Koji Tanaka

<bold>Background:</bold> Coronavirus Disease 2019 (COVID-19) has spread worldwide with collateral damage and therefore might affect the behavior of stroke patients with mild symptoms seeking medical attention. <bold>Methods:</bold> Patients with ischemic stroke who were admitted to hospitals within 7 days of onset were retrospectively registered. The clinical characteristics, including onset-to-door time (ODT), of patients with a transient ischemic attack (TIA)/mild stroke (National Institutes of Health Stroke Scale [NIHSS] score of ≤ 3 on admission) or moderate/severe stroke were compared between those admitted from April 2019 to March 2020 (pre-COVID-19 period) and from April to September 2020 (COVID-19 period). Multivariable regression analysis was performed to identify factors associated with the ODT. <bold>Results:</bold> Of 1,100 patients (732 men, median age, 73 years), 754 were admitted during the pre-COVID-19 period, and 346 were admitted during the COVID-19 period. The number and proportion of patients with TIA/minor stroke were 464 (61.5%) in the pre-COVID-19 period and 216 (62.4%) during the COVID-19 period. Among patients with TIA/mild stroke, the ODT was longer in patients admitted during the COVID-19 period compared with that of the pre-COVID-19 period (median 864 min vs. 508 min, <italic>p</italic> = 0.003). Multivariable analysis revealed the COVID-19 period of admission was associated with longer ODT (standardized partial regression coefficient 0.09, <italic>p</italic> = 0.003) after adjustment for age, sex, route of arrival, NIHSS score on admission, and the presence of hypertension, diabetes mellitus, and wake-up stroke. No significant change in the ODT was seen in patients with moderate/severe stroke. <bold>Conclusions:</bold> The COVID-19 epidemic might increase the ODT of patients with TIA/mild stroke.

<sec id="sec001"> <title>Background and purpose</title> The impact of the paraoxonase-1 (<italic>PON1</italic>) polymorphism, Q192R, on platelet inhibition in response to clopidogrel remains controversial. We aimed to investigate the association between carrier status of <italic>PON1</italic> Q192R and high platelet reactivity (HPR) with clopidogrel in patients undergoing elective neurointervention. </sec> <sec id="sec002"> <title>Methods</title> Post-clopidogrel platelet reactivity was measured using a VerifyNow^® P2Y12 assay in P2Y12 reaction units (PRU) for consecutive patients before the treatment. Genotype testing was performed for <italic>PON1</italic> Q192R and <italic>CYP2C19*2</italic> and <italic>*3</italic> (no function alleles), and <italic>*17</italic>. PRU was corrected on the basis of hematocrit. We investigated associations between factors including carrying ≥1 <italic>PON1</italic> 192R allele and HPR defined as original and corrected PRU ≥208. </sec> <sec id="sec003"> <title>Results</title> Of 475 patients (232 men, median age, 68 years), HPR by original and corrected PRU was observed in 259 and 199 patients (54.5% and 41.9%), respectively. Carriers of ≥1 <italic>PON1</italic> 192R allele more frequently had HPR by original and corrected PRU compared with non-carriers (91.5% vs 85.2%, P = 0.031 and 92.5% vs 85.9%, P = 0.026, respectively). In multivariate analyses, carrying ≥1 <italic>PON1</italic> 192R allele was associated with HPR by original (odds ratio [OR] 1.96, 95% confidence interval [CI] 1.03–3.76) and corrected PRU (OR 2.34, 95% CI 1.21–4.74) after adjustment for age, sex, treatment with antihypertensive medications, hematocrit, platelet count, total cholesterol, and carrying ≥1 <italic>CYP2C19</italic> no function allele. </sec> <sec id="sec004"> <title>Conclusions</title> Carrying ≥1 <italic>PON1</italic> 192R allele is associated with HPR by original and corrected PRU with clopidogrel in patients undergoing elective neurointervention, although alternative results related to other genetic polymorphisms cannot be excluded. </sec>

<sec id="sec001"> <title>Objective</title> Periprocedural thromboembolic events are a serious complication associated with coil embolization of unruptured intracranial aneurysms. However, no established clinical rule for predicting thromboembolic events exists. This study aimed to clarify the significance of adding preoperative clopidogrel response value to clinical factors when predicting the occurrence of thromboembolic events during/after coil embolization and to develop a nomogram for thromboembolic event prediction. </sec> <sec id="sec002"> <title>Methods</title> In this prospective, single-center, cohort study, we included 345 patients undergoing elective coil embolization for unruptured intracranial aneurysm. Thromboembolic event was defined as the occurrence of intra-procedural thrombus formation and postprocedural symptomatic cerebral infarction within 7 days. We evaluated preoperative clopidogrel response and patients’ clinical information. We developed a patient-clinical-information model for thromboembolic event using multivariate analysis and compared its efficiency with that of patient-clinical-information plus preoperative clopidogrel response model. The predictive performances of the two models were assessed using area under the receiver-operating characteristic curve (AUC-ROC) with bootstrap method and compared using net reclassification improvement (NRI) and integrated discrimination improvement (IDI). </sec> <sec id="sec003"> <title>Results</title> Twenty-eight patients experienced thromboembolic events. The clinical model included age, aneurysm location, aneurysm dome and neck size, and treatment technique. AUC-ROC for the clinical model improved from 0.707 to 0.779 after adding the clopidogrel response value. Significant intergroup differences were noted in NRI (0.617, 95% CI: 0.247–0.987, p &lt; .001) and IDI (0.068, 95% CI: 0.021–0.116, p = .005). </sec> <sec id="sec004"> <title>Conclusions</title> Evaluation of preoperative clopidogrel response in addition to clinical variables improves the prediction accuracy of thromboembolic event occurrence during/after coil embolization of unruptured intracranial aneurysm. </sec>

A 44-year-old male was admitted to our hospital because of sudden weakness and sensory loss in both legs following left scapular pain. He had a history of lower back pain but no vascular risk factors. Neurological examination on admission revealed flaccid paraplegia, a loss of both pinprick and vibratory sensations below the Th6 level, and bladder and rectal disturbances. Tendon reflexes were absent in both lower limbs. Diffusion-weighted imaging performed 5 hours after onset revealed an extensive high-intensity lesion at the Th2-6 spine levels, accompanied by a vague high intensity on T2-weighted images. CT angiography showed no abnormalities of the aorta or the artery of Adamkiewicz. Laboratory test results were normal and there was no evidence of coagulopathy. Autoantibodies, including anti-aquaporin-4 and anti-myelin oligodendrocyte glycoprotein antibodies, were negative. The cerebrospinal fluid test was normal. The lesion had expanded to the whole thoracic cord and was markedly swollen on T2-weighted imaging at 5 days after onset. Immunotherapies, including intravenous methylprednisolone pulse therapy and plasma exchange, were ineffective. Although there was no evidence of any source of embolism, we found degenerative calcified changes in the fibrocartilage of the intervertebral discs, with Schmorl's nodes in the thoracic spines. We clinically diagnosed the patient with spinal cord infarction caused by fibrocartilaginous embolism. He developed deep vein thrombosis and was treated with edoxaban. His neurological symptoms did not improve during 55 days of hospitalization. In a case with sudden-onset myelopathy, fibrocartilaginous embolism should be considered.