Clinical neurology and neurosurgery · 2012
Prevalence of cerebrovascular lesions in patients with Lewy body dementia: a neuropathological study.
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De Reuck Jacques, Deramecourt Vincent, Cordonnier Charlotte, Leys Didier, Pasquier Florence, Maurage Claude-Alain
Аннотация
BACKGROUND: The co-existence of vascular pathology in patients with Lewy body dementia (LBD) is still a matter of debate. This study analyses the prevalence and the severity of cerebrovascular lesions in post-mortem brains of patients with LBD.
PATIENTS AND METHODS: Twenty brains of demented patients with autopsy-proven Lewy body disease were compared to 14 brains of age-matched controls.
RESULTS: Associated Alzheimer disease (AD) features, stages I-IV, were present in 70% of the LBD brains and in 7% of the controls (P<0.001). Cerebral amyloid angiopathy (CAA) was only present in 30% and lipohyalinosis in 10%. A semi-quantitative analysis, performed on a coronal section of a whole cerebral hemisphere and on a horizontal section through the pons and the cerebellum, revealed significantly more mini-bleeds in the LBD brains (P=0.007), predominantly in the cerebral cortex (P=0.03). Other cerebrovascular lesions were only rarely observed. Comparison of the LDB brains, with and without moderate AD features and CAA, showed no difference in the severity of the cerebrovascular lesions including mini-bleeds.
CONCLUSIONS: The prevalence of mini-bleeds in LBD brains appears to be independent from the co-existence of moderate AD pathology and CAA. It is more probably due to disturbances of the blood-brain barrier, related to the neurodegenerative process itself.
PATIENTS AND METHODS: Twenty brains of demented patients with autopsy-proven Lewy body disease were compared to 14 brains of age-matched controls.
RESULTS: Associated Alzheimer disease (AD) features, stages I-IV, were present in 70% of the LBD brains and in 7% of the controls (P<0.001). Cerebral amyloid angiopathy (CAA) was only present in 30% and lipohyalinosis in 10%. A semi-quantitative analysis, performed on a coronal section of a whole cerebral hemisphere and on a horizontal section through the pons and the cerebellum, revealed significantly more mini-bleeds in the LBD brains (P=0.007), predominantly in the cerebral cortex (P=0.03). Other cerebrovascular lesions were only rarely observed. Comparison of the LDB brains, with and without moderate AD features and CAA, showed no difference in the severity of the cerebrovascular lesions including mini-bleeds.
CONCLUSIONS: The prevalence of mini-bleeds in LBD brains appears to be independent from the co-existence of moderate AD pathology and CAA. It is more probably due to disturbances of the blood-brain barrier, related to the neurodegenerative process itself.