[A Case of Moyamoya Disease with Postoperative Cerebral Hyperperfusion Syndrome Followed by Cerebral Infarction due to Watershed Shift].

The concept of "watershed shift"(WS)has been proposed as a cause of the ischemic complications following a superficial temporal artery-middle cerebral artery(STA-MCA)bypass operation performed for the management of moyamoya disease. Previous reports have observed that only 1.2-5.7% of the patients who underwent a bypass operation for the management of moyamoya disease developed cerebral infarction secondary to the WS phenomenon. To date, the WS phenomenon has not been objectively proven on imaging studies. We describe a 39-year-old woman who presented with right facial palsy and aphasia. Magnetic resonance imaging revealed cerebral infarction in the left frontal lobe secondary to moyamoya disease. Three days after undergoing the left STA-MCA bypass procedure, she showed deterioration in aphasia secondary to the occurrence of cerebral hyperperfusion syndrome(CHPS). Diffusion-weighted imaging(DWI)performed on postoperative day(POD)1 and 5 showed no area of high signal intensity. DWI performed on POD 8 showed an area of high signal intensity in the deep white matter of the left parietal lobe outside the range of the craniotomy. Postoperative fusion images of computed tomography angiography and DWI performed on POD 8 showed that the blood flow through the MCA from the bypass graft and that through the posterior cerebral artery crossed each other at the surface of the subcortical infarction. In the present case, the WS could be directly confirmed on imaging studies, and the cerebral infarction may have occurred secondary to WS concomitant with CHPS. Clinicians need to be aware of the WS phenomenon even after performing a direct bypass to treat adults with moyamoya disease.

Resolving Thrombus in the Left Atrial Appendage by Edoxaban Treatment after Acute Ischemic Stroke: Report of 2 Cases.

Here we report first 2 cases of patients with nonvalvular atrial fibrillation with acute cardioembolic stroke in whom thrombi in the left atrial appendage (LAA) were resolved by edoxaban administration. Case 1 reports an 86-year-old woman who suddenly showed right hemiparesis and aphasia due to occlusion of the left middle cerebral artery. She received mechanical thrombectomy and recovered neurologically. Transesophageal echocardiography (TEE) performed on day 1 demonstrated thrombus in the LAA. The thrombus was resolved on day 13 after initiation of edoxaban (30 mg once daily) instead of warfarin, which was administered before stroke onset. Case 2 reports a 49-year-old man who was admitted because of the sudden onset of left hemiparesis and aphasia. TEE demonstrated thrombus in the LAA on day 4, and edoxaban therapy (60 mg once daily) was initiated. The thrombus resolution was observed on day 16, and no embolic stroke occurred.