Global hyperperfusion after successful endovascular thrombectomy is linked to worse outcome in acute ischemic stroke.

Patients with stroke may develop hyperperfusion after a successful endovascular thrombectomy (EVT). However, the relationship between post-EVT hyperperfusion and clinical outcomes remains unclear and requires further clarification. We reviewed consecutive patients with anterior circulation occlusion who were successfully recanalized with EVT. Based on post-EVT arterial spin-labeling images, hyperperfusion was categorized as follows: global hyperperfusion (GHP), increased cerebral blood flow (CBF) in ≥ 50% of the culprit vessel territory; focal hyperperfusion (FHP), increased CBF in < 50% of the culprit vessel territory; no hyperperfusion (NHP), no discernible CBF increase. Factors associated with hyperperfusion were assessed, and clinical outcomes were compared among patients under different hyperperfusion categories. Among 131 patients, 25 and 40 patients developed GHP and FHP, respectively. Compared to other groups, the GHP group had worse National Institutes of Health Stroke Scale score (GHP vs. NHP/FHP, 18.1 ± 7.4 vs. 12.3 ± 6.0; p < 0.001), a larger post-EVT infarct volume (98.9 [42.3-132.7] vs. 13.5 [5.0-34.1] mL; p < 0.001), and a worse 90-day outcome (modified Rankin Scale, 3 [1-4] vs. 2 [0-3]; p = 0.030). GHP was independently associated with infarct volume (B = 0.532, standard error = 0.163, p = 0.001), and infarct volume was a major mediator of the association of GHP with unfavorable outcomes (total effect: ß = 0.176, p = 0.034; direct effect: ß = 0.045, p = 0.64; indirect effect: ß = 0.132, p = 0.017). Patients presenting with post-EVT GHP had poorer neurological prognosis, which is likely mediated by a large infarct volume.

Regional Disparities in Prehospital Delay of Acute Ischemic Stroke: The Korean Stroke Registry.

BACKGROUND: Late hospital arrival keeps patients with stroke from receiving recanalization therapy and is associated with poor outcomes. This study used a nationwide acute stroke registry to investigate the trends and regional disparities in prehospital delay and analyze the significant factors associated with late arrivals. METHODS: Patients with acute ischemic stroke or transient ischemic attack between January 2012 and December 2021 were included. The prehospital delay was identified, and its regional disparity was evaluated using the Gini coefficient for nine administrative regions. Multivariate models were used to identify factors significantly associated with prehospital delays of >4.5 h. RESULTS: A total of 144,014 patients from 61 hospitals were included. The median prehospital delay was 460 min (interquartile range, 116-1912), and only 36.8% of patients arrived at hospitals within 4.5 h. Long prehospital delays and high regional inequality (Gini coefficient > 0.3) persisted throughout the observation period. After adjusting for confounders, age > 65 years old (adjusted odds ratio [aOR] = 1.23; 95% confidence interval [CI], 1.19-1.27), female sex (aOR = 1.09; 95% CI, 1.05-1.13), hypertension (aOR = 1.12; 95% CI, 1.08-1.16), diabetes mellitus (aOR = 1.38; 95% CI, 1.33-1.43), smoking (aOR = 1.15, 95% CI, 1.11-1.20), premorbid disability (aOR = 1.44; 95% CI, 1.37-1.52), and mild stroke severity (aOR = 1.55; 95% CI, 1.50-1.61) were found to independently predict prehospital delays of >4.5 h. CONCLUSION: Prehospital delays were lengthy and had not improved in Korea, and there was a high regional disparity. To overcome these inequalities, a deeper understanding of regional characteristics and further research is warranted to address the vulnerabilities identified.

Clonal Hematopoiesis and Acute Ischemic Stroke Outcomes.

