UMLS:C0038454 - FACTA Search

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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our aim was to investigate caspase-3 plasma levels after stroke, its correlation with infarct expansion and neurological outcome. Caspase-3 plasma levels were determined by ELISA at different time points after stroke in 116 t-PA-treated patients and a control group of 40 healthy controls. Neurological status was evaluated by NIHSS scores and functional outcome by modified Rankin Scale. To assess brain infarct growth, serial brain magnetic resonance imaging scans including diffusion- (DWI) and perfusion-weighted (PWI) images were performed in a subgroup of 58 patients. Plasma caspase-3 levels were higher in stroke patients versus the control group throughout the acute phase of stroke. Furthermore, caspase-3 level at 24h was associated with poorer short- and long-term neurological outcome and positively correlated with infarct growth assessed by diffusion-weighted images. Our data suggest that caspase-3 could be involved in recruitment of ischemic brain tissue being a marker of infarct growth.
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PMID:Caspase-3 is related to infarct growth after human ischemic stroke. 1805 16

The purpose of this study is to establish that newborn stroke involving extensive parts of cerebral cortex immediately leads to secondary network injury in pulvinar. Seven term infants with cortical stroke presented with hypersignal in pulvinar on DWI. Stroke types included: complete MCA stroke (n=4); PCA stroke, ICA stroke and multiple artery stroke (1 each). Age range at scanning was between day 2 and 6 after birth (except for 1 infant scanned within 7 days of acute presentation during ECMO). ADC values in secondarily injured pulvinar were significantly higher than in the area with primary (sub)cortical injury (all patients scanned with identical MR image acquisition). In the absence of asphyxia and because pulvinar is outside of the primary area of infarction, we conclude that there are suggestions from imaging for acute secondary injury to pulvinar following primary damage of their cortical targets and/or connecting axons. Acute secondary injury is probably due to excitotoxicity and deafferentiation. The relevance of network injury for prognosis and the impact of early treatment on it have yet to be studied, in stroke but also in other acute perinatal brain disorders.
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PMID:Network injury to pulvinar with neonatal arterial ischemic stroke. 1807 86

Although the perfusion-weighted imaging/diffusion-weighted imaging (PWI/DWI) mismatch model has been proposed to identify acute stroke patients who benefit from reperfusion therapy, the optimal definition of a mismatch is uncertain. We evaluated the odds ratio for a favorable clinical response in mismatch patients with reperfusion compared with no reperfusion for various mismatch ratio thresholds in patients enrolled in the diffusion and perfusion imaging evaluation for understanding stroke evolution (DEFUSE) study. A mismatch ratio of 2.6 provided the highest sensitivity (90%) and specificity (83%) for identifying patients in whom reperfusion was associated with a favorable response. Defining mismatch with a larger PWI/DWI ratio may provide greater power for detecting beneficial effects of reperfusion.
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PMID:Optimal definition for PWI/DWI mismatch in acute ischemic stroke patients. 1818 31

