Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied cerebral oxygen and glucose metabolism as well as cerebral blood flow using positron emission tomography (PET) in a case with MELAS showing dementia, diabetes mellitus, ataxia and lactic acidosis without any signs of stroke. This case, confirmed to have a point mutation at position 3243 in the transfer RNA gene of mitochondrial DNA, developed a stroke-like episode 8 months after the PET study. Uncoupling was observed between cerebral oxygen metabolism and cerebral blood flow with reduced fractional oxygen extraction ratio, indicating "hyperemia", not ischemia. The "hyperemia" may be closely related to the malfunction of mitochondria in aerobic energy production. A drastic decrease in cerebral oxygen metabolism (CMRO2) was found globally in contrast to preserved cerebral glucose metabolism (CMRglu), resulting in a remarkable decrease in the metabolic ratio (CMRO2/CMRglu). The dissociation between cerebral glucose and oxygen metabolism may be characteristic of MELAS.
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PMID:Cerebral metabolism of oxygen and glucose in a patient with MELAS syndrome. 875 Jan 17

Dementia of the Alzheimer type, senile onset (SDAT), and multi-infarct dementia (MID) exhibit differences in cerebrovascular blood flow velocity profiles, which were investigated by means of transcranial Doppler sonography. The pulsatility indices (PI), as angle-independent parameters of peripheral vascular resistance measured in the basal cerebral arteries, were significantly increased in MID patients with respect to SDAT cases. In an analysis of the correlations between several variables and the magnitude of PI, we found strong inverse correlations of the CAMCOG score, and strong direct correlations of the blood pressure and the duration of illness, with the PI of all basal cerebral arteries only in MID patients. In SDAT patients, we found a direct correlation between the Hachinski ischemia score and the PI of all basal cerebral arteries. All 3 ischemia scores (Hachinski, Rosen, Loeb and Gandolfo) were significantly correlated with the PI of the middle cerebral and basilar arteries. By analyzing the correlations of the single items of the 3 different ischemia scores with the PI values obtained, we only found a clearcut correlation with the item focal neurological signs. Thus, our findings stress the relative importance of a concomitant cerebrovascular factor in the development of dementia in old age, even in patients with probable SDAT. A raise of the PI in the basal cerebral arteries allows early suspicion of a cerebrovascular factor even in only slight dementia so that possible risk factors for further aggravation of this type of vascular dementia might be detected and treated early in the course of disease.
Dementia
PMID:Senile dementia of Alzheimer type and multi-infarct dementia investigated by transcranial Doppler sonography. 878 81

The clinical condition known as vascular dementia remains poorly defined. Few studies have attempted a correlative link between the clinical syndrome and the structural abnormalities of the brain. Classically the clinical progression of the vascular dementing process is thought to be a multi-step process punctated by repeated episodes of ischemia, that are clinically expressed as strokes. In most instances it has been assumed that the substrate of vascular dementias consists of atherothrombotic infarcts. The objective of this report is to illustrate 3 cases of progressive (rather than stepwise) cognitive deterioration without clinical evidence of stroke, evolving over a period of several years, in which there were prominent vascular lesions. A complete autopsy and detailed neuropathologic examination demonstrated cerebral vascular lesions involving small arterial vessels (< 200 microns in diameter). The lesions consisted of moderate-to-severe arteriolosclerosis in two cases, and mild-to-moderate arteriolosclerosis in a case of Alzheimer's disease with severe cerebral amyloid angiopathy. Parenchymal lesions consisted of small cortical and subcortical infarcts, most of them smaller than 0.1 cm in average diameter, and subcortical leukoencephalopathy severe in two cases and mild-to-moderate in the third case. Severe atherosclerosis not accompanied by large infarcts was also present in one case. Arterial changes affecting small, distal branches causing sometimes small parenchymal lesions in association with diffuse cerebral white matter disease, appear to be the anatomical substrate that accompanies progressive cognitive impairment in some patients who are frequently diagnosed with Alzheimer's disease because in their clinical records there is neither history of strokes nor stepwise progression of symptoms.
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PMID:Vascular pathology in three cases of progressive cognitive deterioration. 886 69

Antiphospholipid antibodies (aPL) have been associated with a variety of neurological disorders, mostly linked to focal neuroparenchymal ischemia or infarction. Cerebral ischemia associated with the antiphospholipid syndrome (APS) occurs at a younger age than typical atherothrombotic cerebrovascular disease, is often recurrent, and high positive GPL values are usually linked to the presence of a lupus anticoagulant. When other features of the syndrome are not present and cerebral ischemia occurs only associated with anticardiolipin immunoreactivity, there appears to be no discerning features of these patients unless GPL > 40 for which recurrent thrombo-occlusive events appear to occur more frequently. Other neurological manifestations associated with aPL include cerebral venous sinus thrombosis, ocular ischemia, dementia, including ischemic encephalopathy, and chorea. The role of aPL in migrainous events is controversial and may not play a role in recent, large case-controlled studies. Most seizures in patients harboring aPL are associated with focal brain infarction.
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PMID:Neurological aspects of antiphospholipid antibody syndrome. 890 59

