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At least 1,171 records · Page 65Linked to original sources
PubMed1988

Cerebral lactate detected by regional proton magnetic resonance spectroscopy in a patient with cerebral infarction.

Water-suppressed image-guided localized proton magnetic resonance spectroscopy was performed in a 59-year-old woman with two major brain infarcts. Spectra were measured in the infarcts, in an area between the infarcts, and in the healthy hemisphere. The volumes of interest were selected on the basis of a fast T2-weighted image. A 1331-2662 Hahn spin-echo sequence was used to suppress the water in the 8-cm3 volume that was selected by means of spatially resolved spectroscopy or stimulated echoes. The spectra were obtained in 5 minutes' accumulation time. Spectral editing was applied to separate the resonance of lactate from that of other substances. Our results show no increase of lactate concentration within the infarcts after 6 months; however, a resonance was observed at 1.6 ppm, which is assigned to fatty acids. Peak intensities of brain-specific compounds were decreased. Six months after the onset of clinical symptoms (at the time of bypass surgery), a fivefold increase in lactate concentration compared with normal values was observed in the area between the two infarcts. Four months after bypass surgery, the lactate concentration in this area had decreased to only twice normal. We speculate that lactate is a marker of reversible or impending brain damage.

Cerebral Infarction↗
PubMed2003

Early carotid endarterectomy after ischemic stroke improves diffusion/perfusion mismatch on magnetic resonance imaging: report of two cases.

OBJECTIVE AND IMPORTANCE: The functional magnetic resonance imaging techniques of diffusion-weighted imaging and perfusion-weighted imaging allow for ultra-early detection of brain infarction and concomitant identification of blood flow abnormalities in surrounding regions, which may represent brain "at risk." CLINICAL PRESENTATION: We report two patients with acute ischemic stroke associated with ipsilateral high-grade carotid stenosis. The first patient, a 64-year-old woman with a remote history of ischemic stroke and a vertebral artery aneurysm, presented with worsening of her preexisting right hemiparesis. The second patient, another 64-year-old woman with known multiple intracranial aneurysms and bilateral high-grade internal carotid artery stenosis, was admitted for the elective microsurgical clipping of an enlarging giant left carotid-ophthalmic artery aneurysm. Postoperatively, she developed right hemiparesis and mild aphasia. Both patients showed progressive worsening of their neurological deficits in the setting of small or undetected diffusion-weighted imaging abnormalities and large perfusion-weighted imaging defects. INTERVENTION: After prompt carotid endarterectomy, symptoms in both patients resolved or improved. Follow-up magnetic resonance imaging scans demonstrated resolution or significant improvement in the perfusion abnormalities in both patients. CONCLUSION: Carotid endarterectomy in the setting of diffusion-weighted/perfusion-weighted imaging mismatch can lead to improvement in cerebral perfusion as evidenced by resolution of the perfusion-weighted imaging lesion. Diffusion/perfusion magnetic resonance imaging may be useful in identifying patients with severe neurological deficits but without large territories of infarction who may safely undergo early surgical revascularization.

Brain↗
PubMed1998

[Pathological analysis of 180 cases of cerebrovascular disorder in autopsy].

OBJECTIVE: To evaluate the ratio of each kind of causes in 180 cases of cerebrovascular disorder(CVD) in autopsy. RESULTS: In 180 cases of CVD in autopsy: (1)125 (69%) belong to brain hemorrhage including hypertension 36 cases(20%), vascular malformation 28 cases(16%), hemopoitic diseases and blood coagulation disturbances 23 cases(13%), congenital aneurysm and brain tumor 9 cases(5%) each separately. (2) 55 cases (31%) are due to brain infarction, main of them are caused by embolism 29 cases (16%) and thrombosis 17 cases(10%). Thrombosis related to atherosclerosis has 5 cases(3%). CONCLUSION: In CVD in autopsy, brain hemorrhage is more than infarction, the ratio of them is 2.3:1. More than 50% of cases is due to hypertension and vascular malformation. In infarction, embolism is more than thrombosis, the ratio of them is 1.7:1. Vascular malformation is more than congenital aneurysm, the ratio of them is 3:1.

Adult↗
PubMed1992

Large striatocapsular infarcts: clinical presentation and pathogenesis in comparison with lacunar and cortical infarcts.

In a well-defined prospective series of 247 patients with a first-ever supratentorial brain infarct, 15 patients (6%; 95% confidence interval 3-9%) had a large striatocapsular infarct. Twelve (80%) had signs of cortical dysfunction, whereas risk factor profile, frequency of significant carotid stenosis, and frequency of potential cardioembolic sources did not differ between patients with striatocapsular and those with cortical infarction. However, patients with striatocapsular infarction more frequently had potential cardioembolic source and significant carotid stenosis than patients with lacunar infarction. Our findings show that large striatocapsular infarcts differ from lacunar infarcts with regard to both presenting signs and symptoms, and pathogenesis, whereas they resemble infarcts involving the cortex. Such patients should therefore be managed and treated as patients with cortical infarction.

