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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical studies of epilepsy in 137 patients of old age demonstrated that epileptical dementia preserves its nozological specificity. In genuine epilepsy it was not possible to detect symptoms of cerebral atherosclerosis, while in symptomatical epilepsy there were definite signs of arteriosclerotic dementia. Convulsive seizeures in old age become less frequent and are substituted by abortive and psychomotor elementary seizures or are arrested altogether. Epileptic equivalents lose their specifity.
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PMID:[Course of epilepsy in persons of middle and old age with the disease beginning in childhood]. 40 13

A clinicoanatomical study was conducted in 218 cases of atherosclerotic dementia. 12 cases (5,5% of the total amount) showed diagnostic errors. Atherosclerotic dementia with Alzhemier-like symptomatology during life was considered to be Alzheimers disease, while Alzheimers disease, complicated by cerebral atherosclerosis as atherosclerotic dementia. Some objective and subjective factors of diagnostic errors were established. Late detection of such patients is considered as one of the risk factors of diagnostic errors during life.
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PMID:[Several diagnostic errors in cerebral atherosclerosis (clinico-anatomic study)]. 46 65

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

The paper is concerned with a study of confabulation seen in 95 patients. A gradual development of the confabulatory syndrome (from mnemonic confabulations to ecmnestic) was seen in senile dementia (5 cases) and in its combination with vascular atherosclerosis (61 cases). An acute development of confabulations (with a prevalence of mnemonic false reminiscence over ecmnestic) was seen in cerebral atherosclerosis (9 cases). Rudimentary ecmnestic confabulations, without mnemonic were seen in Alzheimer's disease (20 cases). The author established a certain correlation between ecmnestic confabulations and disturbances of fixation, between mnemonic confabulations and disorders of selective reproductivity, between their expressiveness and emotional liveliness and the degree of actualization of the past events. In a complacent-euphoric and anxiety affect the confabulations were spontaneous and were accompanied by psuedoactivity. In depressive states they were fragmentary and were detected only in response to questions. Aphatic disorders and the severity of dementia influence the mnestic confabulations making them poorer and incomplete.
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PMID:[Confabulation in atrophic and vascular disease of old age (clinico-psychopathologic findings)]. 97 23

Cyclandelate, a vasodilator, was administered to 24 patients with dementia. The dementia in these patients was presumed to be due to cerebral ischemia caused by atherosclerosis in cerebral vessels after other possible causes were ruled out. In a double-blind, cross-over study, patients received 200 mg of cyclandelate four times daily for six weeks and a placebo for six weeks. Six psychological tests, which reflect various aspects of higher cortical ability, were used to evaluate the effect of cyclandelate on the dementia. Cyclandelate was found to be no more effective than placebo in improving higher cortical function in these demented patients.
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PMID:Effect of cyclandelate on dementia. 110 57

The influences of endogenous factors (sex, age, premorbid personality traits, heredity) and exogenous factors (somatogenias, cranial injuries and neuroinfections, intoxications, psychogenias) on the origin and course of psychotic syndromes and dementia were regarded on the basis of clinical and epidemiological studies carried out in 523 patients with cerebral atherosclerosis. The leading risk factors were established for each form of mental disorders due to cerebral atherosclerosis.
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PMID:[The correlation of endogenous and exogenous factors in the occurrence and course of mental disorders in cerebral atherosclerosis]. 133 41

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

Postmortem surveys on patients treated for chronic hypertension often fail to demonstrate significant vessel changes. Nevertheless, hypertensive alterations in the brain can include infarcts and hemorrhages. Autopsies in a primary care hospital have shown that hypertension can affect arteries, arterioles, and capillaries in various patterns and degrees in the brain. These vascular lesions may be associated with large and small infarcts and hemorrhages in isolated or diffuse patterns. Widespread cerebral edema can occur with rapidly progressive hypertension. Atherosclerosis, arterial and arteriolar fibrinoid necrosis, and micro-aneurysms may be observed. Chronic hypertensive encephalopathy causes vascular dementia and can be associated with subcortical arterial and arteriolar leukoencephalopathy, leukoaraiosis and/or Binswanger's disease. Epidemiologic evaluations based on complete autopsy studies need to be correlated with compliance of therapy, appropriate diagnosis of hypertension, and its long-term effects on the nervous system. Although persistent poorly controlled hypertension is known to damage the brain both acutely and chronically, the effects of intermittent hypertension remain to be defined.
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PMID:Hypertension and vascular dementia. 173 72

Lacunae are small deep cerebral infarcts which are believed to occur in hypertensive patients, producing characteristic clinical syndromes. Previous reports suggested to differentiate this type of stroke from other cerebrovascular diseases, but failed to provide any evidence that this classification is useful in clinical practice. We reviewed the present literature concerning pathogenesis, clinical features, diagnostic, and therapeutic aspects of lacunae and we established that current concepts in lacunar stroke are inadequately supported. Although lacunar syndromes are reported to be correlated with lacunar infarcts, these syndromes are also described in patients with different pathological findings. The assumption that lacunae always result from a distinct and specific small-vessel arteriopathy is not confirmed; in fact, an atheroma may occlude a single perforating artery at the base of the brain as well as larger arteries. Lipohyalinosis, initially referred to as the underlying pathologic vascular lesion specific for lacunae, is found most commonly in a subset of patients with severe hypertension associated with multilacunar dementia. Large infarcts and hemorrhages are reported to coexist with lacunae in autoptic and neuroradiological studies; intracranial atherosclerosis is associated with lacunae as well as with large superficial infarcts. The percentage of patients with hypertension is approximately the same regardless of type of the infarct, lacunar or cortical. Diagnostic criteria are not clear-cut: clinical onset, neurological examination, and assessment of risk factors are unable to take lacunae apart from other infarcts; the size of the lesion, but not the site or the pathogenesis, determines clinical course, degree of motor deficit, and prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral infarction: lacunae]. 174 36

The subject of the cerebral circulation in the elderly is reviewed. In old age, cerebral blood flow (CBF), which is closely coupled to cerebral oxidative metabolism, decreases along with the amount of brain tissue. In healthy old people, the cerebral circulation is regulated as earlier in life, by autoregulation, metabolic regulation, and chemical and other factors. CBF and its regulation is influenced by disease processes prevailing in old age, such as dementia, atherosclerosis, diabetes mellitus, stroke, and hypertension. Hypertension, apart from being a risk factor for stroke, causes adaptive cerebral vascular changes, leading to a shift of the lower limit of autoregulation towards high pressure, with an impaired tolerance to pressure decrease. In old age, this adaptation may not be reversible. With this background, a conservative approach to elderly hypertensive patients is suggested, aimed at some reduction of pressure but carefully avoiding overtreatment.
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PMID:Cerebral blood flow in the elderly: impact of hypertension and antihypertensive treatment. 200 45


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