A growing amount of data using light and electron microscopy, immunocytochemistry, uptake of brain markers and metabolic studies suggest that the pathogenesis of Alzheimer's disease may be due to impaired vascular delivery of nutrients to the brain. The bulk of this evidence indicates that cerebral capillary transport of glucose, oxygen and other vital nutrients is dysfunctional in Alzheimer brains due to abnormal hemodynamic flow patterns caused by structural deformities of the capillaries. Clinical disorders which can worsen cerebral blood flow, such as head injury, coronary artery disease, cerebrovascular ischemia or the presence of apolipoprotein E4 allele will increase the risk of Alzheimer's dementia. By contrast, activities that increase cerebral blood flow during aging such as complex thinking patterns or the use of drugs to reduce vascular resistance, such as aspirin or NSAIDs, will reduce the risk or improve the status of Alzheimer's disease. The production of neuritic plaques and neurofibrillary tangles may develop from the hypometabolic abnormalities caused by the impaired cerebromicrovasculature in Alzheimer brains. Such metabolic and cerebral blood flow changes are considerably less significant in age-matched control subjects. The major physiological, pathological and cognitive changes reported for Alzheimer's disease appear to have a common denominator which is reflected by the physically distorted cerebromicrovessels and their inability to optimally deliver nutrients to the brain, a condition which ultimately disturbs neurono-glial homeostasis.
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PMID:Cerebromicrovascular pathology in Alzheimer's disease compared to normal aging. 899 28

Cerebrovascular diseases are the second most common cause of dementia. The definitions of vascular dementia (VD) so far proposed in the literature provide little of no information on the etiology of the vascular lesions leading to dementia. An etiology-based classification (e.g. aided by computer tomography) is, however, a must for the development of successful therapeutic strategies. Three kinds of treatment can be differentiated: (1) prevention (before dementia degradation or a stroke occurs), (2) slowing the progress, or prevention, of new infarct, and (3) symptomatic treatment of cognitive and neurological deficits. The treatment strategies are based on three patho-etiological models: (1) recurrent ischemia (i.e. micromboli) which can be treated with aspirin or ticlopidine. (2) Reduce cerebral blood flow, whether so-called vasodilators have any therapeutic benefit remains an open question (3). Reduced perivascular metabolism-which cannot as yet be adequately treated. However, as in all VD-subtypes, rigorous treatment of all cerebrovascular risk factors, such as hypertension and diabetes mellitus is mandatory.
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PMID:[Therapeutic strategies in vascular dementia. From polypragmatic to targeted intervention and research]. 908 91

We report here a unique case of acute-onset dementia caused by a posterior fossa dural arteriovenous fistula (AVF), which was successfully treated by surgical resection of the isolated transverse-sigmoid sinus combined with endovascular procedures. A 70-year-old female was admitted to our hospital with acute-onset dementia and pulsatile tinnitus on the left side. CT scan revealed a low-density area in the parieto-temporal region. Cerebral angiography revealed a dural AVF of the transverse-sigmoid sinus with retrograde drainage into cerebral cortical veins. After transarterial endovascular embolization of the dural AVF, a xenon-CT scan revealed increased cerebral blood flow. Four months postoperatively, however, she was admitted to our hospital again with seizure and aphasia due to recanalizaion of the dural AVF. After trans-arterial embolization, transvenous embolization was attempted, but was unsuccessful due to inaccessibility of the isolated sinus segment. Since this patient could not be cured by endovascular embolization, an open surgical resection of the isolated sinus segment was performed. Following this, CT scans revealed that the low density area present on the first admission had disappeared. The patient's dementia resolved postoperatively. We discuss the pathophysiological mechanism by which venous ischemia due to dural AVF can cause reversible dementia.
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PMID:[Dural arteriovenous fistula presenting as acute-onset dementia: a case report]. 912 19

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in patients with acute ischemic stroke as compared with the controls. The altered CSF NSE levels were well correlated with the infarct size in CT scan. The CSF NSE levels were higher in 6-patients who were diagnosed as multi-infarct dementia (MID) after 6-month follow-up than in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE for dementia related to ischemic stroke is worth further studying.
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PMID:[Neuro-specific enolase in acute ischemic stroke and related dementia patients]. 920 70

We report three patients with dural arteriovenous malformation (DAVM) in the posterior fossa presenting the venous ischemia and the pathophysiology and the clinical characteristics of DAVM presenting the venous ischemia are discussed. Associated with occlusive changes in the venous sinuses, DAVM in the posterior fossa develops the venous hypertension of the straight sinus and the venous ischemia of cerebral white matter and basal ganglia. The venous ischemia presents progressive symptoms consisting of dementia with or without the ensuing consciousness disturbance. Multiple parenchymal lesions and abnormally dilated and tortuous veins are the characteristic findings in MRI/CT.
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PMID:[Dural arteriovenous malformation presenting venous ischemia]. 931 Oct 2

A possible relation between cerebral white-matter injury and dementia was intuitively attributed by Alzheimer to changes affecting the small penetrating vessels that supply the cerebral white matter. Several observations support the view that white-matter changes detectable by neuroimaging may contribute to cognitive deficits in the elderly. But many questions concerning this matter remain partially answered. In this communication we review: (1) Selected anatomic features of the blood vessels supplying the white matter; (2) possible pathogenetic mechanisms responsible for the white-matter changes; (3) observations on humans and animals suggesting a causal relationship between ischemia/hypoxemia and white-matter injury; (4) epidemiologic studies linking white-matter abnormalities with cognitive disorders. We conclude that abnormalities in the small vessels caused by aging and arterial hypertension, or other processes (cerebral amyloid angiopathy, CADASIL) together with systemic circulatory disturbances, such as abrupt variations in blood pressure values or cardiac diseases, may be the substrate of selective white-matter injury. The damage is structurally characterized by incomplete infarction or selective cellular injury.
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PMID:Cognitive impairment and cellular/vascular changes in the cerebral white matter. 932 83


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