OBJECTIVE: The effect of clonal hematopoiesis of indeterminate potential (CHIP) on the manifestation and clinical outcomes of acute ischemic stroke (AIS) has not been fully elucidated. METHODS: Patients with AIS were included from a prospective registry coupled with a DNA repository. Targeted next-generation sequencing on 25 genes that are frequently mutated in hematologic neoplasms was performed. The prevalence of CHIP was compared between patients with AIS and age-matched healthy individuals. A multivariate linear or logistic regression model was used to assess the association among CHIP and stroke severity, hemorrhagic transformation, and functional outcome at 90 days. RESULTS: In total, 380 patients with AIS (mean age = 67.2 ± 12.7 years; 41.3% women) and 446 age-matched controls (mean age = 67.2 ± 8.7 years; 31.4% women) were analyzed. The prevalence of CHIP was significantly higher in patients with AIS than in the healthy controls (29.0 vs 22.0%, with variant allele frequencies of 1.5%, p = 0.024). PPM1D was found to be most significantly associated with incident AIS (adjusted odds ratio [aOR] = 7.85, 95% confidence interval [CI] = 1.83-33.63, p = 0.006). The presence of CHIP was significantly associated with the initial National Institutes of Health Stroke Scale (NIHSS) score (ß = 1.67, p = 0.022). Furthermore, CHIP was independently associated with the occurrence of hemorrhagic transformation (65/110 clonal hematopoiesis positive [CH+] vs 56/270 CH negative [CH-], aOR = 5.63, 95% CI = 3.24-9.77, p < 0.001) and 90-day functional disability (72/110 [CH+] vs 99/270 [CH-], aOR = 2.15, 95% CI = 1.20-3.88, p = 0.011). INTERPRETATION: CH was significantly associated with incident AIS. Moreover, particularly, sequence variations in PPM1D, TET2, and DNMT3A represent a new prognostic factor for AIS. ANN NEUROL 2023;94:836-847.

Lesion Detection Through MRI Postprocessing in Pathology-Proven Focal Cortical Dysplasia: Experience at a Single Institution in the Republic of Korea.

BACKGROUND AND PURPOSE: Focal cortical dysplasia (FCD) is one of the most common causes of drug-resistant epilepsy, and necessitates a multimodal evaluation to ensure optimal surgical treatment. This study aimed to determine the supportive value of the morphometric analysis program (MAP) in detecting FCD using data from a single institution in Korea. METHODS: To develop a standard reference for the MAP, normal-looking MRIs by two scanners that are frequently used in this center were chosen. Patients with drug-resistant epilepsy and FCD after surgery were candidates for the analysis. The three-dimensional T1-weighted MRI scans of the patients were analyzed as test cases using the MAP. RESULTS: The MRI scans of 87 patients were included in the analysis. The radiologist detected abnormal findings correlated with FCD (RAD positive [RAD(+)]) in 34 cases (39.1%), while the MAP could detect FCD in 25.3% of cases. A combination of the MAP (MAP[+] cases) with interpretations by the radiologist increased the detection to 42.5% (37 cases). The lesion detection rate was not different according to the type of reference scanners except in one case. MAP(+)/RAD(-) presented in three cases, all of which had FCD type IIa. The detection rate was slightly higher using the same kind of scanner as a reference, but not significantly (35.0% vs. 22.4% p=0.26). CONCLUSIONS: The results of postprocessing in the MAP for detecting FCD did not depend on the type of reference scanner, and the MAP was the strongest in detecting FCD IIa. We suggested that the MAP could be widely utilized without developing institutional standards and could become an effective tool for detecting FCD lesions.

Clinicoradiologic data of familial cerebral cavernous malformation with age-related disease burden.

