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Patient 1 was a 55-year-old male with cerebral infarction due to obstruction of the left middle cerebral artery during treatment for bacteremia, along with a verruca of infectious endocarditis harvested from endovascular thrombectomy. Patient 2 was a 59-year-old female suffering from cerebral infarction at the terminal branch during intrahepatic cholangiocarcinoma chemotherapy who thereafter developed cerebral infarction again due to obstruction of the left middle cerebral artery, along with a verruca of nonbacterial thrombotic endocarditis (NBTE) harvested from endovascular thrombectomy. In tumor-bearing patients, while NBTE may be more closely related to the development of cerebral infarctions than previously assumed, we also need pay attention to the onset of infectious endocarditis. We need further studies on the effectiveness and safety of thrombolysis therapy and endovascular thrombectomy for cerebral infarctions due to endocarditis in both patients. The harvested emboli may provide clues to the differentiation thereof.

An 82-year-old man with advanced lung cancer who had declined aggressive therapy was transferred to our hospital due to sudden-onset consciousness disturbance, global aphasia, and right hemiplegia. An electrocardiogram showed atrial fibrillation, and brain MRI and MRA revealed acute ischemic lesions of the left hemisphere and occlusion of the left internal carotid artery (ICA), respectively. We diagnosed acute ischemic stroke due to left ICA occlusion and performed endovascular thrombectomy, which resulted in complete recanalization of the left ICA after retrieval of the culprit embolus. Pathological examination of the retrieved thrombus revealed the presence of tumor tissue, as well as fibrin or red blood cells. Treatment was continued after admission, but the patient died of respiratory failure on day 40 of hospitalization. Autopsy revealed invasion of the tumor in the pulmonary vein, but not in the wall of the left atrium where thrombi were present. However, pathological examination of these thrombi in the left atrium revealed tumor tissue, along with fibrin or red blood cells. These findings suggest that the wall of the left atrium, in which lung cancer had not invaded, may be an incubator of a mixed embolus containing tumor tissue and thrombi in a case of cerebral embolism associated with both lung cancer and atrial fibrillation.

A 83 years old woman was slipped and injured with right femoral neck fracture. After three days from the fracture, she underwent an artificial head bone replacement operation. Immediately after surgery, she complained of chest discomfort, nausea and dyspnea. A few hours later, she became comatose. Brain CT showed no abnormality and clinical diagnosis of heart failure was made without pulmonary embolism on enhanced chest CT. Magnetic resonance imaging (MRI) of the brain next day showed multiple small patchy hyperintense lesion in bilateral hemispheres on diffusion-weighted images (DWI), producing a "star field pattern''. Based on Criteria of Gurd, this patient had one major criterion and four minor criteria. And according to the Criteria of Schonfeld, this patient had 5 points, consistent with clinical diagnosis of fat embolism. Because of these criteria, she was diagnosed as cerebral fat embolism syndrome. We started supported care and edaravon. Two weeks after surgery, her condition recovered and remaind to stuporous state even six month after surgery. We experienced a typical case of cerebral fat embolism, after bone surgery with diagnostic findings on MRI-DWI. Diagnosis of cerebral fat embolism syndrome requires a history of long bone fracture and/or replacing surgery with typical finding on MRI images, such as "star field pattern''.

We report a case of spectacular shrinking deficit caused by paradoxical cerebral embolism through pulmonary arteriovenous fistula (AVF). A 79-year-old female suddenly developed right hemiplegia, paresthesia, and speech disturbance symptoms that were improved within 20 min, indicating a diagnosis of spectacular shrinking deficit. Brain magnetic resonance imaging revealed acute cerebral infarcts in the left parietal cortex of the left middle cerebral arterial territory. A contrast-enhanced chest computed tomography scan revealed a pulmonary AVF in the middle lobe of the right lung. The patient had deep venous thrombosis in her left lower leg. She had no clinical signs of telangiectasia, did not exhibit recurrent epistaxis, and had no family history of hereditary hemorrhagic telangiectasia (HHT). Therefore, she was diagnosed with paradoxical cerebral embolism secondary to the pulmonary AVF without HHT. Pulmonary AVF should be considered in patients with cerebral embolism, even when presenting with spectacular shrinking deficit.

A 45-year-old woman, who had had rheumatoid arthritis for 12 years, had three attacks of cerebral embolism over two months and died after the final attack. Intensive clinical laboratory investigations did not disclose any specific origins of emboli, but an autopsy revealed a nodule at the base of the aortic valve which was pathologically proved to be a rheumatoid nodule. The thrombi were present from the distal part of left internal carotid artery up to the proximal part of the left middle cerebral artery. They were rich in fiber, but poorly organized endothelial cell, raising the possibility that they originated from other parts and have recently reached there. On the top of the rheumatoid nodule, a thrombus was present. It was easily ablated and a small amount of fibrin stuck the nodule. Based on these results, we concluded that cerebral emboli were originally generated at the top of a rheumatoid nodule in the heart. In patients with RA, rheumatoid nodules are rarely seen in the heart. If present, they usually cause cardiac failure or atrioventricular block, and seldom result in cerebral infarction. This is the first case in which an autopsy proved rheumatoid nodule in the heart which had caused multiple cerebral emboli. We should consider the possibility of rheumatoid nodules in the heart as an origin of cerebral emboli in patients with rheumatoid arthritis.