Association between Rapid Ventricular Response and Stroke Outcomes in Atrial Fibrillation-Related Cardiac Embolic Stroke.

INTRODUCTION: Patients with atrial fibrillation-related stroke (AF-stroke) are prone to developing rapid ventricular response (RVR). We investigated whether RVR is associated with initial stroke severity, early neurological deterioration (END) and poor outcome at 3 months. METHODS: We reviewed patients who had AF-stroke between January 2017 and March 2022. RVR was defined as having heart rate >100 beats per minute on initial electrocardiogram. Neurological deficit was evaluated with National Institutes of Health Stroke Scale (NIHSS) score at admission. END was defined as increase of ≥2 in total NIHSS score or ≥1 in motor NIHSS score within first 72 h. Functional outcome was score on modified Rankin Scale at 3 months. Mediation analysis was performed to examine potential causal chain in which initial stroke severity may mediate relationship between RVR and functional outcome. RESULTS: We studied 568 AF-stroke patients, among whom 86 (15.1%) had RVR. Patients with RVR had higher initial NIHSS score (p < 0.001) and poor outcome at 3 months (p = 0.004) than those without RVR. The presence of RVR [adjusted odds ratio (aOR) = 2.13; p = 0.013] was associated with initial stroke severity, but not with END and functional outcome. Otherwise, initial stroke severity [aOR = 1.27; p = <0.001] was significantly associated with functional outcome. Initial stroke severity as a mediator explained 58% of relationship between RVR and poor outcome at 3 months. CONCLUSION: In patients with AF-stroke, RVR was independently associated with initial stroke severity but not with END and functional outcome. Initial stroke severity mediated considerable proportion of association between RVR and functional outcome.

Association between renal insufficiency and lesion characteristics of posterior reversible encephalopathy syndrome.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is characterized by cerebral blood flow dysregulation and the blood-brain barrier (BBB) disruption. While renal insufficiency has been considered a factor in BBB fragility, the relationship between renal insufficiency and the PRES lesions volume remains unclear. METHODS: This observational study was performed retrospectively. PRES patients were categorized into two groups with renal insufficiency, defined as an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73m2 on the day of symptom occurrence. Lesion volume was measured using fluid-attenuated inversion recovery (FLAIR) imaging, and the brain was divided into nine regions. The volume of the parietal-occipital-temporal lobe was considered typical, while the other six regions were labeled as atypical. RESULTS: The study included 200 patients, of whom 94 (47%) had renal insufficiency. Patients with renal insufficiency had a larger lesion volume (144.7 ± 125.2 cc) compared to those without renal insufficiency (110.5 ± 93.2 cc; p = 0.032); particularly in the atypical lesions volume (49.2 ± 65.0 vs. 29.2 ± 44.3 cc; p = 0.013). However, there was no difference in the reversibility of the lesions (35.2 ± 67.5 vs. 18.8 ± 33.4 cc; p = 0.129). Multiple regression analysis revealed that decreases in eGFR (ß = -0.34, 95% CI -0.62-0.05, p = 0.020) were positively associated with total lesion volume. CONCLUSION: Our findings suggest that PRES patients with renal insufficiency experience more severe lesion volumes, likely due to the atypical brain regions involvement. The lesions involving atypical regions may have a similar pathophysiology to typical lesions, as the PRES lesions reversibility was found to be similar between individuals with and without renal insufficiency.

Mycobacterium potentiates protection from colorectal cancer by gut microbial alterations.

Not only are many Mycobacteria pathogens, but they can act as strong non-specific immunopotentiators, generating beneficial effects on the pathogenesis of some diseases. However, there has been no direct evidence of the effect of mycobacterial species on colorectal cancer (CRC). Herein, we showed that there may be a meaningful inverse correlation between the incidence of tuberculosis and CRC based on global statistics and that heat-killed Mycobacterial tuberculosis and live Mycobacterium bovis (Bacillus Calmette-Guérin strain) could ameliorate CRC development. In particular, using a faecal microbiota transplantation and a comparison between separate housing and cohousing, we demonstrated that the gut microbiota is involved in the protective effects. The microbial alterations can be elucidated by the modulation of antimicrobial activities including those of the Reg3 family genes. Furthermore, interleukin-22 production by T helper cells contributed to the anti-inflammatory activity of Mycobacteria. Our results revealed a novel role of Mycobacteria involving gut microbial alterations in dampening inflammation-associated CRC and an immunological mechanism underlying the interaction between microbes and host immunity.

