V Perosa1,2,3, T Arts4, A Assmann5, H Mattern6, O Speck2,7,8, J Oltmer5, H-J Heinze5,2,7,8, E Düzel9,2,8,10, S Schreiber5,2, J J M Zwanenburg4. 1. From the Department of Neurology (V.P., A.A., J.O., H.-J.H., S.S.) vperosa@mgh.harvard.edu. 2. German Center for Neurodegenerative Diseases (V.P., O.S., H.-J.H., E.D., S.S.), Magdeburg, Germany. 3. J. Philip Kistler Stroke Research Center (V.P.), Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 4. Department of Radiology (T.A., J.J.M.Z.), University Medical Center Utrecht, Utrecht, the Netherlands. 5. From the Department of Neurology (V.P., A.A., J.O., H.-J.H., S.S.). 6. Institute of Physics (H.M.). 7. Leibniz-Institute for Neurobiology (O.S., H.-J.H.), Magdeburg, Germany. 8. Center for Behavioral Brain Sciences (O.S., H.-J.H., E.D.), Magdeburg, Germany. 9. Institute of Cognitive Neurology and Dementia Research (E.D.), Ottovon-Guericke University, Magdeburg, Germany. 10. Institute of Cognitive Neuroscience (E.D.), University College London, London, UK.
Abstract
BACKGROUND AND PURPOSE: Cerebral small vessel disease contributes to stroke and cognitive impairment and interacts with Alzheimer disease pathology. Because of the small dimensions of the affected vessels, in vivo characterization of blood flow properties is challenging but important to unravel the underlying mechanisms of the disease. MATERIALS AND METHODS: A 2D phase-contrast sequence at 7T MR imaging was used to assess blood flow velocity and the pulsatility index of the perforating basal ganglia arteries. We included patients with cerebral amyloid angiopathy (n = 8; identified through the modified Boston criteria), hypertensive arteriopathy (n = 12; identified through the presence of strictly deep or mixed cerebral microbleeds), and age- and sex-matched controls (n = 28; no cerebral microbleeds). RESULTS: Older age was related to a greater pulsatility index, irrespective of cerebral small vessel disease. In hypertensive arteriopathy, there was an association between lower blood flow velocity of the basal ganglia and the presence of peri-basal ganglia WM hyperintensities. CONCLUSIONS: Our results suggest that age might be the driving factor for altered cerebral small vessel hemodynamics. Furthermore, this study puts cerebral small vessel disease downstream pathologies in the basal ganglia region in relation to blood flow characteristics of the basal ganglia microvasculature.
BACKGROUND AND PURPOSE: Cerebral small vessel disease contributes to stroke and cognitive impairment and interacts with Alzheimer disease pathology. Because of the small dimensions of the affected vessels, in vivo characterization of blood flow properties is challenging but important to unravel the underlying mechanisms of the disease. MATERIALS AND METHODS: A 2D phase-contrast sequence at 7T MR imaging was used to assess blood flow velocity and the pulsatility index of the perforating basal ganglia arteries. We included patients with cerebral amyloid angiopathy (n = 8; identified through the modified Boston criteria), hypertensive arteriopathy (n = 12; identified through the presence of strictly deep or mixed cerebral microbleeds), and age- and sex-matched controls (n = 28; no cerebral microbleeds). RESULTS: Older age was related to a greater pulsatility index, irrespective of cerebral small vessel disease. In hypertensive arteriopathy, there was an association between lower blood flow velocity of the basal ganglia and the presence of peri-basal ganglia WM hyperintensities. CONCLUSIONS: Our results suggest that age might be the driving factor for altered cerebral small vessel hemodynamics. Furthermore, this study puts cerebral small vessel disease downstream pathologies in the basal ganglia region in relation to blood flow characteristics of the basal ganglia microvasculature.
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