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

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

Study of the blood platelet functional activity and intensity of hemolysis in 41 patients with transient disorders of cerebral circulation and comparison of the results with the corresponding indices in healthy individuals, in 40 patients with hypertensive disease free of crisis, and in 25 patients with cerebral atherosclerosis led to the conclusion that the character of cerebral stroke is already determined in the pre-stroke period. It depends on the functional state of the blood platelets in many respects. In patients with hypertensive disease in a period clear of crisis, for instance, there is a tendency towards hypoaggregation possible associated with the presence of latent hemolysis. Platelet hypofunction progresses in the period of hypertensive encephalopathy and still more during its transformation into hemorrhagic stroke. On the contrary, in patients with atherosclerosis but no symptoms of cerebral ischemia the adhesion-aggregation activity of the platelets does not differ essentially from that in healthy individuals. With the development of signs of ischemia of the brain, the platelet activity grows considerably, particularly when transient cerebral circulatory disorders transform into ischemic stroke.
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PMID:[Importance of the thrombocytes and hemolytic syndrome in the pathogenesis of transient cerebral circulatory disorders in hypertension patients]. 63 13

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. Hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.
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PMID:Acute hypertensive encephalopathy in minimal change nephrotic syndrome. 225 60

Circulation to the brain is greatly affected by hypertension and by its treatment. Neurologic dysfunction is prominent among the complications of increased arterial pressure and is also most susceptible to preventive antihypertensive therapy. The upward resetting of the limits of autoregulation of cerebral blood flow in hypertension is probably due largely to structural thickening of the walls (hyaline arteriosclerosis) of the resistance vessels. Other consequences of hypertensive vascular lesions in the brain include increased formation of atheroma, lacunae and lacunar infarction, cerebral infarction, multi-infarct dementia and Binswanger's disease. There is also an association between hypertension and hemorrhagic strokes, namely, subarachnoid and intracerebral hemorrhage. Brain lesions are also prominent in malignant hypertension and hypertensive encephalopathy. Antihypertensive treatment, especially if intensive, can result in boundary zone ischemia in the brain if arterial pressure decreases steeply.
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PMID:Morphologic changes during hypertension. 264 56

In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.
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PMID:Cerebral blood flow and its pathophysiology in hypertension. 275 6

Several new concepts have emerged recently regarding the effects of chronic hypertension on cerebral blood vessels. First, hypertrophy of large cerebral arteries in chronic hypertension attenuates increases in pressure of downstream vessels and protects the cerebral microvasculature. Second, in contrast to large cerebral arteries, which become less distensible during chronic hypertension, distensibility of cerebral arterioles increases during chronic hypertension despite hypertrophy of the arteriolar wall. Third, dilatation of cerebral blood vessels with disruption of the blood-brain barrier, and not vasospasm, appears to be the critical factor in the pathogenesis of hypertensive encephalopathy. This concept is supported by the finding that cerebral edema in stroke-prone spontaneously hypertensive rats is preceded by vasodilatation and disruption of the barrier. Fourth, alterations of endothelium-mediated dilatation may impair vasodilator responses in chronic hypertension and predispose to ischemia. Finally, chronic hypertension impairs dilatation of collateral blood vessels in the cerebral circulation. The implication of this finding is that increased susceptibility to cerebral infarction in chronic hypertension may be related in part to compromised responses of the collateral circulation.
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PMID:Cerebral circulation in chronic arterial hypertension. 304 94

Patients with acute occlusion of a major cerebral artery sequentially call on a hemodynamic reserve quantifiable in terms of rCBF and rCBV and then an oxygen carriage reserve quantifiable in terms of rOER (Fig. 10). If both are exhausted, ischemia supervenes and rCMRO2 becomes linearly related to rCBF. Depending on the degree and duration of fall in rCMRO2, variable degrees of infarction occur. Infarction occurs more rapidly in subcortical than cortical tissue. The phase of maximal rOER is short, and rapid evolution by either reflow or delayed cell death results in an invariable decline of rOER to subnormal levels in the face of a low rCMRO2 (Fig. 11). This combination is characteristic of infarcted tissue. In some instances, partial infarction with a low perfusion reserve is observed with low rCMRO2, high though submaximal rOER, and no increase in rCMRO2 if rCBF is raised. This is a precarious situation predisposing to extension of infarction and suggests blood pressure should not be lowered acutely after a stroke unless the latter is caused by hypertensive encephalopathy. This pattern, however, is rare, short-lived, and usually followed by late reflow or further infarction as a further fall in rCPP occurs, transiently or permanently. Tests of rCPP and the two homeostatic mechanisms involved in maintaining rCMRO2 using non-PET techniques suggest themselves and might form an objective basis for selection of patients for prophylactic revascularization or bypass operations. PET techniques are now becoming available for assessing the blood-brain barrier, tissue pH, and amino acid metabolism, all of which may have relevance to the further understanding of the evolution of infarcts. The rapid study of very early ischemic events is now required to elucidate further the potential for cerebral salvage therapy once ischemia has occurred.
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PMID:Pathophysiology of human cerebral ischemia: studies with positron tomography and 15oxygen. 387 33

