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

An increased distance between the brain surface and the skull causes the appearance of a broad avascular band in the carotid angiogram, which -- apart from other criteria -- has been valued as a sign of cerebral atrophy. 54 patients (60 to 79 years old), suffering from cerebrovascular diseases, were examined. Carotid angiography of the afflicted hemispheres were carried out within 4 to 90 days after the stroke. The initially mentioned distance between the skull and the brain surface, represented by the terminal arterial branches, was measured in frontal and lateral projection. The influence of alterations of the wall of extracranial vessels, of the number of attacks, of the severity of the stroke as well as of the patient's age on the distance was statistically evaluated. The results were compared with those of cranial computerized tomography. Only limited correlations between the mentioned parameters and the distance between the vessels and the skull have been found. Thus the distance is only of limited diagnostic value for the verification of senile cerebral atropy on a vascular basis.
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PMID:[Diagnosis of cerebral atrophy on the basis of the cerebral angiogram (author's transl)]. 46 56

An increased distance between brain surface, represented by the terminal arterial branches, and skull causes the appearance of a broad avascular band in the carotid angiogram, which--apart from other criteria--has been valued as a sign of cerebral atrophy. We investigated 54 patients (ages 60-79 years) suffering from cerebrovascular disease. Carotid angiographies of the afflicted hemispheres were carried out within 4 to 90 days after the stroke. The distance between vessels and skull was measured in frontal and lateral projection. We evaluated statistically the impact on this distance of alterations in extracranial vessel walls, number of attacks, severity of stroke, and patient's age. The results are compared to those of CAT. Only limited correlations have been found between the above-mentioned parameters and the distance between vessels and skull. Thus the distance is only of limited diagnostic value for the verification of senile cerebral atrophy on a vascular basis.
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PMID:The diagnosis of cerebral atrophy on the basis of cerebral angiogram. 74 Jan 58

A derivate of gamma-aminobutyric acid was found to have a favourable therapeutic effect in patients with forced weeping (weeping sickness). All 10 treated cases were shown to have motor neuron lesions resulting from other cerebral changer (cerebrovascular accident, brain atrophy, diffuse vascular changes).
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PMID:[Treatment of forced weeping (author's transl)]. 101 9

Bypass surgery is a safe procedure with low mortality and morbidity, and few reported surgical complications. Three patients developed postoperative chronic subdural hematoma (CSDH): two with stroke after superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis and one with moyamoya disease after STA-MCA anastomosis combined with encephalomyosynangiosis. The factors inducing CSDH after revascularization in the seven reported and present cases included postoperative subdural effusion associated with brain atrophy, and postoperative anticoagulant therapy such as aspirin. CSDH may occur in patients with pre-existing brain atrophy and postoperative subdural effusion. Anticoagulant therapy should be avoided at the early postoperative stage after bypass surgery.
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PMID:Chronic subdural hematoma following bypass surgery--report of three cases. 138 57

In a retrospective study of 624 elderly patients referred with falls and gait disorders, 45 patients were found to have ataxia. Cerebrovascular diseases were the most common underlying cause of ataxia (15 patients, 37%). Nine patients had hereditary/degenerative cerebellar ataxia. History suggesting alcohol as an underlying cause was established in two patients with cerebellar ataxia. Three patients had normal pressure hydrocephalus and their condition improved remarkably after surgery. No definite cause was found in five patients. Cranial computed tomography (CT) showed cerebral atrophy in 16 patients and in three patients there was evidence of atrophy of the cerebellar vermis. Four patients had femoral neck fractures and three patients had other fractures. In a 5-year follow-up five patients died with bronchopneumonia (11% mortality) and patients with dementia showed rapid deterioration. All patients were referred to the day hospital for rehabilitation. The best treatment outcome was achieved in patients who had a single cerebrovascular accident with no cognitive impairment and in those whose ataxia was secondary to medication. Fourteen patients (44%) moved to residential care while 27 (66%) continued to live in their homes with community support. We concluded that there is no evidence of increased mortality in the elderly patients with cerebellar ataxia. CT scan is mainly helpful in diagnosing specific diseases such as tumours or hydrocephalus. A significant proportion of elderly patients with ataxia may have reversible or treatable conditions and can pursue an independent life.
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PMID:Cerebellar ataxia in the elderly. 140 89

Positron emission tomographic studies of cerebral glucose metabolism have shown high diagnostic specificity in distinguishing among the degenerative dementias and differentiating between Alzheimer's disease (AD) and normal aging. The current investigation was undertaken to characterize the regional glucose metabolic deficits in AD, using cross-sectional and longitudinal study designs. All subjects met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for AD (n = 45) or were normal (n = 20), and the AD subjects were subdivided into incipient and mild AD and moderate plus moderately severe subgroups based on the Global Deterioration Scale. The subjects underwent a non-contrast computed tomographic scan and a positron emission tomographic (PETT VI) scan. The AD subjects (n = 14) and normal control subjects (n = 15) received evaluations 2 to 3 years after baseline study. The brain regions that show glucose metabolic deficits cross-sectionally (temporal and parietal association areas, with lesser degrees of deficit in subcortical gray matter structures), over the stages of AD, also show further deficits longitudinally within the same AD subjects. The reduction in glucose metabolism is greater than would be expected from the degree of brain atrophy. The glucose metabolic deficits are discussed in the context of neuropathologic findings and neurotransmitter deficits in AD.
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PMID:Topography of cross-sectional and longitudinal glucose metabolic deficits in Alzheimer's disease. Pathophysiologic implications. 144 81

