Changes in Stroke Patients' Health-Seeking Behavior by COVID-19 Epidemic Regions: Data from the Korean Stroke Registry.

INTRODUCTION: The coronavirus disease 2019 (COVID-19) pandemic has led to changes in stroke patients' healthcare use. This study evaluated changes in Korean stroke patients' health-seeking behaviors and stroke care services using data from the Korean Stroke Registry (KSR). METHODS: We reviewed data from patients with acute stroke and transient ischemic attack (TIA) during 2019 (before COVID-19 period) and 2020 (COVID-19 period). Outcomes included patient characteristics, time from stroke onset to hospital arrival, and in-hospital stroke pathways. Subgroup analyses were performed for an epidemic region (Daegu city and Gyeongsangbuk-do region, the D-G region). RESULTS: The study included 1,792 patients from the pre-COVID-19 period and 1,555 patients from the COVID-19 period who visited hospitals that contribute to the KSR. During the COVID-19 period, the D-G region had two-thirds the number of cases (vs. the pre-CO-VID-19 period) and a significant decrease in the proportion of patients with TIA (9.97%-2.91%). Unlike other regions, the median onset-to-door time increased significantly in the D-G region (361 min vs. 526.5 min, p = 0.016), and longer onset-to-door times were common for patients with mild symptoms and who were in their 60s or 70s. The number of patients who underwent intravenous thrombolysis also decreased during the COVID-19 period, although the treatment times were not significantly different between the 2 periods. DISCUSSION/CONCLUSION: Korean stroke patients in a CO-VID-19 epidemic region exhibited distinct changes in health-seeking behaviors. Appropriate triage system and public education regarding the importance of early treatment are needed during the COVID-19 pandemic.

Lower Glucose Level Associated With Increased Risk for Post-Dural Puncture Headache.

OBJECTIVE AND BACKGROUND: Post-dural puncture headache is the most common significant adverse event following lumbar puncture. In this study, we investigated the possible systemic factors associated with risk for post-dural puncture headache (PDPH). METHODS: We performed a retrospective cohort study in 969 patients who underwent diagnostic lumbar puncture following a standardized protocol. We compared the clinical and laboratory profiles of the post-dural puncture headache group and non-headache group. We also identified independent factors associated with the incidence of post-dural puncture headache. RESULTS: A total of 48 patients (5%) reported headache; 12 of these patients (25%) received a therapeutic epidural blood patch and the remaining 36 patients improved with conservative treatment. After adjusting for other variables that could be related to PDPH, we found that the development of post lumbar puncture headache was independently associated with age (OR: 0.97, 95% CI: 0.95-0.99, P = .001) and serum glucose levels (OR: 0.98, 95% CI: 0.97-0.99, P = .008).When the patients were classified by age, serum glucose levels were persistently lower in patients with PDPH vs those patients without PDPH in all age groups, with more clearly significant differences observed in the elderly (age <30 years, 103.4 mg/dL vs 106.3 mg/dL, P = .716; >60 years, 111.8 mg/dL vs 137.3 mg/dL, P = .023). CONCLUSIONS: Low glucose levels were inversely associated with risk for post-dural puncture headache. Patients with low serum glucose should be carefully monitored for headache after lumbar puncture.

Implications of CHA2DS2-VASc Score in Stroke Patients with Atrial Fibrillation: An Analysis of 938 Korean Patients.