Aged↗
PubMed1989

SPECT analysis of recent cerebral infarction.

We measured regional cerebral blood flow and [123I]iodoamphetamine (IMP) uptake in 16 patients with unilateral brain infarcts during the subacute period (Day 3 to Day 50) and again after 3 months. Our results show that the central and peripheral areas described earlier in the chronic period were already differentiated in the subacute period. The central area presented a short phase of luxury perfusion and a longer phase of IMP hyperfixation. The peripheral area showed both a slight regional cerebral blood flow decrease and an early IMP uptake decrease similar to those previously found in the chronic period. Contralateral regional cerebral blood flow during the subacute period, considered normal, was significantly lower than that during the chronic period.

Acetazolamide↗
PubMed2002

Restricted clinical efficacy of cyclosporin A on rat transient middle cerebral artery occlusion.

The immunosuppressant cyclosporin A (CsA) has been shown to have neuroprotective action. The inhibition of both calcineurin activation and mitochondrial permeability transition pore (mtPTP) opening are considered the primary neuroprotective mechanisms of CsA. Here we have evaluated the effect of CsA on significantly reducing infarct size induced by transient middle cerebral artery occlusion (MCAO) in rats, and examined variable therapeutic applications for brain infarction. Experimental rats were divided into 12 groups according to: CsA administration time (immediately after occlusion or immediately after reperfusion); dosage (between 10 and 50 mg/kg); route (i.v. or i.p.); and with or without needle insertion, which hypothetically disrupts the blood brain barrier (BBB). Neuroprotective effects of CsA were hardly noticeable when administered immediately after occlusion or by i.v. injection. By needle insertion, CsA administration significantly reduced infarct size, although vehicle treatment also reduced infarct size compared with nontreatment animals, i.e. no needle insertion. These results suggest that needle insertion allows endogenous neuroprotective substances to pass into the brain. Furthermore, single dosages over 30 mg/kg CsA were excessive and negated potential neuroprotective effects. However, two i.p. administrations of 20 mg/kg CsA immediately and 24 hrs after reperfusion significantly ameliorated the infarct size compared to the vehicle-treated group. We conclude that CsA exhibits significant neuroprotective activity, although its therapeutic application for stroke may be limited by very strict and precise management requirements.

Animals↗
PubMedDate not supplied

Transient left ventricular dysfunction in childhood sickle cell disease.

For unclear reasons, myocardial infarction is rare in childhood sickle cell disease, whereas lung, bone, and brain infarcts are more common. During vasoocclusive crisis and infection, acute myocardial ischemia and chronic volume overload from anemia may result in myocardial dysfunction. We report a child who had reversible cardiac dysfunction that mimicked myocardial infarction.

Child↗
PubMed2001

Matrix metalloproteinase inhibition prevents oxidative stress-associated blood-brain barrier disruption after transient focal cerebral ischemia.

Oxidative stress generated during stroke is a critical event leading to blood-brain barrier (BBB) disruption with secondary vasogenic edema and hemorrhagic transformation of infarcted brain tissue, restricting the benefit of thrombolytic reperfusion. In this study, the authors demonstrate that ischemia-reperfusion-induced BBB disruption in mice deficient in copper/zinc-superoxide dismutase (SOD1) was reduced by 88% ( P < 0.0001) and 73% ( P < 0.01), respectively, after 3 and 7 hours of reperfusion occurring after 1 hour of ischemia by the inhibition of matrix metalloproteinases. Accordingly, the authors show that local metalloproteinase-generated proteolytic imbalance is more intense in ischemic regions of SOD1 mice than in wild-type litter mates. Moreover, active in situ proteolysis is, for the first time, demonstrated in ischemic leaking capillaries that produce reactive oxygen species. By showing that oxidative stress mediates BBB disruption through metalloproteinase activation in experimental ischemic stroke, this study provides a new target for future therapeutic strategies to prevent BBB disruption and potentially reperfusion-triggered intracerebral hemorrhage.

Animals↗
PubMed1991

Myelin lipids in ischemic stroke.

Slices of ischemic focus (infarct area) and of the contralateral frontal lobe were submitted to histological and biochemical studies. The obtained results indicate that in stroke cases the necrotic focus as well as contralateral brain hemisphere are characterized by a marked decrease of cholesterol and cerebrosides content and an increase of lysophosphatidylcholine and cholesterol esters in the myelin fraction. We conclude that ischemia as well as the degenerative aging process are both responsible for the abnormal lipid pattern in the myelin of the white matter in stroke cases. The long lasting hypoxia resulting from cerebral vessel atheromatosis contributes to biochemical changes in the myelin of the apparently healthy white matter of the contralateral hemisphere in brain infarction.

