Cerebral microhemorrhages, or cerebral microbleeds, are small focal intracerebral hemorrhages, often only visible on susceptibility-sensitive MRI sequences.

Pathology

Common etiologies

• cardiac bypass for surgery ^15,31

• cavernous malformations ^1,8

  • especially Zabramski classification type IV malformations

  • causes include multiple (familial) cavernous malformation syndrome and post-cerebral radiotherapy

• cerebral amyloid angiopathy ^1,8

  • typically involves the grey-white matter junction; usually spares the basal ganglia

• chronic hypertensive encephalopathy ^1,8

  • typically involve the basal ganglia, thalami, brainstem, cerebellum and corona radiata

• diffuse axonal injury (DAI) and other trauma ^1,8

  • typically involves the grey-white matter junction, splenium of the corpus callosum, and dorsolateral brainstem 

Less common etiologies

• acute hemorrhagic leukoencephalitis (AHLE) ⁸

• acute hepatic encephalopathy ⁴¹

• amyloid related imaging abnormalities (ARIA-H) ¹⁶

• cathepsin A-related arteriopathy with strokes and leukoencephalopathy (CARASAL) ^29,30

• cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) ^1,8

  • microhemorrhages have been reported to occur in 25-70% of cases without a characteristic distribution

• cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) ^20,21

• cerebral hyperperfusion syndrome ¹¹

• cerebral vasculitis (primary or secondary) ^1,8

  • microhemorrhages usually located at the corticomedullary junction

• COL4A1 brain small-vessel disease ^5,8

  • microhemorrhages have been reported in up to 53% of cases, characteristically in the centrum semiovale, deep grey matter, or brainstem ^5,8

• Fabry disease ^35,36

• hemorrhagic micrometastases ^1,8

  • especially melanoma or renal cell carcinoma

• heterozygous HTRA1-related cerebral small vessel disease ⁴⁰

• hypoxia and/or being critically ill (e.g. acute respiratory distress syndrome, high-altitude cerebral edema, COVID-19) ^8-10,39

• immune effector cell-associated neurotoxicity syndrome (ICANS) ³²

• intracranial embolism

  • fat embolism

    • usually from fractures ^4,8,14

  • gas embolism ^6,7

    • many causes including: intravenous catheter placement, decompression sickness, extracorporeal membrane oxygenation, hydrogen peroxide ingestion, etc.

  • septic embolism

    • usually from infective endocarditis ^3,8

• intracranial infection (e.g. cerebral malaria, mycotic aneurysm, dengue encephalitis, HSV encephalitis) ^8,37,38

• intravascular lymphoma ^8,17

• linear scleroderma ²⁵

• moyamoya disease and moyamoya syndrome ^22,23

• neurosarcoidosis ^12,13

• pontine autosomal dominant microangiopathy with leukoencephalopathy (PADMAL) ^27,28

• posterior reversible encephalopathy syndrome (PRES) ⁸

• progressive facial hemiatrophy (PFHA) ^1,8

• radiation-induced cerebral vasculopathy ^1,8

• retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) ^33,34

• Sneddon syndrome ^18,19

• thrombotic microangiopathies (e.g. hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP)) ⁸

Radiographic features

MRI

Cerebral microhemorrhages are only seen on MRI and are only seen on susceptibility weighted T2* sequences such as gradient-recalled echo (GRE) and susceptibility weighted imaging (SWI) ²⁴.

They appear as conspicuous 2-10 mm punctate regions of signal drop out with blooming artifact ²⁴. This blooming grossly overestimates the size of the lesions, thus they are usually inapparent on other MRI sequences and CT ²⁴.

Differential diagnosis

• artificial heart valve metallic emboli (very rare) ⁸

• flow voids of veins ⁸

• intracranial calcification ⁸

• punctate regions of signal loss in chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) ²⁶

• pneumocephalus (very rare without preceding surgery) ²