Abdominal aortic aneurysms are rare in children. Causes include mycotic aneurysms, vasculitides (eg, Takayasu's arteritis), connective tissue diseases (eg, Marfan's syndrome, Ehlers-Danlos syndrome, and tuberous sclerosis) and traumatic false aneurysms. Four cases are described. Case 1 was a 12-year-old boy who presented with an acute unheralded rupture of the subdiaphragmatic aorta accompanied by lower limb paralysis and ischemia. Attempted repair failed because of extensive friability of the large arteries. Histological evaluation confirmed cystic medial necrosis despite Marfanoid phenotype. Cases 2 and 3 were boys aged 12 and 11 with Takayasu's arteritis who presented with hypertensive encephalopathy and heart failure. Although both had involvement of the origins of the renal arteries, one aneurysm was predominantly suprarenal and the other infrarenal. Currently both children are being managed successfully with antihypertensive therapy. Case 4 was a 5-year-old girl who presented with hypertension and a pulsatile abdominal mass after treatment of infective endocarditis 18 months previously. Arteriography and three-dimensional computed tomography confirmed an aneurysm (6 x 5 x 4 cm) arising from the aorta and involving the right renal artery. Aneurysmectomy, removal of a small ischemic right kidney, and Gore-Tex grafting resulted in cure of the hypertension and uneventful recovery. The present series confirms that rupture is a fatal complication, renovascular complications are common, and medical control of hypertension is an essential part of management. Management strategies need to be highly individualized, and may be successful without surgical intervention. Close clinical and ultrasound follow-up of those managed nonoperatively is essential.
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PMID:Abdominal aortic aneurysms in children. 898 73

Cerebral microcirculation has a series of complex relationships with arterial hypertension determined, on one hand, by the size and the location of the vessels involved, and on the other hand, by the chronic or acute nature of the hypertension. The small arterial vessels of the cerebral parenchyma react to the effects of chronic hypertension with irreversible structural changes, whose pathologic and radiological correlation is chronic ischemia of the white substance, shown by paleness of the white substance, together with small lacunar infarctions, with a clinical association of dementia, motor disorders and pseudo-bulbar syndrome. With the appearance of an acute rise in arterial pressure, these vessels react with generally reversible changes which lead to an increase in the permeability of the hematoencephalic barrier with formation of cerebral edema and a clinical association generally demonstrating the focal nature of the vascular abnormality (such as in hypertensive encephalopathy with changes in posterior hemispheric predominance) or its unilateral location in cases in which the process occurs in one of the carotid territories (post-endarterectomy).
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PMID:[Hypertensive vascular disease and cerebral microcirculation]. 1037 57

Blood pressure (BP) elevations may correspond to different clinical situations. Hypertensives emergencies are situations that require immediate reduction in BP because of acute or rapidly progressing target organ damage: accelerated malignant hypertension, hypertensive encephalopathy, acute myocardial infarction, acute aortic dissection, acute left ventricular failure, and eclampsia. Hypertensive urgencies are those with marked elevated BP in which it is desirable to reduce BP progressively within few hours, such as severe hypertension, progressive target organ damage, perioperative hypertension. Cerebrovascular accidents have to be individualized. In most patients in the immediate post-stroke period, BP should not be lowered. Caution is advised in lowering BP in these patients because excessive falls may precipitate cerebral ischemia. In situations without symptoms or progressive target organ it is necessary to exclude proximate causes of elevated BP such as pain and elevated BP alone rarely requires antihypertensive treatment. Among parenteral antihypertensive (AH) drugs labetalol, nicardipine, urapidil, and nitroprussiate are generally used, and the choice of AH drug depends on the clinical situation. It is not required to normalize BP immediately but to reduce mean BP no more than 25%, then toward 160/100 mmHg as recommended by JNC VI, in order to avoid an impairment of renal, cerebral or coronary ischemia. Oral long-acting dihydropyridines are often subsequently administrated, except in myocardial ischemia. Therapeutic attitudes vary considerably according to the clinical situation: abstention, immediate decrease or progressive decrease in BP have to be decided.
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PMID:[Acute blood pressure elevations]. 1119 Feb 94


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