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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The terms Binswanger's disease and arteriosclerotic subcortical encephalopathy are often applied to elderly patients with dementia and a diffuse hypodensity of the white matter on CT scan (or increased signal on MRI). Recently, similar white matter abnormalities have been reported in non-hypertensive patients with Alzheimer's disease and in elderly healthy people, casting doubt upon Binswanger's disease as an entity. These findings also suggest that the descriptive term leukoaraiosis meaning rarefied white matter is more appropriate than the term leucoencephalopathy. Nevertheless, within the group of patients with an ischemic stroke, several data suggest that leukoaraiosis is not a fortuitous finding and does not simply reflect ageing. Actually, these patients have a particular clinical profile, with intellectual deterioration, chronic hypertension, usually patent carotid arteries, and a deep location of the presenting infarct. Moreover hypertension seems to be still more strongly associated with leukoaraiosis than with a deep location of the infarct (lacunar infarction).
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PMID:[Leukoencephalopathy, leukoaraiosis and cerebral infarction]. 327 83

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

This paper calls attention to the methodologies designed to investigate the higher cortical functions in order to elicit signis of encephalopathy in apparently normal conditions. This can be done by testing the blobal hemispheric funcionts or the interhemispheric functional balance. This shows up the clinical sequels that may precede or be the outcome both of transient pathological disorders, such as transient global anemia, migraine, TIAs and subarachnoid hemorrhage without apparent clinical consequences and of nontransient pathological conditions, such as epilepsy, occupational diseases, arterial hypertension and cerebral revascularization.
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PMID:Neurobehavioral investigation as a tool for revealing preclinical disorders. 332 25

Of 26 patients with pheochromocytoma treated between 1974 and 1986, two presented with pheochromocytoma crisis. This unusual presentation consists of hyper- and/or hypotension, high fevers (greater than 40 degrees C), encephalopathy, and multiple organ system failure. Both patients had large tumors associated with markedly elevated levels of epinephrine. Although hypertension was adequately controlled in both patients with phenoxybenzamine, phentolamine (1 patient) and nitroprusside, both patients deteriorated rapidly. The first patient expired during attempts to identify a source of sepsis. None was found at autopsy. The second patient underwent urgent adrenalectomy which reversed the multiple organ system failure and resulted in patient survival. We conclude from review of these patients and three others in the literature that (a) crisis is an unusual presentation of pheochromocytoma; (b) its manifestations include vascular lability, high fever, encephalopathy and multiple organ system failure; (c) it may be the result of increased epinephrine secretion; (d) successful treatment of pheochromocytoma crisis demands prompt diagnosis, vigorous medical therapy and emergent tumor removal if the patient continues to deteriorate.
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PMID:Pheochromocytoma crisis. 341 97

Because of recent papers suggesting that subcortical arteriosclerotic encephalopathy (SAE) (Binswanger's disease) is more common than historically assumed, this investigation was initiated to assess the frequency of SAE, to gauge the reliability of CT in making this diagnosis, and to assess the strength of the correlation between SAE and arterial hypertension. Of 202 autopsied patients in a 17-month period, 82 had undergone antemortem CT. Of these, 20 had CT findings thought to represent varying degrees of the disease spectrum of SAE. Microscopy confirmed this diagnosis in 18 cases. The pattern of diminished attenuation in the white matter was periventricular in 16 patients (marked asymmetry in one) and limited to an isolated focus somewhat removed from the ependyma in two. Among the 16 with periventricular disease, the extent of the process by CT appeared mild in nine, moderate in five, and severe only in two. There were two false positive CT diagnoses of SAE. Among a control group of 10 patients with normal white matter by CT, seven had some microscopic evidence of SAE, although it was generally less severe than in those with positive CT scans. Subcortical arteriosclerotic encephalopathy is common and can be identified in its various forms by CT with a high degree of reliability.
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PMID:Subcortical arteriosclerotic encephalopathy: CT spectrum and pathologic correlation. 349 Jul 56

Cerebral neurons can tolerate at least 20 min of normothermic ischemic anoxia. Cerebral recovery from more than 5 min of cardiac arrest is hampered by complex secondary derangements of multiple organ systems after reperfusion. There is increasing support of our hypothesis that this "postresuscitation syndrome" includes the following: secondary cerebral perfusion failure, cerebral reoxygenation injury (cell-necrotizing cascades), and cerebral "intoxication" from derangements of extracerebral organs. To be optimal for the brain, CPR with optimal perfusion pressure must be started as promptly as possible. Significant though inconsistent mitigation of permanent brain damage after prolonged complete global brain ischemia has been achieved in animal outcome preparations with the use of the following treatments initiated at the start of reperfusion: brain-oriented extracerebral life support by protocol, intra-arterial hemodilution, hypertension, and artificial circulation, barbiturates, calcium-entry blockers, free-radical scavengers, and multifaceted treatments. We currently recommend treatment 1 for patient care and treatment 2 for clinical feasibility trials. Treatment 3, thiopental loading (starting 10 to 50 min after restoration of spontaneous circulation), was tested in a randomized clinical trial and was not shown to confer a statistically significant benefit. A calcium-entry blocker is under clinical investigation. Many other novel treatments appear promising but further animal studies are required. The complex multifactorial pathogenesis of postcardiac arrest encephalopathy requires systematic multicenter development of etiology-specific combination therapies.
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PMID:Cerebral resuscitation after cardiac arrest: a review. 353 60

