Cases reported "Brain Ischemia"

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1/11. diffusion MRI in ischemic stroke compared to pathologically verified infarction.

    BACKGROUND: diffusion MRI abnormality correlates with pathology in animal ischemic stroke models. A combined retrospective and prospective analysis of consecutive patients over a 3-year period who had a clinical diagnosis of probable new ischemic stroke, underwent diffusion MRI, and were later studied at autopsy was performed. methods: Inclusion criteria for the retrospective analysis were 1) symptom onset within 14 days of presentation, 2) diffusion MRI within 28 days of symptom onset, and 3) autopsy within 16 weeks of symptom onset. patients with suspected further infarcts between MRI and autopsy were excluded. The locations of all areas of MRI abnormality were identified by a blinded neuroradiologist, and recent infarcts were identified by review of pathologic records and microscopic slides. RESULTS: Eleven patients were identified who fulfilled inclusion criteria, with 25 discrete pathologic infarcts. diffusion MRI abnormality corresponded to pathologically verified infarction in 23 cases, was present in two locations where no pathologic infarct was identified, and was absent in two locations where an infarct was present at autopsy. In two cases, despite clinical suspicion of acute ischemic stroke, no MRI abnormality or pathologic infarct was found. The sensitivity and specificity of diffusion MRI were 88.5% (95% CI, 69.9% to 97.6%) and 96.6% (95% CI, 91.5% to 99.1%). Accuracy was 95.1% (95% CI, 90.2% to 98%). Three further patients who died during the course of the retrospective analysis were studied prospectively, and are described separately. CONCLUSIONS: These findings suggest high accuracy of diffusion MRI for detection of ischemic infarction compared with pathologic examination.
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2/11. Intracarotid abciximab injection to abort impending ischemic stroke during carotid angioplasty.

    BACKGROUND: Abciximab, a platelet glycoprotein IIb/IIIa receptor antagonist, prevents ischemic complications during percutaneous transluminal coronary angioplasty and was recently shown to open occluded vessels in patients with acute myocardial infarction when used alone or in combination with other thrombolytic agents. In an animal model of arterial thrombosis, abciximab was found to be safe and effective for the prevention of carotid artery thrombosis. However, the safety and efficacy of abciximab in the treatment of acute ischemic cerebrovascular events is unknown at present. CASE DESCRIPTION: We describe 3 patients who experienced ischemic cerebrovascular events with symptoms involving the middle cerebral artery territory while undergoing percutaneous angioplasty and stenting to their internal carotid arteries. Abciximab was administered to each patient within 10 min of symptom onset as a bolus (0.25 mg/kg) into the ipsilateral common carotid artery followed by continuous intravenous infusion (9 microg/min) for 12 h. All patients' symptoms resolved completely (by 25 min, 40 min and 5 h, respectively) with no further neurological complications. CONCLUSIONS: Our preliminary observation suggests that abciximab may improve neurological outcome following middle cerebral artery ischemic events associated with carotid angioplasty and stenting. Large prospective studies are warranted to establish the safety and efficacy of abciximab in acute ischemic stroke, either as a primary treatment modality or an adjunct to carotid angioplasty and stenting.
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3/11. Severe ADC decreases do not predict irreversible tissue damage in humans.

    BACKGROUND AND PURPOSE: A mismatch between diffusion- and perfusion-weighted MRI is thought to define tissue at risk of infarction. This concept is based on the assumption that diffusion slowing of and decreases in the apparent diffusion coefficient (ADC) serve as indicator of tissue proceeding to infarction. We tested this hypothesis. methods: MRI (diffusion weighted, perfusion weighted, MRA, T2 weighted) was performed in 15 patients with acute stroke within 2.9 /-0.8 hours (mean /-SD) of onset and on days 1 and 7. After intraindividual realignment of the ADC maps, the development of ADC range volumes and ADC values was determined. RESULTS: An increase (354%, group A1) in the total ADC-based lesion volume below a threshold of < 80% occurred in 4 patients on day 1, persisting on day 7 with a pronounced increase of ADC range volumes with low ADC values. An increase in total ADC-based lesion volume (201%, group A2) followed by a secondary drop to day 7 was found in 7 patients. A significant reduction in total ADC-based lesion volume (14%, group B) was found in 4 patients. ADC-based lesion volume increase was associated with persistent vessel occlusion in group A, whereas recanalization in group B resulted in ADC volume decrease. ADC normalization was observed independently from the degree of the initial ADC decrease on days 1 and 7 in group B. CONCLUSIONS: In line with results from animal experiments, ADC decreases do not reliably indicate tissue infarction Even severely decreased ADC values may normalize in human stroke, and it seems likely that ADC normalization depends on the duration and severity of ischemia rather than the absolute value.
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4/11. Increases in GABA concentrations during cerebral ischaemia: a microdialysis study of extracellular amino acids.

