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

The cranial computerized axial tomography (CAT) findings in groups of patients with epilepsy, migraine, hypertension, and other general medical disorders have been reviewed to assess the frequency and patterns of focal and diffuse brain damage. In addition to demonstrating focal lesions in a proportion of patients with seizures and in patients presenting with a stroke, the CAT scan showed a premature degree of cerebral atrophy in an appreciable proportion of patients with long-standing epilepsy, hypertension and diabetes, and in some patients with migraine, valvular and ischaemic, heart disease, chronic obstructive airways disease, and chronic renal failure. The value of CAT as a means of screening for brain damage in groups of individuals at risk is discussed.
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PMID:Computerized axial tomography in the detection of brain damage. 2. Epilepsy, migraine, and general medical disorders. 746 20

In cerebrovascular disease, progression of brain atrophy may reflect an increase in ischaemic changes. The purpose of this study was to determine whether atrophy of the corpus callosum progresses in association with a deterioration in cerebral cortical oxygen metabolism after occlusion of the carotid artery. Magnetic resonance imaging and PET were used to serially evaluate six patients with occlusion of the unilateral internal carotid artery at intervals ranging from 12 to 50 months. One patient had no symptoms, one had a transient ischaemic attack, and four had a minor stroke. All patients had presented at most only subcortical lesions at the first evaluation. During follow up, no patient showed extension of subcortical lesions or recurrent stroke. The initial total callosal area:skull area ratio for the patients was significantly less than that for 14 age matched normal control subjects. The yearly decrease of callosal size in the patients, which differed significantly from zero and exceeded that in the controls, was significantly correlated with the deterioration in mean cerebral cortical oxygen metabolism. Three of the four patients who showed significant progression of callosal atrophy presented deterioration in haemodynamic states as well. It is concluded that in some patients atrophy of the corpus callosum progresses after occlusion of the carotid artery even in the absence of any overt episode of stroke, and that this atrophy is associated with deterioration in cerebral cortical oxygen metabolism. An increase in cerebral morphological changes with deterioration in cerebral metabolism related to ischaemia may occur after occlusion of the carotid artery, even in the absence of symptoms.
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PMID:Progression of atrophy of the corpus callosum with deterioration of cerebral cortical oxygen metabolism after carotid artery occlusion: a follow up study with MRI and PET. 756 23

To estimate the relationship between aging, dementia and changes observed on magnetic resonance imaging (MRI) seen in elderly patients with cerebral thrombosis, MRI findings in 103 patients with an initial stroke event (thrombosis group) were compared with those of 37 patients with hypertension/diabetes (high risk group) and 78 patients without those disorders (low risk group). In addition to the causative lesions in the thrombosis group, periventricular hyperintensities (PVH), spotty lesions (SL), silent infarctions (SI), ventricular dilatation (VD), and cortical atrophy (CA) were analyzed in these groups. Infarctions located in the internal capsule/corona radiata were the most frequent causative lesion. Compared to the low risk group, a high incidence of patchy/diffuse PVH, SI, and severe CA was seen in both the thrombosis group and the high risk group. Widespread PVH and multiple SL increased with age in the thrombosis group, while severe CA was seen in each group. SI and VD tended to increase after age 60, though they were not significant. Dementia, diagnosed in 40 out of 78 patients, increased with age. Multivariate analysis revealed the degree of the effects of MRI findings on dementia to be marked in PVH, brain atrophy, causative lesions, and SL, in that order. These results indicated that diffuse PVH and brain atrophy, developing with age, promoted dementia in the elderly with vascular lesions. Moreover, they suggested that a variety of silent brain lesions recognized on MRI other than infarction can affect symptoms in the elderly.
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PMID:[Brain MRI findings in patients with initial cerebral thrombosis and the relationship between incidental findings, aging and dementia]. 772 91