A secreted form of chorismate mutase (Rv1885c) in Mycobacterium bovis BCG contributes to pathogenesis by inhibiting mitochondria-mediated apoptotic cell death of macrophages.

BACKGROUND: Mycobacterium tuberculosis is the causative agent of tuberculosis (TB), and its pathogenicity is associated with its ability to evade the host defense system. The secretory form of the chorismate mutase of M. tuberculosis (TBCM, encoded by Rv1885c) is assumed to play a key role in the pathogenesis of TB; however, the mechanism remains unknown. METHODS: A tbcm deletion mutant (B∆tbcm) was generated by targeted gene knockout in BCG to investigate the pathogenic role of TBCM in mice or macrophages. We compared the pathogenesis of B∆tbcm and wild-type BCG in vivo by measuring the bacterial clearance rate and the degree of apoptosis. Promotion of the intrinsic apoptotic pathway was evaluated in infected bone marrow-derived macrophages (BMDMs) by measuring apoptotic cell death, loss of mitochondrial membrane potential and translocation of pore-forming proteins. Immunocytochemistry, western blotting and real-time PCR were also performed to assess the related protein expression levels after infection. Furthermore, these findings were validated by complementation of tbcm in BCG. RESULTS: Deletion of the tbcm gene in BCG leads to reduced pathogenesis in a mouse model, compared to wild type BCG, by promoting apoptotic cell death and bacterial clearance. Based on these findings, we found that intrinsic apoptosis and mitochondrial impairment were promoted in B∆tbcm-infected BMDMs. B∆tbcm down-regulates the expression of Bcl-2, which leads to mitochondrial outer membrane permeabilization (MOMP), culminating in cytochrome c release from mitochondria. Consistent with this, transcriptome profiling also indicated that B∆tbcm infection is more closely related to altered mitochondrial-related gene expression than wild-type BCG infection, suggesting an inhibitory role of TBCM in mitochondrial dysfunction. Moreover, genetic complementation of B∆tbcm (C∆tbcm) restored its capacity to inhibit mitochondria-mediated apoptotic cell death. CONCLUSIONS: Our findings demonstrate the contribution of TBCM to bacterial survival, inhibiting intrinsic apoptotic cell death of macrophages as a virulence factor of M. tuberculosis complex (MTBC) strains, which could be a potential target for the development of TB therapy.

Early Response to Endovascular Thrombectomy after Stroke: Early, Late, and Very Late Time Windows.

BACKGROUND AND PURPOSE: Endovascular thrombectomy (EVT) has benefits in selected patients 6-24 h after stroke onset. However, the response to EVT >24 h after stroke onset is still unclear. We compared the early response to EVT in patients with different time windows. METHODS: Patients who underwent EVT in an emergency setting were enrolled and categorized according to when EVT was performed: within 6 (early), 6-24 (late), and >24 h (very late) after stroke onset. Early neurological improvement (ENI) and deterioration (END) were defined as improvement and worsening, respectively, of National Institutes of Health Stroke Scale (NIHSS) score by ≥4 points after EVT. The three groups' clinical characteristics and response to EVT were compared. We also investigated factors associated with ENI and END. RESULTS: During study period, 274 patients underwent EVT (109 early, 104 late, and 61 very late). Patients who underwent EVT very late were younger (p = 0.007), had smaller ischemic cores, and had lower initial NIHSS scores (8 ± 5) than those who underwent EVT early (14 ± 6) and late (13 ± 7; p < 0.001). Stroke mechanisms also differed according to the time window (p < 0.001): cardioembolism was more common after early EVT, whereas large-artery atherosclerosis was more prevalent among patients who underwent EVT very late. ENI was significantly more common after early (60.6%) and late EVT (51.0%) than after very late EVT (29.5%; p = 0.001); however, rates of END did not differ (11.0%, 13.5%, and 4.9%, respectively). ENI was independently associated with male, higher NIHSS score, and early and late EVT. END was associated with failure of recanalization. CONCLUSIONS: ENI was more observed and associated with early and late EVT. Highly selected patients receiving very late EVT may not benefit from ENI but may still have a chance to prevent END. The occurrence of END was associated not with time window but with failure of recanalization.

