Do cerebral microbleeds affect cognitive functions?

Some studies provide evidence that microbleeds have an impact on cognitive function that is independent of the extent of associated white matter changes and ischemic stroke. It affects executive functions, which is likely to result from tissue damage associated with microbleeds in the frontal lobes and basal ganglia, disrupting frontal-subcortical circuits.

What is the prevalence of CMBs?

Microbleeds prevalence increases with age. It is 6.5% in persons aged 45 to 50 years and up to 40% in persons aged 80 years and older.

INTRACEREBRAL HEMORRHAGE

Cerebral microbleeds

Created 15/04/2021, last revision 25/05/2023

Definition

cerebral microbleeds (CMBs) – hemosiderin deposits caused by small hemorrhages, may serve as a radiologic biomarker of small vessel disease (SVD)
- black, round, or oval lesions on blood-sensitive MRI sequences – (T2*/GRE or SWI)
- 2-5 mm in diameter
often found incidentally on MRI scans; incidence increases with age
- incidence in the general population is approx. 10-15% (Sveinbjornsdottir, 2008)
- 6.5% in the individuals aged 45-50 years
- up to 40% in the population > 80 years [Poels, 2009]
- incidence of CMBs in AD is 20-43%; in vascular dementia up to 85%! [Seo, 2007]
microhemorrhages are associated with:
- older age
- hypertension
- smoking
- white matter disease and lacunar stroke
- previous ischemic stroke or ICH
- COVID-19 leukoencephalopathy (mostly in critically ill patients) (Agarwal, 2020)
a high number of microbleeds is associated with an increased risk of:
- cognitive impairment, which may progress to dementia (Werring, 2004) [Akoudad, 2006]
- intracerebral hemorrhage (especially with antithrombotic or fibrinolytic therapy)
higher risk of progression with:
- severe SVD (Subcortical Vascular Disease or Small Vessel Disease)
- CAA with APOE ε2 and ε4 [McCarron, 2000]

Classification

subcortical (mainly caused by arteriolopathy) → Binswanger´s disease
cortical (mostly caused by CAA – with a higher risk of lobar hemorrhage)
combined (combination of CAA and arteriolosclerosis or rather arteriolosclerosis alone) [Jung, 2020]

Cerebral amyloid angiopathy (CAA) on GRE

Cortical cerebral microbleeds and lobar hematomas in patient with cerebral amyloid angiopathy

Cortical cerebral microbleeds (CMBs) on SWI sequence

Differential diagnosis

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Management

no specific therapy
strict treatment of hypertension
careful indication and monitoring of anticoagulant (preferably use DOACs) and antiplatelet therapy (avoid DAPT if possible)

CMBs and the risk of a hemorrhage

the risk of ICH increases with the number of CMBs
- ≥ 5 CMBs – OR for ICH is 2.8
- ≥ 10 CMBs – OR for ICH is 5.5!
according to the CROMIS-2 trial, the risk of bleeding in patients with CMBs is 9.8/1000 vs. 2.6/1000 patient-years (adjusted hazard ratio 3·67, 95% CI 1·27–10·60) [Wilson, 2018]
the incidence of ICH is up to 5%/year in multiple lobar CMBs [Van Etten, 2014]

CMBs and thrombolysis

the risk of symptomatic intracranial hemorrhage (sICH) may be increased after thrombolytic therapy in patients with cerebral microbleeds (CMBs)
CMBs < 10 ⇒ IVT seems safe (ESO 2021) (AHA/ASA 2019 IIa/B-NR)
CMBs > 10 ⇒ IVT has a higher risk of ICH; the expected benefit of treatment must outweigh the risk – consider IVT in patients with a severe stroke (AHA/ASA 2019 IIb/B-NR)
- the smaller study retrospectively found a slightly increased risk (3%) of bleeding in patients with microbleeds on GRE [Fiehler, 2007]
- increased risk is associated with CAA as a cause of microbleeds
no MRI screening is recommended to assess CMB burden before making a treatment decision regarding IVT (ESO 2021)

CMBs and anticoagulation therapy

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CMBs and antiplatelet therapy

single antiplatelet therapy is a safe and beneficial approach, even in the presence of cerebral microbleeds (RESTART trial subanalysis) [Salman, 2019]