Abstract TP433: Structural, Molecular and Physiologic Alterations in Patients with Lobar Microbleeds

Abstract

Background: Cerebral amyloid angiopathy (CAA) is diagnosed after a lobar intracerebral hemorrhage (L-ICH) but lobar microbleeds (LMB) are increasingly detected on MRIs of patients without L-ICH. We aimed to compare advanced imaging measures of structural brain damage, amyloid load, and cerebrovascular reactivity between CAA patients with L-ICH (CAA-ICH) and those with LMB (LMB-only). Methods: Standard MRI markers (LMB counts, cortical superficial siderosis [cSS], enlarged perivascular spaces [EPVS], white matter hyperintensity [WMH] patterns) and FreeSurfer based advanced volumetric analyses (calculated as percent of total intracranial volume) were obtained in 115 non-demented patients with either CAA-ICH or LMB-only. Pittsburgh compound B PET measures of amyloid deposition and fMRI measures of vascular reactivity (amplitude, time-to-peak, time-to-baseline) were also compared between the 2 groups. Results: LMB-only patients (n=37) presented with transient neurological symptoms or cognitive/gait complaints and stroke/neurodegenerative conditions were ruled out. Age, vascular risk factors, LMB counts, presence of cSS, EPVS counts and WMH patterns were not different between CAA-ICH and LMB-only (Table). Volume of WMH was significantly higher in CAA-ICH as compared to LMB-only patients in univariable and multivariable models (p=0.026). There was no difference in cortical thickness, WM volume, amyloid load/distribution and finally functional MRI markers of vascular reactivity between the two groups (Table). Conclusions: Our results indicate that measures of vascular physiology and amyloid load as well as structural damage of LMB-only patients are not different from CAA-ICH, except a lower WMH load. These data support the view that LMB-only patients represent a non-hemorrhagic stage of the disease and that they can be enrolled in clinical trials aimed at modifying the molecular/physiologic changes to reverse/prevent CAA progression.