Literature DB >> 12154250

Cerebral hypoperfusion generates cortical watershed microinfarcts in Alzheimer disease.

Oda-Christina Suter1, Thanomphone Sunthorn, Rudolf Kraftsik, Joel Straubel, Pushpa Darekar, Kamel Khalili, Judith Miklossy.   

Abstract

BACKGROUND AND
PURPOSE: The watershed cortical areas are the first to be deprived of sufficient blood flow in the event of cerebral hypoperfusion and will be the sites of watershed microinfarcts. Cerebral hypoperfusion is associated with Alzheimer disease (AD), but information regarding the occurrence of watershed cortical infarcts in AD is lacking.
METHODS: Brains of 184 autopsy cases (105 definite AD cases and 79 age-matched controls) were selected and analyzed by histochemical and immunohistochemical techniques. The 3-dimensional reconstruction of the whole cerebrum, with 3-mm spaced serial sections, was performed in 6 AD cases to study the intrahemispheric and interhemispheric distribution of the cortical microinfarcts.
RESULTS: A significant association (P=0.001) was found between the occurrence of watershed cortical infarcts and AD (32.4% versus 2.5% in controls). The microinfarcts were restricted to the watershed cortical zones. Congophilic angiopathy was revealed to be an important risk factor. Perturbed hemodynamic factors (eg, decreased blood pressure) may play a role in the genesis of cortical watershed microinfarcts.
CONCLUSIONS: In AD, cerebral hypoperfusion induces not only white matter changes but cortical watershed microinfarcts as well, further aggravating the degenerative process and worsening dementia. To prevent the formation of watershed cortical microinfarcts in AD, monitoring blood pressure and treating arterial hypotension are essential.

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Year:  2002        PMID: 12154250     DOI: 10.1161/01.str.0000024523.82311.77

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  83 in total

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Review 2.  Cerebral microinfarcts: the invisible lesions.

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9.  [A cerebral watershed infarction after general anaesthesia in a patient with increased anti-cardiolipin antibody level].

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