CMBs are seen as punctate hypointense lesions without surrounding oedema, best detected on susceptibility-weighted imaging (SWI).

* Chronic small vessel disease

Hypertensive microangiopathy

Hypertensive microangiopathy is the most common cause of CMBs and reflects chronic damage to small penetrating arteries related to long-standing arterial hypertension. It is frequently associated with other manifestations of cerebral small-vessel disease and has important prognostic implications. [1]

Imaging features:

• Punctate hypointense foci on SWI, without surrounding oedema
• Predominantly deep distribution
  • Basal ganglia
  • Thalami
  • Brainstem
  • Cerebellum
• Often associated with:
  • White matter hyperintensities
  • Lacunar infarcts
  • Generalized brain atrophy

Fig 1: SWI image showing left temporo‑occipital hypointense foci consistent with cerebral amyloid angiopathy. 1 shows an acute haemorrhage centred in the left basal ganglia and an acute lacunar infarct in the right thalamus. 2 shows an acute right frontal lobar haemorrhage, consistent with cerebral amyloid angiopathy.

Cerebral amyloid angiopathy (CAA)

Cerebral amyloid angiopathy is caused by amyloid-β deposition within cortical and leptomeningeal vessels and is a major cause of lobar haemorrhage and CMBs in elderly patients. Its recognition is clinically relevant due to the increased risk of recurrent haemorrhage and implications for antithrombotic therapy. [1]

On imaging:

• Punctate hypointense foci on SWI
• Lobar and cortico-subcortical distribution
• Relative sparing of:
  • Basal ganglia
  • Thalami
  • Brainstem
• Frequently associated findings:
  • Cortical superficial siderosis
  • Lobar intracerebral haemorrhage

Inflammatory cerebral amyloid angiopathy (iCAA) and amyloid-related imaging abnormalities (ARIA) represent distinct entities within the spectrum of CAA, both related to amyloid-β deposition in cortical and leptomeningeal vessels but with different pathogenic mechanisms and clinical implications.

> Inflammatory CAA

iCAA is an immune-mediated variant of CAA characterised by an inflammatory response against amyloid-β deposited in cortical and leptomeningeal vessels. It typically presents with subacute neurological deterioration, including cognitive decline, seizures or focal deficits, and is clinically relevant because it may respond to immunosuppressive treatment. [2]

Fig 2: A 72-year-old man with a ventriculoperitoneal shunt for chronic adult hydrocephalus underwent follow-up imaging. CT demonstrated bioccipital hypodensities, predominantly on the left (not shown). MRI revealed bioccipital vasogenic oedema (asterisks), more pronounced on the left, with mild mass effect, as well as multiple left occipital cerebral microbleeds. Findings were consistent with iCAA, and the patient had a favourable clinical outcome.

Imaging features:

• Lobar CMBs on SWI
• Asymmetric vasogenic oedema on T2/FLAIR
• Cortical and cortico-subcortical involvement, often extending beyond a single vascular territory
• Variable contrast enhancement
• Possible associated cortical superficial siderosis

> Amyloid-related imaging abnormalities

ARIA are treatment-related imaging findings observed in patients receiving anti-amyloid monoclonal antibodies for Alzheimer’s disease. ARIA is subdivided into ARIA-E (oedema) and ARIA-H (haemorrhagic changes), the latter including CMBs and superficial siderosis. [2]

Fig 3: T2 and SWI images of patients in amyloid-lowering drug trials. The two images on the left show a 75-year-old patient with right temporal (asterisk) and bioccipital vasogenic oedema, with small right temporal microbleeds on SWI (arrowheads), compatible with ARIA‑H. The two images on the right show a 73-year-old patient with right parieto‑occipital juxtacortical oedema (arrow) without microbleeds (circle) on SWI, compatible with ARIA‑E.

• ARIA-H
  • New or increased lobar CMBs on SWI
  • Cortical superficial siderosis
  • Predominantly cortical or cortico-subcortical distribution
• ARIA-E
  • Vasogenic oedema on T2/FLAIR
  • Cortical and subcortical involvement, often asymmetric
  • Possible mild mass effect

* Ischaemic and thromboembolic causes

Haemorrhagic transformation of ischemic stroke

Haemorrhagic transformation occurs when reperfusion follows ischaemic injury, leading to microvascular leakage and petechial haemorrhages. [3]

Fig 4: An 84-year-old man presented with a right occipital stroke. Follow-up CT showed small hyperdense foci in the infarcted region, compatible with petechial haemorrhages (arrowhead). MRI revealed extensive confluent petechial haemorrhages (circle) without mass effect (HI2), along with white matter hyperintensity (asterisks). Multiple dilated perivascular spaces were also observed in the basal ganglia (arrow), representing “état criblé,” a finding typically associated with hypertensive encephalopathy.