    OBJECTIVES: Increases in the extracellular concentration of the excitatory amino acids glutamate and aspartate during cerebral ischaemia in patients are well recognised. Less emphasis has been placed on the concentrations of the inhibitory amino acid neurotransmitters, notably gamma-amino-butyric acid (GABA), despite evidence from animal studies that GABA may act as a neuroprotectant in models of ischaemia. The objective of this study was to investigate the concentrations of various excitatory, inhibitory and non-transmitter amino acids under basal conditions and during periods of cerebral ischaemia in patients with head injury or a subarachnoid haemorrhage. methods: Cerebral microdialysis was established in 12 patients with head injury (n=7) or subarachnoid haemorrhage (n=5). Analysis was performed using high performance liquid chromatography for a total of 19 (excitatory, inhibitory and non-transmitter) amino acids. patients were monitored in neurointensive care or during aneurysm clipping. RESULTS: During stable periods of monitoring the concentrations of amino acids were relatively constant enabling basal values to be established. In six patients, cerebral ischaemia was associated with increases (up to 1350 fold) in the concentration of GABA, in addition to the glutamate and aspartate. Parallel increases in the concentration of glutamate and GABA were found (r=0.71, p<0.005). CONCLUSIONS: The results suggest that, in the human brain, acute cerebral ischaemia is not accompanied by an imbalance between excitatory and inhibitory amino acids, but by an increase in all neurotransmitter amino acids. These findings concur with the animal models of ischaemia and raise the possibility of an endogenous GABA mediated neuroprotective mechanism in humans.
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5/11. MR demonstration of partial lesions of the lateral geniculate body and its functional intra-nuclear topography.

    Two rare cases with a partial lesion of the lateral geniculate body (LGB) presumably due to ischemia are demonstrated on high resolution MR imaging. A 62-year-old woman (case 1) presented with left homonymous superior quadrantanopia on Goldmann perimetry. Heavily T2 weighted MR images showed a localized lesion at the lateral portion of the LGB. The visual field defect was macular and horizontal meridian sparing and persisted for 9 years. A 49-year-old woman (case 2) presented with a sudden onset of left homonymous horizontal sectoranopia on Humphrey automated perimetry and heavily T2 weighted images demonstrated a lesion localized at the more medial part of the right LGB. axons originating from inferior, central and superior retina are essentially located laterally, centrally and medially, respectively, in the LGB, based on the electrophysiological studies of animal experiments and this observation has been applied to humans. This study radiologically shows that a discrete lateral lesion of the LGB produced homonymous upper quadrantanopia in case 1, whereas a more medially located lesion produced homonymous sectoranopia in case 2, and reveals that the axons originating from inferior retina are located more laterally than those from central retina in the human LGB.
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6/11. Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations.

    Progressive ischaemic damage in animals is associated with spreading mass depolarizations of neurons and astrocytes, detected as spreading negative slow voltage variations. Speculation on whether spreading depolarizations occur in human ischaemic stroke has continued for the past 60 years. Therefore, we performed a prospective multicentre study assessing incidence and timing of spreading depolarizations and delayed ischaemic neurological deficit (DIND) in patients with major subarachnoid haemorrhage (SAH) requiring aneurysm surgery. Spreading depolarizations were recorded by electrocorticography with a subdural electrode strip placed on cerebral cortex for up to 10 days. A total of 2110 h recording time was analysed. The clinical state was monitored every 6 h. Delayed infarcts after SAH were verified by serial CT scans and/or MRI. Electrocorticography revealed 298 spreading depolarizations in 13 of the 18 patients (72%). A clinical DIND was observed in seven patients 7.8 days (7.3, 8.2) after SAH. DIND was time-locked to a sequence of recurrent spreading depolarizations in every single case (positive and negative predictive values: 86 and 100%, respectively). In four patients delayed infarcts developed in the recording area. As in the ischaemic penumbra of animals, delayed infarction was preceded by progressive prolongation of the electrocorticographic depression periods associated with spreading depolarizations to >60 min in each case. This study demonstrates that spreading depolarizations have a high incidence in major SAH and occur in ischaemic stroke. Repeated spreading depolarizations with prolonged depression periods are an early indicator of delayed ischaemic brain damage after SAH. In view of experimental evidence and the present clinical results, we suggest that spreading depolarizations with prolonged depressions are a promising target for treatment development in SAH and ischaemic stroke.
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7/11. Diffuse microglial proliferation after global ischemia in a patient with aplastic bone marrow.