Long Sleep Duration and Dissatisfaction with Sleep Quality Are Associated with Ischemic Stroke in Young Patients.

INTRODUCTION: Suboptimal sleep duration and poor sleep quality have been proposed to increase stroke risk. However, their significance in young ischemic stroke is unclear. We aimed to investigate the importance of sleep duration and quality on young ischemic stroke patients. METHODS: A multicenter matched case-control study was performed to evaluate under-recognized risk factors in young (<45 years) ischemic stroke patients in 8 tertiary hospitals in Korea. A total of 225 patients and 225 age- and sex-matched controls were enrolled in the same period. Detailed information about patients' demographics, socioeconomic state, and traditional and nontraditional risk factors including sleep-related factors were obtained using structured questionnaires. Risk of ischemic stroke was estimated using conditional logistic regression analysis. RESULTS: Although average sleep duration was similar in patients and controls, patients were more likely to have long (≥9 h) or extremely short (<5 h) sleep durations. In addition, the proportion of subjects with dissatisfaction with sleep quality was higher in patients than controls (66.2 vs. 49.3%, p < 0.001). In multivariable conditional logistic regression analysis, long sleep duration (OR: 11.076, 95% CI: 1.819-67.446, p = 0.009) and dissatisfaction with sleep quality (OR: 2.116, 95% CI: 1.168-3.833, p = 0.013) were independently associated with risk of ischemic stroke. CONCLUSIONS: Long sleep duration and dissatisfaction with sleep quality may be associated with increased risk of ischemic stroke in young adults. Improving sleep habit or quality could be important for reducing the risk of ischemic stroke.

In-stent restenosis and stented-territory infarction after carotid and vertebrobasilar artery stenting.

BACKGROUND: Prognosis after vertebrobasilar stenting (VBS) may differ from that after carotid artery stenting (CAS). Here, we directly compared the incidence and predictors of in-stent restenosis and stented-territory infarction after VBS and compared them with those of CAS. METHODS: We enrolled patients who underwent VBS or CAS. Clinical variables and procedure-related factors were obtained. During the 3 years of follow-up, in-stent restenosis and infarction were investigated in each group. In-stent restenosis was defined as reduction in the lumen diameter > 50% compared with that after stenting. Factors associated with the occurrence of in-stent restenosis and stented-territory infarction in VBS and CAS were compared. RESULTS: Among 417 stent insertions (93 VBS and 324 CAS), there was no statistical difference in in-stent restenosis between VBS and CAS (12.9% vs. 6.8%, P = 0.092). However, stented-territory infarction was more frequently observed in VBS than in CAS (22.6% vs. 10.8%; P = 0.006), especially a month after stent insertion. HbA1c level, clopidogrel resistance, and multiple stents in VBS and young age in CAS increased the risk of in-stent restenosis. Diabetes (3.82 [1.24-11.7]) and multiple stents (22.4 [2.4-206.4]) were associated with stented-territory infarction in VBS. However, in-stent restenosis (odds ratio: 15.1, 95% confidence interval: 3.17-72.2) was associated with stented-territory infarction in CAS. CONCLUSIONS: Stented-territory infarction occurred more frequently in VBS, especially after the periprocedural period. In-stent restenosis was associated with stented-territory infarction after CAS, but not in VBS. The mechanism of stented-territory infarction after VBS may be different from that after CAS.

rt269L-Type hepatitis B virus (HBV) in genotype C infection leads to improved mitochondrial dynamics via the PERK-eIF2α-ATF4 axis in an HBx protein-dependent manner.