OBJECTIVE: Familial cerebral cavernous malformation (FCCM) is an autosomal dominant disease induced by loss-of-function mutations in three CCM genes, KRIT1, CCM2, and PDCD10. However, previous studies paid little attention to analyzing the radiologic features and age-related disease burden according to the genes. Therefore, we retrospectively reviewed the genetic tests of our center's clinical FCCM patients. METHOD: This study investigated clinical FCCM patients with multiple lesions or a family history of CCMs who underwent the FCCM gene (KRTI1, CCM2, and PDCD10) panel test. The clinical, genetic, and radiologic features were analyzed. RESULT: Among the patients (n = 34) undergoing the FCCM gene test, twenty-seven patients had CCM confirmed by brain MRI, and twenty-one patients were considered to have FCCM (cohort 1). In cohort 1, thirteen patients had mutations in the FCCM gene, but eight did not. Cohort 2 comprised cohort 1 and four family members with the same mutation as the probands. Six novel variants in CCM genes were detected (KRIT1 c.22_26del, c.815dup, c.1094_1098del, c.1147-2A>G, c.2124dup, and PDCD10 c.150 + 1dup). Cohort 1 demonstrated that brainstem lesions were mostly associated with the mutation detection in CCM genes (brainstem, lateral temporal, and parietal lesions vs. lateral temporal and parietal lesions, AUC 0.928 vs. 0.779, P = 0.0389). The radiologic severity worsened according to age in the KRIT1 group compared with the Mutation not detected group (correlation coefficient 0.75 (P < 0.001) versus 0.53 (P = 0.004)). CONCLUSION: The brainstem lesion could be the radiologic marker for FCCM with the mutation detected. The age-related disease burden regarding FCCM according to genetic information was demonstrated.

Classification of white matter lesions and characteristics of small vessel disease markers.

OBJECTIVES: Radiological markers for cerebral small vessel disease (SVD) may have different biological underpinnings in their development. We attempted to categorize SVD burden by integrating white matter signal abnormalities (WMSA) features and secondary presence of lacunes, microbleeds, and enlarged perivascular spaces. METHODS: Data were acquired from 610 older adults (aged > 40 years) who underwent brain magnetic resonance imaging exam as part of a health checkup. The WMSA were classified individually by the number and size of non-contiguous lesions, distribution, and contrast. Age-detrended lacunes, microbleeds, and enlarged perivascular space were quantified to further categorize individuals. Clinical and laboratory values were compared across the individual classes. RESULTS: Class I was characterized by multiple, small, deep WMSA but a low burden of lacunes and microbleeds; class II had large periventricular WMSA and a high burden of lacunes and microbleeds; and class III had limited juxtaventricular WMSA and lacked lacunes and microbleeds. Class II was associated with older age, diabetes, and a relatively higher neutrophil-to-lymphocyte ratio. Smoking and higher uric acid levels were associated with an increased risk of class I. CONCLUSION: The heterogeneity of SVD was categorized into three classes with distinct clinical correlates. This categorization will improve our understanding of SVD pathophysiology, risk stratification, and outcome prediction. KEY POINTS: • Classification of white matter signal abnormality (WMSA) features was associated with different characteristic of lacunes, microbleeds, and enlarged perivascular space and clinical variability. • Class I was characterized by multiple, small, deep WMSA but a low burden of lacunes and microbleeds. Class II had large periventricular WMSA and a high burden of lacunes and microbleeds. Class III had limited juxtaventricular WMSA and lacked lacunes and microbleeds. • Class II was associated with older age, diabetes, and higher neutrophil-to-lymphocyte ratio. Smoking and higher uric acid levels were associated with an increased risk of class I.

Increased pulsatility index of the basilar artery is a risk factor for neurological deterioration after stroke: a case control study.

BACKGROUND: Higher pulsatility of the middle cerebral artery (MCA) is known to be associated with stroke progression. We investigated whether pulsatility index (PI) of the basilar artery (BA) can predict neurological deterioration (ND) after acute cerebral infarction. METHODS: A total of 708 consecutive patients with acute ischemic stroke who had undergone transcranial Doppler (TCD) ultrasonography were included. ND was defined as an increase in the National Institutes of Health Stroke Scale scores by two or more points after admission. The patients were categorized into quartiles according to BA PI. Multivariable logistic regression analysis was performed to examine whether BA PI is independently associated with ND. RESULTS: BA PI was well correlated with the right (n = 474, r2 = 0.573, P < 0.001) by Pearson correlation analysis although MCA PI could not be measured from right MCA (n = 234, 33.05%) and left MCA (n = 252, 35.59%) by TCD owing to insufficient temporal bone window. Multivariable logistic regression analysis including age, sex, cerebral atherosclerosis burden, National Institutes of Health Stroke Scale at admission, and the proportion of patients with current smoking status, hypertension, diabetes mellitus, atrial fibrillation revealed that the higher BA PI (odds ratio, 3.28; confidence interval, 1.07-10.17; P = 0.038) was independently associated with ND. CONCLUSIONS: BA PI, which would be identified regardless of temporal window, could predict ND among acute stroke patients.

