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Search Results: 1 - 10 of 4117 matches for " cerebral ischemia "
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Prospective Evaluation of Post-Traumatic Vasospasm and Post-Injury Functional Outcome Assessment: Is Cerebral Ischemia Going Unrecognized in Patients with Traumatic Brain Injury?  [PDF]
Cherisse Berry, Jamila Torain, Joseph A. Kufera, Peter F. Hu, Thomas M. Scalea, Deborah M. Stein
Journal of Behavioral and Brain Science (JBBS) , 2017, DOI: 10.4236/jbbs.2017.78025
Abstract: Background: Secondary injury processes such as posttraumatic vasospasm (PTV) play a critical role in the development of cerebral ischemia/infarction after traumatic brain injury (TBI). The objectives of this study were to evaluate the incidence of cerebral vasospasm in patients with moderate to severe TBI and to assess post-injury functional outcome. Study Design: A prospective observational study was conducted in patients with moderate and severe blunt TBI. Transcranial Doppler (TCD) ultrasound was performed within the first 72 hours and then daily for up to 7 days. Patient characteristics and outcome data including functional outcome as assessed by the Extended Glasgow Outcome Scale (GOS-E) were collected and compared between patients with and without PTV. Results: Twenty-three patients met our inclusion criteria. While there was a 47.8% incidence of vasospasm as detected by TCD, there was no significant difference in hospital LOS or mortality between patients with and without PTV. Of the two patients with PTV who died, both had a cerebral infarct or cerebral ischemia. In evaluating overall GOS-E among patients with a cerebral focal injury, patients with PTV had a significantly higher GOS-E score when compared to patients without PTV (8.0 vs. 6.8, p = 0.01). Conclusions: The high incidence of PTV and the role of clinically significant vasospasm after TBI remain unclear. While functional outcome was better in patients with a focal injury and vasospasm, patients who died had cerebral ischemia or infarction. We hypothesize that there is an interaction between impaired cerebral autoregulation, PTV and poor outcomes in patients with TBI.
Hypertensive-Nimodipine Therapy for Middle Cerebral Artery Vasospasm after Resection of Glioblastoma Multiforme: A Case Report and Literature Review  [PDF]
Peter Yat Ming Woo, Ka Wing Michael See, Jason Kwan Ho Chow, Yung Chan, Hoi Tung Wong, Kwong Yau Chan
Open Journal of Modern Neurosurgery (OJMN) , 2015, DOI: 10.4236/ojmn.2015.53013
Abstract: Delayed cerebral ischemia (DCI) due to post-brain tumor resection vasospasm is an often unrecognized yet debilitating complication. We present a patient with DCI after the resection of glioblastoma multiforme (GBM). To our knowledge, this is the first report on DCI after GBM resection. A 52-year-old female patient with headache for one month underwent subtotal resection of a left temporal GBM encasing the proximal middle cerebral artery (MCA). She was well during the immediate postoperative period but developed right upper limb dense monoparesis on postoperative day four with computed tomographic angiography confirming left MCA vasospasm. Symptoms were significantly alleviated with weeklong hypertensive therapy and nimodipine administration; however they recurred soon after cessation of treatment. A high index of clinical suspicion is needed for the diagnosis of post-tumor resection DCI. Any new postoperative neurological deficit that cannot be explained by hemorrhage, seizures or infection should be expeditiously investigated by angiography or transcranial Doppler sonography. Prompt initiation of hypertensive and nimodipine therapy can possibly reverse neurological deficit. Treatment should be guided by Doppler, angiographic or perfusion imaging studies and not by clinical improvement alone.
