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. 2021 Nov;191(11):1888–1905. doi: 10.1016/j.ajpath.2021.07.004

Table 1.

Radiological and Pathologic Features of Spectrum of Small Vessel Disease in AD Dementia

Clinical features SVD feature Imaging marker Key pathologic features Degree of change in AD (compare aging or neurological controls)
Stroke(s)/vascular origin Silent infarcts WMHs on T2W, FLAIR, ↑ high signal Unclear ++
Transient Ischemic attacks WMHs on DWM; high signal Unclear +
White matter attenuation WMHs (pvWMH, dWMH), WM atrophy in CAA; high signal Demyelination in deep WM; axon damage +++
Lacunar infarcts Hyperintense lesions on T2W/FLAIR Lacunes (<1.5 cm) in BG, thalamus, WM ++
Cortical Infarcts Hyperintense lesions on T2W/FLAIR Cortical infarcts +
Microinfarcts Tiny hyperintense lesions on T2W (3T, 7T) Microinfarcts (<0.5 cm) in GM and WM +++
Microbleeds T2W or GRE signal lobar and deep bleeds; hypointense lesions on T2W Hemosiderin deposits in cortex (CAA) and subcortical structures (hypertensive) ++
Intracerebral hemorrhages Hyperintense on CT; hypointense lesions on T2W ICH, microaneurysms +
Cerebral siderosis Hypointense signal on GRE SAH +
Vascular pathologies Perivascular spaces (enlarged Virchow-Robin spaces) Hyperintense rounded lesions on T2W/FLAIR PVS in WM; GM of BG ++
Intracranial atherosclerosis Unclear Occasional microatheromas in branches of MCA, ACA +
Arteriolosclerosis Unclear Moderate-severe arteriolosclerosis +++
CAA Posterior WMHs, lobar microbleeds Moderate-severe CAA in cortex; predominance in occipital lobe +++
Vascular Function CBF Resting CBF Parietal, temporal lobes, BG +++
BBB function Permeability on MRI (contrast agents, Gd) EC damage, ↓ capillary density +++
PVW Phase contrast MRI; pulse sequence with retrospective peripheral pulse gating sequences Arteriosclerotic vessels; collagen fibers +++
Autonomic function (hypoperfusion) Tilt table, carotid sinus supersensitivity (OH, CSH) WMLs, arteriolosclerosis, microinfarcts in BG ++

Neuroimaging and pathologic changes involving SVD in AD.

ACA, anterior cerebral artery; AD, Alzheimer disease; BG, basal ganglia; CAA, cerebral amyloid angiopathy; CBF, cerebral blood flow; CSH, carotid sinus hypersensitivity; DWM, deep white matter; dWMH, deep white matter hyperintensities; EC, endothelial cell; FLAIR, fluid attenuated inversion recovery; Gd, gadolinium; GM, grey matter; GRE, gradient echo; ICH, intracerebral hemorrhage; MCA, middle cerebral artery; MRI, magnetic resonance imaging; OH, orthostatic hypotension; PVS, perivascular space; pvWMH, periventricular white matter hyperintensities; PVW, pulse wave velocity; SAH, subarachnoid hemorrhage; SVD, small vessel disease; WM, white matter; WMH, white matter hyperintensities; WML, white matter lesion.

Changes found in AD type of dementia above and beyond normally aging healthy subjects. Arrow (↑) indicates increase. Scale of change means scores: +, mild (1); ++ moderate (2), severe +++ (3). Microhemorrhages may be caused by leakage by two mechanisms: microaneurysms and rupture of walls due to deposition of fibrillar proteins or iron.28