Neuroimaging features of antiphospholipid antibody-related stroke compared with atrial fibrillation-related stroke.

Recognizing the lesion pattern of antiphospholipid antibody-related stroke (aPL-stroke) may contribute to establishing the cause in patients with cryptogenic stroke. We aimed to describe the neuroimaging features of aPL-stroke compared with atrial fibrillation-related stroke (AF-stroke), a major hidden cause of cryptogenic stroke. Using a prospective stroke registry, we identified consecutive aPL- and AF-stroke patients without other potential causes of stroke. Neuroimaging features based on diffusion-weighted imaging and angiographic findings at admission were compared. A total of 56 and 333 patients were included in the aPL- and AF-stroke groups, respectively. aPL-stroke patients more often presented with single small lesions (aPL-stroke, 30.4% vs. AF-stroke, 7.5%, p < 0.001), while the predominant pattern in AF-stroke patients was large territorial lesions (26.8% vs. 56.5%, p < 0.001). aPL-stroke patients had smaller infarct volume (1.58 mL [0.45; 9.41] vs. 11.32 mL [2.82; 33.08], p < 0.001) and less experience of relevant artery occlusion (17.9% vs. 54.7%, p < 0.001). The proportion of multi-territory lesions, an embolic pattern, was similar between the two groups (28.6% vs. 22.8%, p = 0.44). In comparison only including patients with multi-territory lesions as well, aPL-stroke patients showed small lesion dominance and smaller infarct volume. Multivariate analyses showed independent associations between mild neuroimaging features (small lesion prevalence, smaller infarct volume, and absence of relevant artery occlusion) and aPL-stroke. Patterns of small lesion prevalence, small infarct volume, and absence of relevant artery occlusion were suggestive of aPL-stroke rather than AF-stroke. Cryptogenic stroke patients with such neuroimaging features may benefit from aPL testing for a precise diagnosis.

Neuropsychiatric symptoms and seizure related with serum cytokine in epilepsy patients.

Neuroinflammation contributes to epileptogenesis and ictogenesis. Various signals of neuroinflammation lead to neuronal hyper-excitability. Since an interplay between epilepsy, psychiatric comorbidities and neuroinflammation has been suggested, we explored psychiatric symptoms in epilepsy patients, and the relationship with neuroinflammation. We screened epilepsy patients who were admitted for video-EEG monitoring between July 2019 and December 2020. Enrolled patients were asked to respond to neuropsychiatric questionnaires (Hospital Anxiety and Depression Scale (HADS) and Neuropsychiatric Inventory-Questionnaire (NPI-Q)) on admission. Serum cytokines (IL-1ß, IL-2, IL-6, IFN-γ, CCL2, and CCL5) were measured by ELISA on admission, and within 6 h after a seizure. We enrolled 134 patients, and 32 patients (23.9%) had seizures during monitoring. Cytokine levels did not change after seizures, but IL-2 and IL-6 increased in cases of generalized tonic-clonic seizures. The HADS-A score was lower in Q4 of CCL5 (p-value = 0.016) and anxiety was also less common in Q4 of CCL5 (p-value = 0.042). NPI-Q question 4 (depression) severity was higher in CCL2 (p-value = 0.024). This suggested that psychiatric symptoms may also be related to inflammatory processes in epilepsy patients. Further large, standardized studies are necessary to underpin the inflammatory mechanisms in epilepsy and psychiatric symptoms.

Isolated CNS involvement in eosinophilic granulomatosis with polyangiitis treated with mepolizumab: A case report.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a systemic vasculitis disease involving small-sized vessels. The literature has reported involvement of the central nervous system (CNS) in 5% cases, and isolated CNS involvement is extremely rare. Due to its rarity and scarcity of clinical data, standardized treatment of isolated CNS involvement in EGPA is unclear. Mepolizumab, an anti-interleukin-5 monoclonal antibody, was previously introduced to treat EGPA with longer remission period, more patients showing remission, and reduction in prednisolone dose of those who already taking prednisolone compared to placebo. We describe a case of isolated CNS involvement in EGPA, confirmed by brain biopsy and treated with mepolizumab, which was refractory to conventional immunotherapy.

