blood fat,cholesterol,fibrinogen and et al),were compared between the two groups.Results Of all the 60 patients,HT rate was 35％ (21/60).Incidence of HT was higher in patients with past and present hypertension and hyperglycemia(P =0.009,0.013,0.005,0.008,0.017),and in patients with atrial fibrillation,anti-platelet therapy,infarction in cortex,and hypocholesterolemia (P =0.020,0.037,0.003,0.009).But gender,age,histories of drink and smoke and history of coronary disease were not significantly different between the two groups(P=0.935,0.309,0.196,0.717,0.058).Conclusion Hypertension,hyperglycemia,atrial fibrillation,hypocholesterolemia,anti-platelet therapy could be independent risk factors for HT in patients with acute massive cerebral infarction. Key words: Hemorrhagic transformation; Brain infarction; Risk factors

Plasma copeptin levels in elderly victims of massive cerebral infarction and its relationship to early death

To investigate copeptin levels in elderly patients who have suffered massive cerebral infarction, and to establish its correlation with early death. Forty-nine elderly patients with acute massive cerebral infarction and an age-matched control group of thirty normal people were established. Plasma copeptin levels of patient group were measured by ELISA at 24 h, 36 h, 5 d, and 14 d after onset of infarction. Glasgow-Pittsburgh coma scale (GPCS) were recorded within 24 h after onset, and both results were graded. Based on the 14-day mortality, the patient was divided into a death group and a survival group, and the correlations between graded copeptin level and GPCS to mortality were analyzed, as well as the consistency and accuracy of prognosis. Plasma copeptin levels in the patient group were no differences between the 24 h, 36 h and 5 d point, and that of the 14 d was lower than that of the other points. Copeptin levels were significantly higher than in the control group at each test point (P< 0.01 or P< 0.05). The copeptin level at 24 h among those dead by 14 days was higher than in those of the survival group (P<0.01). There were significant associations of early death (within 14 d) with copeptin levels and with GPCS grade(r=0.58, P<0.001, r=0.46, P<0.001, respectively). Copeptin level of the third-grade (>25.0 pmol/L) showed better consistency and coincidence rate than GPCS score (< 20) in predicting early death. Plasma copeptin level was increased in early phases of acute massive cerebral infarction in elderly patients; it may have predictive value for early death.

Expression of nitric oxide and nitric oxide synthase in patients with acute massive cerebral infarction

Objective To study the expression of nitric oxide (NO) and nitric oxide synthase (NOS) in patients with acute massive cerebral infarction. Methods Sixteen patients (cerebral infarction group) with acute massive cerebral infarction were subjected to craniotomy decompression craniectomy under the anesthesia, and part of the infarct frontal lobe was removed. The normal frontal lobe from 6 cases of severe brain injury receiving the intracranial decompression served as control group. The ultrastructures of frontal lobe cells were observed under the electron microscopy. Serum NO content and NOS activity were measured. The protein expression patterns of eNOS, nNOS and iNOS were analyzed by Western blotting.Results The consciousness in 16 patients with acute massive cerebral infarction was improved after operation to varying degrees, and there were no deaths. The NO contents and NOS activities in cerebral infarction group and control groups were 85.4 and 36. 2 U/mi, and 63.2 and 37.2 μmol/L ( all P ＜ 0. 05). As compared with control group, the expression of eNOS, nNOS and iNOS in cerebral infarction group was significantly increased, especially the expression of iNOS ( all P ＜ 0. 05). Conclusion Craniotomy decompression craniectomy was the effective treatment to cure the acute massive cerebral infarction. It could reduce mortality. NO and NOS participated in and influenced the complex pathophysiological process of massive cerebral infarction. After craniotomy decompression craniectomy the regional cerebral blood was effectively improved, and NOS activity, especially iNOS, and the synthesis of NO were reduced, resulting in the reduction to neurotoxicity and improvement in clinical symptoms. Key words: Cerebral infarction; Nitric oxide synthase; Decompressive craniectomy

Clinical research of edaravone on high sensitivity C-reaction protein in patients with acute massive cerebral infarction

Objective To explore the effects of edaravone on high sensitivity C-reaction protein (hsCRP) in patients with acute massive cerebral infarction. Methods 86 cases with acute massive cerebral infarction were selected from December 2006 to December 2008. all the cases were divided into two groups, control group and cure group. routine treatment was used to the control group, on the basis of control group'therapy,edaravone was given to cure group. the level of hsCRP was detected before and after treatment, and the results of cure was compared. Results ①the total effective rate in two groups existed statistical difference (P<0.05);② the level of hsCRP in two groups before treatment and in the 7th and the 14th of treatment existed statistical difference(P<0.01), the level of hsCRP in the 7th and the 14th of treatment in cure group existed statistical difference(P<0.05). Conclusion Edaravone can decrease the level of hsCRP in patients with massive cerebral infarction, and has significant clinical efficacy,which should be the reference for the doctors. Key words: Massive cerebral infarction; Edaravone; C-reaction protein

Massive cerebral infarctions in main cerebral arteries.

This study was designed to investigate the outcomes in patients with massive cerebral infarction, and to determine the risk factors associated with worse outcomes in the patients with massive cerebral infarction. Twenty-seven patients with acute massive cerebral infarction were hospitalized in our institution. These 10 men and 17 women had an average age of 77.8 years (range, 42 to 97 years). Some patients had multiple infarctions. Thirteen patients had infarctions of the middle cerebral artery, 12 patients had internal carotid artery infarctions, 6 patients had anterior cerebral artery infarctions, and 3 patients had vertebro-basilar artery infarctions. The causes of the main cerebral arterial infarctions were cardiac embolism in 22 patients, atherothrombosis in 4 patients, and unknown in one patient. Fifteen (55%) of the 27 patients died from transtentorial herniation caused by massive cerebral infarction or from general complications. Of the 12 patients (45%) who survived, 8 patients were moderately disabled, 1 patient was severely disabled, and 3 patients existed in a vegetative state. Worse outcomes were more frequent in younger patients with internal carotid artery infarctions related to cardiogenic embolism.

Outcome after external decompression for massive cerebral infarction.

Acute ischemic stroke involving the entire vascular distribution of a carotid or middle cerebral artery can cause massive cerebral edema. This study evaluated external decompression for the treatment of massive stroke and analyzed possible prognostic factors. Twenty-four patients with acute massive cerebral infarction, which had progressed to tentorial herniation and impending death, underwent external decompression after medical therapy failed to achieve an effective response. The neurological outcome 2 months after surgery using the Glasgow Outcome Scale was severe disability in 14 patients, vegetative state in two, and death in eight. The overall mortality was 33%. Various characteristics (age, sex, etiology, side of hemispheric infarction, pupillary asymmetry, Japan Coma Scale, distribution of infarction, hemorrhagic infarction, midline shift, tentorial herniation) were evaluated to determine the factors associated with high mortality after surgical intervention. There was no statistically significant relationship between any variable and mortality. Mortality was especially high in the patients with preoperative consciousness level of 200, anterior, middle, and posterior cerebral artery territory infarction, and stage III of tentorial herniation. Postoperatively, all patients with severe disability returned to a clear level of consciousness. Six patients with dominant hemisphere stroke had some measure of communicative skills in spite of aphasia. External decompression is a life-saving treatment for patients with massive cerebral infarction and can provide a reasonable quality of life even for those with dominant hemisphere strokes. Decompressive surgery should be considered and performed as soon as possible if computed tomography demonstrates signs of descending tentorial herniation.

Hemicraniectomy for acute massive cerebral infarction

Hemicraniectomy for acute massive cerebral infarction