General Features of Cerebral Emboli

Emboli travel distally through progressively narrower arteries before lodging where the blood vessel becomes too small for further progression, especially at branching points. Chung and colleagues have shown that large emboli strongly favor the middle cerebral artery (MCA), while smaller emboli are carried proportionally to flow volume in the MCA and anterior cerebral artery (ACA) territories.

Emboli lodging in the proximal intracranial arteries result in territorial cortical infarcts, whereas smaller emboli lodging distally in terminal cortical branches result in small wedge-shaped peripheral infarcts centered at the gray-white matter interface. Uncommonly, embolic lacunar infarcts may occur in conditions causing massive showers of emboli. Overall, emboli are more likely to travel toward the leptomeningeal arteries rather than to the small perforators due to the smaller caliber and sharp angles of the perforators as they arise from parent vessels.

A multiplicity of acute small infarcts in different vascular territories suggests emboli and is best appreciated on the diffusion-weighted imaging (DWI) ( Fig. 1 ). However, multiple acute infarcts can also be seen with watershed infarcts, vasculitis, hypercoagulable states, and in presence of anatomic variants connecting the anterior and posterior circulations (eg, fetal posterior cerebral artery [PCA] and persistent trigeminal artery) or connecting both hemispheres (eg, azygos A2 supplying the ACA territories bilaterally). Of note, multiple acute infarcts exclusively affecting the posterior circulation are, in most cases, related to large-artery atherosclerosis.

Typical pattern of embolic infarcts: ( A – D ) Axial diffusion-weighted MR images demonstrate multiple acute small infarcts in different vascular territories in the supratentorial and infratentorial compartments bilaterally.

Hemorrhagic transformation is a common feature of embolic infarcts and is best seen on susceptibility blood-sensitive MR imaging sequences as petechial hemorrhage as opposed to the larger parenchymal hematomas that develop more commonly in territorial infarcts such as those involving the MCA.

Cerebral Fat Embolism

Cerebral fat embolism (CFE) is a consequence of fractures, especially those involving the lower extremity long bones and the pelvis, orthopedic procedures, as well as nontraumatic conditions including bone infarcts in sickle cell disease and acute hemorrhagic pancreatitis. It presents as a triad of pulmonary and neurologic dysfunction and petechial rash. The neurologic presentation varies from asymptomatic to subclinical to headache, confusion, and coma. The onset varies from a few hours up to 48 hours after trauma with a mean of 29 hours. Clinically apparent fat embolism occurs in 0.5% to 3.5% of isolated long bone fractures and in 5% to 10% of polytrauma patients. Subclinical fat embolism is thought to occur in all cases of lower extremity and pelvic fractures. The incidence of CFE is 0.9% to 2.2% of patients with a long bone fracture.

CFE is thought to result from the exposure of medullary fat to damaged blood vessels with fat mechanically forced into the venous system. An alternative theory suggests that stored fat is mobilized into the plasma due to increased levels of catecholamines and plasma lipase, resulting in fat droplets throughout the entire circulation. Fat emboli cross the pulmonary circulation and reach the intracranial circulation even without an intracardiac shunt being present.

Intracranially, fat emboli lodge in and mechanically occlude capillaries, producing ischemia and cytotoxic edema. However, the fat globules are deformable and tend to break up into smaller ones, which recycle through the pulmonary circulation. Hence, occlusions tend to be temporary, and changes may be reversible. Cytotoxic edema may also result from the release of toxic metabolites (oleic acid and triglyceride triolein). The release of toxic metabolites also results in opening of the blood-brain barrier (BBB), causing vasogenic edema and enhancement on contrast studies.

Imaging Findings

The “star field” appearance ( Fig. 2 ) is the most common imaging pattern found, and yet it remains nonspecific. It is seen on DWI early in the acute phase as multiple foci of high signal scattered throughout the brain predominantly in the border zones and deep gray nuclei bilaterally. These foci are thought to represent cytotoxic edema in acute cerebral infarcts. As the occlusions are temporary, the findings can be reversible, leading to better outcome compared with other cerebral embolic events. A second pattern seen on DWI, usually in the subacute phase, is the confluent bilateral symmetric periventricular and subcortical white matter cytotoxic edema and diffusion restriction. This pattern portrays a worse prognosis.

