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

Memory is an intellectual function that is initially and consistently impaired in patients with vascular dementia. Experimental approaches to vascular dementia have so far been confined to investigations of memory impairments in rodent ischemic models. Unilateral middle cerebral artery (MCA) occlusion, multiple small embolization or transient four-vessel occlusion in rats produced acute single or multiple infarctions. In such rats, significant memory impairments occurred during the subacute or chronic phases, but were partially reversible. Permanent stenosis of both common carotid arteries in gerbils caused no ischemic changes at 1 day after stenosis but induced multiple infarctions after 1 week of stenosis, probably due either to chronic recurrent ischemia resulting from transient repetitive obstruction of the carotid arteries or to chronic low perfusion. The memory impairments in this model were persistent. Permanent bilateral common carotid artery occlusion in rats produced multiple infarctions plus white matter changes after 1 week of occlusion. Marked memory impairment was also observed in this model. The results of the above studies suggest that memory impairments due to ischemic causes may be partially reversible provided that the infarctions occur only once and are followed by flow recovery. Memory impairments, however, appear to persist if the brain is exposed to chronic recurrent ischemia or chronic moderately low perfusion. A repetitive or persistent low-flow state appears to be an important factor in determining the irreversibility of cognitive impairments.
Alzheimer Dis Assoc Disord 1991
PMID:Experimental basis of multi-infarct dementia: memory impairments in rodent models of ischemia. 205 2

In the last 40 years, blood flow and metabolism in the brain have been measured by many methods of varying resolution and reliability. Modern methods have helped to answer some basic pathophysiologic questions, in particular disproving ongoing global ischemia as a cause for dementia. But much of this physiologic work is confounded by swiftly changing clinical and pathologic understandings of ischemic and other forms of dementia: the field remains limited as much by unresolved clinical questions as by technologic feasibility.
Alzheimer Dis Assoc Disord 1991
PMID:Cerebral blood flow and metabolism studies in multi-infarct dementia. 205 5

In this study, vascular dementia (VD, 31 cases), senile dementia of Alzheimer type (DAT, 36 cases) and mixed type dementia (14 cases) were studied by means of magnetic resonance imaging (MRI). Diagnosis of dementia was made according to DSM-III and Hachinski's ischemic score. The areas of periventricular high intensity lesions (PVH) and those of brain parenchyma were measured by digitizer which was connected to a computer. The PVH score was obtained by dividing the areas of PVH by those of brain parenchyma at the level of the body of the lateral ventricule. A multiple variable analysis was applied to the PVH scores and risk factors for dementia using Hayashi's quantification method I. The multiple correlation coefficient between the PVH and the risk factors was 0.685. The most significant correlation was found between Hachinski's ischemic score and the PVH score (partial correlation coefficient: 0.58). Significant correlations were also found between ADL and the PVH score (0.25), as well as between the Hasegawa dementia score and the PVH score (0.24). Using the student T test, it was shown that the large PVH group was significantly correlated to poor ADL, whereas the small PVH group was not. The large PVH group in VD showed lower Hasegawa score than the small PVH group. On the other hand, there was no such correlation in DAT. PVH with prolongation of T2 could exist in various pathological states irrespective of their causes. Diffuse PVH tended to be frequently observed in VD together with poor ADL. It was therefore thought that brain ischemia was the main cause of PVH.
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PMID:[Clinical significance of periventricular high intensity lesions on magnetic resonance imaging in dementia]. 206 92

Evidence from experimental and clinical studies suggests the involvement of the endogenous opioid system in several neurologic and psychiatric disorders (Alzheimer's, Huntington's and Parkinson's diseases, drug-induced movement disorders, Gilles de la Tourette syndrome, stroke, ischemia, brain and spinal cord injury, epilepsy, schizophrenia and affective disorders). However, its involvement is rather a secondary one, perhaps being a severe consequence of a primary, nonopioid disturbance. Thus, treatment of an opioidergic manifestation of a disorder of nonopioidergic origin is necessarily symptomatic and targets only the restoration of the opioid system; such treatment may be beneficial in ameliorating the clinical symptoms of the disorder.
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PMID:The opioid system in neurologic and psychiatric disorders and in their experimental models. 218 70

