[A case of cerebral embolism with Coronavirus disease 2019].

A 63-year-old man, who had persistent fever for a month, was admitted to the hospital with sudden left arm palsy with a National Institutes of Health Stroke Scale score of 3. Consequently, brain MRI showed hyperintensity of the bilateral occipital, right parietal, and right frontal lobes on diffusion-weighted imaging. Moreover, FLAIR presented hyperintensity of the left occipital lobe. Magnetic resonance angiography detected the deficit of the blood-flow signal of the horizontal segment of the middle cerebral artery. He was diagnosed with acute ischemic stroke. In addition, chest CT showed ground-glass opacities, and test to detect SARS-CoV-2 was positive. Cerebral embolism was suspected. However, the source was unknown. His ischemic stroke was possibly associated with coagulation abnormality caused by coronavirus disease 2019.

Clinically overt and silent cerebral embolism in the course of infective endocarditis.

The data on cerebral embolism prevalence in the course of infective endocarditis (IE) are most probably underestimated. Part of the cerebral embolism episodes are clinically silent. The objective of this study was to assess the prevalence of clinically silent cerebral embolism in the course of IE and to correlate hematological, inflammatory, and echocardiography parameters with the presence of clinically overt or silent cerebral embolisms. For this purpose, we examined 65 patients with IE by blood test, cultures, echocardiography, and MRI/CT imaging. Clinically overt cerebral embolism was found in 13 patients; 52 patients had no clinically overt cerebral embolism. MRI/CT examinations revealed that among patients with no clinically overt cerebral embolism, 24 had clinically silent cerebral embolism. Thus, 37 patients in all were diagnosed with a cerebral embolism episode (overt + clinically silent). Clinically silent cerebral embolism was diagnosed in 36.9% of all patients, being as high as 64.8% of cerebral embolism cases. Silent or overt embolism development did not depend on the localization of the inflammatory process in either native or artificial valves. The type of cerebral embolism was not found to be influenced by leukocytosis, platelet count, ESR, or hsCRP levels. Neither was the type of embolism found to be influenced by the etiologic factor. Nine patients died. In three patients, the cause of death was hemorrhage from a cerebral apoplectic focus. These results suggest that clinically silent central nervous system embolism is a common complication of infective endocarditis and each patient should undergo a neuroimaging examination.