By Improving Regional Cortical Blood Flow, Attenuating Mitochondrial Dysfunction and Sequential Apoptosis Galangin Acts as a Potential Neuroprotective Agent after Acute Ischemic Stroke
Shaojing Li,Chuanhong Wu,Li Zhu,Jian Gao,Jing Fang,Defeng Li,Meihong Fu,Rixin Liang,Lan Wang,Ming Cheng,Hongjun Yang
Molecules , 2012, DOI: 10.3390/molecules171113403
Abstract: Ischemic stroke is a devastating disease with a complex pathophysiology. Galangin is a natural flavonoid isolated from the rhizome of Alpina officinarum Hance, which has been widely used as an antioxidant agent. However, its effects against ischemic stroke have not been reported and its related neuroprotective mechanism has not really been explored. In this study, neurological behavior, cerebral infarct volumes and the improvement of the regional cortical blood flow (rCBF) were used to evaluate the therapeutic effect of galangin in rats impaired by middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia. Furthermore, the determination of mitochondrial function and Western blot of apoptosis-related proteins were performed to interpret the neuroprotective mechanism of galangin. The results showed that galangin alleviated the neurologic impairments, reduced cerebral infarct at 24 h after MCAO and exerted a protective effect on the mitochondria with decreased production of mitochondrial reactive oxygen species (ROS). These effects were consistent with improvements in the membrane potential level (Dym), membrane fluidity, and degree of mitochondrial swelling in a dose-dependent manner. Moreover, galangin significantly improved the reduced rCBF after MCAO. Western blot analysis revealed that galangin also inhibited apoptosis in a dose-dependent manner concomitant with the up-regulation of Bcl-2 expression, down-regulation of Bax expression and the Bax/Bcl-2 ratio, a reduction in cytochrome c release from the mitochondria to the cytosol, the reduced expression of activated caspase-3 and the cleavage of poly(ADP-ribose) polymerase (PARP). All these data in this study demonstrated that galangin might have therapeutic potential for ischemic stroke and play its protective role through the improvement in rCBF, mitochondrial protection and inhibiting caspase-dependent mitochondrial cell death pathway for the first time.
Camara, RLB;Roselino, JES;Colli, BO;
Acta Cirurgica Brasileira , 2001, DOI: 10.1590/S0102-86502001000500010
Abstract: cerebral ischemia has been extensively studied in order to obtain effective therapeutic measures that might minimize its effects, since a large number of clinical or surgical patients frequently suffer irreversible consequences of this condition. the choice of a satisfactory experimental model to be used in research on neuroprotective agents has been the basis of these studies. in the present investigation, the cat was chosen as an experimental model of ischemia and the condition was evaluated on the basis of two parameters, i.e., mitochondrial respiration and swelling. the animals used in the experiment (n = 32) were divided into four groups; three groups of 10 animals each were submitted to progressively increasing periods of ischemia (15, 30 and 60 minutes), and the last group (n = 2) was not submitted to ischemia. clear changes in the curves of energized mitochondrial swelling were observed in the animals submitted to 60 minutes of ischemia when the ischemic side was compared to the control, and this occurrence was even clearer when the antibiotic alameticin was added during the laboratory assays of swelling. it is possible to find these conclusions: swelling is an indicator of mitochondrial differentiation between tissues; brain mitochondrion when exposed to effects of alameticin presents a different sensibility if is comparison to other tissues; brain mitochondria submitted to ischemia during 60 minutes became more sensibility to alameticin; and finally, brain mitochondria have an extremely fast installation of reversion swelling.
Leading factors of cerebral ischemia in newborns
Yakovleva O.V.,Muzurova L.V.,Zryachkin N.I.