Mismatches between tissue perfusion-weighted imaging (PWI; an index of blood flow deficit) and cellular diffusion-weighted imaging (DWI; an index of tissue injury) provide information on potentially salvageable penumbra tissue in focal stroke and can identify "treatable" stroke patients. The present pre-clinical studies were conducted to: a.) Determine PWI (using perfusion delay) and DWI measurements in two experimental stroke models, b.) Utilize these measurements to characterize selective ET(A) receptor antagonism (i.e., determine efficacy, time-to-treatment and susceptibility to treatment in the different stroke models), and c.) Determine if increasing the reduced blood flow following a stroke is a mechanism of protection. Permanent middle cerebral artery occlusion (MCAO) or sham surgeries were produced in Sprague Dawley rats (SD; proximal MCAO; hypothesized to be a model of slowly evolving brain injury with a significant penumbra) and in spontaneously hypertensive rats (SHR; distal MCAO; hypothesized to be a model of rapidly evolving brain injury with little penumbra). Infusions of vehicle or SB 234551 (3, 10, or 30 microg/kg/min) were initiated at 0, 75, and/or 180 min post-surgery and maintained for the remainder of 24 h post-surgery. Hyper-intense areas of perfusion delay (PWI) in the forebrain were measured using Gadolinium (Gd) bolus contrast. DWI hyper-intense areas were also measured, and the degree of forebrain DWI-PWI mismatch was determined. Region specific analyses (ROI) were also conducted in the core ischemic and low perfusion/penumbra areas to provide indices of perfusion and changes in the degree of tissue perfusion due to SB 234551 treatment. At 24 h post-surgery, final infarct volume was measured by DWI and by staining forebrain slices. Following SD proximal MCAO, there was a significant mismatch in the ischemic forebrain PWI compared to DWI (PWI>DWI) at 60 min which was maintained up to 150 min (all p<0.05). By 24 h post-stroke, infarct volume was identical to the area of early perfusion deficit/PWI, suggesting a slow progression of infarct development that expanded into the significant, earlier cortical penumbra (i.e., model with salvageable tissue with potential for intervention). When SB 234551 was administered within the period of peak mismatch (i.e., at 75 min post-stroke), SB 234551 provided significant dose-related reductions in cortical (penumbral) progression to infarction (p<0.05). Cortical protection was related to an increased/normalization of the stroke-induced decrease in tissue perfusion in cortical penumbra areas (p<0.05). No SB 234551-induced changes in reduced tissue perfusion were observed in the striatum core ischemic area. Also, when SB-234551 was administered beyond the time of mismatch, no effect on cortical penumbra progression to infarct was observed. In comparison and strikingly different, following SHR distal MCAO there was no mismatch between PWI and DWI (PWI=DWI) as early as 60 min post-stroke, with this early change in SHR DWI being identical to the final infarct volume at 24 h, suggesting a rapidly occurring brain injury with little cortical penumbra (i.e., model with little salvageable tissue or potential for intervention). In distal MCAO, SB 234551 administered immediately at the time of stroke did not have any effect on infarct volume in SHR. These data demonstrate that selective blockade of ET(A) receptors is protective following proximal MCAO in SD (i.e. a model similar to "treatable" clinical patients). The protective mechanism appears to be due to enhanced collateral blood flow and salvage of penumbra. Therefore, the use of PWI-DWI mismatch signatures can identify treatable stroke models characterized by a salvageable penumbra and can define appropriate time to treatment protocols. In addition, tissue perfusion information obtained under these conditions might clarify mechanism of protection in the evaluation of protective compounds for focal stroke.
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PMID:SB 234551 selective ET(A) receptor antagonism: perfusion/diffusion MRI used to define treatable stroke model, time to treatment and mechanism of protection. 1846 20

Intravenous administration of tissue plasminogen activator (t-PA) can improve clinical outcome in patients with acute ischemic stroke. In our country, use of t-PA for acute brain infarction within 3 hours of onset was approved by Japanese government from October, 2005. About 5,700 patients were treated with t-PA for these two years. Analysis of 2,484 patients (mean 70 years old, median NIHSS Score 15) showed that mRS 0-1 was 32%, the death was 20% and symptomatic brain hemorrhage was 5.2%. We had 63 patients (median 74 years old, median NIHSS score 14) treated with t-PA thrombolysis by November, 2007. Immediately after t-PA therapy 8 patients (12.7%) had dramatic recovery. On day 7 after t-PA therapy, excellent recovery was 49.2%, good recovery was 15.9%, and worsening was 12.7%. Within one hour after t-PA therapy, rate of recanalization for occluded arteries was 43.5%, which was strongly associated with excellent and good neurological recovery on day 7. Atrial fibrillation was an independent factor associated with no early recanalization. When we evaluated baseline DWI findings before t-PA infusion using DWI-ASPECTS and NIHSS score at day 7 after rt-PA therapy, bad outcome was seen more frequently in patients with an DWI ASPECTS < or = 5 (6 of 8 patients) than in patients with an DWI ASPECTS > 5 (2 of 41 patients; P < 0.0001). Patients with an ASPECTS-DWI > 5 should be considered eligible for t-PA therapy.
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PMID:[IV t-pA thrombolysis in acute stroke patients]. 1854 Mar 77

