RÉSUMÉ
Introduction: Brachiocephalic artery stenosis rarely causes right hemispheric infarction with associated left hemiparesis. To date, there have been no reported cases of stroke associated with brachiocephalic artery stenosis that were successfully treated with recombinant tissue-type plasminogen activator (rt-PA), alteplase.Case Report: An 80-year-old woman presented with left hemiparesis. Brain computed tomography showed no hemorrhage, and computed tomography angiography demonstrated brachiocephalic artery stenosis. Alteplase was administered based on a diagnosis of ischemic stroke. Brain magnetic resonance imaging showed multiple acute infarctions. Thereafter, the blood pressure of the right arm was found to be lower than that of the left arm. The patient’s neurological deficits gradually improved; she was eventually able to walk again and was thus discharged home.Conclusion: While the combination of left hemiparesis and a decrease in blood pressure in the right arm are well known in patients with stroke associated with Stanford type A aortic dissections, it may also occur in patients with stroke due to brachiocephalic artery stenosis. Unlike stroke associated with Stanford type A aortic dissections, stroke due to brachiocephalic artery stenosis may be treated with alteplase.
RÉSUMÉ
The Trail Making Test (TMT) is a widely used measure of attention impairment. The time needed to complete the TMT (TMT score) is longer with greater impairment of attention in patients with brain diseases. TMT score becomes large in a proportion of patients with minor ischemic stroke. The Japanese version of the TMT- (TMT-J) was published in 2019. The purpose of this study was to clarify serial changes in TMT-J scores in patients with minor ischemic stroke. We retrospectively reviewed the TMT-J scores in those patients who completed the test both 8-14 days and 29-35 days after stroke onset. On initial evaluation, 1 of 21 patients could not complete TMT-J Part A. TMT-J Part A scores had a mean of 67 s and were abnormally large in 45% of the 20 patients who completed this part. Two of these 20 patients could not complete TMT-J Part B. TMT-J Part B scores had a mean of 135 s and were abnormally large in 61% of the 18 patients who completed this part. On second evaluation, scores on Part A and Part B improved in 76% and 73% of patients, respectively. This study demonstrated that abnormal TMT-J scores 8-14 days after onset of minor ischemic stroke improved over time in most patients.
RÉSUMÉ
Based on previous reports, we propose a practical guide to choose dabigatran 150 mg twice daily or apixaban 5 mg twice daily for patients with atrial fibrillation. We recommend the use of dabigatran 150 mg twice daily for patients with atrial fibrillation who have a high risk of embolism (e.g., ischemic stroke on other oral anticoagulants, presence of left atrial appendage thrombus) and a low risk of bleeding. However, the prevalence of such patients with atrial fibrillation is considered low because patients with atrial fibrillation with a high risk of embolism usually have a high risk of bleeding. In most other patients with atrial fibrillation, the use of apixaban 5 mg twice daily should be considered.
RÉSUMÉ
We summarized recent findings regarding the clinical features and treatment of patients with essential thrombocythemia (ET), in particular, those with calreticulin (CALR ) mutations. CALR mutations are frameshift mutations of exon 9, which are mainly composed of a 52-bp deletion (Type 1) or 5-bp insertion (Type 2). ET with CALR mutations is associated with younger age, male sex, higher platelet count, lower hemoglobin level, lower leukocyte count, and lower incidence of thrombosis compared with ET with Janus kinase 2 (JAK2 ) mutations. There is no transformation to polycythemia vera in ET patients with CALR mutations. Patients with ET who have CALR type 1 mutations are at higher risk of thrombosis and myelofibrotic transformation compared with ET with CALR type-2 mutations. The standard treatment of CALR-mutated ET patients is currently based on the treatment algorithm of JAK2-unmutated ET patients. Further studies are necessary to clarify whether the appropriate treatment differs between type 1 and 2 mutations of CALR-mutated ET patients.