BACKGROUND: In our previous report, the rt269I type versus the rt269L type in genotype C2 infection led to poor clinical outcomes and enhanced mitochondrial stress in infected hepatocytes. Here, we sought to investigate differences between the rt269L and rt269I types in mitochondrial functionality in hepatitis B virus (HBV) genotype C2 infection, mainly focusing on endoplasmic reticulum (ER) stress-mediated autophagy induction as an upstream signal. METHODS: Mitochondrial functionality, ER stress signaling, autophagy induction, and apoptotic cell death between rt269L-type and rt269I-type groups were investigated via in vitro and in vivo experiments. Serum samples were collected from 187 chronic hepatitis patients who visited Konkuk or Seoul National University Hospital. RESULTS: Our data revealed that genotype C rt269L versus rt269I infection led to improved mitochondrial dynamics and enhanced autophagic flux, mainly due to the activation of the PERK-eIF2α-ATF4 axis. Furthermore, we demonstrated that the traits found in genotype C rt269L infection were mainly due to increased stability of the HBx protein after deubiquitination. In addition, clinical data using patient sera from two independent Korean cohorts showed that, compared with rt269I, rt269L in infection led to lower 8-OHdG levels, further supporting its improved mitochondrial quality control. CONCLUSION: Our data showed that, compared with the rt269I type, the rt269L type, which presented exclusively in HBV genotype C infection, leads to improved mitochondrial dynamics or bioenergetics, mainly due to autophagy induction via activation of the PERK-eIF2α-ATF4 axis in an HBx protein-dependent manner. This suggests that HBx stability and cellular quality control in the rt269L type predominating in genotype C endemic areas could at least partly contribute to some distinctive traits of genotype C infection, such as higher infectivity or longer duration of the hepatitis B e antigen (HBeAg) positive stage.

Spatiotemporal association between air pollution and stroke mortality in South Korea.

BACKGROUND: Air pollutant concentrations in South Korea vary greatly by region and time. To assess temporal and spatial associations of stroke subtypes with long-term air pollution effects on stroke mortality, we studied ischemic stroke (IS), intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). METHODS: This was an observational study conducted in South Korea from 2001-2018. Concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter ≤10 µm in diameter (PM10) were determined from 332 stations. Average air pollutant concentrations in each district were determined by distance-weighted linear interpolation. The nationwide stroke mortality rates in 249 districts were obtained from the Korean Statistical Information Service. Time intervals were divided into three consecutive 6-year periods: 2001-2006, 2007-2012, and 2013-2018. RESULTS: The concentrations of air pollutants gradually decreased from 2001-2018, along with decreases in IS and ICH mortality rates. However, mortality rates associated with SAH remained constant. From 2001-2006, NO2 (adjusted odds ratio [aOR]:1.13, 95% confidence interval: 1.08-1.19), SO2 (aOR: 1.10, 1.07-1.13), and PM10 (aOR: 1.12, 1.06-1.18) concentrations were associated with IS mortality, and SO2 (aOR: 1.07, 1.02-1.13) and PM10 (aOR:1.11,1.06-1.22) concentrations were associated with SAH-associated mortality. Air pollution was no longer associated with stroke mortality from 2007 onward, as the air pollution concentration continued to decline. Throughout the entire 18-year period, ICH-associated mortality was not associated with air pollution. CONCLUSIONS: Considering temporal and spatial trends, high concentrations of air pollutants were most likely to be associated with IS mortality. Our results strengthen the existing evidence of the deleterious effects of air pollution on IS mortality.

Enlarged left atrium may be associated with laterality of anterior circulation cardioembolic stroke.

BACKGROUND: Propensity for lesion lateralization in atrial fibrillation-related cardiac embolic stroke (AF-stroke) remains controversial. In this study, we compared the hemispheric differences among patients with AF-stroke and identified factors associated with lesion laterality. METHODS: We retrospectively reviewed patients with acute AF-stroke admitted from January, 2017 to March, 2022. Patients were grouped based on whether lesions were right or left hemispheric in the anterior circulation territory, based on diffusion-weighted imaging. Factors associated with right-side propensity were analyzed. RESULTS: Among 385 patients, the mean age was 74±11 years and 52.5 % were male. Right and left hemispheric lesions were observed in 189 (49.1 %) and 196 (50.9%) patients, respectively. In the multivariate analysis, enlarged left atrium (LA) (adjusted odds ratio [aOR]=1.03, 95% confidential interval [CI], 1.007-1.061; p=0.013) and single confluent lesion pattern (aOR= 1.55, 95% CI, 1.012-2.381; p=0.044) were associated with right hemispheric lesions. CONCLUSIONS: Enlarged LA and single confluent lesion pattern were strongly related to right-sided propensity in patients with AF-stroke.

Mycobacterium abscessus infection leads to enhanced production of type 1 interferon and NLRP3 inflammasome activation in murine macrophages via mitochondrial oxidative stress.