Proportion of peripheral regulatory T cells in patients with autoimmune encephalitis.

Purpose: Regulatory T cells (Tregs) play a crucial role in maintaining immune tolerance. Any deficiency or dysfunction of the Tregs can influence the pathogenesis of autoimmune disease. This study aimed to assess the role of Tregs among patients with autoimmune encephalitis (AE) with different autoantibody types and to evaluate their association with clinical features. Methods: This was a cross-sectional observational study involving 29 patients with AE. Peripheral blood was sampled from each patient for flow cytometric analysis. Proportions of CD4+CD25+ and CD4+CD25+Foxp3+ Tregs were calculated and compared between the antibody types (synaptic, paraneoplastic, and undetermined). Associations between the proportion of Tregs and clinical features were also evaluated. Results: Five patients had synaptic autoantibodies, five had paraneoplastic autoantibodies, and the others were of an undetermined type. The proportion of CD4+CD25+ Tregs tended to be higher in those with paraneoplastic antibodies than in those with synaptic antibodies (post-hoc p = 0.028) and undetermined antibody status (post-hoc p = 0.043). A significant negative correlation was found between the proportion of Tregs and the initial modified Rankin score (r = -0.391, p = 0.036). Those who received intravenous immunoglobulin had lower proportions of Tregs than those who did not. Conclusion: The results of the present study suggest that Tregs may play different roles according to the type of AE and may be linked to disease severity.

Refractory neuro-Sweet disease successfully treated with tocilizumab and mycophenolate mofetil.

Sweet syndrome, or acute febrile neutrophilic dermatosis, is mainly a dermatologic condition presenting with erythematous plaques; however, neutrophils infiltrate multiple systems. Neuro-Sweet disease is a neurological manifestation of Sweet syndrome and a rare cause of recurrent aseptic meningoencephalitis, which needs to be distinguished from neuro-Behçet disease. Although neuro-Sweet disease generally responds well to corticosteroids, relapsing neuro-Sweet disease is not an exceptional case. Herein, we present a case of a 51-year-old male with recurrent encephalitis followed by erythematous plaques. The patient was confirmed as Sweet syndrome based on skin biopsy and showed partial response to corticosteroids. With intravenous immunoglobulin, rituximab, tocilizumab, and mycophenolate mofetil, his neurologic symptoms were fully recovered.

Patterns of pontine strokes mimicking Bell's palsy.

BACKGROUND: Peripheral-type facial palsy very rarely arises from pontine stroke. We attempted to identify unique clinico-radiologic patterns associated with this condition. CASE PRESENTATION: Patients with pontine tegmentum stroke and acute onset of peripheral-type facial weakness were reviewed from the acute stroke registry of a tertiary hospital. The clinico-radiologic patterns of 10 patients were classified into one of three types based on the respective stroke mechanism. Type A (n = 5) was characterized by relatively diverse clinical presentations and larger, multiple infarctions resulting from large-artery atherosclerosis. Three cases with small lacunar infarcts were classified to type B (small vessel occlusion), and they showed only limited symptoms including horizontal gaze disturbance and facial paralysis. The two hemorrhagic cases (type C) presented with a focal pontine hemorrhage, likely due to a cavernous hemangioma. CONCLUSIONS: Peripheral-type facial palsy often occurs in pontine stroke with specific patterns. Type recognition helps to determine the underlying mechanism and the appropriate clinical approach. In particular, focal pontine tegmental infarctions showing stereotypic combinations of ophthalmoplegia and peripheral-type facial weakness (type B) might be recognized as a new type of lacunar syndrome.

Radiological features and outcomes of essential thrombocythemia-related stroke.