Saratov Journal of Medical Scientific Research , 2010,
Abstract: The research goal is to study the causes of perinatal hypoxic impairments of Central Nervous System (CNS) in fetus and newborn. Risk factors of cerebral ischemia development in fetus and newborn are likely to be found anemia, chronic adnexitis in mothers, threatened abortions, athletic type of pregnant women, loop of cord during the pregnancy course, rapid parturition and acute respiratory diseases during the II and III trimesters of pregnancy
Aminoguanidine reduces infarct volume and improves neurological dysfunction in transient model of focal cerebral ischemia in rat
Abedin Vakili,Aliakbarar Nekooeian,Gholam Abbas Dehghani
DARU : Journal of Pharmaceutical Sciences , 2006,
Abstract: Focal cerebral ischemia (Stroke) is the cessation or severe reduction of blood flow to an area of the brain that through activation of a complex cytotoxic cascade results in neuronal cell death. The present study was designed to examine the effects of post-ischemic treatment with aminoguanidine (AG) on cortical, striatal infarct volume as well as neurological dysfunctions. Rats (n=23) were allocated to sham, saline or AG (300 mg/kg)-treated groups. Ischemia was induced by 90 minutes middle cerebral artery occlusion, followed by 24 hrs reperfusion. Saline or AG was administered intraperitoneal at one hour after induction of ischemia. At the end of 24hrs reperfusion, neurological deficit score was tested and cortical, striatal infarct volumes were determined by Triphenyltetrazolium chloride staining. Administration of AG (300 mg/kg) at one hours after ischemia resulted in a significantly lower cortical (85±25 vs. 210±13 mm3), striatal (35±5 vs. 58±10 mm3) infarct volumes, and neurological deficit score (1.88±0.23 vs. 2.67±0.21). Our findings indicate that aminoguanidine is a potent neuroprotective in rat model of transient focal cerebral ischemia. The future studies are required to clear cerebroprotective mechanism of aminoguanidine and possible use of this agent as a therapeutic target in stroke patients.
Neuroprotective Effect of a Prostacyclin Agonist (ONO-1301) with Thromboxane Synthase Inhibitory Activity in Rats Subjected to Cerebral Ischemia  [PDF]
Mai Hazekawa, Yoshiki Sakai, Miyako Yoshida, Tamami Haraguchi, Takahiro Uchida
Pharmacology & Pharmacy (PP) , 2011, DOI: 10.4236/pp.2011.24039
Abstract: ONO-1301 has been developed as a novel long-acting prostacyclin agonist with thromboxane synthase inhibitory activity. In the present study, we investigated the cerebroprotective effect of ONO-1301 on post-ischemic injury induced by cerebral ischemia in rats. ONO-1301 (1 and 10 mg/kg) was administrated orally at reperfusion and then twice a day for 42 days. The cell damage induced by cerebral ischemia in the hippocampal CA1 was evaluated using both Nissl staining and proliferating cell nuclear antigen (PCNA) staining on the 42 days after cerebral ischemia. Activated astrocytes were evaluated using immunofluorescence staining with GFAP on the 42 days after cerebral ischemia. Spatial learning was assessed using a Morris water maze (MWM) task on the 56 days (i.e. after a 14 days washout period). ONO-1301- treated rats (1 and 10 mg/kg) significantly improved cell death in the hippocampal CA1, the number of PCNA-positive cells and astrocyte activation. The spatial learning of ONO-1301-treated rats compared with vehicle- treated rats in the MWM task. These results suggest that repeated treatment with oral ONO-1301 could prevent or limit post-ischemic brain damage. In particular, treatment with ONO-1301 within 7 days after ischemia is most effective to improve ischemic damage.
Experimental Hyperthermia during Cardiac Arrest and CPR Is Associated with Severe Spontaneous Hypothermia in Mice  [PDF]
Ruediger R. Noppens, Julia Kofler, Richard Traystman
Neuroscience & Medicine (NM) , 2012, DOI: 10.4236/nm.2012.33035
Abstract: Background: Since genetically engineered mice are becoming more and more available, these animals become of high interest to study physiologic and pathophysiologic pathways of brain ischemia. The aim of this study was to examine body temperature (Tb), physical activity variation and neurohistopathology in mice exposed to normothermic and hyperthermic cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Methods: Male C57Bl/6 mice weighing 22 - 27 g were implanted intraperitoneally with a radio telemeter and subjected to 10 min cardiac arrest followed by cardiopulmonary resuscitation. Normothermia (37.5°C) or hyperthermia (39.0°C) was induced by controlling pericranial temperature during the arrest period. Results: Hyperthermia during the arrest resulted in a Tb decrease during early recovery to a nadir of 28°C ± 0.8°C (mean ± SE) and partially recovered to 34.4°C ± 1°C 36 hrs after CA/CPR. With normothermia during the arrest, Tb depression was less pronounced (nadir of 32.3°C ± 0.3°C) and recovered to physiologic levels within 24 hrs. Coupling of physical activity and body temperature was absent in all animals after CA/CPR. Neuronal injury in the caudoputamen was greater in the hyperthermia group. Conclusions: This study demonstrates that CA/CPR eliminates normal connectivity between body temperature and physical activity and induces long-lasting hypothermia, the depth of which is related to severity of brain injury. Long term temperature monitoring is required in survival murine experiments, if body temperature is a study variable.
