Table 3

Postmortem studies on characterisation of microbleeds using postmortem MRI–pathology correlation

ReferenceSubjectsHistochemistryMRIMain findings
Fazekas 19998411 subjects with intracerebral haemorrhageHE, Masson trichrome, KB, Congo Red, iron1.5T

  • MRI signal loss in 7/11 subjects. 2 pts: only cortical–subcortical, 1 pt only basal ganglia/infratentorial, 4 pts both locations. WMH in all patients, lacunes in 5/7 pts.

  • In 62% of MRI signal loss: focal accumulation of hemosiderin-containing macrophages adjacent to small blood vessels, sometimes minute areas of tissue necrosis. The remainder of MRI signal loss: no pathological substrate.

  • Also MR negative hemosiderin deposits: smaller, only a few perivascular, hemosiderin laden macrophages. No calcification or vascular malformations.

  • 2 subjects had cerebral amyloid angiopathy of variable extent in multiple vessels, associated with foci of remote blood leakage. Brains with fibrohyalinosis showed microbleeds preferentially in the basal ganglia/thalami, but also cortical–subcortical.

Tanaka 1999853 neur (+) controls, with MRI signal lossHE, Masson trichrome, KB, Berlin Blue

  • 1.0T

  • In vivo MRI

  • Foci of old haemorrhages caused by rupture of arteriosclerotic microvessels <200 μm, surrounded by gliosis and incomplete ischaemic necrosis. Identified as hemosiderin pigments within the perivascular space and as an organised pseudoaneurysm (1 case).

Tatsumi 2008861 neur (+) controlHE, Berlin Blue1.5T, both postmortem and in vivo MRI

  • 9 MRI hypointensities: all could be identified as brown spots on the cut surface.

  • 8 hemosiderin laden macrophages, 1 vascular pseudocalcification (left pallidum).

  • 5/8 had vascular abnormalities: degenerated endothelial lining and hyalinosis.

  • Size of hemosiderin deposit similar with MRI hypointensity.

  • Associated with tissue rarefaction, gliosis or arteriolar changes. Some hemosiderin deposits not observed on MRI. Ante- and postmortem MRI comparable.

Schrag 2009878 AD (of which 6 advanced CAA), 2 neur (-) controlsAβ1–42, CD68, HO-1, complement C6, CD3, CD20, Prussian Blue, fluorescent study (HO-1 + MAP-2), TUNEL3.0T

  • 38 MBs: correspond to variety of pathological changes=16 old haematomas, 7 small cavities, 3 microscopic hemosiderin granules+haematoidin deposition, 1 dissection vessel wall, 1 microaneurysm.

  • Location: 79% grey–white junction, 21% superficial cortex.

  • CAA related vascular damage: thickened, acellular, arteriolar walls with βamyloid deposition and lacking muscularis layer.

  • Activated microglia (CD68), evidence of haeme degradation (HO-1), late complement activation, apoptosis. Inflammatory reaction along local microvasculature.

  • AD, Alzheimer's disease; CAA, cerebral amyloid angiopathy; CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; EvG, Elastic van Gieson; HE, haematoxylin-eosin; HO-1, haeme oxygenase 1; KB, Klüver–Barrera; MB, microbleed; MAP-2, microtubule associated protein 2; neur (−) controls, non-demented subjects without neurological disease; neur (+) controls, non-demented patients with neurological disease; WMH, white matter hyperintensities.