Multiple cerebral emboli from caseous necrosis of the mitral annulus calcification

Case contributed by Dr Jayanth Keshavamurthy


Dizziness, ataxia and difficulty walking.

Patient Data

Age: 65 years
Gender: Female

Note: This case has been tagged as "legacy" as it no longer meets image preparation and/or other case publication guidelines. Images should be presented as scrollable stacks. 

The CT on our left is 18 months after the right.

Can you see the tiny new fleck of calcium on the left side of brain?

There is another fleck of calcium in right frontal lobe. Which was seen 18 months before also.

Incidentally seen is mitral valve annulus calcification. Tortuous descending thoracic aorta. 

A mass described below: possible etiologies include extension of ectopic calcification from significant mitral annular calcification (MAC), other possibilities include calcified myxoma or other tumors. The mass appears to have a mobile surface component noted.
The left ventricle is normal size with moderate concentric left ventricular hypertrophy; the basal septum appears to have moderate-severe hypertrophy.
Normal global LV function with ejection fraction 60%.
A moderately sized 7 x 6 mm calcified, irregular mass with small mobile surface component is seen in the left atrium. It appears attached to either atrial aspect of the calcified mitral annulus or the adjacent atrial septum.
No thrombus is detected in the left atrial appendage.
The mitral leaflets appear mildly thickened with trace mitral regurgitation.
There moderate mitral annular calcification.
There is trace to mild tricuspid regurgitation.
Injection of agitated saline contrast documented no interatrial or intrapulmonary shunt.

A low signal is seen in the mitral annulus suggestive of mitral annular calcification. There is a small mass 5 x7 mm arising from the posterior part of the mitral annular calcification on the atrial side and has mild mobility. These findings are correlated with transesophageal echocardiogram findings significant mitral annular calcification with a mobile component was seen on the transesophageal echocardiogram. MRI is not best for evaluation of calcification.
However, these findings appear to be consistent with significant mitral annular calcification with a mobile component. There is no evidence of left atrial mass or myxoma. The mitral leaflets appear to be normal.

3D heart and SSFP sequences obtained.

Since the most recent examination, there is now multiple supra and infratentorial punctate areas of diffusion restriction consistent with lacunar infarcts. The cerebellar hemispheres are predominantly involved right more than left with a focal lesion that
appears more chronic in the left middle cerebellar peduncle. Small focal lesions are seen within the left occipital lobe as well as within the left basal ganglia head of the caudate nucleus and very tiny one in the left frontal as well as right frontal orbital frontal gyrus, right basal ganglia and right temporal lobe in the region of the amygdala and anterior temporal pole and right frontal opercular

An old right cerebellar infarct is again identified with gliotic changes of the subjacent white matter appears unchanged.

There is again very extensive focal and confluent hyperintensity within the corona radiata with extension into the centrum semiovale consistent with microvascular ischemic changes with involvement now of the splenium of the corpus callosum but without diffusion restriction.

Severe progressive microvascular ischemic changes as seen in patient with chronic hypertension and/or diabetes with extensive infra and supratentorial punctate areas of diffusion restriction most likely representing embolic phenomena. Rule out a central cause.

Case Discussion

The MRI brain showed embolic strokes. So a search for central or cardiac source was performed. Transthoracic echocardiography, transesophageal echocardiography, then finally a cardiac MRI to confirm the source of emboli.

Based on multiple imaging modalities the source of central embolic stroke is caseous necrosis of mitral valve annular calcifications causing multiple embolic strokes.

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