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

Outcome following stroke is difficult to measure because the behavioral response to infarction is variable. We hypothesized that cognitive function, such as spatial learning, may be a reproducible and sensitive outcome variable. We developed an animal model of multifocal cerebral ischemia in order to study the effects of infarction on learning. To cause ischemia, several hundred microspheres were injected into the internal carotid arteries of rats. After ischemia, behavior was measured using a global rating and a Morris water maze. Postmortem serial brain sections were stained and the size of the infarctions was measured. We found that intracerebral microspheres caused cortical infarction and an impairment of spatial learning. This impairment was not due to occlusion of the internal carotid artery and was not found in animals who received a sham injection of saline. The degree of learning impairment was not correlated with the volume density of the infarctions or with the volume density of the remaining cerebral hemisphere. The learning impairment clearly differentiated normal from lesioned animals, and the impairment was probably due to a delay in acquisition of spatial information rather than a defect in retention or retrieval. Measurement of learning deficit after cerebral ischemia is an efficient and sensitive method for evaluating new stroke treatments and possibly for exploring structure function relationships.
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PMID:Quantitative effects of cerebral infarction on spatial learning in rats. 157 20

The spin-lattice relaxation time (T1) of water protons and the cross-relaxation time (TIS) between irradiated protein protons and observed water protons were measured in order to study water-macromolecular interactions in ischemic rat brain tissues. Tissues were obtained by bilateral common carotid artery occlusion from stroke-prone spontaneously hypertensive rats. Water, Na, and K contents were measured in ischemic brain tissue at the same time. Water and Na content increased while the TIS value and K content decreased following ischemic insults. The T1 value did not change until 180 min after ischemia had been induced. Changes in the TIS value occurred earlier than changes observed for the T1 value, water, and electrolyte contents. Results indicate that the value of TIS may be useful for detecting cerebral ischemia and that the physical structure of water-macromolecular interaction may be altered soon after ischemic onset in brain tissue.
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PMID:Proton NMR studies on ischemic rat brain tissue. 159 59

Intravoxel incoherent motion (IVIM*)-MRI has been performed on a clinical system at 0.5 tesla with a b gradient factor of 100 s/mm2, in a feline focal model of cerebral ischaemia. Images were obtained in 26 cats from less than 1 hour and up to 7-12 hours after stroke. The apparent diffusion coefficient (ADC) was decreased at the site of injury when compared to the contralateral normal side, by 30% in the first, 33% in 1-2 h and 27% in 2-4 h; it increased at 7-12 h, when vasogenic oedema occurred. IVIM*-MRI demonstrated early changes, due to cytotoxic oedema, during the acute phase of cerebral ischaemia to which conventional T2-weighted spin-echo imaging was not sensitive.
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PMID:Experimental focal cerebral ischaemia assessed with IVIM*-MRI in the acute phase at 0.5 tesla. 160 12

To investigate the basis of ambiguous reports of the validity and utility of processed electroencephalogram (EEG) detection of cerebral ischemia, 19 patients monitored during surgical procedures requiring clamping of the carotid artery were studied. The EEG was recorded and observed for detection of alteration of spectral edge frequency versus EEG power. Electrodes were positioned at the P3-C3' locations over the left hemisphere and P4-C4' areas over the right hemisphere (10-20 system of electrode placement). Maximum sensitivity was used for recordings of the processed EEG. Twelve of 19 patients had bilateral carotid vascular stenosis. Nine of 19 patients studied with EEG monitoring had EEG changes suggestive of cerebral ischemia during interruption of carotid artery blood flow by surgical manipulation, defined as a decline in EEG power of greater than 40% or a decline in spectral edge frequency of at least 3 Hz. Eight of these episodes occurred at the time of carotid vascular clamp placement. These changes were confirmed by the raw EEG. Whereas power band monitoring detected 9 episodes of suspected ischemia, alteration of spectral edge frequency was sufficient to detect only 2 of these episodes. One patient sustained a right hemispheric stroke detected intraoperatively by a 47% decline in EEG power; however, these changes were unaccompanied by intraoperative alteration of spectral edge frequency. It is concluded that monitoring of EEG power with processed EEG devices is a more sensitive indicator of cerebral ischemia than monitoring only the spectral edge frequency of the EEG.
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PMID:EEG power changes are more sensitive than spectral edge frequency variation for detection of cerebral ischemia during carotid artery surgery: a prospective assessment of processed EEG monitoring. 161 Sep 93