BACKGROUND AND AIMS: The aim of this study was to investigate the stroke mechanisms and associated conditions influencing the decision regarding stroke thromboprophylaxis in patients with atrial fibrillation (AF) plus ischemic stroke, according to the CHA2DS2-VASc score. METHODS: We evaluated 938 consecutive patients with a diagnosis of AF plus transient ischemic attack/ischemic stroke. Based on the CHA2DS2-VASc scores, patients were stratified as score 0 or 1 (n = 151), score 2 (n = 146), score 3 (n = 213), score 4 (n = 185), or score ≥5 (n = 243). RESULTS: Patients with a higher CHA2DS2-VASc score were more likely to have noncardioembolic stroke mechanism (p = 0.001). Large-artery atherosclerosis causing stenosis >50% was more frequently observed in the high CHA2DS2-VASc group (p < 0.001). Coronary artery disease and the use of antiplatelet agents were more prevalent in the higher group (p < 0.001). A high CHA2DS2-VASc score was associated with a higher frequency of cerebral microbleeds and a higher Fazekas grade for leukoaraiosis (p < 0.001). The HAS-BLED score was correlated with the CHA2DS2-VASc score (γ = 0.650; p < 0.001). CONCLUSIONS: A higher CHA2DS2-VASc score is associated with noncardioembolic mechanisms of stroke and with a higher risk of bleeding. Strategies to treat macro/microangiopathy such as use of statin for plaque stabilization, as well as oral anticoagulants with a lower bleeding risk, are needed in these patients.

Previous Statin Use and High-Resolution Magnetic Resonance Imaging Characteristics of Intracranial Atherosclerotic Plaque: The Intensive Statin Treatment in Acute Ischemic Stroke Patients With Intracranial Atherosclerosis Study.

BACKGROUND AND PURPOSE: Although statin use has been linked to the stabilization of systemic atherosclerosis, its effect on symptomatic intracranial atherosclerotic plaques has yet to be explored. We hypothesized that premorbid statin use is associated with plaque instability in intracranial arteries and may lead to differential patterns (size and distribution) of ischemic lesions in patients with acute intracranial atherosclerotic stroke. METHODS: One hundred and thirty-six patients with acute infarcts caused by intracranial atherosclerotic stroke underwent high-resolution magnetic resonance imaging. Patients were categorized into 3 groups based on their premorbid statin use: nonuser, low-dose user, and high-dose user, according to the 2013 American College of Cardiology/American Heart Association guidelines on blood cholesterol. Symptomatic lesions in intracranial arteries were analyzed using high-resolution magnetic resonance imaging for vascular morphology (degree of stenosis, remodeling index, and wall index) and plaque activation (pattern and volume of enhancement). The cortical distribution and volume of ischemic brain lesions were measured using diffusion-weighted imaging. RESULTS: Among the enrolled patients, 38 (27.94%) were taking statins before the index stroke (22 low-dose statins and 16 high-dose statins). The degree of stenosis, remodeling index, and wall index did not differ between the 3 groups. However, the volume of plaque enhancement was significantly lower in statin users (nonuser, 33.26±40.72; low-dose user, 13.15±17.53; high-dose user, 3.13±5.26; P=0.002). Premorbid statin use was associated with a higher prevalence of nonembolic stroke and a decrease in large cortical infarcts (P=0.012). CONCLUSIONS: Premorbid statin usage is independently associated with reduced plaque enhancement and a decrease in large cortical lesions in patients with intracranial atherosclerotic stroke.

Echoing Plaque Activity of the Coronary and Intracranial Arteries in Patients With Stroke.

BACKGROUND AND PURPOSE: Atherosclerosis is a systemic disease, and both coronary and intracranial atherosclerosis are common in the elderly. Unlike coronary artery disease (CAD), intracranial atherosclerotic disease can cause intracranial atherosclerotic stroke by branch occlusive disease (B-type) and coronary-type rupture of plaque (C-type). We hypothesized that plaque characteristics of intracranial arteries are associated with those of coronary arteries. METHODS: Eighty-one patients with acute cerebral infarcts caused by intracranial atherosclerotic disease without history of CAD were analyzed. Asymptomatic CAD burden (number and degree of stenosis) and plaque characteristics (calcified, mixed, and noncalcified) were measured with multidetector computed tomography, whereas the asymptomatic intracranial atherosclerotic disease burden was measured using magnetic resonance angiography. The symptomatic intracranial artery was analyzed using high-resolution magnetic resonance imaging for vascular morphology (stenosis degree, remodeling index, and wall index) and plaque activation (enhancement pattern and volume). RESULTS: The asymptomatic CAD burden was correlated with the asymptomatic intracranial atherosclerotic disease burden. The overall CAD burden did not differ between B- and C-type intracranial atherosclerotic stroke. However, the prevalence of noncalcified coronary plaque was much higher in C-type intracranial atherosclerotic stroke and the presence of coronary noncalcified plaque was independently associated with C-type intracranial atherosclerotic stroke (odds ratio, 3.38; 95% confidence interval, 1.05-10.85; P=0.041). As the number of coronary noncalcified plaques increased, positive remodeling and plaque enhancement increased in the symptomatic intracranial artery on high-resolution magnetic resonance imaging. CONCLUSIONS: Plaques within the intracranial and coronary arteries behave in similar ways. Our results suggest the need to evaluate and treat other vascular trees in patients with vulnerable plaques within a single arterial system.