Mycobacterium abscessus (MAB) is a rapidly growing mycobacterium (RGM), and infections with this pathogen have been increasing worldwide. Recently, we reported that rough type (MAB-R) but not smooth type (MAB-S) strains enhanced type 1 interferon (IFN-I) secretion via bacterial phagosome escape, contributing to increased virulence. Here, we sought to investigate the role of mitochondrial oxidative stress in bacterial survival, IFN-I secretion and NLRP3 inflammasome activation in MAB-infected murine macrophages. We found that live but not heat-killed (HK) MAB-R strains increased mitochondrial ROS (mtROS) and increased release of oxidized mitochondrial DNA (mtDNA) into the cytosol of murine macrophages compared to the effects of live MAB-S strains, resulting in enhanced NLRP3 inflammasome-mediated IL-1ß and cGAS-STING-dependent IFN-I production. Treatment of the infected macrophages with mtROS-modulating agents such as mito-TEMPO or cyclosporin A reduced cytosolic oxidized mtDNA, which inhibited the MAB-R strain-induced production of IL-1ß and IFN-I. The reduced cytosolic oxidized mtDNA also inhibited intracellular growth of MAB-R strains via cytosolic escape following phagosomal rupture and via IFN-I-mediated cell-to-cell spreading. Moreover, our data showed that mtROS-dependent IFN-I production inhibited IL-1ß production, further contributing to MAB-R intracellular survival in murine macrophages. In conclusion, our data indicated that MAB-R strains enhanced IFN-I and IL-1ß production by inducing mtROS as a pathogen-associated molecular pattern (PAMP). These events also enhance bacterial survival in macrophages and dampen inflammation, which contribute to the pathogenesis of MAB-R strains.

Allergenic characterization of Bomb m 4, a 30-kDa Bombyx mori lipoprotein 6 from silkworm pupa.

BACKGROUND: Silkworm pupa (SWP) food anaphylaxis has been described frequently in Asian countries. However, false-positive reactions by skin pricks and serum IgE (sIgE) tests to the extract complicate diagnosis, requiring identification of clinically relevant major allergens. OBJECTIVES: In this study, we characterized a novel SWP allergen, Bomb m 4, a 30-kDa lipoprotein, and evaluated its diagnostic sensitivity. METHODS: Bomb m 4 was identified by a proteomic analysis. This recombinant (r)Bomb m 4 was overexpressed in Escherichia coli, and the IgE reactivity by ELISA was compared with other reported allergenic proteins: Bomb m 1 (arginine kinase), 27-kDa glycoprotein, Bomb m 3 (tropomyosin) using the serum samples from 17 SWP allergic patients and 11 asymptomatic sensitized subjects. RESULTS: rBomb m 4-specific IgE was recognized by all 17 SWP allergic patients. The 27-kDa glycoprotein and Bomb m 1 sIgE were found in 35.3% and 0%, respectively, in the SWP allergic patients. ELISA sIgE reactivity increased significantly, when 4 M urea was added in serum samples. However, only 16% inhibition of sIgE reactivity to the whole SWP extract was exhibited by rBomb m 4, whereas more than 93% of self-inhibition of rBomb m 4 sIgE was obtained, possibly due to the low abundance of Bomb m 4 in the extract. Three linear epitopes (81-95, 191-205 and 224-238 residues) of rBomb m 4 were identified. These epitopes are shown to be released by pepsin digestion. Receiver operator characteristic (ROC) analysis showed the highest diagnostic value of Bomb m 4 followed by Bomb m 1, 27-kDa glycoprotein and Bomb m 3. CONCLUSION: Bomb m 4 is the major allergen of SWP allergic patients. It has cryptic epitopes which are exposed to IgE antibodies with digestive enzymes. This recombinant Bomb m 4 allergen permits exact diagnosis of SWP allergy.

Basilar Artery Tortuosity May Be Associated with Early Neurological Deterioration in Patients with Pontine Infarction.