Embolic causes

CMBs may result from various embolic events, including endovascular procedures, fat, septic, or gaseous embolism. Patient history, including recent interventions, trauma, or infections, is essential to identify the underlying source and guide management. [1]

Fig 5: A 75-year-old patient, following hip arthroplasty, presented with reduced consciousness and acute dyspnoea. SWI shows multiple hypointense foci compatible with fat microemboli, diffusely distributed throughout the brain parenchyma. DWI demonstrates several microinfarcts (arrows).

Fig 6: A 54-year-old patient with endocarditis developed bradypsychia and headache during hospitalisation. MRI demonstrated a right parietal lesion with vasogenic oedema and peripheral diffusion restriction (arrow). Hyperintense lesions on FLAIR were also identified in both thalami (asterisk), showing avid contrast enhancement (circle). Multiple associated cerebral microbleeds were observed on SWI (arrowheads). These findings are consistent with embolic ischaemic lesions with associated CMBs.

Non-ischaemic cerebral enhancing (NICE) lesions

NICE lesions are rare post‑endovascular complications caused by microembolisation of catheter materials, leading to focal endothelial injury, microvascular inflammation, and petechial haemorrhages. [4]

Fig 7: A 65-year-old woman presenting for follow-up 7 months after embolization of a middle cerebral artery aneurysm. T1 post-contrast shows right frontoparietal enhancing foci (arrows). DWI demonstrates juxtacortical diffusion-restricted foci (arrowhead). T2 reveals multiple juxtacortical vasogenic oedema foci (asterisk). SWI shows cortical hypointense foci in the frontoparietal region.

Imaging features:

• Punctate enhancing foci on post-contrast MRI, often within the treated vascular territory
• T1 hypointense, T2 hyperintense, with microhaemorrhages on SWI
• Minimal or mild vasogenic oedema; diffusion usually not restricted

* Vascular

Cavenous malformations

> Sporadic cavernomas

Sporadic cavernomas are low-flow vascular malformations composed of dilated capillary channels, generally solitary and asymptomatic. [1]

Fig 8: The CT image shows a small hyperdense focus (arrowhead) without associated vasogenic oedema, compatible with a cavernoma. On MRI, multiple hypointense foci are seen, consistent with cavernomas and microbleeds.

>Familial multiple cavernomas

Familial multiple cavernomas are a genetic vascular malformation disorder, often inherited in an autosomal dominant pattern. Patients may present with seizures, focal neurological deficits, or be asymptomatic, with microbleeds representing chronic small haemorrhages from cavernous malformations. [1]

Imaging features:

• Multiple punctate or “popcorn-like” hypointense foci on SWI, often with mixed signal on T1/T2 reflecting blood products of different ages
• Predominantly supratentorial, but brainstem and cerebellar involvement is common
• Typically no surrounding oedema unless recent haemorrhage has occurred

Mineralizing microangiopathy

Mineralizing microangiopathy is an acquired, post-radiotherapy small-vessel complication. It typically presents with punctate microbleeds on SWI in previously irradiated regions, sometimes associated with subtle white matter changes. [1]

Fig 9: A patient treated with radiotherapy in the nasosinusal region in 2001 shows multiple hypointense foci on SWI in the cerebellar hemispheres (arrowhead) and temporal lobes (arrow), located around the previously irradiated area. These foci are consistent with small microbleeds and cavernomas. There are also calcifications in the pons (not shown).

Dural arteriovenous fistulas (DAFVs)

DAFVs are acquired connections between dural arteries and venous sinuses or cortical veins. They may present with headache, tinnitus, or focal deficits. Cortical or subcortical microbleeds on SWI indicate prior haemorrhage, often associated with cortical venous reflux. [5]

Fig 10: 3D TOF shows arterialisation of cortical veins (arrow), and 4D MRV demonstrates rapid contrast passage through the transverse sinus (arrowheads). SWI shows microbleeds in an area with tortuous vessels.