Can CT Perfusion Guide Patient Selection for Treatment of Delayed Cerebral Ischemia?  [PDF]
Rachel Gold, Pina C. Sanelli, Nikesh Anumula, Austin Ferrone, Carl E. Johnson, Joseph P. Comunale, Apostolos J. Tsiouris, Howard Riina, Halinder Mangat, Axel Rosengart, Alan Z. Segal
Advances in Computed Tomography (ACT) , 2013, DOI: 10.4236/act.2013.21002

Purpose: To evaluate qualitative and quantitative CT perfusion (CTP) for different treatment options of delayed cerebral ischemia (DCI) in aneurysmal SAH. Methods: Retrospective study of consecutive SAH patients enrolled in a prospective IRB-approved clinical trial. Qualitative analysis of CTP deficits were determined by two blinded neuroradiologists. Quantitative CTP was performed using standardized protocol with region-of-interest placement sampling the cortex. DCI was assessed by clinical and imaging criteria. Patients were classified into treatment groups: 1) hypertension-hemodilution-hypervolemia (HHH); 2) intra-arterial (IA) vasodilators and/or angioplasty; 3) no treatment. Mean quantitative CTP values were compared using ANOVA pairwise comparisons. Receiver operating characteristic (ROC) curves, standard error (SE) and optimal threshold values were calculated. Results: Ninety-six patients were classified into three treatment groups; 21% (19/96) HHH, 34% (33/96) IA-therapy and 46% (44/96) no treatment. DCI was diagnosed in 42% (40/96); of which 18% (7/40) received HHH, 80% (32/40) IA-therapy, and 2% (1/40) no treatment. CTP deficits were seen in 50% (48/96); occurring in 63% (12/19) HHH, 94% (31/33) IA-therapy, and 11% (5/44) no treatment. Presence of CTP deficits had 83% sensitivity, 89% specificity, 90% positive predictive and 81% negative predic

To Optimize the Therapeutic Dose and Time Window of Picroside II in Cerebral Ischemic Injury in Rats by Orthogonal Test  [PDF]
Hui Huang, Li Sun, Ling Wang, Lei Fang, Li Zhao, Yan Li
Neuroscience & Medicine (NM) , 2013, DOI: 10.4236/nm.2013.43027

The paper aims to optimize the therapeutic dose and time window of picroside II by orthogonal test in cerebral ischemic injury in rats. The forebrain ischemia models were established by bilateral common carotid artery occlusion (BCCAO) methods. The successful models were randomly divided into sixteen groups according to orthogonal experimental design and treated by injecting picroside II intraperitonenally at different ischemic time with different dose. The concentrations of neuron-specific enolase (NSE), neuroglial marker protein S100B and myelin basic protein (MBP) in serum were determined by enzyme linked immunosorbent assay to evaluate the therapeutic effect of picroside II in cerebral ischemic injury. The results indicated that best therapeutic time window and dose of picroside II in cerebral ischemic injury were ischemia 1.5 h with 20 mg/kg body weight according to the concentrations of NSE, S100B and MBP in serum. It is concluded that according to the principle of lowest therapeutic dose with longest time window, the optimized therapeutic dose and time window are injecting picroside II intraperitonenally with 20 mg/kg body weight at ischemia 1.5 h in cerebral ischemic injury in rats.

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