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[Modern concepts of "cerebrovascular dementia"].
Encephale. 1977; 3(4):357-72.E

Abstract

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.

Authors

No affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

fre

PubMed ID

611016

Citation

Bousser, M G.. "[Modern Concepts of "cerebrovascular Dementia"]." L'Encephale, vol. 3, no. 4, 1977, pp. 357-72.
Bousser MG. [Modern concepts of "cerebrovascular dementia"]. Encephale. 1977;3(4):357-72.
Bousser, M. G. (1977). [Modern concepts of "cerebrovascular dementia"]. L'Encephale, 3(4), 357-72.
Bousser MG. [Modern Concepts of "cerebrovascular Dementia"]. Encephale. 1977;3(4):357-72. PubMed PMID: 611016.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Modern concepts of "cerebrovascular dementia"]. A1 - Bousser,M G, PY - 1977/1/1/pubmed PY - 1977/1/1/medline PY - 1977/1/1/entrez SP - 357 EP - 72 JF - L'Encephale JO - Encephale VL - 3 IS - 4 N2 - 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. SN - 0013-7006 UR - https://www.unboundmedicine.com/medline/citation/611016/[Modern_concepts_of_"cerebrovascular_dementia"]_ L2 - https://medlineplus.gov/dementia.html DB - PRIME DP - Unbound Medicine ER -