After large CT-based clinical trials have failed to prove the benefits of intravenous tissue plasminogen activator (tPA) administration for ischemic stroke patients beyond 3 hours of the onset of the concept of PWI/DWI mismatch which is the volume difference between a PWI lesion and DWI lesion on MRI scans, has been proposed to facilitate the selection of patients with a salvageable area. PWI/DWI mismatch is considered to represent the tissue that is not irreversibly injured and can respond to early reperfusion therapy. When an ischemic lesion is divided into 4 regions, namely, ischemic core, reversible DWI lesion, penumbra and benign oligemia, both the reversible DWI lesion and penumbra are considered to be an optimal targets for thrombolysis. In order to clarify the clinical significance of PWI/DWI mismatch in the selection of candidates for tPA therapy, some multicenter trials were performed. The results of DIAS (desmoteplase in acute ischemic stroke)/DEDAS (dose escalation of desmoteplase for acute ischemic stroke)/DIAS-2 did not difinitly demonstrate the clinical benefits of desmoteplase administration in patients with PWI/DWI mismatch between 3 to 9 hours of onset; in fact, DIAS-2 could not prove any effect of the drug. DEFUSE (diffusion and perfusion imaging evaluation for understanding stroke evolution), in which tPA was administered to all participants between 3 to 6 hours of stroke onset, showed that the occurrence of early reperfusion led to a favorable clinical response in patients with PWI/DWI mismatch. In contrast, early reperfusion was not beneficial in patients without PWI/DWI mismatch. In EPITHET (echoplanar imaging thrombolysis evaluation trial), stroke patients who showed PWI/DWI mismatch after 3 to 6 hours of the onset were assigned to receive either alteplase or placebo administration: lesion growth was lesser in patients with alteplase than in those who received placebo, although the difference was not statistically significant because of a small number of participants. Although these results supported the importance of the PWI/DWI concept, there still remain some issues to be resolved. Regarding the definition of PWI/ DWI mismatch, a larger mismatch ratio than the one that has been typically used seems to be recommended. Most useful parameters of PWI should be determined to standardize volume evaluation using MRI scans. For the institutes where MRI scans are not available 24 hours a day, clinical DWI mismatch has been proposed as an alternative to of PWI/DWI mismatch. The application of MRI-based decision making strategy for stroke patients may facilitate the assessment and treatment of stroke patients beyond 3 hours of stroke onset, and is expected to allow the use of tPA for a substantially greater number of patients.
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PMID:[Intravenous administration of a tissue plasminogen activator beyond 3 hours of the onset of acute ischemic stroke--MRI-based decision making]. 1897 5

Most clinical trials have focused on the presence of perfusion- and diffusion-weighted imaging (PWI-DWI) mismatch by more than 20%, and different stroke subtypes were lumped together. We hypothesized that intracranial large artery atherosclerotic stroke (IC-LAA) would show different PWI-DWI and magnetic resonance angiography (MRA)-DWI mismatch profiles, compared with other stroke subtypes. Consecutive patients underwent pretreatment multiparametric magnetic resonance imaging for the acute middle cerebral artery infarcts within 6 h of symptom onset. We assessed the difference in the DWI-PWI mismatch ratio, severity of hypoperfusion, and MRA-DWI mismatch among the stroke subtypes. Of 86 patients, 19 (22.1%) had IC-LAA; 42 (48.8%) cardioembolic stroke, 15 (17.4%) extracranial-LAA, and 10 (11.6%) had cryptogenic embolic stroke. Although the volume of the penumbra was not different among the groups, the mismatch ratio was higher (P=0.003) and the severity of hypoperfusion was lower in the IC-LAA group (P=0.001). The MRA-DWI mismatch was more prevalent in the IC-LAA group than in other groups (P<0.001). Collateral grading, assessed in 41 patients, was more likely to be intermediate/excellent in the IC-LAA group (P<0.001). Multivariate testing revealed that a larger mismatch ratio and less severe hypoperfusion, and MRA-DWI mismatch were independently associated with IC-LAA. Our data show that patients with IC-LAA had different mismatch profiles, which were related to better collaterals, compared with other subtypes.
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PMID:MR mismatch profiles in patients with intracranial atherosclerotic stroke: a comprehensive approach comparing stroke subtypes. 1936 94

Posterior cerebral artery (PCA) territory infarcts account for only 5-10% of all infarcts in stroke registries. Moreover, the clinical features and etiology of such infarcts have not been studied as extensively as those in other vascular territories.We describe two patients with recurrent episodes of visual symptoms and headache due to probable transitory PCA vasospasm. MR angiography in the acute phase revealed incomplete visualization of PCA, conventional MRI showed mild T2 signal alterations and MR perfusion showed the presence of marked hypoperfusion in the same regions. Diffusion weighted MR images were normal. All these findings resolved after therapy. These cases suggest that reversible signal alterations associated with reversible vessel and perfusion abnormalities may be observed in patients with visual symptoms and headache. Normal DWI-MR may help distinguish these patients from those affected by non-reversible ischemic attacks.
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PMID:Headache and visual symptoms in two patients with MRI alterations in posterior cerebral artery territory. 1945 1