In this study we evaluated the effect of the competitive N-methyl-D-aspartate (NMDA) antagonist D-(E)-4-(3-phosphonoprop-2-enyl)piperazine-2-carboxylic acid (CGP 40116) on both early (2 days) and late (28 days) ischemic brain damage in a rodent model of focal cerebral ischemia by means of magnetic resonance imaging (MRI) and conventional histology. Immediately after occlusion of the left middle cerebral artery (MCA), rats received either CGP 40116 (20 mg/kg i.p.) or isotonic saline. Two MRI scans were performed in each animal 2 and 28 days after MCA occlusion. After the second scan, rats were perfusion fixed for histological evaluation. The volume of lesioned brain tissue as determined by MRI or histology was calculated from the damaged area in single sections and the distance between them. CGP 40116 reduced acute infarct volume as measured by MRI 2 days after MCA occlusion by 44% (p < 0.05, analysis of variance). After 28 days the lesion detected by MRI was still significantly smaller in the drug-treated animals. This finding was confirmed by the histological analysis showing a 64% reduction in the volume of brain atrophy in the CGP 40116 group (p < 0.05, analysis of variance). There was a good correlation between the MRI data and the results of the histological evaluation (r = 0.9). Our results indicate that (a) the competitive NMDA antagonist CGP 40116 permanently protects brain tissue from the consequences of cerebral ischemia in a rat model for human stroke and (b) early and late pathological changes can be accurately measured by MRI.
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PMID:The competitive NMDA antagonist CGP 40116 permanently reduces brain damage after middle cerebral artery occlusion in rats. 779 Apr 8

A 50-year-old woman with subacute dementia and brain atrophy on CT showed periodic synchronous discharge (PSD) on electroencephalogram (EEG) and myoclonus. She was initially suspected of suffering from Creutzfeldt-Jakob disease (CJD), but dramatically recovered over 5 months. Based on further investigations, the final diagnosis was mitochondrial encephalomyopathy with an A-to-G substitution at nucleotide position 3243 in mitochondrial DNA (mtDNA), commonly seen in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). This case suggests that patients suspected of suffering from CJD should be evaluated for mitochondrial encephalomyopathy.
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PMID:A MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) mtDNA mutation that induces subacute dementia which mimicks Creutzfeldt-Jakob disease. 800 Jan 5

The data of topographic EEG brain mapping were compared to neurological evidence and CT data in 6 patients with organic lesions (sequelae of vertebrobasilar ischemic stroke, brain atrophy, brain tumor). Cortical activity typical for these nosological entities appeared on the EEG maps. In 5 out of 6 patients foci of alpha- and delta-activity indicated the location of the lesion. The authors suggest that EEG brain mapping of the large number of patients with neural and mental diseases will provide insight into pathogenetic mechanisms of these diseases. The authors also think it necessary for patients undergoing EEG brain mapping to be examined neurologically.
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PMID:[A comparison of the results of topographic EEG mapping with the data from a neurological examination and computed tomography of the brain]. 800 28

MELAS is a mitochondrial cytopathy characterized by encephalopathy with stroke-like episodes and lactic acidosis. Most patients exhibit an A-G transition mutation at np 3243 of mitochondrial DNA (tRNA(Leu)(UUR)). We present a family of four in which the mutation was discovered in blood and in muscle mt DNA. Two patients had the classic MELAS syndrome with multiple stroke-like episodes. Some episodes were precipitated by metabolic stress. The remaining two patients had an oligosymptomatic disease with mild chronic encephalopathy, small stature and hearing loss. MRI was followed over a period of 4-8 years, during which the MELAS patients showed progression from nonspecific multifocal signal change to typical extensive cortico-subcortical parieto-occipital lesions and progressive cerebral atrophy. MRI in the oligosymptomatic cases was normal, or showed non-progressive cerebellar atrophy. Biochemical findings were non-specific, indicating increased mitochondrial volume in all cases, and a relatively complex IV defect in one case. All patients were treated with coenzyme Q with varying clinical response. The percentage of mutant mt DNA in blood and muscle did not correlate with clinical severity. Pathogenetic theories based on molecular genetics, and the therapeutic regimen in terms of the underlying biochemical concepts are discussed.
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PMID:[MELAS syndrome. Clinical aspects, MRI, biochemistry and molecular genetics]. 801 33