Edoxaban for the treatment of hypercoagulability and cerebral thromboembolism associated with cancer: A randomized clinical trial of biomarker targets.

BACKGROUND: This study aimed compare efficacy of edoxaban and enoxaparin upon biomarkers of hypercoagulability in patients with cancer-related embolic stroke of undetermined source (ESUS). METHODS: In this open-label, randomized, pilot trial, patients with cancer-related ESUS within 30 days of diagnosis were randomly assigned (1:1) to receive edoxaban (60 mg once daily) or enoxaparin (1 mg/kg twice daily) for 90 days. The primary endpoint was interval change of serum D-dimer level between days 0 and 7. The secondary endpoints were microembolic signals detected by transcranial Doppler at 7 and 90 days, the modified Rankin scale score, and stroke recurrence during 90 days. Safety outcomes included major bleeding and all-cause death at 90 days. RESULTS: Of 303 patients with ischemic stroke and cancer, 40 fully met enrollment criteria and were randomized. Baseline D-dimer levels were numerically higher in the edoxaban group (22.9 ± 15.9 µg/mL vs 16.9 ± 16.9 µg/mL). D-dimer level change (%) between days 0 and 7 was similar in the two groups (53.2 ± 25.7 vs 52.2 ± 52.0; P = 0.11). Microembolic signals were detected in 41.1% and 43.8% at baseline, 41.2% and 42.9% at day 7, and 25.0% and 28.6% at day 90 in the edoxaban and enoxaparin groups, respectively. Non-significantly higher major bleeding (35.0% vs 10.0%, P = 0.06) and 90-day mortality (40.0% vs 25.0%, P = 0.31) were noted in the edoxaban group. CONCLUSION: Edoxaban and enoxaparin were comparable with respect to the biomarkers of hypercoagulability and cerebral thromboembolism. Larger trials are warranted to compare effects of edoxaban and enoxaparin upon recurrent stroke and major bleeding in patients with cancer-related ESUS. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT03570281 (https://clinicaltrials.gov/ct2/show/NCT03570281).

Microembolic signals in acute posterior circulation cerebral ischemia: sources and consequences.

BACKGROUND AND PURPOSE: The clinical significance of microembolic signals (MES) in the posterior circulation remains unclear. The aim of this study was to investigate the sources and consequences of MES in acute posterior circulation cerebral ischemia. METHODS: We evaluated a total of 140 consecutive patients (93 males, mean age 62.9 years) who had acute posterior circulation cerebral ischemia. The MES monitoring was conducted at the basilar artery through the suboccipital window for a 30-minute period. RESULTS: MES were detected in 18 (12.9%) of the 140 patients. Clinical characteristics and laboratory data did not differ between the MES-positive and MES-negative groups. Intracranial vertebrobasilar artery (VBA) stenosis was independently associated with the presence of MES (odds ratio, 9.85; 95% confidence interval, 1.22-79.48; P=0.032), whereas the patients with vertebral artery stenosis that was limited to the extracranial portion did not show an association. Microembolic signals occurred significantly more frequently in patients with severe degree of VBA stenosis compared to those with nonsignificant stenosis (odds ratio, 9.88; 95% confidence interval, 1.23-79.07; P=0.031). In a subgroup analysis of the 79 patients who had lesions on diffusion-weighted images and relevant VBA stenosis, the MES-positive group showed more frequent embolic infarction (P=0.010) and multiple lesion patterns (P=0.007) than single perforating infarctions. CONCLUSIONS: In acute posterior circulation cerebral ischemia, intracranial and severe VBA stenosis is associated with MES and may be its root causes. The presence of MES in VBA stenosis suggests that multiple and embolic type infarctions are the mechanisms of stroke.

