Neuro_MR_Brain: 66 M, history of CABG, aortic valve endocarditis.


CLINICAL HISTORY: 66 years of age, Male, history of CABG, aortic valve replacement, recent diagnosis of aortic valve endocarditis, concern for mycotic aneurysm/septic emboli. 


Parenchyma: Mild global volume loss with commensurate enlargement of the sulci and ventricles. Multiple enhancing lesions scattered throughout the cerebral hemispheres: cluster within the left occipital lobe, cluster within the right occipital lobe, multiple foci within the left globus pallidus and insula. Some of these foci are associated with restricted diffusion, however there are additional small restricting foci do not have associated enhancement, for example the right insula. Left insular and opercular lesion is tubular morphology, adjacent M2 branches in the sylvian fissure without direct communication demonstrated. Irregular rim-enhancing lesion measures 9 mm in the left parasagittal occipital lobe with focal susceptibility artifact centrally, which may represent internal hemorrhage or mineralization.

Other scattered foci of periventricular and subcortical white matter FLAIR signal abnormality are nonspecific and may represent chronic microvascular ischemic changes. Few scattered foci of of susceptibility artifact may represent microhemorrhage from infection, amyloid, or hypertension, for example small focus within the right thalamus (series 11 image 20). Possible developmental venous anomaly within the left cerebral hemisphere.

Ventricles and extra-axial spaces: No midline shift. Mild prominence of the temporal horn of the right lateral ventricle, with appropriate configuration of the remaining ventricles. No extra-axial hemorrhage. 

Orbits: Normal. 

Visualized paranasal sinuses: Clear. 

Mastoid air cells: Right mastoid effusion. 

Bones: Normal. 


Anterior circulation: No flow-limiting stenosis or aneurysm. 

Posterior circulation: Focal high-grade stenosis in the left mid V4 segment of the vertebral artery, corresponding to prominent atherosclerotic calcification on prior PET/CT. 

Dural venous sinuses: Patent. 

Additional comment: None. 

Perfusion: Decreased signal within the right temporal lobe, and focal increased signal in region of the right pterygopalatine fossa without anatomic correlate, likely artifactual. 


1.  Findings most compatible with multifocal septic emboli evolving bilateral cerebral hemispheres given history of infectious endocarditis, with multiple scattered enhancing nodules, dominant rim-enhancing lesion measuring 9 mm with central susceptibility in the left occipital lobe, and few foci of restricted diffusion without definite enhancement. Tubular focus of enhancement and restricted diffusion in the left insula and frontal operculum raises possibility of vascular structure given morphology, however larger than adjacent vasculature and no clear connection to adjacent vessels. No definite mycotic aneurysm.  

2.  Additional associated scattered foci of susceptibility artifact without enhancement or restricted diffusion are nonspecific, may represent hypertensive angiopathy, amyloid angiopathy, or microhemorrhage associated with small emboli. Absence of comparisons makes determining chronicity difficult. 

(Septic emboli)

Accession: CL27388659

Study description: MR BRAIN W/WO