Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.
The diagnostic key is blood-sensitive MRI: the gradient-recalled echo (GRE) sequence, also called T2-star, and susceptibility-weighted imaging (SWI). These sequences detect hemosiderin from old microbleeds that are invisible on CT and on standard T1, T2, and FLAIR images. Microbleeds appear as small dark foci of signal loss, and their lobar distribution is what points toward amyloid angiopathy rather than hypertensive disease.
Imaging features
- Lobar microbleeds distributed across cortical territories, often multiple.
- Lobar intracerebral haemorrhage, frequently occipital or parietal in acute presentations.
- Cortical superficial siderosis as linear hemosiderin along the cortical surface.
- White matter hyperintensities on FLAIR and enlarged perivascular spaces in the centrum semiovale, which support the diagnosis without proving it on their own.
Boston version 2.0 framework
The Boston criteria grade diagnostic certainty from definite disease (full postmortem examination) through pathology-supported and clinical levels. Version 2.0 applies to patients aged 50 years or older presenting with intracerebral haemorrhage, transient focal episodes, or cognitive impairment, with no deep haemorrhagic lesions and no other cause.
It added two white matter features alongside the haemorrhagic lesions: severely enlarged perivascular spaces in the centrum semiovale and a multispot pattern of subcortical white matter hyperintensities.
In outline, probable disease requires either at least two strictly lobar haemorrhagic lesions (haemorrhage, microbleed, or superficial siderosis) or one such lesion combined with a qualifying white matter feature. Possible disease requires a single strictly lobar haemorrhagic lesion or a single qualifying white matter feature. In practice, a clinical diagnosis of probable disease is sufficient to guide management decisions such as antithrombotic avoidance.
Amyloid angiopathy versus hypertensive bleeding
| Feature | Amyloid angiopathy | Hypertensive small-vessel disease |
|---|---|---|
| Haemorrhage location | Lobar (cortical) | Deep (basal ganglia, thalamus, pons) |
| Typical age | Usually past 70 | Often 50 to 70 |
| Microbleeds on blood-sensitive MRI | Lobar distribution | Deep distribution |
| Management implication | Generally avoid antithrombotics | Blood pressure control central |
The table describes typical patterns rather than absolute rules, and mixed disease occurs: an older hypertensive patient can carry both pathologies, in which case the strictly lobar lesions still argue for coexisting amyloid angiopathy.
Evidence anchors
- Charidimou A, et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy. Lancet Neurol. 2022: https://pubmed.ncbi.nlm.nih.gov/35841910/
- Greenberg SM, et al. 2022 Guideline for the management of patients with spontaneous intracerebral hemorrhage: https://pubmed.ncbi.nlm.nih.gov/35579034/