Characterization of the infarct pattern caused by vulnerable aortic arch atheroma: DWI and multidetector row CT study.

BACKGROUND: Aortic arch atheroma (AAA) has been accepted as a possible embolic source in patients with ischemic stroke, especially cryptogenic stroke. However, despite its well-known role as a risk factor for stroke, research focused on the mechanism or characteristics of stroke caused by AAA is insufficient. In this study, we aimed to evaluate clinical and radiological characteristics including lesion pattern on DWI in acute stroke patients associated with vulnerable AAA detected by multidetector row computed tomography (MDCT). METHODS: From September 2008 through May 2011, patients who presented with acute ischemic stroke and underwent MDCT were found in a prospective stroke registry. Patients without evident stroke etiology were included and classified by presence of vulnerable AAA. Vulnerable AAA was defined as (i) at least 6 mm thick adjacent to the aortic wall; (ii) ulcerated plaque, or (iii) soft plaque. Soft plaque was defined as the presence of clearly visualized area of hypoattenuation (<80 Hounsfield units) suggestive of thrombus. The patients without vulnerable AAA were classified as no/simple AAA group. The characteristics of diffusion-weighted MRI (DWI) lesions were analyzed in terms of the number and size of the lesions, and the involved vascular territories. RESULTS: A total of 63 cryptogenic stroke patients were included in this study. Vulnerable AAA was observed in 15 (23.8%) patients. The patients with vulnerable AAA were older than those with no/simple AAA (p = 0.026). DWI analysis revealed that the vulnerable AAA group had a greater chance of having multiple and small lesions in multiple vascular territories that were mainly located in cortical and border-zone regions than the no/simple AAA group. Multiple logistic regression analysis showed that age (odds ratio 1.17; 95% confidence interval 1.02-1.34) and multiple small lesions in multiple vascular territories (odds ratio 33.18; 95% confidence interval 4.26-258.45) were independently associated with vulnerable AAA. CONCLUSION: Vulnerable AAA is independently associated with a DWI pattern characterized by multiple small scattered lesions in multiple vascular territories in conjunction with age. It may help determine stroke mechanism quickly and easily, and provide more information about the pathomechanism of vulnerable AAA-related stroke.

Serum neurofilament light chain levels are correlated with the infarct volume in patients with acute ischemic stroke.

Neurofilament light chains (NfLs) are promising biomarkers of neuroaxonal damage in stroke patients. We investigated the correlations between NfL levels and infarct volume, initial stroke severity, and functional outcomes at discharge in patients with acute ischemic stroke. We prospectively included 15 patients with first-ever acute ischemic stroke and 8 age- and sex-matched healthy controls without other neurological disorders. Serum NfL levels were measured using the single-molecule array (Simoa) technique twice within 24 hours of admission (NfL1D) and on the seventh hospital day (NfL7D) in patients with stroke and once in healthy controls. We assessed the infarct volume on diffusion-weighted magnetic resonance imaging using the free software ITK-SNAP. Serum NfL1D levels in stroke patients were significantly higher (28.4 pg/mL; interquartile range [IQR], 43.0) than in healthy controls (14.5 pg/mL; IQR, 3.2; P = .005). Temporal pattern analyses demonstrated that NfL7D levels were increased (114.0 pg/mL; IQR, 109.6) compared to NfL1D levels in all stroke patients (P = .001). There was a strong correlation between NfL7D levels and infarct volume (R = 0.67, P = .007). The difference between NfL1D and NfL7D (NfLdiff levels) was strongly correlated with the infarct volume (R = 0.63; P = .013). However, there was no statistically significant correlation between NfL levels and the initial stroke severity or functional outcomes at discharge. NfL levels in the subacute stage of stroke and the NfL difference between admission and 7th day of hospital were correlated with infarct volume in patients with acute ischemic stroke.

