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Background: Calcitonin gene-related peptide monoclonal antibodies (CGRP mAbs) are a breakthrough migraine treatment, but long-term compliance under limited public insurance coverage has not been well known. This study explores one-year treatment patterns and outcomes of CGRP mAbs using real-world data. Methods: This multicenter retrospective study included migraine patients treated with CGRP monoclonal antibodies (CGRP mAbs) from July 2022 to June 2023. Treatment discontinuation was defined as a gap of over 60 days between injections. Among patients with 12 months of follow-up, adherence was measured using the Proportion of Days Covered (PDC), calculated as the ratio of days covered to the follow-up duration, with PDC ≥ 80% indicating good adherence. Efficacy was also assessed, defined as a ≥50% reduction in monthly headache days and acute medication use. Results: The study included 140 patients (mean age 44.6 ± 12.1 years; 82.9% female). Migraine without aura was predominant (93.6%), and 65.0% had chronic migraine. CGRP mAbs discontinuation occurred in 71.4% of patients, primarily due to headache improvement (22.9%) or lack of efficacy (15.0%). Among 81 patients with 12 months of follow-up, good adherence was observed in 40.7% of patients. Among these patients, 60.6% achieved a ≥50% reduction in monthly headache days, and 51.9% showed a ≥50% reduction in monthly acute medication use. Conclusions: More than two-thirds of patients discontinued the CGRP mAb within 1 year, so these findings emphasize the need for strategies to improve adherence and optimize follow-up plans to enhance patient support. [ABSTRACT FROM AUTHOR]

Objective Methods Results Interpretation This study aimed to evaluate the potential of exercise as an abortive treatment for patients with cluster headache (CH).A cross‐sectional survey was conducted among CH patients at a single center in Korea. Demographics and headache characteristics were compared between those who found exercise effective and those who did not. We analyzed the type and intensity of exercise used. Headache improvement was measured as intensity reduction, with ≥50% improvement defined as a reduction in intensity by half or more. Exercise intensity was categorized as moderate (“possible to talk but hard to sing”) or high (“difficult to speak without pausing”). Case reports of patients exercising during CH attacks were also reviewed.Among 167 registered CH patients, 136 patients provided responses about exercise during CH attacks; 39.7% (54/136) attempted exercise as treatment. Improvement was reported by 42.6% (23/54), with ≥50% improvement in 29.6% (16/54). Patients who found exercise effective had lower Headache Impact Test‐6 scores. Effective exercises included running (39.1%), squats (30.4%), and stair climbing (21.7%), with high‐intensity exercise effective for 52.2% and moderate intensity for 43.5%. Among the 23 patients who benefited from exercise, 18 reported their most effective treatment, which were exercise alone in 50% (9/18), followed by exercise with triptans in 38.9% (7/18), and oxygen with or without triptans in 5.5% (1/18).About 40% of CH patients attempted exercise for acute CH management, with 30% experiencing over 50% improvement. While evidence is limited, exercise may help alleviate headaches and could be considered an adjunctive treatment for CH attacks. [ABSTRACT FROM AUTHOR]

Objective: Epilepsy is a suitable target for gene panel sequencing because a considerable portion of epilepsy is now explained by genetic components, especially in syndromic cases. However, previous gene panel studies on epilepsy have mostly focused on pediatric patients. Methods: We enrolled adult epilepsy patients meeting any of the following criteria: family history of epilepsy, seizure onset age ≤ 19 years, neuronal migration disorder, and seizure freedom not achieved by dual anti‐seizure medications. We sequenced the exonic regions of 211 epilepsy genes in these patients. To confirm the pathogenicity of a novel MTOR truncating variant, we electroporated vectors with different MTOR variants into developing mouse brains. Results: A total of 92 probands and 4 affected relatives were tested, and the proportion of intellectual disability (ID) and/or developmental disability (DD) was 21.7%. As a result, twelve probands (13.0%) had pathogenic or likely pathogenic variants in the following genes or regions: DEPDC5, 15q12‐q13 duplication (n = 2), SLC6A1, SYNGAP1, EEF1A2, LGI1, MTOR, KCNQ2, MEF2C, and TSC1 (n = 1). We confirmed the functional impact of a novel truncating mutation in the MTOR gene (c.7570C > T, p.Gln2524Ter) that disrupted neuronal migration in a mouse model. The diagnostic yield was higher in patients with ID/DD or childhood‐onset seizures. We also identified additional candidate variants in 20 patients that could be reassessed by further studies. Significance: Our findings underscore the clinical utility of gene panel sequencing in adult epilepsy patients suspected of having genetic etiology, especially those with ID/DD or early‐onset seizures. Gene panel sequencing could not only lead to genetic diagnosis in a substantial portion of adult epilepsy patients but also inform more precise therapeutic decisions based on their genetic background. Plain Language Summary: This study demonstrated the effectiveness of gene panel sequencing in adults with epilepsy, revealing pathogenic or likely pathogenic variants in 13.0% of patients. Higher diagnostic yields were observed in those with neurodevelopmental disorders or childhood‐onset seizures. Additionally, we have shown that expanding genetic studies into adult patients would uncover new types of pathogenic variants for epilepsy, contributing to the advancement of precision medicine for individuals with epilepsy. In conclusion, our results highlight the practical value of employing gene panel sequencing in adult epilepsy patients, particularly when genetic etiology is clinically suspected. [ABSTRACT FROM AUTHOR]

Microgels were prepared by taking advantage of electrostatic interaction between poly(N-isopropylacrylamide- co-methacrylic acid) and poly( N-isopropylacrylamide- co-dimethylaminoethylmethacrylate). The maximum interaction, investigated by measuring the size of complex and the turbidity of the mixture, took place at pH = 6.5. The microgel prepared at pH = 6.5 using the copolymer ratio of 1/1 (w/w) was globular on scanning electron microscopy, and the size was a few to tens of micrometer. The phase transition of the microgel, observed by turbidometry and differential scanning calorimetry, occurred around 31°C. % Release, in 24 h at room temperature, of FITC-dextran from the microgel was higher under an acidic (64% at pH = 4.0) and an alkali condition (69 % at pH = 9.0) than the % release at pH = 6.5 (41%). The disintegration of microgels would be responsible for the higher % release. The % releases, in 24 h at pH = 6.5, were lower at higher temperatures (53% at 35°C, 50% at 40°C) than at lower temperatures (71% at 25°C, 61% at 30°C). The suppressed release at higher temperatures is possibly due to the skin formation on the surface of microgel. © 2012 Wiley Periodicals, Inc. J Appl Polym Sci, 2012 [ABSTRACT FROM AUTHOR]