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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In"cerebral arteriosclerosis" the diffuse sclerotic involvement of the cerebral vessels may produce acute softening of cerebral tissue. However this paper concentrates mainly on the clinical symptomatology which, in the absence of major vascular accidents, is characterized from the psychopathologic viewpoint by acute confusional states, aggressive behaviour, fluctuating loss of memory, disturbances of concentration and finally dementia. The chief neurologic symptoms are motor disturbance with short-stepping gait, stooped position of the body, pseudobulbar symptoms with dysarthric speech and disturbances of swallowing, and increased perioral reflexes. A complete case history and a thorough neurologic and psychopathologic examination are the most important factors in diagnosis, while ancillary methods are of value only for differential diagnosis. Prophylaxis and therapy (cardiotherapy, treatment of diabetes and hypertension, lowering of serum cholesterol and sedation) are discussed. In the differential diagnosis of dementia in the elderly patient consideration should be given to chronic vascular diseases, degenerative cerebral atrophies, brain tumors, low pressure hydrocephalus, progressive paralysis and some other rare brain conditions.
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PMID:[Cerebral sclerosis. Diagnostic criteria and differential diagnostic consideration in practice]. 23 20

The survival of 305 patients with chronic renal failure treated at the Vancouver General Hospital by centre and home peritoneal dialysis, centre and home hemodialysis and cadaver renal transplantation over a 12-year period was analysed. There was decreasing survival with age except in patients undergoing home dialysis. Hypertension and analgesic nephropathy as primary causes of renal disease were associated with a poor prognosis. Hence age and diagnosis appear to be two of the main determinants of survival. Cardiovascular disease was the commonest cause of death but seven deaths were due to dialysis dementia. The results compare favourably with other published statistics.
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PMID:Results of 12 years' treatment of chronic renal failure by dialysis and transplantation. 34 97

Arterial hypertension causes the formation of small lacunes, or ischemic brain infarcts, which may result in transient ischemic attacks, hemiparesis, sensory loss, ataxic hemiparesis, or dysarthria. Usually these effects are reversible with physical therapy, but multiple lesions may lead to dementia. Prevention of lacunar disease is possible with vigorous control of hypertension.
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PMID:Lacunar strokes. 39 51

Serial EEGs with early and progressive bilateral periodic activity were recorded from a patient with clinically "atypical" but pathologically confirmed subcoritcal arteriosclerotic encephalopathy (Binswanger's type). This disease should be considered as a diagnostic possibility when periodic EEG activity is encountered, particularly when dementia, hypertension, and focal neurologic signs coexist. At times, white matter lesions may contribute to the production of periodic EEG activity.
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PMID:Periodic EEG activity in subcortical arteriosclerotic encephalopathy (Binswanger's type). 50 60

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

The subcortical arteriosclerotic encephalopathy of Binswanger is characterized clinically by hypertension, dementia, spasticity, syncope, and seizures. It is usually diagnosed pathologically by the finding in white matter of diffuse demyelination or foci of necrosis plus arteriosclerotic and hypertensive vasculopathy. We present a case in which the diagnosis was made on the basis of the clinical course and a computerized tomogram which demonstrated extensive white matter degeneration. Postmortem examination confirmed both the diagnosis and the extent of the degeneration as shown by CT scan.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger): computerized tomography. 57 97

