Abstract T P407: Functional MRI-measured Vascular Reactivity is Preserved in CADASIL, but not Cerebral Amyloid Angiopathy

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Objectives: Previous studies have demonstrated that the magnitude of the blood oxygen dependent level (BOLD) functional MRI (fMRI) response to visual stimulation is reduced in cerebral amyloid angiopathy (CAA) relative to controls, reflecting impaired vascular reactivity. We wished to determine if BOLD responses were reduced in an associated small vessel disease, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Methods: BOLD fMRI data were collected using a visual stimulus (contrast-reversing checkerboard) and motor task (finger-tapping). BOLD responses in the visual cortex (visual stimulus) and motor cortex (motor task) were compared between 5 CADASIL (55.0 ±12.9 years; 3 females), 18 CAA (72.1 ± 7.2 years; 6 females) and 22 control subjects (67.0 ±10.0 years; 9 females). One-way analysis of variance and multivariable-adjusted generalized models, controlling for age and hypertension, were used to compare groups with Tukey-Kramer’s correction for multiple comparisons. Results: BOLD response varied by group for the visual stimulus (p<0.001) but not the motor task (p=0.48). After adjusting for age and hypertension, the estimated mean visual cortex BOLD response was 3.91% in CADASIL (95% confidence interval, CI, 3.12-4.70%), 1.71% in CAA (95% CI 1.23-2.20%), and 2.84% (95% CI 2.44-3.24%) in controls. In CADASIL, the BOLD response was greater than in CAA (p<0.001) and controls (p=0.04). In CAA, the BOLD response was less than controls (p=0.009). No significant differences were observed for the motor task (p=0.51). Conclusions: We observed increased and unchanged BOLD responses in the visual and motor cortices of CADASIL patients, respectively. This suggests that cortical blood flow regulation by neuronal activity may be relatively preserved in CADASIL, in contrast to CAA where occipital vascular reactivity is impaired. Preserved reactivity in CADASIL may be because damage is primarily subcortical, whereas increased activation may reflect compensatory mechanisms for subcortical damage.