Cerebral vasculitis

Cerebral vasculitis involves inflammation of small and medium sized vessels, causing multifocal microbleeds, infarcts, and white matter changes. Early recognition is critical for immunosuppressive therapy. [6]

On imaging:

• Multiple punctate hypointense foci on SWI, often cortical and subcortical
• May coexist with small infarcts or leukoencephalopathy
• Distribution is multifocal and asymmetric

* Traumatic

Diffuse axonal injury (DAI)

Diffuse axonal injury is a severe form of traumatic brain injury caused by rotational and acceleration–deceleration forces, leading to widespread axonal disruption. The corpus callosum is one of the most commonly affected structures, particularly the splenium, due to its central location and dense white matter composition. Callosal involvement is associated with severe trauma and poor neurological outcome. [1]

Fig 11: Axial SWI images show multiple hypointense foci with diffuse distribution, predominantly at the cortico‑subcortical junction, in a 37-year-old patient who sustained severe trauma in a car accident. Coronal FLAIR reconstruction demonstrates white matter hyperintensities extending towards the corpus callosum, suggestive of non‑haemorrhagic lesions.

Imaging features:

• Punctate or linear lesions within the corpus callosum, classically involving the splenium
• Restricted diffusion on DWI in the acute phase, reflecting axonal injury
• Variable haemorrhagic components on SWI

Diffuse vascular injury (DVI)

DVI is a traumatic microvascular pathology that results from high-energy acceleration-deceleration forces applied to the brain. Although historically grouped with DAI, recent evidence suggests that axonal and vascular lesions have distinct pathological responses to tissue deformation and often occur in differing regional patterns rather than complete overlap. [7]

DVI reflects traumatic damage to blood vessels and capillaries with consequent petechial haemorrhages and microvascular disruption, whereas DAI represents mechanical shearing of axons. The two often coexist in severe blunt force trauma, but they each contribute independently to injury burden and clinical outcome. 

On imaging:

• SWI: numerous punctate haemorrhages throughout the white matter, not confined to classic DAI locations
• Minimal diffusion restriction
• CT is often normal

> Differentiating DVI from DAI:

• DAI is characterised by microhemorrhages and non-haemorrhagic lesions along typical white matter tracts such as the splenium of the corpus callosum, brainstem and parasagittal regions, with prominent acute restricted diffusion. 
• DVI shows more widespread punctate haemorrhagic lesions that are less associated with diffusion restriction and may occur in regions not typical for axonal shearing.

* Tumoral

Metastases

Haemorrhagic-prone metastases, such as those from renal cell carcinoma or melanoma, can cause CMBs. These are typically cortical or cortico-subcortical in distribution and may coexist with larger metastatic lesions or post-radiosurgery changes. Vasogenic oedema is usually minimal. [1]

Fig 12: A 49-year-old man with melanoma of unknown primary and known systemic metastases presented with recurrent headaches. MRI revealed multiple punctate T1-hyperintense lesions with peripheral FLAIR hyperintensity and associated vasogenic oedema (arrow). Some lesions appeared hypointense on SWI, while others were associated with small white matter CMBs (arrowheads).

Primary CNS lymphoma (intravascular large B-cell type)

Intravascular large B-cell lymphoma is a rare subtype of primary CNS lymphoma characterised by malignant lymphocytes within small vessels, leading to microvascular obstruction and microbleeds. [8]

Fig 13: A 73-year-old man with B symptoms was found unconscious at home. CT demonstrated several hypodense areas in the white matter (not shown), with subtle peripheral enhancement. MRI revealed multiple hyperintense white matter lesions, predominantly in the left frontal region (asterisk) and bioccipital regions, showing peripheral enhancement (circle). These lesions contained internal foci of diffusion restriction (arrow) and were associated with multiple CMBs (arrowheads). The patient experienced very rapid clinical deterioration, prompting consideration of acute haemorrhagic leukoencephalitis and primary central nervous system lymphoma in the differential diagnosis. The patient subsequently died, and autopsy revealed intravascular large B-cell lymphoma.

* Infectious

Herpes simplex virus encephalitis

HSV encephalitis is a severe viral infection, classically affecting the medial temporal lobes and orbitofrontal regions. Clinical presentation includes fever, headache, seizures, and altered mental status. [9]

Fig 14: A 63-year-old woman presented with confusion and disorientation. She was found to have a urinary tract infection and started on treatment; however, her condition failed to improve and she began behaving unusually. CT revealed a left temporal hypodensity with an associated haemorrhagic component (arrowhead). Subsequent MRI demonstrated cytotoxic oedema (asterisk) with diffusion restriction (arrow), as well as CMBs on SWI. A diagnosis of herpes encephalitis was suspected and later confirmed by cerebrospinal fluid analysis.