BACKGROUND: Essential thrombocythemia (ET) is known to be associated with an increased vascular event, but the stroke patterns and prognosis have not been studied. METHODS: Between January 2013 and December 2017, acute ischemic stroke patients with ET who were admitted to two tertiary hospital stroke centers in Seoul, Korea were included. We retrospectively reviewed their clinical, laboratory and imaging data. Stroke mechanism was determined as ET-only when no atherosclerotic, cardioembolic, or lacunar stroke etiology was demonstrated and as ET-plus group when any specific etiology was combined. Each group was analyzed to ascertain stroke patterns and outcomes. RESULTS: A total of 26 patients were included, and their mean age was 66 ±â€¯17 years, including 12 female patients. There were 12 ET-only cases and 14 ET-plus cases per stroke mechanism. The ET-plus group included 7 large artery atherosclerosis, 5 small vessel occlusion, and 2 cardioembolic cases. Multiple scattered lesions involving multiple vascular territories were more prevalent in the ET-only group. Poor outcome (modified Rankin scale >2 at discharge) was noted in 13 cases (50.0%), and old age, female sex, prior diagnosis of ET to stroke and low hemoglobin level were associated with poor outcome. CONCLUSION: ET-related stroke displayed a characteristic infarction pattern, such as multiple embolisms.

Development of the clinical assessment scale in autoimmune encephalitis.

OBJECTIVE: There is no scale for rating the severity of autoimmune encephalitis (AE). In this study, we aimed to develop a novel scale for rating severity in patients with diverse AE syndromes and to verify the reliability and validity of the developed scale. METHODS: The key items were generated by a panel of experts and selected according to content validity ratios. The developed scale was initially applied to 50 patients with AE (development cohort) to evaluate its acceptability, reproducibility, internal consistency, and construct validity. Then, the scale was applied to another independent cohort (validation cohort, n = 38). RESULTS: A new scale consisting of 9 items (seizure, memory dysfunction, psychiatric symptoms, consciousness, language problems, dyskinesia/dystonia, gait instability and ataxia, brainstem dysfunction, and weakness) was developed. Each item was assigned a value of up to 3 points. The total score could therefore range from 0 to 27. We named the scale the Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The new scale showed excellent interobserver (intraclass correlation coefficient [ICC] = 0.97) and intraobserver (ICC = 0.96) reliability for total scores, was highly correlated with modified Rankin scale (r = 0.86, p < 0.001), and had acceptable internal consistency (Cronbach α = 0.88). Additionally, in the validation cohort, the scale showed high interobserver reliability (ICC = 0.99) and internal consistency (Cronbach α = 0.92). INTERPRETATION: CASE is a novel clinical scale for AE with a high level of clinimetric properties. It would be suitable for application in clinical practice and might help overcome the limitations of current outcome scales for AE. ANN NEUROL 2019;85:352-358.

LGI1 expression and human brain asymmetry: insights from patients with LGI1-antibody encephalitis.

BACKGROUND: While brain asymmetry has been a fascinating issue in neuroscience, the critical mechanism remains to be elucidated. Based on some index cases with asymmetric 18F-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) uptake in leucine-rich glioma-inactivated 1 (LGI1)-antibody encephalitis, we hypothesized LGI1 expression could be asymmetrically distributed in the human brain. METHODS: We enrolled 13 patients who were diagnosed with LGI1-antibody encephalitis between June 2012 and January 2018 at Seoul National University Hospital. Their pretreatment 18F-FDG-PET images were analyzed to find asymmetry between the left and right hemispheres. Guided by these observations, expression of LGI1 in the human hippocampus and the globus pallidus of both cerebral hemispheres was studied in nine post-mortem human brains. RESULTS: Eleven of the 13 LGI1-antibody encephalitis patients (84.6%) showed asymmetrical FDG high uptake in the hippocampus: nine (81.8%) on the left hippocampus and two (18.2%) on the right. In the basal ganglia, seven patients (53.8%) showed asymmetry: four (57.1%) on the left and three (42.9%) on the right. The asymmetry was not evident in the laterality of faciobrachial dystonic seizures, brain MRI, and EEG. When the expression of LGI1 protein was analyzed in nine post-mortem human brains by western blotting, LGI1 expression was higher on eight left globus pallidus samples (88.89%, P = 0.019) and on four left hippocampal samples (44.44%, P = 0.652), compared to their right hemisphere samples. CONCLUSIONS: Imaging parameters from patients with LGI1-antibody encephalitis and studies of LGI1 protein expression suggest that LGI1 is asymmetrically distributed in the human brain. These observations have implications for our understanding of human brain development.

