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The aim of the study was to evaluate the concomitant psychiatric disorders of anxiety and depression in patients with epilepsy caused by low-grade brain tumors (LBTs). We retrospectively reviewed the clinical data of patients who underwent preoperative neuropsychological evaluations of anxiety and depression and subsequent epilepsy surgery for LBTs. The univariate and multivariate analyses were conducted to analyze the risk factors of the occurrence of anxiety and depression. Of the 107 patients included in the study, 42 patients (39.3%) were female, and 28 patients (26.2%) were children. The median age at surgery was 22 years (interquartile range [IQR]: 17–27 years old), the median age of seizure onset was 12 years (IQR: 6–18 years old), and the median duration of epilepsy was 84 months (IQR: 42–180 months). In total, 21 patients (19.6%) had psychiatric disorders of anxiety, and 26 patients (24.3%) had psychiatric disorders of depression. Through univariate and multivariate analysis, discordant (vs. concordant) interictal electroencephalogram (EEG) findings were found to be related to the presence of anxiety (P = 0.035, odds ratio [OR] = 3.35). Discordant (vs. concordant) ictal EEG findings (P = 0.015, OR = 4.44) and temporal location of tumor (P = 0.015, OR = 13.52) were found to be associated with the presence of depression. Psychiatric disorders of anxiety and/or depression could frequently occur in patients with epilepsy caused by LBTs. Thus, early screening and mental intervention are necessary, especially for those with discordant or wider epileptic discharges and temporal invasion of tumors. [ABSTRACT FROM AUTHOR]

Aims: Previous studies suggest potential associations between epilepsy, anti‐epileptic drugs (AEDs), and levels of vitamin D and vitamin D‐binding protein (VDBP). This study aims to investigate the causal relationships among these variables using Mendelian Randomization (MR) methods. Methods: Using summary data from genome‐wide association studies on serum 25‐hydroxyvitamin D [25(OH)D] levels (N = 417,580), VDBP concentrations (N = 65,589), and various types of epilepsy (Ncases = 27,559), MR analyses were conducted to determine bidirectional causal relationships among these variables. Additionally, eQTL data from eQTLGen (N = 31,684) were employed to model the effects of AEDs and evaluate their causal impact on both biomarkers. Results: No causal relationships were found between serum 25(OH)D or VDBP levels and epilepsy. Although genetically predicted focal epilepsy risk was potentially associated with increased serum 25(OH)D levels (OR 1.031, 95% CI: 1.006–1.058, p = 0.017), and a higher genetic risk of juvenile myoclonic epilepsy was linked to lower VDBP levels (OR 0.977, 95% CI: 0.961–0.993, p = 0.004), both associations lost significance after multiple correction. Furthermore, significant associations were observed between serum 25(OH)D levels and AED target genes SCN4A, GABBR1, CA13, ALDH5A1, and CA8. No significant associations were found between AED target genes and VDBP levels after correction. Conclusion: No causal relationships were found between genetically determined serum 25(OH)D levels, VDBP, and epilepsy or its subtypes. Furthermore, the use of AEDs, such as Carbamazepine, Oxcarbazepine, Progabide, and Valproic Acid, reduces serum 25(OH)D levels, while not affect VDBP levels. [ABSTRACT FROM AUTHOR]

Introduction: The centromedian nucleus (CM) of the thalamus is essential for arousal, attention, sensory processing, and motor control. Neuromodulation targeting CM dysfunction has shown efficacy in various neurological disorders. However, its individualized precise transcranial magnetic stimulation (TMS) remains unreported. Using resting‐state functional MRI, we mapped CM‐based functional connectivity (CM‐FC) to develop a personalized TMS scheme for neurological conditions. Methods: We first analyzed the CM‐FC patterns of healthy subjects via 10 scanning sessions in three MRI scanners spanning two subject groups: one from the Human Connectome Project (n = 20, four sessions) dataset and the other from Hangzhou Normal University (n = 20, three sessions of 3 T MRI and three sessions of 1.5 T MRI). Pearson's correlation was used for CM‐FC evaluation. Then, we proposed an overlapping index ranging from 1 to 10, and group‐level clusters with the highest overlapping index located 4 cm beneath the scalp were identified. In the individual CM‐FC map, watershed image segmentation was used to obtain an individual cluster. The peak voxel with the highest FC value within the individual cluster was defined as a potential individualized target for future TMS. Results: The spatial FC patterns were remarkably similar between the left and right CMs. CMs have widespread positive connectivity with cortical areas, including the sensorimotor cortex, supplementary motor area, middle frontal cortex, medial temporal cortex, and middle cingulate. Among the group‐level FC patterns of the left and right CMs, only the left CM had a group cluster in the left primary sensorimotor cortex (PSMC, cluster size = 51) with an overlapping index of 10, that is, 10 sessions showed significant CM‐FC. Conclusions: The left PSMC exhibited reproducible FC with the left CM. The individual peak FC location in the left PSMC could be used as a TMS target for indirect modulation of CM activity and aid in the treatment of CM‐related neurological disorders. [ABSTRACT FROM AUTHOR]