The value of TCD in clinical practice is well established since it can be used to measure cerebral vasomotor reactivity and to detect and grade vasospasm (VSP) following subarachnoid haemorrhage and cerebral blood perfusion consequences of extracranial ICA stenosis or occlusion. Intracranial steno-occlusive disease can be detected more reliably by transcranial color-coded imaging (TCCI) that provides a two-dimensional imaging of parenchymal and vascular anatomy of brain too. In patients with suspected brain TCD diagnostic criteria for brain death have a sensitivity of 91 to 100% and specificity of 97 to 100% and they are particularly useful when clinical and EEG evaluations are difficult. TCD is a sensitive technique for real time detection of microembolic signals (MES) from prosthetic cardiac valves, myocardial infarction site, atrial fibrillation, aortic arch atheroma and this suggests the use of TCD for monitoring response to antithrombotic therapy. There is also a high correlation between contrast-enhanced TCD and trans-esophageal echocardiography for detecting paradoxical embolism through right-to-left cardiac or pulmonary shunts. Microembolization detected by TCD monitoring may confirm features of unstable carotid artery plaques as imaged by Duplex scanning and there is an increasing evidence that asymptomatic MES from unstable carotid plaques are an independent factor for ischemic stroke. TCD can be used as a monitoring tool during cardiac surgery and cerebrovascular operations to determine critical hemodynamic changes in cerebral arteries and to identify high-intensity transients referred to air or particulate emboli. Several research studies of the past 10 years have shown that MES may be detected by TCD during all phases of CEA and CAS and that sustained microembolism after carotid flow restoration is an indication of impending postoperative or post-procedural occlusion. Our series showed a clear difference between the number of patients with MES and the incidence rate of MES in each patient submitted to CAS (100% of cases with 35-250 MES in each case) and to CEA (74% of cases with 2-30 MES in each case). We also observed a decrease in the incidence rate of microembolic events by TCD during CAS with or without brain protection devices , 18.% and 40%, respectively. There is a statistically significant difference between the neurological deficit related to embolism during CEA (1.8% of cases) and during CAS(9 %). Furthermore DWI has shown a higher prevalence of postoperative small areas of brain ischemia due to asymptomatic embolism occurring during CAS than after carotid surgery according with a higher incidence of patients suffering from neuropsychological impairment after CAS as compared with those submitted to CEA . The use of TCD can provide new insights into pathophysiology of cerebral steno-occlusive and functional diseases, it can helps in risk stratifications of patients with cardio-embolic sources and in the choice and monitoring of medical, surgical or endovascular treatment. TCD monitoring during carotid revascularization either surgical or endovascular can alert the operator to take appropriate measures to avoid brain ischemia and provides useful data for choice and control of the different brain protection devices.
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PMID:Trancranial Doppler: value in clinical practice. 1964 67

The time course of changes in apparent diffusion coefficient (ADC) and signal intensity on diffusion-weighted magnetic resonance imaging (DW MR) imaging in acute ischemic stroke is a very dynamic event. There is an initial reduction in ADCs with no change on T2-W imaging but signal intensity increase on T2-weighted takes place about 6-12 hours after onset of stroke. As necrosis begins to set in, there is a gradual reversal of ADC change, and around 3-10 days post-onset, ADC pseudonormalizes. Twenty-four patients of acute stroke underwent diffusion MR imaging in addition to conventional T1W, T2W, and Fluid Attenuated Inversion Recovery (FLAIR) sequence performed within 12 hours, at 30 days, and at 90 days. The mean signal intensity at b = 0 s/mm2 and at b = 1000 s/mm2 were significantly higher than control values for all time periods. The ratio of signal intensity at b = 0 (rSI b=0) significantly increased from 1.63 +/- 0.20 in the acute stage to 2.19 +/- 0.24 in the chronic stage (P < 0.001). The ratio of signal intensity on DWI (r SIDWI) decreased from 2.54 +/- 0.46 to 1.54 +/- 0.22. The mean ADC in the lesion was found to be 41% lower than the mean ADC in the contralateral hemisphere .Linear regression analysis between rADC and log hours showed that pseudonormalization occurred at 6.61 days (P < 0.001). We conclude that the above information could be useful in the management of very early stroke.
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PMID:Studies on the time course of apparent diffusion coefficient and signal intensities on T2- and diffusion-weighted MR Imaging in acute cerebral ischemic stroke. 1989 11

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