The Role of Factor Xa-Independent Pathway and Anticoagulant Therapies in Cancer-Related Stroke.

BACKGROUND: The optimal strategy for stroke prevention in cancer patients is unknown. We compared the underlying mechanisms of coagulopathy and the effects of anticoagulants in patients with active cancer and atrial fibrillation (AF). METHODS: We retrospectively enrolled 46 consecutive patients with embolic stroke of unknown source and active cancer (cancer stroke). We consecutively screened patients with cancer patients without stroke (n = 29), AF stroke (n = 52), and healthy subjects (n = 28), which served as controls. Patients with cancer stroke were treated with either enoxaparin (a low-molecular-weight heparin) or a factor Xa inhibitor, and those with AF stroke were treated with factor Xa inhibitors. D-dimer, factor Xa, and circulating cell-free DNA (cfDNA), a marker of neutrophil extracellular traposis, were measured at both before and after anticoagulation. RESULTS: In AF stroke, factor Xa activity and cfDNA and D-dimer levels were decreased by treatment with factor Xa inhibitors. In contrast, in cancer stroke, factor Xa activity was decreased, D-dimer levels were unchanged, and cfDNA levels were increased by treatment with factor Xa inhibitors. In cancer stroke patients treated with enoxaparin, D-dimer levels were decreased (p = 0.011) and cfDNA levels were unchanged. CONCLUSION: The anticoagulation effects of factor Xa inhibitors differed between cancer stroke and AF stroke.

Dramatic thrombolysis after rapid injection of tissue plasminogen activator: A case report.

RATIONALE: The regimen of the recombinant tissue plasminogen activator (rt-PA) is identical in every case where it is indicated in the treatment of cerebral infarction. We report a case of efficient recanalization of large arterial occlusion after rapid injection of rt-PA. PATIENT CONCERNS: A 78-year-old man was admitted with right-sided hemiplegia and global aphasia that occurred an hour ago. DIAGNOSES: His brain computed tomography (CT) revealed no hemorrhage, suggesting cerebral infarction. INTERVENTIONS: Ten percent of a total rt-PA dose was injected over 1 minute promptly. The remainder of rt-PA was designed to be infused for 60 minutes. Unexpectedly, during the study of CT angiography, administration of rt-PA was completed within 5 minutes. CT angiography showed occlusion from carotid bifurcation to the middle cerebral artery. OUTCOMES: After 2 hours of rt-PA administration, the patient began to regain strength in his right arm and leg. By the next day, he had only mild dysarthria and aphasia. Follow-up CT angiography revealed recanalized internal cervical artery and severe residual stenosis with a plaque. He was discharged without any neurologic symptoms. LESSONS: The infusion protocol of rt-PA administration is established in 1995 and has not changed. Successful recanalization of long segmental large vessel occlusion with only intravenous rt-PA is relatively low. In our case, a high concentration of rt-PA may have influenced the successful dissemination of large thrombus in the whole internal cervical artery. Our case is of significance as it raises the question of unanswered efficacy of diverse injection protocol according to thrombus size and bleeding risk.

Comparison of Clopidogrel and Ticlopidine/Ginkgo Biloba in Patients With Clopidogrel Resistance and Carotid Stenting.