Using formalized documentation and computerized techniques, the authors analyzed clinical, electrophysiological, and biochemical semiotics in 2180 individuals--healthy subjects, patients with subclinical and initial manifestations of cerebral circulation insufficiency, initial dyscirculatory encephalopathy developing in the presence of neurocirculatory dystonias, atherosclerosis, and arterial hypertension. The author has established characteristics of the semiotics which depend on the nature of the underlying vascular disease, the stage of the process and the patient's age. Tabulated methods and a computerized system of the diagnosis of cerebrovascular disease have been developed. They are based on the employment of a bank of clinical and physiological information used for prophylactic examinations and population screening. The social, medical and economic effectiveness of the proposed methods of the diagnosis and prevention of cerebrovascular diseases allows their recommendation for wide introduction into health care practice.
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PMID:[Semeiotics of incipient forms of vascular diseases of the brain and their diagnosis during preventive examinations of the population]. 354 80

Progressive subcortical vascular encephalopathy (PSVE) usually occurs in elderly individuals, suffering from hypertension. We here describe a male, born of consanguineous parents, who first showed signs of PSVE at the age of 30. Despite the absence of hypertension or known metabolic causes, the degenerative cerebral vascular disease developed progressively. Several cases, surprisingly identical to the one reported here, were traced using Japanese medical records. They are clinically characterized by: early onset of PSVE (at age 25-30), absence of persistent hypertension, diffuse alopecia since youth, spondylitis deformans with early onset, often so severe as to necessitate surgery, and the possible existence of an autosomal recessive transmission. Cases with these features appear to constitute a distinct clinical entity, possibly a new form of premature aging syndrome.
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PMID:Subcortical vascular encephalopathy in a normotensive, young adult with premature baldness and spondylitis deformans. A clinicopathological study and review of the literature. 357 55

The encephalopathy is characterized by an important arteriosclerotic involvement of the vessels of the cerebral white matter and a diffuse subcortical demyelination, sparing the cortex. The diagnosis is presently possible, ante mortem, by connecting the clinical picture with the CT scan findings, which are essential. Three cases with Binswanger encephalopathy are reported and the following picture was found: age 50 to 70 years old at the onset; dementia with scanty neurological signs; systemic arterial hypertension; subacute course of the disease; and a CT scan, highly characteristic, that shows bilateral and symmetric subcortical hypodensity. In one of the patients, that eventually died, an angiography disclosed a right internal carotid thrombosis and a diminished flow in the thalamic striate arteries in both sides. The other two patients are apparently stabilized with anti-hypertensive medication. Binswanger encephalopathy is still seldom described in spite of being a very well defined entity. This diagnosis should be considered much more frequently because it is possible to prevent the encephalopathy avoiding systemic hypertension that is probably intimately linked with the genesis of the disease.
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PMID:[Binswanger's subcortical arteriosclerotic encephalopathy: a special form of dementia associated with systemic arterial hypertension]. 359 34

Twenty-three infants suffering the effects of moderate or severe hypoxic-ischaemic encephalopathy were continuously monitored for intracranial pressure (ICP) by means of a subarachnoid catheter for a total of 1083 hours. Cerebral perfusion pressure (CPP) was also continuously monitored for 21 of the infants. The median age at the start of ICP monitoring was 17 hours, and the opening pressure correlated poorly with maximum sustained pressures. Maximum sustained ICP allowed the infants to be divided into three groups: (1) those with no elevation of ICP (nine), of whom two died and five had a normal outcome; (2) those with sustained rises in ICP which were resistent to treatment (nine), of whom seven died and two survivors are severely handicapped; and (3) those in whom the pressure was elevated but could be controlled medically (five), of whom two survived to be quite normal. No infant with a sustained elevation of ICP of 15mmHg or more survived to be normal, nor any who had had a CPP below 20mmHg for one hour or more. Hypotension was the cause of low CPP in most cases. There was a highly significant correlation between sustained elevation of ICP above 10mmHg and poor outcome, but no correlation between outcome and minimum CPP. It was not possible to predict clinically which infants would develop intracranial hypertension, and some infants with very severe perinatal asphyxia did not develop intracranial hypertension, and some infants with very severe perinatal asphyxia did not develop raised intracranial pressure at any time.
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PMID:Value of intracranial pressure monitoring of asphyxiated newborn infants. 359 67


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