BACKGROUND: Early neurological deterioration (END) occurs in patients with pontine infarction that is adversely associated with a long-term functional outcome. As basilar artery (BA) tortuosity may alter hemodynamics, we investigated whether factors including BA tortuosity are associated with END and poor outcome at 3 months. METHODS: We reviewed patients with acute (<7 days from stroke onset) unilateral pontine infarction mainly involving the pontine base and/or tegmental regions from January 2017 through April 2021. END was defined as increase of ≥2 in total National Institutes of Health Stroke Scale (NIHSS) score or ≥1 in motor NIHSS score within first 72 h. A poor clinical outcome was defined as modified Rankin Scale (mRS) 3-6 at 3 months. The BA tortuosity index (TI) was measured: ([actual/straight length -1] x 100). To assess interobserver agreement, TI measurements were obtained by 2 independent raters. RESULTS: The study included 245 patients; END occurred in 72 (29.3%) and 35 (14.2%) showed poor outcome at 3 months. Old age (odds ratio [OR] = 1.03, 95% confidence interval [CI] 1.004-1.062; p = 0.027), previous stroke history (OR = 2.36, 95% CI: 1.176-4.717; p = 0.016), lower initial NIHSS (OR = 0.72, 95% CI: 0.628-0.827; p < 0.001), and high BA TI (OR = 1.17, 95% CI: 1.062-1.295; p = 0.002) were associated with END. On the other hand, old age (OR = 1.04, 95% CI: 1.002-1.073; p = 0.037) and END (OR = 3.03, 95% CI: 1.429-6.403; p = 0.004) were associated with poor outcome at 3 months. CONCLUSIONS: High BA tortuosity may be a factor associated with END in patients with pontine infarction. As END was related to unfavorable clinical outcome, this risk may have to be carefully considered in patients with high BA tortuosity.

Clinical-Diffusion Mismatch Is Associated with Early Neurological Improvement after Late-Window Endovascular Treatment.

BACKGROUND: Clinical-diffusion mismatch (CDM) and perfusion-diffusion mismatch (PDM) are used to select patients for endovascular thrombectomy (EVT) in the late-window period. As CDM well reflects true penumbra, we hypothesized that patients with CDM and PDM would respond better to EVT than those with PDM only at the late-window period. METHODS: Acute ischemic stroke patients who received EVT 6-24 h after stroke onset were included. PDM (perfusion-/diffusion-weighted image (DWI) lesion volume >1.8) was used to select candidates for EVT in this time-period in our center. CDM was defined according to the DAWN trial criteria. Response to EVT was compared between patients with and without CDM. Early neurological improvement (ENI) was defined as improvement >4 points on National Institutes of Health Stroke Scale (NIHSS) score 1 day after EVT. Multivariable analysis was performed to investigate independent factors associated with ENI. The correlation between DWI lesion volume and NIHSS score was investigated in those with and without CDM. RESULTS: Among 94 patients enrolled, all patients had PDM and 44 (46.3%) had CDM. Forty-eight patients (51.1%) showed ENI. The prevalence of hypertension, initial NIHSS score, improvement in NIHSS score after EVT, and prevalence of ENI were greater in patients with CDM than those without. ENI was independently associated with onset-to-door time (odds ratio [95% confidence interval]: 0.998 [0.997-1.000]; p = 0.042), complete recanalization (23.912 [2.238-255.489]; p = 0.009), initial NIHSS score (1.180 [1.012-1.377]; p = 0.034), and the presence of CDM (5.160 [1.448-18.386]; p = 0.011). The correlation between DWI lesion volume and initial NIHSS score was strong in patients without CDM (r = 0.731) but only moderate in patients with CDM (r = 0.355). CONCLUSION: Patients with both CDM and PDM had a better response to late-window EVT than those with PDM only.

Intramedullary parasite eggs, latent for three decades, mimicking acute transverse myelitis.

BACKGROUND: Intramedullary parasitic infection is extremely uncommon, and clinical presentation of Brown-Sequard syndrome is even rarer. CASE PRESENTATION: The authors report a case involving a 57-year-old woman with Brown-Sequard syndrome, in whom magnetic resonance imaging and clinical and epidemiological features were similar to those of acute transverse myelitis. Myelotomy suggested inflammation caused by latent parasite eggs in the spinal cord. Antiparasitic and steroid therapies were administered postoperatively. To the author's knowledge, this is the first report to describe a surgical experience for Taenia solium eggs in the spinal cord. CONCLUSION: Intramedullary parasitic infection is a diagnostic challenge that requires careful discrimination from other diseases. If parasite infection is suspected in a progressively deteriorating patient, myelotomy should be considered for rapid and accurate treatment.

High serum total cholesterol associated with good outcome in endovascular thrombectomy for acute large artery occlusion.

