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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A man of 19 years of age was found to have a diffuse livedo, a quadruple asphyxic acrosyndrome, and dementia. Angiography confirmed the presence of distal ischemia with multiple circulatory blocks and a reduced distal network. The patient died at the age of 25 years and histopathological examinations of the vessels demonstrated obstructive atheromatous lesions in the medium sized and small arteries of the brain and viscera. By comparing these findings with those observed in three other cases, in which biopsy of the pulp of the toe was also performed, the hypothesis can be advanced that these juvenile encephalic ischemic accidents are caused by atheroma, which can be detected, at an early stage, by studying the distal arteries in the finger or toe pulp.
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PMID:[Successive encephalic ischemic accidents in a young patient: Buerger's disease, buergerian syndrome, or juvenile atheroma? A report in clinical, angiographic, and anatomical findings in one case, compared to three other ones, in which a biopsy of the pulp of the toes was also performed (author's transl)]. 49 84

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.
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PMID:Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease). 56 79

Topographic analysis was performed of the distribution of Alzheimer's neurofibrillary tangles and the granulovacuolar degeneration of Simchowicz in the hippocampal cortex of patients with Alzheimer's dementia and mentally normal aged controls. A semiautomated scanning stage microscope was linked potentiometrically to an XY pen recorder in order to plot cytoarchitectonic "scattergrams" from the sequentially screened hippocampal formations. The density of both lesions per cubic mm of pyramidal cortex was quantified by measuring the area of each of six "zones", using a digitizer and programmable calculator. In elderly normal brains as well as those of Alzheimer's disease, the statistically most representative ranking order of predilection for neurofibrillary tangles (in decreasing severity) was: entorhinal cortex greater than subiculum greater than H1 greater than end-plate greater than presubiculum greater than H2. For granulovacuolar degeneration the best rank order was: subiculum greater than H1 greater than H2 greater than end-plate greater than entorhinal cortex greater than presubiculum. The notable similarities of both such orders of predilection to the well-recognized "selective vulnerability" of certain hippocampal neurones in clinical conditions of hypoxia, ischemia and epilepsy suggest some common, focally accentuated cytotoxic mechanism may underlie all these regional predispositions.
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PMID:Topographic distribution of neurofibrillary tangles and granulovacuolar degeneration in hippocampal cortex of aging and demented patients. A quantitative study. 65 88

Regional blood flow and oxygen metabolism were determined by positron emission tomography, using the steady state technique with 15O, in the hypothalamus and in the whole brain of fifty two normal persons and patients suffering from cerebral ischemia and degenerative dementia. During normal ageing regional blood flow and oxygen consumption appeared to increase slightly in the hypothalamus and to decrease in the whole brain in 24 persons. In the young age group the hypothalamus was more protected against ischemia than in the elderly group. In the aged group with cerebral ischemia and degenerative dementia regional blood flow and oxygen consumption were decreased in the hypothalamus to the same extent as in the whole brain.
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PMID:Positron emission tomography study of the human hypothalamus during normal ageing and in ischemic and degenerative disorders. 132 8

Parallel determinations of muscarinic cholinergic M1 receptor (M1-R) binding and of M1-R mRNA levels were carried out in the gerbil hippocampus 14 days after 5 min of transient ischemia. Both were reduced in the ischemic tissue to about 50% of the levels found in sham-operated controls, indicating that the late loss of M1-R is probably dependent on decreased synthesis. Three administrations of bifemelane hydrochloride (15 mg/kg, i.p., just after ischemia and 6 and 12 h later) completely prevented neuronal death in the hippocampus and ischemia-induced losses of hippocampal M1-R and its mRNA. Since vascular dementia may depend upon the ischemia-induced losses in cholinergic communication in the hippocampus, these findings suggest that it may be possible to prevent its occurrence by post-ischemic treatment with bifemelane hydrochloride.
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PMID:Post-ischemic administration of bifemelane hydrochloride prohibits ischemia-induced depletion of the muscarinic M1-receptor and its mRNA in the gerbil hippocampus. 144 28

To delineate the pathophysiology of periventricular hemodynamics in normal pressure hydrocephalus, we performed quantitative and three-dimensional measurements of cerebral blood flow (CBF) by using xenon-enhanced computed tomographic scans. Measurements were made on 7 patients in whom normal pressure hydrocephalus after subarachnoid hemorrhage had been confirmed by clinical improvement after shunting. We compared mean CBF values in the white matter and cortex of the frontal, temporal, parietal, and occipital lobes and in the thalamus before and after shunting, with an evaluation of dementia and the extent of ventricular dilation and periventricular lucency on computed tomographic scans. CBF returned to within normal limits in the white matter of the frontal and temporoparieto-occipital lobes. CBF restoration closely correlated with clinical improvement and reduction in ventricular dilation and periventricular lucency. We speculate that ischemia occurs initially in the periventricular white matter as a result of diffused cerebrospinal fluid and then extends of the cortex and to the thalamus, causing a "misery perfusion" state with neuronal dysfunction. Incomplete improvement of dementia and CBF in the cortex and thalamus may be explained by preexisting arteriosclerosis in aged patients, coexisting brain damage caused by subarachnoid hemorrhage and subsequent surgical insult in aneurysm patients, and delayed recovery of cortical function that has been secondarily impaired by the periventricular lesions.
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PMID:Significance of periventricular hemodynamics in normal pressure hydrocephalus. 158 81

