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Results for “Brain Infarction”

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At least 505 records · Page 28Linked to original sources
PubMed1990

A semiautomated method for measuring brain infarct volume.

An accurate, reproducible method for determining the infarct volumes of gray matter structures is presented for use with presently available image analysis systems. Areas of stained sections with optical densities above that of a threshold value are automatically recognized and measured. This eliminates the potential error and bias inherent in manually delineating infarcted regions. Moreover, the volume of surviving normal gray matter is determined rather than that of the infarct. This approach minimizes the error that is introduced by edema, which distorts and enlarges the infarcted tissue and surrounding white matter.

Animals↗
PubMed1999

CADASIL: hereditary disease of arteries causing brain infarcts and dementia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) begins with migraine with aura in approximately one-third of the patients. More severe symptoms of recurrent strokes usually appear at 30-50 years of age. However, well before the first stroke, CADASIL may be diagnosed on the basis of characteristic hyperintensities in T2-weighted magnetic resonance images. Multiple lacunar infarcts located mainly in the basal ganglia and frontal white matter lead to a cognitive decline and finally to dementia. These infarcts result from a thickening and fibrosis of the walls of the small and medium-sized penetrating arteries with consequent obliteration and/or thrombosis. Although the symptoms are almost exclusively neurological, the arteriopathy is generalized. Thus, basophilic, periodic acid-Schiff-positive and, in electron microscopy, osmiophilic material accumulates between degenerating smooth muscle cells. This occurs even in dermal arteries, which renders skin a useful target for diagnostic biopsy. Presently, no specific therapy is available. CADASIL is caused by missense point mutations in the Notch3 gene, which encodes a transmembrane receptor protein. Each gene defect leads to either a gain or loss of a cysteine residue in the extracellular, N-terminal domain of the molecule, which most probably results in conformational alteration. The function of Notch3 in adults and the pathogenesis of CADASIL are still unknown.

Cerebral Arterial Diseases↗
PubMed1977

Brain infarction in young adults (with particular reference to pathogenesis).

Sixty-four young adults (aged 16 to 40 years) with ischemic stroke were analyzed in retrospect with regard to possible pathogenetic mechanisms. In older patients various predisposing factors emerge (arterial hypertension, hyperlipidemia etc.) which are rare among younger age groups. In patients lacking predisposing causes the stroke incidence exhibits a seasonal variation. It is suggested that infection may be important for the development of ischemic stroke.

Adolescent↗
PubMed1981

Serial measurements of quantitative EEG and cerebral blood flow and circulation time after brain infarction.

The quantitative EEG (QEEG), regional cerebral blood flow (rCBF) and circulation time of 17 patients were examined semisimultaneously thrice during the first 3 months after a cerebral supratentorial infarction. The EEG was quantified according to normalized slope descriptor technique in nine patients and by means of a combined period and amplitude analysis in eight patients. Intravenously injected isotopes 133Xenon and 99TcmO4 were used for blood flow and circulation time measurements. The QEEG-values improved during the whole follow-up period. Cerebral blood flow stayed low for all 3 months and did not alter during this period, while initially prolonged circulation time to some extent improved within 2 weeks remaining, however, prolonged even thereafter. A tendency for a positive correlation between QEEG and rCBF values in the infarcted hemisphere could be seen.

Adult↗
PubMed1976

Combined dexamethasone and low-molecular-weight dextran in acute brain infarction: double-blind study.

Intramuscular dexamethasone combined with intravenous low-molecular-weight dextran (dextran 40) was compared with placebo in 40 patients with acute ischaemic cerebral infarction. A double-blind procedure was used. Dexamethasone was given for up to 14 days and dextran 40 for up to three days after the infarction. A weighted scoring system was used to evaluate neurological state and mobility. There were no differences in mortality or in improvement of the neurological or mobility scores between the two groups.

Clinical Trials as Topic↗
PubMed2005

Early signs of brain infarction at CT: observer reliability and outcome after thrombolytic treatment--systematic review.

PURPOSE: To review systematically all reported early computed tomographic (CT) signs in acute ischemic stroke to determine interobserver agreement and the relationship between early CT signs and patient outcome with or without thrombolysis. MATERIALS AND METHODS: A systematic review of the literature was conducted by using Cochrane Stroke Group methodology to identify studies published between 1990 and 2003 that were performed to assess interobserver agreement about early signs of infarction on CT scans obtained within 6 hours after onset of stroke symptoms and determine the relation of early signs of infarction to clinical outcome, including any interactive effect of thrombolysis. Interobserver agreement was measured with the kappa statistic, sensitivity, and specificity. The relation of early signs to clinical outcome with or without thrombolysis was assessed with calculated odds ratios and 95% confidence intervals. RESULTS: In 15 studies of interobserver agreement (median of 30 CT scans and six raters), the prevalence of all early infarction signs was 61% +/- 21 (standard deviation). Interobserver agreement (kappa statistics) ranged from 0.14 to 0.78 for any early infarction sign. The mean sensitivity and specificity for detection of early infarction signs with CT were 66% (range, 20%-87%) and 87% (range, 56%-100%), respectively. Experience improved detection, but knowledge of symptoms did not. In 15 studies of early infarction signs and outcome (including seven thrombolysis trials) in 3468 patients, any early infarction sign increased the risk of poor outcome (odds ratio, 3.11; 95% confidence interval: 2.77, 3.49). Two studies that sought interaction between early infarction signs and thrombolysis found no evidence that thrombolysis given in the presence of early infarction signs resulted in worse outcome than that due to early signs alone. CONCLUSION: Further work is required to determine which signs are most reliably detected, whether scoring systems help to improve detection, and whether any early infarction sign should influence decisions concerning thrombolysis.

Acute Disease↗