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Copyright of Česká a Slovenská Neurologie a Neurochirurgie is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Česká a Slovenská Neurologie a Neurochirurgie is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Česká a Slovenská Neurologie a Neurochirurgie is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Status epilepticus (SE) is a common neurological emergency in children and a well-known epileptogenic insult. Neonates are extremely susceptible to seizures in the neonatal period due to the higher vulnerability. Neonatal SE is associated with significant mortality and morbidity. There is an evident need for attention on neonatal SE in research due to the incredibly limited diagnostic and treatment options in current neonatology, and its serious long-term consequences. The aim of the present study was to characterize the glycoprofiles in the pilocarpine-induced SE model in immature rats to assess the overall N-glycans composition. To induce lithium-pilocarpine (Li-Pilo) SE male Wistar rat pups were pretreated with lithium chloride (127 mg/kg, n=11) on the 11th postnatal day. After 24 hours, the lithium pre-treated pups were administered either with pilocarpine intraperitoneally (i.p.) (35 kg/g, n=6) or saline (n=5) in the control group (Control). On the 19th postnatal day, serum was collected and the analytical procedures were done by mass spectrometry (MS) analytics on matrix-assisted laser desorption/ionization in combination with a time-of-flight detector (MALDI-TOF/MS). Analyzed data were processed by FlexAnalysis (Bruker Daltonics) and GlycoWorkbench software. There were 21 N-glycans that were identified, appointed, and sorted with special emphasis on their structure. We have demonstrated the significant changes in terms of N-glycans sialylation in Li-Pilo compared to the Control. We also observed some other remodelation trends in different portions of relative intenstities of N-glycan clusters according to their glycan type. Our preliminary findings have laid the foundation for additional investigation into glycosylation alterations in the SE in immature rats.

Neonatal hypoxic-ischemic insult (HII) is one of the leading causes of morbidity and mortality in newborns. It has long-term consequences and represents a socioeconomic burden. It is an urgent issue in current neonatology. The aim of the present pilot study was to evaluate the possible effect of sulforaphane on brain glucose uptake expressed as 18F-fluorodeoxyglucose (18F-FDG) activity at the acute, subacute, and subchronic time intervals after the experimental perinatal HII in rats. Significant protection has been observed in the hippocampus 5 weeks after the insult as represented by normalisations of interhemispheric ratio of measured 18F-FDG activity. In conclusion, positron emission tomography (PET) with 18F-FDG revealed a protective effect of SFN on glucose metabolism in the subchronic phase after HII. Further research within the field of neonatal HII in newborn rats will be necessary.

This review aims to describe a novel method in the field of electromyography (EMG), established and improved upon in the last three decades that is able to observe specific parameters of muscle units (MUs). This concept is called the decomposition method, based on its ability to decompose a surface EMG signal to describe muscle activity on the level of individual muscle units in contrast to the level of the whole muscle, as is customary for regular surface electromyography. We provide a brief overview of its history, constituent parts regarding both hardware and software and possible applications. We also acknowledge the state of the research, regarding the background of the decomposition algorithm, the main software component responsible for identifying individual motor units and their parameters. As a result of the ability to describe the behavior of individual motor units during muscle contractions, key concepts in neuromuscular physiology have been put forward, pertaining to the hierarchy of MUs during their recruitment. Together with the recent application for cyclic contractions and gait, the decomposition method is beginning to open up wider possibilities of enquiry.

This study aimed to investigate changes in the H-reflex recruitment curve in compressive radiculopathy, specifically assessing differences between symptomatic and asymptomatic limbs in patients with unilateral S1 radiculopathy through derived parameters. A total of 24 volunteers (15 male and 9 female, aged between 22 and 60 years) with confirmed nerve root compression in the L5/S1 segment participated. Nerve root compression was verified through clinical MRI examination and attributed to disc protrusion, spinal canal stenosis, or isthmic spondylolisthesis of L5/S1. Analysis revealed no difference in M-wave threshold intensity between symptomatic and non-symptomatic limbs. However, the H-reflex exhibited a trend toward increased threshold intensity in the symptomatic limb. Notably, a significant decrease in the slope of the H-reflex was observed on the symptomatic side, and the maximal H-reflex amplitude proved to be markedly different between the two limbs. The Hmax/Mmax ratio demonstrated a significant decrease in the symptomatic limb, indicating reduced effectiveness of signal translation. In conclusion, our findings emphasize the importance of H-reflex parameters in evaluating altered recruitment curves, offering valuable insights for neurological examinations. The observed differences in maximal values of M-wave, H-reflex, and their ratio in affected and unaffected limbs can enhance the diagnostic process for lumbosacral unilateral radiculopathy and contribute to a standardized approach in clinical assessments.