    Abundant proliferation of cells having the histologic and tinctorial features of microglia, were seen in the brain of 34-year old man who suffered cardiac arrest 10 days before death and whose bone marrow was nearly totally depleted of white-blood-cell precursors. It is suggested, that in adult human brains there are native microglial precursors which can take on a phagocytic function. Therefore, brain macrophages do not have to originate from circulating monocytes, as suggested by some animal studies.
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8/11. hyperglycemia and hemorrhagic transformation of cerebral infarcts.

    BACKGROUND: Identification of factors that predispose to bleeding into ischemic brain could lead to safer use of thrombolytic agents in the setting of ischemic stroke. Recently de Courten-Meyers and colleagues reported that occluding the middle cerebral artery of markedly hyperglycemic cats was associated with 5-fold more frequent and 25-fold more extensive hemorrhage into infarcts than in normoglycemic animals. Hemorrhage associated with hyperglycemia in cats was much more pronounced with reperfusion than with permanent middle cerebral artery occlusion. CASE DESCRIPTION: We describe two patients with a unique presentation of diffuse hemorrhagic infarction of the caudate and lentiform nuclei associated with initially marked hyperglycemia and the subsequent development of hemichorea. CONCLUSIONS: We hypothesize that the marked hyperglycemia due to poor control of diabetes contributed to the hemorrhagic change of the caudate and lenticular nuclei. Because the hemorrhage in hyperglycemic cats was more pronounced in the setting of reperfusion, hemorrhagic risk associated with hyperglycemia should be investigated, particularly in ongoing thrombolytic treatment trials for acute ischemic stroke. We encourage other acute stroke investigators to prospectively look at the risk of brain hemorrhage in stroke patients with marked hyperglycemia.
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9/11. Visualization of damaged brain tissue after ischemic stroke with cobalt-55 positron emission tomography.

    In animal experiments, the radionuclide 55Co2 has been shown to accumulate in degenerating cerebral tissue similar to Ca2 . methods: The potential role of 55Co2 for in vivo brain PET imaging was investigated in four patients after ischemic stroke. RESULTS: PET showed uptake of 55Co2 in damaged brain tissue irrespective of blood-brain barrier integrity, as affirmed by CT and MRI. CONCLUSION: Our preliminary results indicate that 55CoCl2 may prove to be a useful and relatively inexpensive PET radiopharmaceutical for visualization of degenerative processes in brain tissue.
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10/11. The rationale for, and effects of oxygen delivery enhancement to ischemic brain in a feline model of human stroke.

    Reduced brain tissue oxygenation is frequently seen in severe head injury and after subarachnoid hemorrhage, and this is considered a major cause of secondary ischemic brain injury. In fact, in a previous study, we found a tight correlation between low brain tissue oxygen tension and poor outcome. Therefore, we tested the hypothesis that an allosteric modifier of hemoglobin, which improves oxygen transport to tissue, could reduce the size of an acute infarct in a feline model of human stroke. This compound produces a shift in the hemoglobin dissociation curve to the right and therefore facilitates the unloading of oxygen during low oxygen tension. Seventeen adult cats were studied. Ischemic stroke was induced through a transorbital, permanent, middle cerebral artery occlusion. Seven animals received saline, and 10 received the allosteric Hb modifier RSR-13. Three different endpoints were used to determine the effect of the allosteric modifier. Delta p50 values were measured in the arterial blood; the intra-infarct oxygen tension was measured, and finally, the volume of the infarct was assessed using TTC staining. Mean delta p50 changes varied from 10.4 /- 9.2 mmHg up to 15.0 /- 6.8 mmHg. Mean intra-infarct oxygen tension was 27 /- 6 mmHg for the control group and 33 /- 7 mmHg for the drug-treated animals. The mean infarct size (measured as percentage of hemisphere volume) in the control group was 32 /- 9% and for the RSR-13 animals 22 /- 10% (p < 0.05). A definitive trend towards improvement in brain oxygen tension was seen, such that animals pretreated with RSR-13 showed a higher infarct oxygen tension. Infarct size was significantly reduced in the drug group. Therefore, RSR-13 is potentially beneficial in the treatment of brain ischemia. Since human studies with this compound are already completed, and other compounds which increase oxygen delivery, such as perfluorocarbons, are already being evaluated, it is likely that oxygen delivery enhancement will rapidly become the first 'neuroprotective' modality, employed in patients with severe brain injury, stroke and subarachnoid hemorrhage.
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