Pneumococcal meningoencephalitis

Severe bacterial infection can lead to microvascular damage and CMBs. Patients often present with fever, neck stiffness, altered consciousness and signs of sepsis. [10]

Fig 15: A 72-year-old woman admitted to the neurology department with pneumococcal meningitis. MRI demonstrated a left occipital wedge-shaped area of diffusion restriction with FLAIR hyperintensity, vasogenic oedema, and leptomeningeal and gyral enhancement, consistent with an area of cerebritis (arrowheads). Punctate foci of diffusion restriction were also identified in both corona radiata (arrow), compatible with small infarcts secondary to meningitis. Bilateral white matter hyperintensity (asterisk) and multiple hypointense foci on SWI, consistent with CMBs (circle), were also observed.

* Systemic causes

Critical illness-associated microvascular damage

Severe critical illness, including sepsis, respiratory failure, or multi-organ dysfunction, can result in widespread microvascular injury in the brain. The underlying mechanisms include endothelial dysfunction, hypoxia, systemic inflammation, and coagulopathy, which together lead to small vessel disruption and petechial haemorrhages. Clinically, patients may present with altered mental status, delirium, or diffuse neurological deficits, although findings can be subtle. [1]

Fig 16: CMBs in critically ill patients represent a distinct entity that does not always show abnormalities on other sequences (for example, T2 in our case), presenting as multiple microbleeds most frequently located in the corpus callosum and juxtacortical regions. The splenium is the most commonly affected structure (circle).

Radiological findings:

• Numerous punctate hypointense foci on SWI, often diffuse and involving both cortical and deep regions
• May be associated with leukoencephalopathy, small infarcts or chronic microvascular changes
• Surrounding oedema is typically minimal or absent
• CT is often normal or shows only nonspecific hypodensities

Coagulopathies in chronic liver disease

Patients with chronic liver disease may develop coagulopathies leading to CMBs. These result from impaired synthesis of clotting factors, thrombocytopenia, and fragile microvasculature. [11]

Fig 17: A 60-year-old man with alcohol-related liver cirrhosis presented to the emergency department with confusion. Clinical management of his liver disease did not improve his level of consciousness, prompting CT evaluation. CT demonstrated small juxtacortical intraparenchymal haemorrhages with mild vasogenic oedema (arrowheads). MRI revealed multiple cerebral microbleeds with diffuse distribution throughout the brain parenchyma. These findings were consistent with microbleeds secondary to the patient’s coagulopathy.

* Genetic diseases

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)

CADASIL is an inherited small-vessel disease caused by NOTCH3 mutations, leading to recurrent microvascular injury, lacunar infarcts, and cognitive decline. Patients often present with recurrent lacunar strokes, migraine with aura, mood disturbances or early cognitive decline. [1]

Fig 18: 1 and 2 show small microbleeds in both thalami (arrows). 3 and 4 are FLAIR images in axial and coronal planes, respectively, demonstrating vasogenic oedema extending between the internal and external capsules (asterisks). 5 is a T2 image showing bitemporal vasogenic oedema, a classic finding in CADASIL.

Imaging features:

• Deep and periventricular punctate hypointense foci on SWI
• Frequently associated with white matter hyperintensities and lacunar infarcts
• Predominantly affects basal ganglia, thalami, brainstem and temporal lobes

Deficiency of Adenosine Deaminase 2 (DADA2)

DADA2 is a rare autosomal recessive vasculopathy caused by ADA2 mutations. It typically affects children or young adults, presenting with recurrent strokes, systemic inflammation, and sometimes livedo reticularis/racemosa. Imaging may show multiple CMBs, small lacunar infarcts, and features of small / medium vessel vasculitis. [12]

Fig 19: A 56-year-old woman with a complex medical history, including Crohn’s disease, sensorineural hearing loss of probable autoimmune origin, autoimmune-related medullary hypoplasia, transient ischaemic attacks, aortitis, and acute myopericarditis. MRI demonstrated multiple cerebral microbleeds involving the cortex of both cerebellar hemispheres, cerebellar peduncles, the splenium of the corpus callosum, and grey and white matter of the frontal, parietal, and occipital lobes. Several white matter ischaemic lesions were also present.