Background and Purpose: Patients undergoing carotid artery stenting (CAS) who show low responsiveness to clopidogrel may have a higher risk of peri-procedural embolic events. This study aimed to compare the effectiveness and safety of clopidogrel and ticlopidine plus Ginkgo biloba in clopidogrel-resistant patients undergoing CAS. Methods: In this multi-center, randomized, controlled trial, we used platelet reactivity test to select patients undergoing CAS who showed clopidogrel resistance, and compared treatments using clopidogrel and ticlopidine plus ginkgo. The primary outcome was the incidence of new ischemic lesion in the ipsilateral hemisphere of CAS. Detection of microembolic signal on transcranial Doppler was the secondary outcome. The clinical outcomes were also monitored. Results: This trial was discontinued after 42 patients were randomized after preplanned interim sample size re-estimation indicated an impractical sample size. The primary endpoint occurred in 12/22 patients (54.5%) in the clopidogrel group and 13/20 patients (65.0%) in the ticlopidine-ginkgo group (P = 0.610). No significant differences in the presence of microembolic signal (15.0 vs. 11.8%, P = 0.580), clinical outcomes (ischemic stroke or transient ischemic attack, 0.0 vs. 5.5%; acute myocardial infarction 0.0 vs. 0.0%; all-cause death, 4.5 vs. 0.0%), or incidence of adverse events were found in the two groups. In terms of resistance to clopidogrel, treatment with ticlopidine-ginkgo significantly increased the P2Y12 Reaction Units (difference, 0.0 [-0.3-3.0] vs. 21.0 [6.0-35.0], P < 0.001). Conclusions: In patients who showed clopidogrel resistance, ticlopidine-ginkgo treatment was safe and increased P2Y12 Reaction Units; however, compared to clopidogrel, it failed to improve surrogate and clinical endpoints in patients undergoing CAS. This multimodal biomarker-based clinical trial is feasible in neurointerventional research. Clinical Trial Registration: http://www.clinicaltrials.gov. Unique identifier: NCT02133989.

Therapeutic-induced hypertension in patients with noncardioembolic acute stroke.

OBJECTIVE: To evaluate the safety and efficacy of induced hypertension in patients with acute ischemic stroke. METHODS: In this multicenter randomized clinical trial, patients with acute noncardioembolic ischemic stroke within 24 hours of onset who were ineligible for revascularization therapy and those with progressive stroke during hospitalization were randomly assigned (1:1) to the control and intervention groups. In the intervention group, phenylephrine was administered intravenously to increase systolic blood pressure (SBP) up to 200 mm Hg. The primary efficacy endpoint was early neurologic improvement (reduction in NIH Stroke Scale [NIHSS] score of ≥2 points during the first 7 days). The secondary efficacy endpoint was a modified Rankin Scale score of 0 to 2 at 90 days. Safety outcomes included symptomatic intracranial hemorrhage/edema, myocardial infarction, and death. RESULTS: In the modified intention-to-treat analyses, 76 and 77 patients were included in the intervention and control groups, respectively. After adjustment for age and initial stroke severity, induced hypertension increased the occurrence of the primary (odds ratio 2.49, 95% confidence interval [CI] 1.25-4.96, p = 0.010) and secondary (odds ratio 2.97, 95% CI 1.32-6.68, p = 0.009) efficacy endpoints. Sixty-seven (88.2%) patients of the intervention group exhibited improvements in NIHSS scores of ≥2 points during induced hypertension (mean SBP 179·7 ± 19.1 mm Hg). Safety outcomes did not significantly differ between groups. CONCLUSION: Among patients with noncardioembolic stroke who were ineligible for revascularization therapy and those with progressive stroke, phenylephrine-induced hypertension was safe and resulted in early neurologic improvement and long-term functional independence. CLINICALTRIALSGOV IDENTIFIER: NCT01600235. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that for patients with acute ischemic stroke, therapeutic-induced hypertension increases the probability of early neurologic improvement.

NIHSS sub-item scores predict collateral flow in acute middle cerebral artery infarction.

BACKGROUND AND PURPOSE: The status of collateral vessels has important clinical implications in acute ischemic stroke. To evaluate which components of ischemic symptoms were predictive of pretreatment collateral status, we tested the hypothesis that sub-item scores from the National Institutes of Health Stroke Scale (NIHSS) are associated with leptomeningeal collateral status in acute ischemic stroke with middle cerebral artery (MCA) occlusion. METHODS: This study included consecutive patients with acute M1 occlusion who underwent revascularization treatment for acute MCA infarction. We evaluated clinical factors and the NIHSS score according to the collateral status assessed by multiphase perfusion computed tomography. RESULTS: Eighty-six patients were included (48 good collateral status, 38 poor collateral status). The patients with poor collateral status were more likely to have a higher total NIHSS score (18 versus 11, p < 0.001) and atrial fibrillation (65.8% versus 41.7%, p = 0.026) than patients with good collateral flow. In a multiple logistic regression, the NIHSS sub-items such as profound "facial palsy" (score 2 versus 0-1) and "visual field defect" (score 2 versus 0-1) were independently associated with poor collateral status. CONCLUSION: Among the NIHSS sub-items, severe facial palsy and visual field defect were associated with poor collateral status in acute MCA stroke with M1 occlusion. Decision on whether to treat these patients endovascularly should be made more cautiously due to the possibility of a poor outcome.

