Background and purpose: Four direct oral anticoagulants (DOACs) can be used clinically to prevent cardioembolic stroke (CE) caused by atrial fibrillation (AF). However, the yearly changes in the proportion and outcome of CE remain unknown. We thus investigated the CE trends after the introduction of DOACs. Methods: Yearly changes of CE rate in cerebral infarction (CI) were evaluated using data from 2011 to 2017. CE (738) trends for previously prescribed antithrombotic drugs were investigated over the past 7 years. Additionally, we examined the severity of patients at the time of admission and the outcome at discharge. Results: The proportion of CE in CI decreased (p<0.01). The increase in DOACs (p<0.01) and anticoagulant prescriptions (p<0.01), the decrease in antiplatelet drug prescriptions (p<0.01) were significantly different in trend analysis over the past 7 years. Inadequate DOAC medication (poor adherence or inadequate low-dose prescription) was the problem in the last 3 years. Conclusion: The proportion of CE patients in CI decreased in 7 years after DOACs were introduced. The patients with poor adherence and inadequate low-dose DOAC prescriptions require careful attention.

Purpose and Method: We investigated prothrombin time (PT) and activated partial thromboplastin (APTT) tests using two different reagents and the relationship between PT and APTT and anti-factor Xa activity (AXA) in patients treated with edoxaban. Results: Two reagents had the high correlation with PT (R =0.95, p<0.001), but not APTT (R =0.55, p =0.001). AXA provided the correlation with both PT tests. However, APTT was different between the two reagents. One reagent did not have the relationship between APTT and AXA. Conclusion: In clinical practice, PT test was suggested to be better to estimate the drug effects for edoxaban if AXA was available.

An 86-year-old woman was admitted to the hospital because of disturbed consciousness and aphasia 8^th day after carotid artery stenting for left severe internal carotid artery stenosis. Head MRI showed high signal intensity in the left temporooccipital cerebral cortex and ¹²³I-IMP SPECT showed severe hyperperfusion in the same area. She was diagnosed delayed hyperperfusion syndrome (HPS), and she was treated with strict blood pressure control. Disturbed consciousness of the patient gradually improved, although persistent right hemiplegia and mild aphasia remained in the chronic state. Delayed HPS is rare after carotid artery stenting (CAS) however, we should take account of this complication.

An 84-year-old female was admitted to our hospital with dysarthria and gait disturbance. Magnetic resonance imaging demonstrated acute ischemic stroke in bilateral cerebellar hemisphere. A few days later, paresis of both upper limbs and right lower limb emerged due to cervical cord infarction. Computed tomography angiography revealed an aberrant right subclavian artery and its calcified stenosis at the part traveling behind the esophagus. Transesophageal echocardiography showed irregular surface of the calcified plaque. We diagnosed that the etiology of brain and spinal cord infarction was the artery-to-artery embolism to the right vertebral artery and the anterior spinal artery from the aberrant right subclavian artery stenosis.

Here we describe a case of narcolepsy-like hypersomnia associated with moyamoya disease. A 16-year-old girl presented with excessive daytime sleepiness during conservative treatment for her bilateral moyamoya disease. Her symptoms were diagnosed as central disorders of hypersomnolence because her clinical presentation and electroencephalography were similar to those of narcolepsy but her examinations did not meet criteria for narcolepsy. Because her hypersomnia disappeared immediately after unilateral surgical revascularization, her symptoms were finally diagnosed as symptomatic hypersomnia. Association between cerebral ischemia of moyamoya disease and hypersomnia is unclear. However, hemodynamics characteristic to moyamoya disease including bilateral and perforator region ischemia may cause symptomatic hypersomnia.

A 75-year-old man was admitted to our hospital for the assessment of progressive weakness of four extremities. In the past 1 year, he suffered from cerebral infarction two times. No cervical and intracerebral vascular stenosis was seen, and no obvious embolic sources were found. He was diagnosed as vitamin B12 deficiency polyneuropathy due to low value of vitamin B12 and abnormal nerve conduction study (NCS). Vitamin B12 was administered but symptoms progressed. Lower limb distal muscle weakness, areflexia of four extremities, glove and stocking type sensory disorder, gynecomastia, hepatosplenomegaly, pigmentation and edema in the skin were observed. A few days after hospitalization, dysarthria and left upper limb paralysis appeared and MRI showed infarction of right middle cerebral artery (MCA) and right MCA occlusion. Serum vascular endothelial growth factor (VEGF) was markedly elevated, and NCS showed demyelination and axonal degeneration. He was eventually diagnosed as POEMS syndrome. After starting thalidomide therapy, the progression of symptoms temporarily stopped, but recurred. After changing to bortezomib therapy, the progression of symptoms stopped. In this case, initially no major artery stenosis was observed, but sudden occlusion of MCA occurred in the early stage of POEMS syndrome. We report this case regarding the relation among POEMS syndrome, Vitamin B12 deficiency, and cerebrovascular disorder with some literature review.