Purpose: Sturge-Weber syndrome (SWS), a rare congenital neurological and skin disorder, is frequently associated with drug-resistant epilepsy. Translocation of high mobility group box 1 (HMGB1) protein from the nucleus to the cytoplasm or extracellular milieu has been implicated in neuroinflammatory processes contributing to the development of epileptogenesis. This study aimed to explore the expression and distribution of HMGB1 in brain tissue from SWS patients with drug-resistant epilepsy, with the goal of elucidating its potential involvement in the pathogenesis of epilepsy. Patients and Methods: The study enrolled eight patients with drug-resistant epilepsy who underwent hemispherectomy. Brain tissue specimens were obtained and analyzed using immunofluorescence staining to detect HMGB1 distribution in microglia, astrocytes, or different neuronal subtypes. Correlation analyses were performed to investigate the potential relationship between HMGB1 translocation within cells and the clinical characteristics of SWS patients. Results: In lesional tissues of SWS patients, we observed significantly higher cytoplasmic HMGB1 levels. Meanwhile, HMGB1 was widely distributed in the cytoplasm of microglia and neurons, while in astrocytes, it was primarily localized in the nucleus. This translocation occurred across many neuronal subtypes, including excitatory glutamatergic, inhibitory GABAergic, and cholinergic neurons. The lower proportion of HMGB1-translocated cholinergic neurons was seen compared to the other two neuronal subtypes. Furthermore, no correlation was found between cytoplasmic HMGB1 levels and clinical characteristics of SWS patients. Conclusion: The results suggest the involvement of HMGB1 in the pathogenesis of drug-resistant epilepsy in SWS patients. Additional research is required to elucidate the precise mechanisms and potential therapeutic targets associated with HMGB1 that underlie the epilepsy linked to SWS. [ABSTRACT FROM AUTHOR]

Aims: Deep brain stimulation (DBS) is not routinely performed in elderly patients (≥75 years old) to date because of concerns about complications and decreased benefit. This study aimed to evaluate the safety and efficacy of DBS in elderly patients with Parkinson's disease. Methods: A retrospective analysis was performed using data from 40 elderly patients from four centers who were treated with neurosurgical robot‐assisted DBS between September 2016 and December 2021. These patients were followed up for a minimum period of 2 years, with a subgroup of nine patients followed up for 5–7 years. Patient demographic characteristics, surgical information, pre‐ and postoperative motor scores, non‐motor scores, activities of daily living, and complications were retrospectively analyzed. Results: The mean surgical procedure duration was 1.65 ± 0.24 h, with a mean electrode implantation duration of 1.10 ± 0.23 h and a mean pulse generator implantation duration of 0.55 ± 0.07 h. The mean pneumocephalus volume, electrode fusion error, and Tao's DBS surgery scale were 16.23 ± 12.81 cm3, 0.81 ± 0.23 mm, and 77.63 ± 8.08, respectively. One patient developed a skin infection, and the device was removed. The Unified Parkinson's disease rating scale, Unified Parkinson's disease rating scale of Part III, tremor, rigidity, bradykinesia, axial, and Barthel index for activities of daily living (ADL‐Barthel) scores significantly improved at the 2‐year follow‐up (p < 0.05). The levodopa equivalent daily dose (LEDD) was significantly reduced at the 2‐year follow‐up (p < 0.05). However, the Montreal cognitive assessment, Hamilton depression scale, and Hamilton anxiety scale scores did not significantly change during the 2‐year follow‐up (p > 0.05). Additionally, in the subgroup with a 5‐year follow‐up, the motor symptoms, ADL‐Barthel score, and cognitive function worsened over time compared to baseline. However, there was still an improvement in motor symptoms and ADL with DBS on‐stimulation compared with the off‐stimulation state. The LEDD increased 5 years after surgery compared to that at baseline. Eleven patients had passed away during follow‐up, the mean survival time was 38.3 ± 17.3 months after surgery, and the mean age at the time of death was 81.2 (range 75–87) years. Conclusion: Robot‐assisted DBS surgery for the elderly patients with Parkinson's disease is accurate and safe. Motor symptoms and ADL significantly improve and patients can benefit from long‐term neuromodulation, which may decrease the risk of death. [ABSTRACT FROM AUTHOR]

Objectives We aimed to investigate the clinicopathologic features of and genetic changes in Sturge-Weber syndrome (SWS) in patients with refractory epilepsy. Methods Clinical data were retrospectively analyzed. H&E and immunohistochemistry were performed to assess pathologic changes. Targeted amplicon sequencing was applied to investigate the somatic GNAQ (c.548G>A) mutation. The potential predictors of seizure outcomes were estimated by univariate and multivariate statistical analyses. Results Forty-eight patients with SWS and refractory epilepsy were enrolled. According to the imaging data and pathologic examination, ipsilateral hippocampal sclerosis (HS), calcification of leptomeningeal arteries, and focal cortical dysplasia were found in 14 (29.2%), 31 (64.6%), and 37 (77.1%) patients, respectively. A high frequency of GNAQ alteration was detected in both cerebral cortex (57.7%) and ipsilateral hippocampus (50.0%) from patients with SWS. During follow-up, 43 of 48 patients (85.4%) had achieved seizure control (Engel class I). Statistically, HS signs on imaging were found to be independent predictors of unfavorable seizure outcomes (P =.015). Conclusions Calcification of leptomeningeal arteries, focal cortical dysplasia, and GNAQ alteration are common features in SWS pathology. Patients with refractory epilepsy caused by SWS can achieve satisfactory seizure control after surgery, but seizure control was compromised in patients with comorbid HS. [ABSTRACT FROM AUTHOR]