Abstract
Introduction Spontaneous calcified cerebral emboli (CCE) secondary to aortic valve calcification is a rare pathologic phenomenon. Currently, only five cases of spontaneous CCE secondary to bicuspid aortic valve calcification have been reported. It was previously assumed that most CCE occurred after procedures such as aortic/mitral valve replacement. Conversely, recent evidence demonstrates the overwhelming majority of CCE occurs spontaneously, most commonly from the aortic valve.
Case A 54-year-old male was found collapsed at home, last seen well 24 hours prior. Previously, he was fully independent with a medical history including epilepsy, dyslipidaemia and illicit substance use. His regular medications included carbamazepine 400mg BD, levetiracetam 500mg BD, rosuvastatin 10mg daily and suboxone 8/2mg daily. On presentation, his NIHSS was 10 for aphasia, right partial facial palsy and right hemiparesis. Examination revealed an ejection systolic murmur. CT brain demonstrated a 6mm CCE in M1, left middle cerebral artery. Diffusion-weighted MRI demonstrated left hemispheric cortical hyperintensity (‘cortical ribbon sign’) with corresponding hypointensity on apparent diffusion coefficient images. Transoesophageal echocardiogram revealed bicuspid aortic valve stenosis with a large vegetation. Subsequently, the patient underwent aortic valve replacement. Histopathological evaluation of the large ulcerated calcific leaflet lesion revealed dystrophic calcification. Investigations for infective endocarditis were consistently negative. Treatment included aspirin and the patient made minor recovery with persisting neurological deficits.
Conclusion This case demonstrates a rare stroke presentation. Upon CCE identification, undertaking a rigorous search for an embolisation source is critical to prevent recurrence. Further studies addressing CCE management are required, especially comparing thrombolysis to mechanical thrombectomy.