“Star field” appearance of CFE: ( A ) Lateral radiograph of the left femur demonstrates a displaced diaphyseal fracture. ( B ) Anteroposterior (AP) radiograph of the chest shows patchy bilateral airspace disease. ( C , D ) Axial diffusion-weighted MR images show multiple bilateral scattered foci of high signal, which on the apparent diffusion coefficient (ADC) maps (not shown) demonstrated restricted diffusion, predominantly in the deep border zones.

T2* sequences may reveal innumerable foci of blooming low signal in the white matter ( Fig. 3 ). This pattern is best appreciated on susceptibility-weighted images (SWI) and is to be pathognomonic of CFE. The diffuse microhemorrhages can be secondary to microscopic hemorrhagic infarcts and vessel wall rupture due to embolism or leakage of red blood cells because of abnormal BBB. Alternatively, Suh and colleagues suggested decreased blood flow secondary to embolism, leading to local increased deoxyhemoglobin levels as an underlying explanation for the extensive abnormalities seen on SWI.

Diffuse microhemorrhage in CFE: ( A – D ) Axial SWI MR images demonstrate innumerable tiny white matter blooming foci in the supratentorial and infratentorial compartments and through the splenium of the corpus callosum ( arrow in B ). Larger blooming areas in the frontal lobes are due to associated hemorrhagic contusions and diffuse axonal injury.

White-matter T2/FLAIR (fluid attenuation inversion recovery sequence) hyperintense foci with no diffusion restriction can be seen, can reflect vasogenic edema, and may show contrast enhancement. T2 abnormalities appear later than the DWI changes and are nonspecific. However, the number of white matter lesions on T2-weighted images correlates with the patient’s Glasgow coma scale score. Magnetic resonance (MR) spectroscopy shows the presence of lipid peaks within the lesions, a finding related to the nature of the emboli or associated necrosis.

General Features of Cerebral Emboli

Emboli travel distally through progressively narrower arteries before lodging where the blood vessel becomes too small for further progression, especially at branching points. Chung and colleagues have shown that large emboli strongly favor the middle cerebral artery (MCA), while smaller emboli are carried proportionally to flow volume in the MCA and anterior cerebral artery (ACA) territories.

Emboli lodging in the proximal intracranial arteries result in territorial cortical infarcts, whereas smaller emboli lodging distally in terminal cortical branches result in small wedge-shaped peripheral infarcts centered at the gray-white matter interface. Uncommonly, embolic lacunar infarcts may occur in conditions causing massive showers of emboli. Overall, emboli are more likely to travel toward the leptomeningeal arteries rather than to the small perforators due to the smaller caliber and sharp angles of the perforators as they arise from parent vessels.

A multiplicity of acute small infarcts in different vascular territories suggests emboli and is best appreciated on the diffusion-weighted imaging (DWI) ( Fig. 1 ). However, multiple acute infarcts can also be seen with watershed infarcts, vasculitis, hypercoagulable states, and in presence of anatomic variants connecting the anterior and posterior circulations (eg, fetal posterior cerebral artery [PCA] and persistent trigeminal artery) or connecting both hemispheres (eg, azygos A2 supplying the ACA territories bilaterally). Of note, multiple acute infarcts exclusively affecting the posterior circulation are, in most cases, related to large-artery atherosclerosis.

Typical pattern of embolic infarcts: ( A – D ) Axial diffusion-weighted MR images demonstrate multiple acute small infarcts in different vascular territories in the supratentorial and infratentorial compartments bilaterally.

Hemorrhagic transformation is a common feature of embolic infarcts and is best seen on susceptibility blood-sensitive MR imaging sequences as petechial hemorrhage as opposed to the larger parenchymal hematomas that develop more commonly in territorial infarcts such as those involving the MCA.

