OBJECTIVES: Thirty seven vascular dementia (VAD) patients were categorized into eight subtypes based on clinical, radiological, and pathogenetic features. Cerebral vasodilator responses to acetazolamide were then compared with age-matched normal controls and stroke patients without dementia. METHODS: VAD results were compared with 42 normals and 19 cognitively intact stroke patients. Regional cerebral vasodilator responses were quantitated utilizing xenon contrasted computed tomography measures of local cerebral blood flow (LCBF) before and after oral administration of acetazolamide. LCBF changes (DeltaLCBF) before and after acetazolamide were calculated within cortical and subcortical, gray and white matter. Clinical VAD subtypes were: type 1, multi-infarct dementia (MID); type 2, strategically placed infarcts; type 3, subcortical lacunar infarcts; type 4, Binswanger's subcortical arteriosclerotic leukoencephalopathy; type 5, subcortical infarctions due to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), inflammatory angitis, or antiphospholipid antibodies; type 6, admixtures of above types; type 7, cerebral hemorrhagic lesions; and type 8, VAD combined with Alzheimer's disease (DAT). The group with subcortical VAD comprised types 3-5. The group with cortical VAD comprised the remainder (types 1, 2, and 6-8). Cerebral vasodilator responses were also compared between these two main groups. RESULTS: Cerebral vasodilator responses identified differences between the two main groups of VAD patients, those with cortical and those with subcortical dementia. Leukoaraiosis was measurably greater in subcortical VAD compared with cortical VAD. Among subcortical VAD patients, cortical LCBF increases after administration of acetazolamide were greater compared with cortical VAD and with normal controls. CONCLUSIONS: Cognitive impairments in subcortical VAD are attributable to cortical disconnection syndromes. This concept is supported by reduced perfusion in deactivated cortex. In patients with subcortical VAD, deactivated cortical LCBF becomes promptly activated by acetazolamide resulting in marked cortical LCBF increases. Leukoaraiosis is greater among VAD patients and leukoaraiosis contributes to cortical disconnections, confirmed by excessive cortical vasodilator responses to acetazolamide.
OBJECTIVES: Thirty seven vascular dementia (VAD) patients were categorized into eight subtypes based on clinical, radiological, and pathogenetic features. Cerebral vasodilator responses to acetazolamide were then compared with age-matched normal controls and strokepatients without dementia. METHODS: VAD results were compared with 42 normals and 19 cognitively intact strokepatients. Regional cerebral vasodilator responses were quantitated utilizing xenon contrasted computed tomography measures of local cerebral blood flow (LCBF) before and after oral administration of acetazolamide. LCBF changes (DeltaLCBF) before and after acetazolamide were calculated within cortical and subcortical, gray and white matter. Clinical VAD subtypes were: type 1, multi-infarct dementia (MID); type 2, strategically placed infarcts; type 3, subcortical lacunar infarcts; type 4, Binswanger's subcortical arteriosclerotic leukoencephalopathy; type 5, subcortical infarctions due to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), inflammatory angitis, or antiphospholipid antibodies; type 6, admixtures of above types; type 7, cerebral hemorrhagic lesions; and type 8, VAD combined with Alzheimer's disease (DAT). The group with subcortical VAD comprised types 3-5. The group with cortical VAD comprised the remainder (types 1, 2, and 6-8). Cerebral vasodilator responses were also compared between these two main groups. RESULTS: Cerebral vasodilator responses identified differences between the two main groups of VAD patients, those with cortical and those with subcortical dementia. Leukoaraiosis was measurably greater in subcortical VAD compared with cortical VAD. Among subcortical VAD patients, cortical LCBF increases after administration of acetazolamide were greater compared with cortical VAD and with normal controls. CONCLUSIONS:Cognitive impairments in subcortical VAD are attributable to cortical disconnection syndromes. This concept is supported by reduced perfusion in deactivated cortex. In patients with subcortical VAD, deactivated cortical LCBF becomes promptly activated by acetazolamide resulting in marked cortical LCBF increases. Leukoaraiosis is greater among VAD patients and leukoaraiosis contributes to cortical disconnections, confirmed by excessive cortical vasodilator responses to acetazolamide.