Selective Application of High-Resolution 3 T MRI in the Evaluation of Intracranial Vertebral Artery Dissection.

BACKGROUND AND PURPOSE: Although high-resolution magnetic resonance imaging (HR-MRI) is considered optimal for the diagnosis of intracranial vertebral artery dissection (IVAD), it is not readily available for all patients with suspected IVAD. The purpose of our study was to determine the factor related to IVAD lesions that are not definitively diagnosed by conventional MRI. METHODS: This study included IVAD lesions that were evaluated with both of 3 T conventional MRI and HR-MRI. Definitive dissection was defined as the presence of one or more pathognomonic radiological findings including crescentic intramural hematoma, intimal flap, and double lumen. A total of 30 IVAD lesions definitively diagnosed by HR-MRI were included and grouped into a conventional MRI true-positive group (n = 17) or false-negative group (n = 13) based on the presence of definitive findings on conventional MRI. RESULTS: Clinical characteristics did not differ between the two groups. The absence of vertebral artery aneurysmal dilatation was more common in the conventional MRI false-negative group (84.6% vs. 35.3%; P = .010). Ipsilesional vertebral hypoplasia was observed more frequently in the conventional MRI false-negative IVAD group (53.8% vs. 17.6%; P = .056). In logistic regression, absence of vertebral artery aneurysmal dilatation was independently associated with conventional MRI false-negative IVAD (OR, 16.37; 95% CI, 1.39-192.30; P = .026). Ipsilesional vertebral artery hypoplasia showed only a trend as a predictor of conventional MRI false-negative IVAD (OR, 7.24; 95% CI, .73-71.51; P = 0.090). CONCLUSIONS: HR-MRI may be useful for diagnosing IVAD without aneurysmal dilatation or with ipsilesional vertebral hypoplasia.

Presence of anti-Ro/SSA antibody may be associated with anti-aquaporin-4 antibody positivity in neuromyelitis optica spectrum disorder.

BACKGROUND: Neuromyelitis optica (NMO) is often associated with systemic autoimmune diseases or serological markers of non-organ-specific autoimmunity, and has been most frequently associated with Sjögren's syndrome and anti-Ro/SSA antibody (SSA-Ab) positivity in Asian populations. OBJECTIVE: We evaluated the clinical significance of anti-Ro/SSA antibody positivity in patients with NMO spectrum disorder (NMOSD). METHODS: We retrospectively collected data from 106 consecutive patients with NMOSD and reviewed clinical features and laboratory findings. All patients underwent tests for SSA-Ab and anti-aquaporin-4 antibody (AQP4-Ab) using cell-based indirect immunofluorescence assays. RESULTS: Among 106 patients, 20 (18.9%) were positive for SSA-Ab. Of 48 AQP4-Ab-positive patients, 18 (37.5%) had SSA-Ab. AQP4-Ab seropositivity was 90.0% in patients positive for SSA-Ab, and 32.6% in patients without SSA-Ab (p<0.001). Presence of SSA-Ab was associated with systemic autoimmune diseases, including Sjögren's syndrome (p<0.001) and systemic lupus erythematosus (p=0.003), and with the presence of non-organ-specific autoantibodies such as anti-nuclear antibody and anti-dsDNA antibody in patients with NMOSD, but was not associated with annualized relapse rate or final Expanded Disability Status Scale score independent of AQP4-Ab positivity. CONCLUSION: We found that the presence of SSA-Ab was highly associated with seropositivity for AQP4-Ab in patients with NMOSD.