Cerebral Fat Embolism

Cerebral fat embolism (CFE) is a consequence of fractures, especially those involving the lower extremity long bones and the pelvis, orthopedic procedures, as well as nontraumatic conditions including bone infarcts in sickle cell disease and acute hemorrhagic pancreatitis. It presents as a triad of pulmonary and neurologic dysfunction and petechial rash. The neurologic presentation varies from asymptomatic to subclinical to headache, confusion, and coma. The onset varies from a few hours up to 48 hours after trauma with a mean of 29 hours. Clinically apparent fat embolism occurs in 0.5% to 3.5% of isolated long bone fractures and in 5% to 10% of polytrauma patients. Subclinical fat embolism is thought to occur in all cases of lower extremity and pelvic fractures. The incidence of CFE is 0.9% to 2.2% of patients with a long bone fracture.

CFE is thought to result from the exposure of medullary fat to damaged blood vessels with fat mechanically forced into the venous system. An alternative theory suggests that stored fat is mobilized into the plasma due to increased levels of catecholamines and plasma lipase, resulting in fat droplets throughout the entire circulation. Fat emboli cross the pulmonary circulation and reach the intracranial circulation even without an intracardiac shunt being present.

Intracranially, fat emboli lodge in and mechanically occlude capillaries, producing ischemia and cytotoxic edema. However, the fat globules are deformable and tend to break up into smaller ones, which recycle through the pulmonary circulation. Hence, occlusions tend to be temporary, and changes may be reversible. Cytotoxic edema may also result from the release of toxic metabolites (oleic acid and triglyceride triolein). The release of toxic metabolites also results in opening of the blood-brain barrier (BBB), causing vasogenic edema and enhancement on contrast studies.

Imaging Findings

The “star field” appearance ( Fig. 2 ) is the most common imaging pattern found, and yet it remains nonspecific. It is seen on DWI early in the acute phase as multiple foci of high signal scattered throughout the brain predominantly in the border zones and deep gray nuclei bilaterally. These foci are thought to represent cytotoxic edema in acute cerebral infarcts. As the occlusions are temporary, the findings can be reversible, leading to better outcome compared with other cerebral embolic events. A second pattern seen on DWI, usually in the subacute phase, is the confluent bilateral symmetric periventricular and subcortical white matter cytotoxic edema and diffusion restriction. This pattern portrays a worse prognosis.

“Star field” appearance of CFE: ( A ) Lateral radiograph of the left femur demonstrates a displaced diaphyseal fracture. ( B ) Anteroposterior (AP) radiograph of the chest shows patchy bilateral airspace disease. ( C , D ) Axial diffusion-weighted MR images show multiple bilateral scattered foci of high signal, which on the apparent diffusion coefficient (ADC) maps (not shown) demonstrated restricted diffusion, predominantly in the deep border zones.

T2* sequences may reveal innumerable foci of blooming low signal in the white matter ( Fig. 3 ). This pattern is best appreciated on susceptibility-weighted images (SWI) and is to be pathognomonic of CFE. The diffuse microhemorrhages can be secondary to microscopic hemorrhagic infarcts and vessel wall rupture due to embolism or leakage of red blood cells because of abnormal BBB. Alternatively, Suh and colleagues suggested decreased blood flow secondary to embolism, leading to local increased deoxyhemoglobin levels as an underlying explanation for the extensive abnormalities seen on SWI.

Diffuse microhemorrhage in CFE: ( A – D ) Axial SWI MR images demonstrate innumerable tiny white matter blooming foci in the supratentorial and infratentorial compartments and through the splenium of the corpus callosum ( arrow in B ). Larger blooming areas in the frontal lobes are due to associated hemorrhagic contusions and diffuse axonal injury.

White-matter T2/FLAIR (fluid attenuation inversion recovery sequence) hyperintense foci with no diffusion restriction can be seen, can reflect vasogenic edema, and may show contrast enhancement. T2 abnormalities appear later than the DWI changes and are nonspecific. However, the number of white matter lesions on T2-weighted images correlates with the patient’s Glasgow coma scale score. Magnetic resonance (MR) spectroscopy shows the presence of lipid peaks within the lesions, a finding related to the nature of the emboli or associated necrosis.