Sixteen patients (8 female, 8 male) with primary angiitis of the CNS (PACNS), were followed prospectively in a vasculitis clinic. Diagnosis was by angiography in patients without underlying disease. Median age at diagnosis was 36.5 years, and median duration of follow-up was 28 months. Onset was acute in 14 patients (88%), with 3.5 weeks (median) from onset symptoms to diagnosis. Three women developed symptoms within 3 weeks postpartum. The most frequent symptoms were severe headaches (12, 75%), stroke (6, 30%), transient ischaemic attack (TIA) (4, 28%), seizures (7, 44%), visual aberration (3, 19%), and cognitive impairment (5, 31%). Laboratory data included high ESR (2, 13%), leucocytosis (8, 80%), thrombocytosis (1, 6%), positive antinuclear antibody titre (3, 15%), and high levels of complement (5, 31%). Lumbar puncture was performed in 12 patients (75%). CSF analysis was abnormal in five patients (42%). EEG was abnormal in 5/9 patients. The major CT/MRI scan findings were cerebral haemorrhage (4, 25%), brain infarcts (5, 31%), brain atrophy (2, 13%) and non-specific lesions (2, 13%). Four patients had normal studies. All patients received corticosteroids (CS), and five were treated with oral cyclophosphamide. Two patients relapsed despite CS and cyclophosphamide therapy. All patients are alive, and at the last assessment, eight had a permanent neurological deficit, which included paresis (3, 19%), neurocognitive abnormalities (2, 13%), visual loss (2, 13%) and seizure activity (5, 31%). Our data suggest a non-progressive, non-fatal course in those PACNS patients diagnosed angiographically and treated with CS with or without cyclophosphamide.
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PMID:Primary angiitis of the CNS diagnosed by angiography. 804 67

In recent years, interest in vascular causes of dementia has increased and it has been proposed that vascular dementia (VAD) may be more common than previously supposed. This may have important implications, because VAD at present may be more amenable to prevention and treatment than Alzheimer's disease (AD). Several vascular factors have been related to cognitive decline and dementia in the elderly, including stroke and white matter disease. However, while numerous case-control studies have been concerned with the risk factors for AD, studies on risk factors for VADs are rare. The problems inherent in the diagnostic criteria make it difficult to interpret the results from the few studies that have been performed. Generally, risk factors for multi-infarct dementia are supposed to be the same as those for stroke, and include hypertension, diabetes mellitus, advanced age, male sex, smoking and cardiac diseases. White matter dementia has mainly been related to hypertension. Recent research suggests that vascular factors may also be important in AD, especially in the late-onset type. In stroke patients, dementia has been associated with higher age, less formal education, cerebral atrophy, left-sided or bilateral infarcts, volume of macroscopic infarcts, bilateral symptoms, previous stroke and white matter lesions. The pathogenetic mechanism through which these factors cause dementia is still not clear. Furthermore, it is not known if risk factors for VAD differ from those found in stroke patients. There is now an urgent need for further research on risk factors for VAD and on factors related to dementia in subjects with cerebrovascular disorders.
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PMID:Risk factors for vascular dementia: a review. 808 68

The clinical features and long-term outcome of seven patients with delayed cerebral radiation necrosis (DCRN) are described. Radiotherapy had been given for pituitary tumour (1), astrocytoma (2), pinealoma (2), craniopharyngioma (1) and parotid carcinoma (1). The mean latency to onset of the first neurological symptoms was 22 months (range 6-40 months), and mean duration of follow-up was 86 months (range 60-126). Three patients died at a mean of 84 months after radiotherapy (range 62-98). A fourth patient probably died from metastatic disease. Three patients remain alive, albeit severely disabled, after 5-10 years. The illness typically ran a stepwise course, with fits and stroke-like episodes occurring against a background of progressive dementia and somnolence. CT and MRI scans showed progressive ventricular dilatation associated with cerebral atrophy and diffuse or focal changes in the white matter. Four patients had had two or more neurosurgical procedures after the radiotherapy. In only one of the seven patients was the diagnosis made at presentation. DCRN produces a distinctive clinical picture, yet remains a poorly recognized complication of cranial irradiation.
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PMID:Delayed cerebral radiation necrosis. 815 88


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