Abstract TP441: Neurovascular Coupling is Impaired in Cerebral Amyloid Angiopathy

Introduction: Cerebral amyloid angiopathy (CAA) is marked by accumulation of vascular beta-amyloid which is toxic to smooth muscle cells. An animal study and a pilot study in humans suggest decreased vasodilation in CAA. We studied patients with CAA and matched controls to determine whether neurovascular coupling is impaired in CAA. Methods: Patients with CAA and controls underwent task-related fMRI with a visual task (viewing a flashing alternating checkerboard pattern) or a motor task (tapping the fingers of the dominant hand) using a block design, and visual evoked potentials (VEPs). CAA patients were diagnosed by Boston criteria and had normal corrected visual acuity, no visual field deficits and no paresis of the dominant arm. Controls were recruited by community advertising and were matched by gender and age (±5 years) to CAA cases. Results: Eighteen CAA patients (12 M, 6F; 72±7 yrs) and eighteen controls (12 M, 6F; 70±7 yrs) were studied. For the visual task, CAA patients had reduced activity in the occipital lobe (Figure) and lower amplitude of the BOLD response vs. controls (28% reduced, p=0.005). By contrast, for the motor task CAA patients had a similar response of the primary motor cortex vs. controls (9.6% reduced BOLD response, p=0.53). VEP P100 latencies and amplitudes did not differ between CAA and controls (p=0.49 and p=0.74). Lower visual cortex BOLD amplitudes were correlated with greater white matter lesion volumes in CAA (r=-0.66, p=0.003). Conclusions: Neurovascular coupling is impaired in the occipital lobe in CAA. BOLD signal amplitudes are reduced despite normal evoked potentials, suggesting impaired vasodilation. The association with white matter lesion volume raises the possibility that impaired vasodilation may be involved in the pathogenesis of these lesions. BOLD responses in the primary motor cortex in CAA were not reduced, likely reflecting the known posterior predominance of CAA with lesser involvement of the frontal lobe.