Victor J. Del Brutto, MD
Cerebral Amyloid Angiopathy (CAA) results from the deposition of amyloid β-protein in the media and adventitia of small vessels in the leptomeninges and cerebral cortex. CAA is tightly associated with aging and is known to be a major cause of intracranial hemorrhage (ICH) and cognitive decline in the elderly. On pathological examination, vessels affected by CAA show degeneration of the smooth muscle cells, splitting of the vessel wall, microaneursymal dilation and perivascular hemorrhages. These pathological changes lead to the development of hemorrhagic lesions including lobar ICH, cerebral microbleeds (CMBs) and cortical superficial siderosis (cSS), as well as ischemic changes such as cortical infracts and white matter disease. All of them contribute to neuronal loss and development of global brain atrophy.
In vivo diagnosis of CAA is based on brain MRI findings that can be complemented by amyloid-binding positron emission tomography or cerebrospinal fluid markers. The distinctive neuroimaging findings in CAA are the presence of cortical CMBs and focal cSS. On the other hand, pathological studies have shown that cortical microinfarcts (CMIs) are common in CAA and their incidence might be even higher than CMBs or lobar hemorrhages in these patients. These cortical CMIs appear to be related to impaired cerebral autoregulation associated with CAA and are thought to be clinical silent and be part of the ongoing pathology of the disease. However, the relevance on diagnosis and prognosis of CMIs detected by traditional brain imaging in patients with CAA is unknown.
In the present study, Li Xiong and colleagues assessed the frequency of CMIs detected by brain MRI in a cohort of non-demented patients diagnosed with CAA and determined their baseline cognitive function as well as the association of CMIs with other imaging markers of CAA. In addition, they presented follow-up data of cognitive performance in a substantial portion of the population studied. The investigators found that CMIs were a common MRI finding in patients with CAA (40%). CMIs were independently associated with total brain atrophy and cSS, but no association was found between CMIs and CMBs or white matter disease. Additionally, CMIs had worse baseline cognitive performance on executive function and processing speed, as well as higher incidence of dementia on follow up. This later finding was not independent of other CAA neuroimaging markers including total brain atrophy.
Previous studies on CMIs and CAA have been based on pathological specimens or high-resolution 7-T MRI. Patients in the present study underwent detection of CMIs either by 1.5- or 3-T MRI, which is probably a more pragmatic way of assessing these lesions in real practice. The current findings suggest that CMIs detected by brain MRI is an important marker of disease burden and cognitive decline in patients with CAA; however, total brain volume seems to be a stronger predictor of dementia in this population.