Brief periods of cerebral ischemia result in prolonged inhibition of protein synthesis. In CA1 sector of hippocampus inhibition is irreversible, leading to delayed death of pyramidal neurons. In order to study the possible role of gene transcription in this process, expression of four individual RNAs was investigated in the gerbil brain after 5 min of global cerebral ischemia by in situ hybridization with the following nucleic acid probes: plasmid pMr100 (ribosomal RNA sequences), plasma pAG82 (cytochrome c oxidase sequences), plasmid p629 (amyloid A4 precursor protein of Alzheimer's disease, pre-A4 protein), and plasmid pHF beta A-1 (beta-actin sequences). Cytochrome c oxidase mRNA and ribosomal RNA did not show any changes in expression up to 48 hr after ischemia. After longer recirculation times they gradually declined in the CA1 sector of hippocampus in parallel with the morphological manifestation of delayed neuronal death. The pre-A4 mRNA transiently decreased after 8 hr of recirculation of the CA1 sector but then recovered before it finally disappeared in parallel with delayed neuronal death. The beta-actin mRNA transiently appeared to increase after 8 hr of recirculation in the stratum radiatum of hippocampus but then also declined and disappeared when CA1 neurons began to disintegrate. The possible significance of these changes in the pathogenesis of ischemic neuronal damage is discussed.
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PMID:Determination of RNA content in postischemic gerbil brain by in situ hybridization. 248 Dec 24

We reviewed the clinical histories and autopsy records of 35 pediatric patients (ranging in age from 9 months to 18 years) who underwent orthotopic liver transplantation using ciclosporin and corticosteroids for immunosuppression. At the time of death, 19 children (54%) had encephalopathy, 16 (46%) were lethargic or in coma, 10 (29%) had seizures, and 10 were normal. Neuropathological lesions were found on postmortem examination in all 35 patients. Vascular lesions such as infarction, ischemia, thrombosis, and hemorrhage were the most common neuropathological findings (86%) followed by infectious processes (29%). Candida albicans (2 patients) and Aspergillus fumigatus (3 patients) were the only offending organisms identified, both causing meningoencephalitis. Alzheimer type II astrocytes, a characteristic feature of chronic liver disease, were the single most common autopsy finding (69%). Central pontine myelinolysis was seen in 3 children and basilar artery thrombosis affected 1 child. Neurological complications and their subsequent neuropathology are a significant cause of morbidity and mortality after pediatric liver transplantation. Vascular insults, electrolyte abnormalities, and infections that involve the central nervous system are directly related to liver function and the immunosuppression necessary to maintain graft viability. Only with continued observation after surgery combined with rapid medical and surgical treatment can we hope to improve the prognosis following liver transplantation in the pediatric population.
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PMID:Neuropathology of pediatric liver transplantation. 248 84

The overstimulation of receptors for L-glutamate, particularly those of the N-methyl-D-aspartate (NMDA) type, has been suggested to play a role in mediating damage in a variety of neurodegenerative conditions or disorders ranging from ischemia/hypoxia to senile dementia of the Alzheimer's type (SDAT). We report here that the functional deficits and histological damage mediated by the overactivation of NMDA receptors in the Fischer 344 rat hippocampus can be blocked effectively by systemic administration of the noncompetitive NMDA antagonist, MK-801. These results suggest that MK-801 may be effective clinically in attenuating memory loss and hippocampal damage in disorders associated with the overstimulation of NMDA receptors.
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PMID:MK-801 prevents cognitive and behavioral deficits produced by NMDA receptor overstimulation in the rat hippocampus. 254 91

N-Methyl-D-Aspartate (NMDA) receptors are believed to play a critical role in excitotoxic cell death in the CNS. The distribution of NMDA-preferring binding sites is compared here with the patterns of selective neuronal death observed in Alzheimer's disease and following transient ischemia. The distribution of NMDA receptors, by itself, is unable to account for the characteristic patterns of selective neuronal vulnerability observed in conjunction with these types of neuropathology.
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PMID:Selective neuronal vulnerability and the distribution of N-methyl-D-aspartate (NMDA) receptors. 255 70

Binswanger's encephalopathy is reviewed in respect to history, computed tomography, magnetic resonance imaging, epidemiology, pathology, clinical picture, laboratory findings, differential diagnosis, and treatment. The various viewpoints on the pathogenesis of the process are discussed, in particular the role of ischemia, vascular disease, high blood pressure, lacunar infarction, hypoxia, edema, and hydrocephalus. The white matter hypomyelination of congophilic angiopathy and Alzheimer's disease should provide clues. A unifying hypothesis has not been attained.
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PMID:Binswanger's encephalopathy: a review. 265 69

Subcortical arteriosclerotic encephalopathy (SAE) is a common though infrequently recognized dementia of the elderly. The unique vascular anatomy of the subcortical white matter and central brain stem probably predisposes those regions to chronic ischemia and incomplete infarction in the presence of various cardiovascular and hemodynamic insults. Recent studies have begun to define the risk factors for SAE, and others have shown it to be a condition frequently comorbid with the dementias of Alzheimer's disease, the multi-infarct state, and normal pressure hydrocephalus. Recent research into the etiologies of these disorders suggest certain pathogenetic links between them, strongly implying that they are not neatly distinct disease entities, as is commonly believed, and accounting for some of the overlap between these dementing illnesses seen clinically.
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PMID:Binswanger's disease (Part II): Pathogenesis of subcortical arteriosclerotic encephalopathy and its relation to other dementing processes. 269 55


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