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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

In a large autopsy series of elderly individuals, organic dementia was attributed to (pre-) senile atrophy in 52.8%, to cerebrovascular disease in 22.5%, while 13.6% were of mixed senile and vascular origin, and 1.3% showed communicating hydrocephalus with meningopathies or were of undetermined origin. A survey is given of the morphological criteria of dementia resulting from disorders of cerebral blood supply and CSF circulation. The anatomic basis of vascular dementias are: atherosclerotic encephalopathy with lacunar state or multiple infarcts; granular cortical atrophy resulting from local microcirculation disorders; hypertensive cerebrovascular disease with the common "mixed" cortico-subcortical type, and the rare Binswanger's subcortical type. Atypical cerebral hemorrhage in old individuals rather results from congophilic (amyloid) angiopathy than from hypertensive arteriosclerosis. Multiple infarct dementia may also result from thrombotic microangiopathy, thromboembolic disease or cerebral vasculitides. The anatomical features of dementia associated with communicating "normal-pressure" hydrocephalus (NPH) are meningopathy at the basis or on the convexity, and fibrosis of the choroid plexus and/or arachnoid villi of post-inflammatory or undetermined origin, and other non-specific changes (periventricular gliosis). This condition is also associated with hypertensive cerebrovascular disease and Alzheimer's disease. Cerebral biopsies in NPH as well as in other types of hydrocephalus show enlarged extracellular spaces with otherwise normal neuropil probably resulting from increased transcapillary filtration. In some cases of "idiopathic" NPH no causative anatomical changes are found. The relationship between cerebral tissue changes, abnormal blood and CSF dynamics in these conditions remains to be clarified.
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PMID:Neuropathological aspects of dementias resulting from abnormal blood and cerebrospinal fluid dynamics. 96 75

Cerebral microangiopathies based on arteriosclerosis are frequent. In most cases, microangiopathy is the result of long standing hypertension. Other risk factors, however, such as diabetes mellitus or disturbances of fatty metabolism, may also be responsible. The sequels of cerebral microangiopathy can be lacunar infarcts or subcortical arteriosclerotic encephalopathy. Both status lacunaris and subcortical arterioslerotic encephalopathy can result in development of dementia if they last for a long time. Particularly in these disorders, however, it is imperative to carry out preventive measures by influencing the vascular risk factors. Another approach to therapy is offered by influencing the haemorrheological properties of the blood by means of vasoactive preparations.
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PMID:The significance of microcirculatory disturbances in the pathogenesis of vascular dementia. 306 8

The pathological changes in the brains of seven patients who had been clinically diagnosed as normal pressure hydrocephalus (NPH) are described and the possible etiological mechanisms are discussed. The pathological findings in all cases consisted of demyelination akin to Binswanger's type of encephalopathy, especially in the frontal lobes. Arteriosclerosis accompanied by occasional organized thrombi and scattered microinfarcts in the periventricular white matter were seen. Focal leptomeningeal fibrosis, diminution of arachnoidal granulations, and non-specific aging processes were noted. Among the above of particular interest, was the degeneration of both periventricular and deep white matters with microinfarcts, and moderate to severe arteriosclerosis. On the basis of these observations, we assume that the degeneration in the white matter is not merely a secondary change due to the result of enlargement of ventricle, but plays an important role in the development of NPH. The development of NPH requires not only the disturbance of cerebrospinal fluid, but also the pre- or coexisting vulnerability in the white matter caused by variables such as ischemia, hypoxia, and trauma.
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PMID:Normal pressure hydrocephalus. Neuropathological study. 357 65

Five patients with variable clinical symptoms were diagnosed as having--subcortical arteriosclerotic encephalopathy (Binswanger disease) based on the presence of lacunar infarcts in basal ganglia, various abnormalities of subcortical white matter and severe thickening and hyalinization of penetrating arteries and arterioles. One case had a classical clinical picture while in the others the course of the disease was short and was associated with severe systemic abnormalities. The variability of the clinical features, the identify of "classical" clinical symptoms with other forms of cerebral arteriosclerosis, the similarity between "atypical" cases and other entities, and the high frequency of associated conditions makes it difficult to characterize the clinical pathological entity called subcortical arteriosclerotic encephalopathy.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's disease): a report of five patients. 361 6