To determine whether hypertension, the predominant risk factor for stroke and vascular dementia, is associated with brain atrophy, magnetic resonance imaging (MRI) scans were performed to quantify brain volumes and cerebrospinal fluid spaces. Eighteen otherwise healthy, cognitively normal older hypertensive men (mean +/- SD age, 69 +/- 8 years, duration of hypertension 10-35 years) and 17 age-matched healthy, normotensive male control subjects were studied in a cross-sectional design. Axial proton-density image slices were analyzed using region-of-interest and segmentation analyses. The hypertensive subjects had significantly larger mean volumes of the right and left lateral ventricles (p less than 0.05, both absolute volume and volume normalized to intracranial volume) and a significantly smaller normalized mean left hemisphere brain volume (p less than 0.05) with a trend toward significance for a smaller normalized mean right hemisphere volume (p less than 0.09). Four hypertensive subjects and one healthy control subject were found to have severe periventricular hyperintensities on T2-weighted MRI images. When data for these subjects were removed from the analyses, the normalized lateral ventricle volumes remained significantly larger in the hypertensive group. Lateral ventricle enlargement was not related to age or use of diuretics in the hypertensive group nor to duration of hypertension between 10 and 24 years. Our findings suggest that long-standing hypertension results in structural changes in the brain. Longitudinal studies will determine whether MRI-associated changes are progressive and if such changes identify hypertensive subjects at increased risk for clinically apparent brain dysfunction.
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PMID:Brain atrophy in hypertension. A volumetric magnetic resonance imaging study. 151 53

A 64-year-old man developed hallucinations, delusions, and agitation after a right hemispheric cerebrovascular accident (CVA) in the occipital, inferior temporal, and parietal regions of the posterior cerebral artery. A review of the literature suggests that psychotic behavior is rare after CVA, but when such behavior does occur, the lesion is usually in the right hemisphere. Two clinical presentations are seen. One presentation involves patients free of chronic disease who develop episodic psychotic behavior at a time remote from their CVA. Electroencephalogram often demonstrates epileptogenic foci, and these patients often improve with anticonvulsant medication. Another presentation involves patients with one or more chronic diseases, often resulting in brain atrophy, who display continuous abnormal behavior soon after their CVA; these patients respond variably to antipsychotic agents.
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PMID:Psychotic behavior after right hemispheric cerebrovascular accident: a case report. 155 13

Point mutation of mitochondrial DNA has been described in the blood from a MELAS patient. The 39-year-old patient developed progressive dementia, stroke-like episodes, heart conduction defect (Lown-Ganong-Levin syndrome) and cortical blindness. CT scan revealed brain atrophy and low density areas in the bilateral occipital lobes. Laboratory tests showed hyperglycemia and lactic acidosis. Muscle biopsy showed ragged red fibers on Gomori trichrome staining. He was clinically diagnosed as having MELAS and insulin-dependent diabetes mellitus. Onset of diabetes mellitus and MELAS was almost same. Family history showed his mother's brother and sisters had also insulin-dependent diabetes mellitus. We amplified the leucine (UUR) tRNA gene from the patient's blood with polymerase chain reaction (PCR) and analysed it by restriction enzyme analysis and sequencing. Genetic analysis showed A-to-G substitution at the nucleotide position 3243 in the leucine (UUR) tRNA gene. This substitution made a new restriction site Apa I. Mutant DNA coexisted with wild type DNA (heteroplasmy). It is shown that in some types of mitochondrial encephalomyopathies, especially patients of Kearns-Sayre syndrome (KSS), diabetes mellitus is often complicated. And in KSS patients insulin receptor in normal, but insulin secretion from beta cells of pancreas is decreased. In MELAS patients, however, has diabetes mellitus been reported to be rarely complicated and relationship between MELAS and diabetes mellitus is not done. As far as we know, two cases, including ours, with genetically diagnosed MELAS have been reported to have diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[MELAS associated with diabetes mellitus and point mutation in mitochondrial DNA]. 159 Nov 3

There is little information available regarding management of apraxic gait. We present a 61-year-old man with a five-year history of right-sided cerebrovascular accident, apraxic gait, difficulty in walking, and frequent falls. A CT head scan revealed moderate cerebral atrophy, a small lacunar infarction. The patient was unable to initiate walking, was bed ridden and housebound. Traditional gait training and balance exercises failed to improve his gait. Two straight canes were modified by fixing florescent horizontal projections approximately two inches up from the tip of the cane. The patient was instructed to step over the horizontal projected portion, making use of visual cues from the florescent painted projections. The patient became independent with safe ambulation after practicing for approximately three weeks and was discharged home.
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PMID:Management of apraxic gait in a stroke patient. 172 82


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