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Either vascular disease due to large artery ischemia or to small artery ischemia disease can lead to vascular dementia. Small arteryischemia can provoke subcortical ischemic disease.
Any patients hospitalized in the USA for first stroke, the majority is due to large artery ischemia. But 10 – 30 % of cases may be due to subcortical ischemic vascular disease. However, this latter disease may be responsible for 36% to 67% of cases of vascular dementia. This figure is still little precise because almost all epidemiological studies, existing up to now, fail to assess the prevalence of the disease by subtypes. At present, mostly the broad category of vascular dementia has been considered. However, the more precise identification of the type of vascular dementia may be important, since one subcategory leads far much often to dementia.
The basic pathology of subcortical ischemic vascular disease is atherosclerosis, which is accelerated by hypertension or/and diabetes. The hypoperfusion of the brain due to this disease leads to the progressive degeneration of the white matter, the end stage causing lacunar state and Binswanger’s syndrome. Asian people may have a higher prevalence of this disease than Westerners, partially linked to a higher prevalence of hypertension. When compared to patients with Alzheimer’s disease, patients with vascular dementia retain better recognition and memory but are worse with regard to executive functions.
This very interesting paper can be retrieved in full at the Medscape website shown below, provide that one has registered, which is free of charge.

Up to now, promising neuroprotectants in animal models have produced deceiving results in humans. Single agents have been usedto block one segment of the ischemic cascade, but parallel pathways remained so that neuronal cell death continued to occur. A more comprehensive and in-depth understanding of the various pathways may lead to more effective strategies including the combination of different types of neuroprotective measures.
This paper represents an updated description of the various steps of the ischemic cascade, which lead either to necrosis or to apoptosis, the latter taking place during reperfusion. This phenomenon introduces the concept of delayed cell death, taking place in the penumbra. This delayed cell death produces the rationale of neuroprotection in stroke. Variouspossibilities of neuroprotection are summarized in that concise review paper,that can be recommended for to every medical student interesting in strokeand its treatment. This concise and clear paper can be found under the website:
http://www.cme-reviews.com/CMEReviews/stroke/CNS300_Felberg.html
JF 07.01.01

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