The health condition of 615 disabled persons--in result of occupational CS2 poisoning--has been checked. The diseases yielding grounds for qualification into one of disability groups have been established. In all the disabled people one of the nervous system diseases was diagnosed, which gave grounds for disability certification. Most frequently diagnosed was encephalopathy, less frequently--pseudoneurotic syndrome, polyneuropathy and psychoorganic syndrome. In 75% of disabled persons at least one of the circulatory system diseases was diagnosed, the intensity of which affected also the psycho-physical status of those examined. Among the circulation organ diseases, clinical syndromes of arteriosclerosis were diagnosed, such as heart ischaemia and vascular diseases of the brain. At present, occupational CS2 poisoning is diagnosed when irreversible changes in the nervous system are found, accompanied by advanced changes in the circulatory system, thus--when the workers' health condition calls for disability qualification. It seems advisable to establish such diagnostic criteria for CS2 poisoning that a worker unable to work in exposure to neurotoxic substances (preventive elimination) can get compensation for health detriment when he can still work at other workplaces so that there is no need for disability qualification.
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PMID:[Causes of disability related to occupational exposure to carbon disulfide]. 383 32

Since Binswanger's description of subcortical arteriosclerotic encephalopathy in 1894, numerous cases have been reported. Several authors doubt the validity of this malady, although the majority consider it to be a disease entity. We report seven cases with this type of pallor of myelin, only two of which are accompanied by a history of dementia. Among the seven cases, two had arteriosclerosis of penetrating arteries and arterioles in cerebral white matter. Electron microscopy showed splitting of myelin sheaths, probably the result of edema. In reviewing the blood supply of the cerebral white matter, we conclude that no pathological alterations of medullary branches of the cerebral arteries, the same vessels supplying the white matter, can give rise to such diffuse pallor of white matter and spare the arcuate fibres. This pallor can only be due to cerebral edema, most likely of hypoxic-ischemic, hypotensive, or acidotic origin. We also contend that arteriosclerosis can only cause dementia through multiple infarcts or lacunae, if it indeed leads to dementia.
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PMID:Binswanger's disease: progressive subcortical encephalopathy or multi-infarct dementia? 401 96

Twenty-three elderly patients were found to have a consistent pattern of leukoencephalopathy by computed tomography and nuclear magnetic resonance imaging. Eight patients presented with vague, nonspecific symptoms and had no neurologic deficits. The other 15 patients had neurologic deficits that presented in one of three ways: stroke, seven patients; slowly progressive dementia and gait disturbance, five patients; or slowly progressive dementia alone, three patients. Risk factors for arteriosclerosis (hypertension, diabetes) were present in 18 patients (78%). The necropsy of one patient revealed arteriosclerotic vasculopathy characteristic of subcortical arteriosclerotic encephalopathy (SAE) or Binswanger's disease. Subcortical arteriosclerotic encephalopathy may be a relatively common affliction of elderly patients, most of whom have risk factors for arteriosclerosis. The modes of presentation and associated clinical signs are variable, and more than one third may have no neurologic deficit. In some cases SAE overlaps with normal pressure hydrocephalus by clinical and neuroimaging criteria. Some patients with normal pressure hydrocephalus who do not respond to ventricular shunting may actually have SAE.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's disease). Computed tomographic, nuclear magnetic resonance, and clinical correlations. 403 2

A 49-year-old normotensive man died after a series of strokes, slowly evolving dementia and personality change occurring over a period of 23 years. CT scan showed large infarcts involving the cortex and white matter of the temporo-occipital areas, small subcortical infarcts and low attenuation in the white matter of the frontal and parietal lobes. Neuropathological examination revealed large cortical and small subcortical infarcts corresponding to the radiological findings as well as degeneration/demyelination of central white matter corresponding to the areas of low attenuation seen on CT. The basic underlying pathological process was hyaline arteriosclerosis and atheroma which diffusely affected the small intracerebral arteries and to a lesser extent the arteries of the circle of Willis. Though usual because of the absence of hypertension, the very early age at onset of the syndrome and the presence of large cortical infarcts this case illustrates the clinical, radiological and neuropathological features of subcortical arteriosclerotic encephalopathy (Binswanger's type).
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's type) and cortical infarcts in a young normotensive patient. 708 53

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.
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PMID:Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly. 709 54


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