Advances in imaging hardware for positron emission tomography and single-photon emission CT, coupled with a wide variety of radiopharmaceutical agents, have allowed these techniques to be used in the evaluation of neoplasm, stroke, epilepsy, and dementia. Cerebral perfusion agents continue to be the mainstay of single-photon emission CT imaging but, in addition to the evaluation of ischemia, it has seen an increasing role in the study of dementia, neuropsychiatric disorders, and seizures. Positron emission tomography scanning has had similar applications but it is playing a greater part in the evaluation of neoplasms, including primary gliomas and pituitary adenomas. Stable-xenon CT has shown value in the study of ischemia associated with meningitis, sickle cell disease, chronic subdural hematomas, and cerebral arteriovenous malformations. MR diffusion imaging shows promise in the evaluation of white matter pathology and some tumors.
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PMID:Physiologic imaging of the brain. 173 6

The differential diagnosis of vascular dementia (VD) and Alzheimer's disease (AD) based on clinical assessment and neuropsychologic testing is still associated with a relatively high degree of inaccuracy compared to neuropathology standards. This is especially true in the identification of mixed forms between AD and VD. The present study investigates the potential of neuroimaging methods in providing additional information in dealing with this problem. Magnetic resonance imaging (MRI) of the brain identified a relatively high percentage (39%) of patients with AD (with ischemia scores of 4 and less) with basal ganglia hyperintensities and also demonstrated basal ganglia lacunae and infarcts in some of these patients. These findings indicate that in these cases a vascular component, consistent with the mixed form of dementia, may contribute to the etiology of the disease. These findings also underscore the clinical usefulness of MRI in the further differentiation of the dementias.
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PMID:Does cerebrovascular insufficiency contribute to Alzheimer's disease? 177 62

A total of 87 patients with mild or moderate degree of dementia of the Alzheimer type (AD) or vascular dementia (VD) was identified (DSM-III criteria), and their cognitive capacity was evaluated by means of rating scales and psychometric tests. Three years later 30 patients (34%) were dead. Significantly more VD than AD patients died. Eight of the survivors declined to participate in a follow-up study, and 1 patient was excluded by mistake. Of the survivors, 17 had indisputably suffered cognitive decline during the follow-up period (4 VD and 13 AD, 35%). In the case of 11 patients (2 VD and 9 AD) cognitive decline remained doubtful, and 20 patients (9 VD and 11 AD, 42%) underwent no intellectual deterioration during the follow-up period. The results underline the problems of early diagnosis of dementia according to DSM-III criteria. For both sexes a high ischemia score and a low body mass index predicted death. A low score on a verbal fluency test predicted death for men but not for women, and a high difference between systolic and diastolic blood pressure increased the risk of death for men but not for women.
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PMID:The accuracy of early diagnosis and predictors of death in Alzheimer's disease and vascular dementia--a follow-up study. 195 Jun 29

Acute neurological injury from hypoxia-ischemia, hypoglycemia, and trauma is thought to be predominantly mediated by activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor in the brain and the subsequent influx of calcium ions through receptor-operated channels. Several chronic degenerative diseases, such as Huntington's disease and the amyotrophic lateral sclerosis-Parkinsonism-dementia complex found on Guam, may share a similar pathogenesis due to a glutamate-like toxin. This laboratory recently reported that exposure to a reducing agent, such as dithiothreitol (DTT), selectively increases ionic current flow through NMDA-activated channels in several types of central neurons; conversely, oxidizing agents reverse this effect. To investigate the novel influence of redox modulation on NMDA neurotoxicity, in the present in vitro study we monitored survival of an identified central neuron, the retinal ganglion cell, approximately 24 h after a brief exposure to DTT. To determine the degree of killing specifically related to activation of the NMDA receptor, 2-amino-5-phosphonovalerate (APV, a selective NMDA antagonist) was added to sibling cultures. APV-preventable, glutamate-induced death was increased 70 +/- 9% with DTT treatment. This effect was totally blocked by the concomitant addition of an oxidizing agent, 5,5-dithiobis-2-nitrobenzoic acid (DTNB). These findings suggest that the enhanced killing following chemical reduction with DTT is mediated at the NMDA receptor site, and that the redox state of the NMDA receptor is crucial for the survival of neurons facing glutamate-related injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Redox modulation of NMDA receptor-mediated toxicity in mammalian central neurons. 197 Jan 45


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