TY - JOUR
T1 - Vasodilator responses to acetazolamide tested in subtypes of vascular dementia
AU - Meyer, John Stirling
AU - Konno, Shizuko
AU - Margishvili, Gaiane M.
AU - Terayama, Yasuo
N1 - Funding Information:
From the Cerebrovascular Research Laboratories, Veterans Affairs Medical Center, and the Department of Neurology, Baylor College of Medicine, Houston, TX. Received October 24, 1997; accepted April 9, 1998. Supported by Department of Veterans Affairs, Central Office, Washington, DC; Harry K. Smith; and the Gordon and Mary Cain Foundation, Houston, TX. Address reprint requests to John Stifling Meyer, MD, Director, Cerebrovascular Research Laboratories, Bldg 110, Room 225, VAMC, 2002 Holcombe Blvd-151A,H ouston, TX 77030. Copyright 9 1998 by National Stroke Association 1052-3057/ 98 / 0705-001053.00/ 0 In the United States and Europe, vascular dementia (VAD) is a common cause of dementia among the elderly, second only to Alzheimer's disease (DAT). >3 In developing countries, VAD is more common than DAT. 4,s VAD is a form of late-life dementia that is preventable and remediable. 6-n With advancing age, causes of VAD become more multifactoriaU a VAD in the elderly should not be considered homogeneous, but heterogeneous. For these reasons, subclassification of VAD according to its clinical and pathogenetic features is important before undertaking
PY - 1998/9
Y1 - 1998/9
N2 - 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 (ΔLCBF) 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.
AB - 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 (ΔLCBF) 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.
KW - Acetazolamide
KW - Local cerebral blood flow
KW - VAD subtypes
KW - Vascular dementia
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U2 - 10.1016/S1052-3057(98)80050-5
DO - 10.1016/S1052-3057(98)80050-5
M3 - Article
C2 - 17895108
AN - SCOPUS:70249098999
SN - 1052-3057
VL - 7
SP - 323
EP - 329
JO - Journal of Stroke and Cerebrovascular Diseases
JF - Journal of Stroke and Cerebrovascular Diseases
IS - 5
ER -