Intraoperative transcranial Doppler monitoring of cerebral ischemia during carotid clamping under general anesthesia was done in 238 carotid artery operations, mostly endarterectomy. Depending on the severity of reduction of middle cerebral artery mean velocity, patients were classified as no, mild, or severe ischemia at clamping. With a carotid shunt, velocity was always in the "no ischemia" category during shunting. For patients with no ischemia, stroke was significantly lower without a shunt (2/175 no shunt versus 2/12 shunt). For mild ischemia, shunting did not affect the stroke rate (1/20 no shunt versus 0/9 shunt). For severe ischemia, strokes were less frequent with a shunt (4/9 no shunt versus 0/13 shunt). Intraoperative electroencephalogram predicted most, but not all severely ischemic cases. Carotid back pressure correlated with Doppler velocity, but transcranial Doppler was more helpful. Transcranial Doppler is a new and valuable technique in carotid surgery.
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PMID:Carotid endarterectomy monitored with transcranial Doppler. 161 88

Cerebral ischemic injury is uncommon in children, but the effects are long-lasting with significant implications for the child's development. The precipitating event in ischemic infarct is generally occlusion of the cerebral vessels. This occlusion may the result of direct injury of the cerebral vasculature, thrombus formation, or emboli from more distant sources. A wide variety of conditions are known to predispose to cerebral infarcts in children. However, even in recent studies, the underlying condition is unknown in as many as half the children who suffer an ischemic stroke. To care for these children effectively, it is imperative that extensive evaluations be performed to determine the cause of the cerebral infarct. Furthermore, increasing attention will need to be directed toward the metabolic events of cerebral ischemia. A better understanding of these mechanisms may provide clues to some of the causes of ischemic injury and should lead to more effective treatments.
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PMID:Ischemic stroke syndromes in childhood. 162 May 62

To investigate the role of glutamate release in cerebral ischemia, the amounts of amino acids (glutamate, taurine, alanine, glycine and glutamine) released in the hippocampal CA1 region of stroke-prone SHR (SHRSP), stroke-resistant SHR (SHRSR) and normotensive rats (WKY) were determined during and after cerebral ischemia by the microdialysis method under halothane anesthesia. Cerebral ischemia was produced by the occlusion of both common carotid arteries for 20 min. The basal amino acids release did not differ among the three strains of rats, but ischemic glutamate and taurine releases were more marked in SHRSP than in other strains. These results suggest that the massive glutamate release during cerebral ischemia of SHRSP might be related with severe neuronal cell injury.
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PMID:Changes in extracellular concentration of amino acids in the hippocampus during cerebral ischemia in stroke-prone SHR, stroke-resistant SHR and normotensive rats. 162 92

The medical community has not yet identified cerebrovascular pathophysiological factors that distinguish patients at high risk for stroke or aid in selecting patients for microvascular cerebral bypass. In this study, we describe the courses of 13 patients, all of whom suffered recurrent episodes of transient cerebral ischemia after previous cerebral infarction. These patients underwent regional cerebral blood flow studies using xenon inhalation with a CO2 challenge before and at various times after extracerebral-to-intracerebral microvascular anastomosis. Collateral circulation was assessed in all patients before surgery using four-vessel cerebral angiography. Patients were followed for a mean of 30 months (range, 1-7 yr) after the anastomosis. Measurements of mean cortical cerebral blood flow, as measured using the initial Slope Index, and CO2 cerebrovascular reactivity of these 13 patients were compared with those in a group of 20 patients designed as controls. Hemispheric cortical blood flow was significantly depressed in these patients before surgery compared with those in the control group (P less than 0.05). After the bypass, the mean resting Initial Slope Index in these patients increased 14% (P = 0.0005). Cerebral blood flow both before and after CO2 inhalation improved significantly in these patients after surgery (P = 0.001). Detectors bordering computed tomographic or magnetic resonance image documented infarctions, identified as peri-infarct regions, and demonstrated significant mean increases in both cerebral blood flow (38.8-43.2 ml/min/100 g, P = 0.05) and CO2 cerebrovascular reactivity in these patients after bypass (1.71 + 1.91% to 4.00 + 2.38% change Initial Slope Index/mm Hg CO2, P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved cerebral blood flow and CO2 reactivity after microvascular anastomosis in patients at high risk for recurrent stroke. 164 Nov 7