The incidence of both atherosclerosis and demential increases with age and therefore the terms "cerebral atherosclerosis" or "cerebro-vascular dementia" are commonly used for any mental deterioration in elderly persons. These names depend on the proposition of a gradual narrowing of cerebral arteries as an inevitable accompaniement of ageing which ends in dementia through a progressive reduction of cerebral blood flow. This apparently reasonnable hypothesis has now been shown to be wrong. ;t has been established that first, senile dementia is not due to cerebral atherosclerosis in spite of the frequent coexistence of degenerative and vascular lesions; and secondly, true cerebro vascular dementia results from the destruction of brain tissue following cerebral infarction; hence the proper term is "multi-infarct dementia". This neuronal destruction leads to decrease in cerebral metabolism and blood flow and to intellectual deterioration. The diagnostic criteria are therefore those of cerebral infarcts i.e: arterial hypertension and/or signs of atherosclerosis, sudden onset and/or stepwise progression, and focal neurological signs. If one follow those criteria, multi-infarct dementia accounts for only about 10% of all dementias; if one does not, the diagnosis will continue to be made to the exclusion of other potentially curable causes of dementias. Five clinico-pathological forms can be distinguished according to the size, number and site of the infarcts: lacunar state, large multiple infarcts, watershed infarction, single infarct and Binswanger's encephalopathy. This distinction is always arbitrary because the association of lacunes and large infarcts is very common in multi-infarct dementia. The almost invariable failure of all therapeutic measures once multi-infarct dementia has been established stresses the importance of prevention. This depends on prevention of cerebral infarcts, i.e. on the correction of risk factors amongst which arterial hypertension is by far, the most important. Some cases benefit also from carotid surgery, anticoagulants, and antiplatelet drugs but antihypertensive drugs are the most essential part. It is very likely that if all cases of arterial hypertension are properly treated, the incidence of multi-infarct dementia will decrease greatly.
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PMID:[Modern concepts of "cerebrovascular dementia"]. 61 Oct 16

An elderly man suffering from dementia associated with hypertension developed right-sided parkinsonism marked by rigidity and flexion. At autopsy the brain showed generalized vascular changes chiefly in the white matter, diffuse plaque and neurofibrillary tangle formation in the temporal cortex, and a discrete gliotic scar in the right substantia nigra. Hemiparkinsonism with a strictly unilateral lesion confined to the substantia nigra has, to our knowledge, not been described before, and the fact that it was ipsilateral adds to its theoretical interest.
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PMID:Hemiparkinsonism with infarction of the ipsilateral substantia nigra. 70 30

Senile dementia of the Alzheimer type is becoming one of the most common of the malignant diseases as our society ages. Currently, research has identified several pathophysiological changes, including the bihelical filament and the loss of the enzyme choline acetyltransferase from the cortex. Although genetic factors play some role in this disease, the important environmental risk factors have not yet been identified and there is, at present, no specific treatment. The second most common cause of dementia, cerebrovascular disease, produces dementia only when there is destruction of brain tissue, as in individuals who have multiple strokes or who have hypertensive vascular disease leading to multiple lacunae. In both multi-infarct dementia and in the lacunar state, hypertension appears to play a greater role than it does in other forms of vascular disease. Many of the other causes of dementia, including normal pressure hydrocephalus, CNS infections or tumors, metabolic disorders produced by thiamine or vitamin B12 deficiency or thyroid dysfunction, are often reversible. Every patient, whatever the age, with a developing dementia deserves a thorough workup to identify these treatable disorders.
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PMID:Dementias. 75 96

Amyotrophic lateral sclerosis and Parkinsonism-dementia are unusually prevalent on Guam. Carbohydrate metabolism was studied in 110 patients with evidence diagnostic of or suspecious for these diseases. The combined incidence of known diabetes in 29 per cent of them plus a high percentage of glucose tolerance tests interpreted as abnormal, even when most age-related criteria were considered, was considerably higher than the incidence of abnormal carbohydrate metabolism reported elsewhere in the general population of the United States, the tropical Pacific area, or in recent surveys on Guam itself. The diabetes was generally mild in nature and noteworthy for a lack of retinopathy and other complications. Hypertension, hypercholesterolemia, and hyperuricemia, although highly prevalent, were not consistently associated with abnormal glucose metabolism. Similarly, no consistent association was demonstrated with such factors as age, muscle atrophy, or physical activity.
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PMID:Abnormal carbohydrate metabolism in amyotrophic lateral sclerosis and Parkinsonism-dementia on Guam. 99 26


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