Acute Disease↗
PubMed1994

Apolipoprotein E-4 gene dose in clinically diagnosed Alzheimer's disease: prevalence, plasma cholesterol levels and cerebrovascular change.

The prevalence of the apolipoprotein E-4 allele (ApoE-4) was significantly higher in a referral population of 40 patients with clinically diagnosed Alzheimer's disease than in a sample of non-demented elderly controls (P < 0.01). The highest plasma cholesterol levels were found in demented patients homozygotic for Apo E-4, but no significant increases of glucose, triglycerides and thyroxine or of leuko-araiosis and brain infarcts were verified in this preliminary study.

Aged↗
PubMed1996

Potassium-induced cortical spreading depressions during focal cerebral ischemia in rats: contribution to lesion growth assessed by diffusion-weighted NMR and biochemical imaging.

In focal ischemia of rats, the volume of ischemic lesion correlates with the number of peri-infarct depolarizations. To test the hypothesis that depolarizations accelerate infarct growth, we combined focal ischemia with externally evoked spreading depression (SD) waves. Ischemic brain infarcts were produced in halothane-anaesthetized rats by intraluminal thread occlusion of the middle cerebral artery (MCA). In one group of animals, repeated SDs were evoked at 15-min intervals by microinjections of potassium acetate into the frontal cortex. In another group, the spread of the potassium-evoked depolarizations was prevented by application of the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801). The volume of ischemic lesion was monitored for 2 h by diffusion-weighted imaging (DWI) and correlated with electro-physiological recordings and biochemical imaging techniques. In untreated rats, each microinjection produced an SD wave and a stepwise rise of the volume and signal intensity of the DWI-visible cortical lesion. The volume of this lesion increased between 15 min and 2 h of MCA occlusion from 19 +/- 15% to 66 +/- 16% of ipsilateral cortex. In dizocilpine-treated animals, microinjections of potassium did not evoke SDs, nor did the volume and signal intensity of the DWI-visible cortical lesion change. At 15 min after MCA occlusion, the DWI-visible lesion was larger than in untreated animals-43 +/- 16% of the ipsilateral cortex; however, after 2 h, it increased only slightly further to 49 +/- 21%. Slower lesion growth in the absence of SDs was also reflected by the volume of ATP-depleted tissue, which, after 2 h of MCA occlusion, involved 26 +/- 12% of the ipsilateral cortex in treated and 49 +/- 9% in untreated animals (p < 0.01). These observations support the hypothesis that peri-infarct depolarizations accelerate cerebral infarct growth.

Animals↗
PubMed2003

[The role of polymorphic variants of renin-angiotensin system genes in the development of ischemic stroke in Moscow population].

Polymorphic variants of genes for angiotensin-converting enzyme (ACE) and angiotensinogen (ATG) were studied in 110 patients with different types of brain ischemic disease--carotid atherothrombotic ischemic stroke (one of the pathogenic brain infarction variants) as well as in 119 their siblings with the main risk factors of cerebrovascular pathology development being taken into account. No association has been found between ACE and ATG genes polymorphisms and carotid atherothrombotic ischemic stroke. However, the presence of a homozigous DD ACE genotype was shown to be an independent risk factor for development of hemodynamically relevant stenosis of the major brain arteries. The absence of differences in genetic variants distribution in patients with acute ischemic stroke, comparing to those with prolonged chronic brain ischemic disease (without infarction formation) and the highest frequency of this polymorphism in "longevity" group (without lifetime stroke) imply a relatively independent character of the atherothrombogenic process, which may probably underlie a further development of pathological process.

Aged↗
PubMed1994

Effects of lecithin-emulsified perfluorochemical compounds in ischemic brain injury.

A lecithin-emulsified "Pluronic F-68"-free perfluorochemical compound, named F-1,3-DMA, was tested as a new agent in the prevention of central nervous tissue ischemia. A permanent ischemia leading to cerebral infarction was induced after microsurgical exposure and occlusion of the internal carotid, anterior, and middle cerebral arteries in the rabbit. Following arterial occlusion, F-1,3-DMA was administered intravenously, in a solution rendered isotonic to plasma, over a 30 minute period. The F-1,3-DMA was well tolerated. Hemodynamic, cardiovascular and metabolic parameters were not affected by the infusion of F-1,3-DMA. Although PO2 remained virtually unchanged, animals treated with F-1,3-DMA (n = 9), had smaller infarct volume by 61 percent as compared to the control (n = 8) group (P < 0.04, Student's t-test). Histopathology did not reveal any F-1,3-DMA related damage in the non-infarcted brain. These results suggest that F-1,3-DMA has nervous tissue ischemia protective properties possibly because of microflow effects although O2 transport to "local" tissue may be enhanced as well. We believe that further research is necessary in order to make clinical trials of F-1,3-DMA possible.

Adamantane↗