An open angiography-based, dose rate escalation study on the effect of intravenous infusion of recombinant tissue plasminogen activator (rt-PA) on cerebral arterial recanalization in patients with acute focal cerebral ischemia was performed at 16 centers. Arterial occlusions consistent with acute ischemia in the carotid or vertebrobasilar territory in the absence of detectable intracerebral hemorrhage were prerequisites for treatment. After the 60-minute rt-PA infusion, arterial perfusion was assessed by repeat angiography and computed tomography scans were performed at 24 hours to assess hemorrhagic transformation. Of 139 patients with symptoms of focal ischemia, 80.6% (112) had complete occlusion of the primary vessel at a mean of 5.4 +/- 1.7 hours after symptom onset. No dose rate response of cerebral arterial recanalization was observed in 93 patients who completed the rt-PA infusion. Middle cerebral artery division (M2) and branch (M3) occlusions were more likely to undergo recanalization by 60 minutes than were internal carotid artery occlusions. Hemorrhagic infarction occurred in 20.2% and parenchymatous hematoma in 10.6% of patients over all dose rates, while neurological worsening accompanied hemorrhagic transformation (hemorrhagic infarction and parenchymatous hematoma) in 9.6% of patients. All findings were within prospective safety guidelines. No dose rate correlation with hemorrhagic infarction, parenchymatous hematoma, or both was seen. Hemorrhagic transformation occurred significantly more frequently in patients receiving treatment at least 6 hours after symptom onset. No relationship between hemorrhagic transformation and recanalization was observed. This study indicates that site of occlusion, time to recanalization, and time to treatment are important variables in acute stroke intervention with this agent.
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PMID:Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke. 164 75

Two different techniques were utilized to identify the infiltration of polymorphonuclear leukocytes (PMN) into cerebral tissue following focal ischemia: histologic analysis and a modified myeloperoxidase (MPO) activity assay. Twenty-four hours after producing permanent cortical ischemia by occluding and severing the middle cerebral artery of male spontaneously hypertensive rats, contralateral hemiparalysis and sensory-motor deficits were observed due to cerebral infarction of the frontal and parietal cortex. In hematoxylin-and-eosin-stained histologic sections, PMN, predominantly neutrophils, were identified at various stages of diapedesis from deep cerebral and meningeal vessels at the periphery of the infarct, into brain parenchyma. When MPO activity in normal brain tissue was studied initially, it could not be demonstrated in normal tissues extracted from non-washed homogenates. However, if tissue was homogenized in phosphate buffer (i.e., washed), MPO activity was expressed upon extraction. Utilizing this modified assay, MPO activity was significantly increased only in the infarcted cortex compared to other normal areas of the brain. This was observed in non-perfused animals and after perfusion with isotonic saline to remove blood constituents from the vasculature prior to brain removal. The increased PMN infiltration and MPO activity were not observed in forebrain tissue of sham-operated control rats. Also, MPO activity was not increased in the ischemic cortex of MCAO rats perfused immediately after middle cerebral artery occlusion, indicating that blood was not trapped in the ischemic area. By using a leukocyte histochemical staining assay, activity of peroxidases was identified within vascular-adhering/infiltrating PMN in the infarcted cortex 24 hr after focal ischemia. An evaluation of several blood components indicated that increased MPO activity was selective for PMN. The observed increase of approximately 0.3 U MPO/g wet weight ischemic tissue vs. nonischemic cerebral tissues probably reflects the increased vascular adherance/infiltration of approximately 600,000 PMN/g wet weight infarcted cortex 24 hr after focal ischemia. This combined biochemical and histological study strongly suggests that PMN adhere within blood vessels and infiltrate into brain tissue injured by focal ischemia and that the associated inflammatory response might contribute to delayed progressive tissue damage in focal stroke. This modified MPO assay is a useful, quantitative index of PMN that can be utilized to elucidate the potential deleterious consequences of neutrophils infiltrating into the central nervous system after cerebral ischemia, trauma, or other pro-inflammatory stimuli.
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PMID:Polymorphonuclear leukocyte infiltration into cerebral focal ischemic tissue: myeloperoxidase activity assay and histologic verification. 165 59


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