BACKGROUND: The effect of cholesterol on the functional outcome after endovascular thrombectomy (EVT) is still controversial. This study aimed to investigate whether the lipid profile is associated with the EVT prognosis. METHODS: We retrospectively analyzed patients with emergent large vessel occlusion who underwent EVT. The blood lipid levels were measured in the fasting state, 1 day after admission. We divided patients into terciles of serum total cholesterol (TC) levels and compared the clinical characteristics among the groups. The factors associated with a good outcome at 3 months (modified Rankin scale 0-2) were investigated, considering the stroke mechanism and recanalization status. RESULTS: Among 274 patients, good outcomes were observed in 108 (39.4%) patients. Low initial severity (odds ratio (OR), 0.91, 95% confidence interval (CI), 0.858-0.954; p < 0.001) and high TC level (1.35, 1.034-1.758; p = 0.041) were associated with good outcomes. In patients with cardioembolism, young age (0.95, 0.915-0.991; p = 0.021), low initial severity (0.92, 0.857-0.988; p = 0.024), and high TC level (1.60, 1.019-2.499; p = 0.036) were associated with good outcomes. The lipid profile was not associated with a functional outcome in those with large artery atherosclerosis. In patients with complete recanalization, young age (0.97, 0.941-0.994; p = 0.016), low initial severity (0.91, 0.864-0.961; p = 0.001), absence of diabetes (0.45, 0.218-0.947; p = 0.035) or any hemorrhage (0.33, 0.142-0.760; p = 0.009), and high TC level (1.40, 1.031-1.879; p = 0.031) were associated with good outcomes. CONCLUSIONS: A high TC level was associated with favorable outcomes after EVT, especially in patients with cardioembolism and complete recanalization.

Structural Changes of Intra and Extracranial Artery Dissection: a Study of High-Resolution Magnetic Resonance Imaging.

OBJECTIVES: The prognosis of a cerebral artery dissection is known to be benign, but the structural changes of vessel wall at follow-up are not well known. The natural course of an intracranial and extracranial artery dissection may differ due to structural differences. We aimed to figure out how stenosis and other wall features change, according to the dissection location. MATERIALS AND METHODS: We retrospectively enrolled patients who suffered an ischemic stroke or transient ischemic attack due to a dissection and who had undergone both initial and follow-up high-resolution magnetic resonance imaging (HRMRI). Patients were dichotomized to intracranial or extracranial dissection group. The clinical and HRMRI characteristics of two groups were compared. Factors associated with stenosis changes were also investigated. RESULTS: A total of 57 patients (intracranial, n = 43; and extracranial, n = 14) were enrolled. The mean age (45.6 vs. 32.2, p < 0.001) was higher and hypertension (37.2% vs. 7.1%, p = 0.04) was more frequent in the intracranial dissection group. In HRMRI analysis, stenosis improvement (27.9% vs. 85.7%, p < 0.001) were more frequent whereas residual wall enhancement (86.0% vs. 46.2%, p = 0.006) and intramural hematoma (62.8% vs. 21.4%, p = 0.007) were less frequent in the extracranial dissection group. Multivariate analysis indicated that extracranial location was the only independent factor (odds ratio 8.98, 95 % confidence interval 1.45-55.65; p = 0.02) associated with stenosis improvement. CONCLUSIONS: Younger age, stenosis improvement, disappearance of wall enhancement and intramural hematoma were more frequent in an extracranial dissection compared with an intracranial dissection. An extracranial location is independently associated with stenosis improvement in dissection patients.

Atherosclerotic Burden and Vascular Risk in Stroke Patients With Atrial Fibrillation.