Increased adverse events associated with antiepileptic drugs in anti-leucine-rich glioma-inactivated protein 1 encephalitis.

Anti-leucine-rich glioma-inactivated protein 1 (LGI1) encephalitis is a rare autoimmune condition presenting mainly as altered mental state, cognitive dysfunction, and seizure. Antiepileptic drugs (AEDs) are usually initiated to control seizures despite their limited efficacy; however, accumulating clinical experience suggests a high incidence of adverse reactions to AEDs in anti-LGI1 encephalitis. We reviewed the medical records of patients who were diagnosed with anti-LGI1 encephalitis to analyze the adverse effects of AEDs in these patients. Among the 20 patients who were treated with AEDs, 10 (50%) changed their AEDs due to adverse cutaneous drug reaction. Eight of them presented with maculopapular eruption, one with drug rash with eosinophilia and systemic symptoms syndrome, and one with eczema. Causative agents mostly consisted of aromatic AEDs. Oxcarbazepine was discontinued in two additional patients due to hyponatremia. Six patients (30%) discontinued their dose of levetiracetam because of psychiatric manifestations including irritability/aggressive behavior (four patients), insomnia (one patient), and depressive mood (one patient). Clinicians should consider adverse cutaneous drug reaction, psychiatric adverse events, and hyponatremia when selecting AEDs for the treatment of anti-LGI1 encephalitis.

Case of Rickettsia typhi-induced Brain Abscess Mimicking Brain Tumor.

Murine typhus is one of the most prevalent rickettsial infections in the world, caused by the bacterial genus Rickettsia. Though the disease manifests a relatively benign clinical course with fever, rash, and headache being the 3 classic symptoms, neurological complications may arise in patients that could become permanent. In this case study, a patient with a brain abscess caused by R typhi infection is described. Based upon the recent reemergence of arthropod-borne disease, the findings in this case are significant; R typhi can cause a brain abscess that mimics a brain tumor, which delays the diagnosis and appropriate management of the disease. Murine typhus should always be considered when performing the differential diagnosis of brain abscesses in South Korea.

Assessing Impact of High-Dose Pitavastatin on Carotid Artery Elasticity with Speckle-Tracking Strain Imaging.

AIM: Speckle-tracking imaging has been introduced for the precise assessment of vessel mechanics. However, there are no data on the role of this imaging tool in assessing the changes in vasculature with statin therapy, which is known to enhance vascular elasticity. METHODS: This study was a prospective study including 48 statin-naïve patients (age, 58.2±8.4 years; 29.2% male) with hypercholesterolemia. Circumferential carotid artery strain (CAS) and stiffness index (ß2) were measured using speckle-tracking imaging before and after 3 months of high-dose pitavastatin treatment (4 mg daily). For the comparison, we measured conventional carotid elasticity parameters and intima-media thickness using B-mode ultrasound at the same time points. RESULTS: Compared with baseline, there was significant improvement in circumferential CAS (2.98%±1.18% to 3.40%±1.43%, p=0.008) and ß2 (0.19±0.07 to 0.17±0.08, p=0.047) after statin therapy. Contrariwise, there were no significant changes in all conventional carotid elasticity metrics and intima-media thickness. When stratifying patients into two subgroups by 10 year atherosclerotic cardiovascular disease (ASCVD) risk, speckle-tracking-derived circumferential CAS and ß2 improved significantly only in patients with ASCVD risk ≥ 7.5%. CONCLUSIONS: Short-term treatment with high-dose pitavastatin improved carotid artery elasticity measured by speckle-tracking method, but not conventional parameters by B-mode ultrasound. Speckle-tracking-based measurements may allow the early noninvasive assessment of statin effects on vascular function in hypercholesterolemic patients.