Background and Purpose: Data on the effect on vascular outcomes of concomitant atherosclerotic vascular disease (ASVD) with atrial fibrillation (AF) after stroke are limited. This study evaluated the effect of ASVD with AF versus AF only on the risk of vascular events. Methods: We retrospectively analyzed a prospectively registered multicenter database involving 3213 stroke patients with AF. ASVD included extracranial atherosclerosis measured in the proximal portion of the internal carotid artery, intracranial atherosclerosis (all ≥50% stenosis), coronary artery disease, and peripheral artery disease and was categorized into 4 strata depending on the number of ASVDs (0, 1, 2, and 3­4). The independent associations of ASVD with major adverse cardiovascular events, stroke, and all-cause death were assessed. Results: A total of 2670 patients were included (mean age, 73.5±9.8 years; median CHA2DS2-VASc score, 5; interquartile range, 4−6). During the follow-up (mean, 1.7 years), a total of 672 (25.2%) major adverse cardiovascular events, 170 (6.4%) stroke events, and 501 (18.8%) all-cause deaths were noted. The adjusted hazard ratio for major adverse cardiovascular events versus no ASVD was 1.25 (95% CI, 1.00­1.56) for ASVD 1, 1.34 (95% CI, 1.02­1.76) for ASVD 2, and 1.93 (95% CI, 1.24­2.99) for ASVD 3­4. The adjusted hazard ratio for all-cause death versus no ASVD was 1.32 (1.01­1.74), 1.47 (1.06­2.03), and 2.39 (1.47­3.89), respectively. Among ASVD components, the presence of symptomatic or asymptomatic extracranial atherosclerosis was a more potent predictor of major adverse cardiovascular events (1.27 [1.05­1.54]) and all-cause death (1.45 [1.17­1.81]). Conclusions: ASVD burden with AF can be a cumulative marker of a high risk for untoward vascular outcomes. Among ASVD components, extracranial atherosclerosis seems to have a predominant effect.

The cerebellum could serve as a potential imaging biomarker of dementia conversion in patients with amyloid-negative amnestic mild cognitive impairment.

BACKGROUND AND PURPOSE: As part of network-specific neurodegeneration, changes in cerebellar gray matter (GM) volume and impaired cerebello-cerebral functional networks have been reported in Alzheimer disease (AD). Compared with healthy controls, a volume loss in the cerebellum has been observed in patients with continuum of AD. However, little is known about the anatomical or functional changes in patients with clinical AD but no brain amyloidosis. We aimed to identify the relationship between cerebellar volume and dementia conversion of amyloid-negative mild cognitive impairment (MCI). METHODS: This study was a retrospective cohort study of patients over the age 50 years with amyloid-negative amnestic MCI who visited the memory clinic of Asan Medical Center with no less than a 36-month follow-up period. All subjects underwent detailed neuropsychological tests, 3 T brain magnetic resonance imaging scans including three-dimensional T1 imaging, and fluorine-18[F18 ]-florbetaben amyloid positron emission tomography scans. A spatially unbiased atlas template of the cerebellum and brainstem was used for analyzing cerebellar GM volume. RESULTS: During the 36 months of follow-up, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The converter group had more severe impairments in all visual memory tasks. In terms of volumetric analysis, reduced crus I/II volume adjusted with total intracranial volume, and age was observed in the converter group. CONCLUSIONS: Significant cerebellar GM atrophy involving the bilateral crus I/II may be a novel imaging biomarker for predicting dementia progression in amyloid-negative amnestic MCI patients.

Pre-Admission CHADS2 and CHA2DS2-VASc Scores on Early Neurological Worsening.

BACKGROUND: Stroke risk scores (CHADS2 and CHA2DS2-VASc) not only predict the risk of stroke in atrial fibrillation (AF) patients, but have also been associated with prognosis after stroke. OBJECTIVE: The aim of this study was to evaluate the relationship between stroke risk scores and early neurological deterioration (END) in ischemic stroke patients with AF. METHODS: We included consecutive ischemic stroke patients with AF admitted between January 2013 and December 2015. CHADS2 and CHA2DS2-VASc scores were calculated using the established scoring system. END was defined as an increase ≥2 on the total National Institutes of Health Stroke Scale (NIHSS) score or ≥1 on the motor NIHSS score within the first 72 h of admission. RESULTS: A total of 2,099 ischemic stroke patients with AF were included. In multivariable analysis, CHA2DS2-VASc score (adjusted odds ratio [aOR] = 1.17, 95% confidence interval [CI] = 1.04-1.31) was significantly associated with END after adjusting for confounders. Initial NIHSS score, use of anticoagulants, and intracranial atherosclerosis (ICAS) were also found to be closely associated with END, independent of the CHA2DS2-VASc score. Multivariable analysis stratified by the presence of ICAS demonstrated that both CHA2DS2-VASc (aOR = 1.20, 95% CI = 1.04-1.38) and CHADS2 scores (aOR = 1.24, 95% CI = 1.01-1.52) were closely related to END in only patients with ICAS. In patients without ICAS, neither of the risk scores were associated with END. CONCLUSIONS: High CHA2DS2-VASc score was associated with END in ischemic stroke patients with AF. This close relationship is more pronounced in patients with ICAS.