Background: Evaluation of molecular markers ( IDH , p TERT , 1p/19q codeletion, and MGMT ) in adult diffuse gliomas is crucial for accurate diagnosis and optimal treatment planning. Dynamic Susceptibility Contrast (DSC) and Arterial Spin Labeling (ASL) perfusion MRI techniques have both shown good performance in classifying molecular markers, however, their performance has not been compared side-by-side., Methods: Pretreatment MRI data from 90 patients diagnosed with diffuse glioma (54 men/36 female, 53.1 ± 15.5 years, grades 2-4) were retrospectively analyzed. DSC-derived normalized cerebral blood flow/volume (nCBF/nCBV) and ASL-derived nCBF in tumor and perifocal edema were analyzed in patients with available IDH -mutation ( n = 67), p TERT -mutation ( n = 39), 1p/19q codeletion ( n = 33), and MGMT promoter methylation ( n = 31) status. Cross-validated uni- and multivariate logistic regression models assessed perfusion parameters' performance in molecular marker detection., Results: ASL and DSC perfusion parameters in tumor and edema distinguished IDH -wildtype (wt) and p TERT- wt tumors from mutated ones. Univariate classification performance was comparable for ASL-nCBF and DSC-nCBV in IDH (maximum AUROCC 0.82 and 0.83, respectively) and p TERT (maximum AUROCC 0.70 and 0.81, respectively) status differentiation. The multivariate approach improved IDH (DSC-nCBV AUROCC 0.89) and p TERT (ASL-nCBF AUROCC 0.8 and DSC-nCBV AUROCC 0.86) classification. However, ASL and DSC parameters could not differentiate 1p/19q codeletion or MGMT promoter methylation status. Positive correlations were found between ASL-nCBF and DSC-nCBV/-nCBF in tumor and edema., Conclusions: ASL is a viable gadolinium-free replacement for DSC for molecular characterization of adult diffuse gliomas., Competing Interests: There are no conflicts of interest to disclose., (© The Author(s) 2024. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.)

Epilepsy is the most common chronic neurological disease, affecting nearly 1%-2% of the world's population. Current pharmacological treatment and regimen adjustments are aimed at controlling seizures; however, they are ineffective in one-third of the patients. Although neuronal hyperexcitability was previously thought to be mainly due to ion channel alterations, current research has revealed other contributing molecular pathways, including processes involved in cellular signaling, energy metabolism, protein synthesis, axon guidance, inflammation, and others. Some forms of drug-resistant epilepsy are caused by genetic defects that constitute potential targets for precision therapy. Although such approaches are increasingly important, they are still in the early stages of development. This review aims to provide a summary of practical aspects of the employment of in vitro human cell culture models in epilepsy diagnosis, treatment, and research. First, we briefly summarize the genetic testing that may result in the detection of candidate pathogenic variants in genes involved in epilepsy pathogenesis. Consequently, we review existing in vitro cell models, including induced pluripotent stem cells and differentiated neuronal cells, providing their specific properties, validity, and employment in research pipelines. We cover two methodological approaches. The first approach involves the utilization of somatic cells directly obtained from individual patients, while the second approach entails the utilization of characterized cell lines. The models are evaluated in terms of their research and clinical benefits, relevance to the in vivo conditions, legal and ethical aspects, time and cost demands, and available published data. Despite the methodological, temporal, and financial demands of the reviewed models they possess high potential to be used as robust systems in routine testing of pathogenicity of detected variants in the near future and provide a solid experimental background for personalized therapy of genetic epilepsies. PLAIN LANGUAGE SUMMARY: Epilepsy affects millions worldwide, but current treatments fail for many patients. Beyond traditional ion channel alterations, various genetic factors contribute to the disorder's complexity. This review explores how in vitro human cell models, either from patients or from cell lines, can aid in understanding epilepsy's genetic roots and developing personalized therapies. While these models require further investigation, they offer hope for improved diagnosis and treatment of genetic forms of epilepsy., (© 2024 The Authors. Epilepsia Open published by Wiley Periodicals LLC on behalf of International League Against Epilepsy.)

Background: Electroporation is an effective technique for genetic manipulation of cells, both in vitro and in vivo. In utero electroporation (IUE) is a special case, which represents a fine application of this technique to genetically modify specific tissues of embryos during prenatal development. Commercially available electroporators are expensive and not fully customizable. We have designed and produced an inexpensive, open-design, and customizable electroporator optimized for safe IUE. We introduce NeuroPorator., Method: We used off-the-shelf electrical parts, a single-board microcontroller, and a cheap data logger to build an open-design electroporator. We included a safety circuit to limit the applied electrical current to protect the embryos. We added full documentation, design files, and assembly instructions., Result: NeuroPorator output is on par with commercially available devices. Furthermore, the adjustable current limiter protects both the embryos and the uterus from overcurrent damage. A built-in data acquisition module provides real-time visualization and recordings of the actual voltage/current pulses applied to each embryo. Function of NeuroPorator has been demonstrated by inducing focal cortical dysplasia in mice., Significance and Conclusion: The simple and fully open design enables quick and cheap construction of the device and facilitates further customization. The features of NeuroPorator can accelerate the IUE technique implementation in any laboratory and speed up its learning curve., Competing Interests: Declaration of Competing Interest The authors have no financial or non-financial interests to disclose., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Despite the rising global burden of stroke and its socio-economic implications, the neuroimaging predictors of subsequent cognitive impairment are still poorly understood. We address this issue by studying the relationship of white matter integrity assessed within ten days after stroke and patients' cognitive status one year after the attack. Using diffusion-weighted imaging, we apply the Tract-Based Spatial Statistics analysis and construct individual structural connectivity matrices by employing deterministic tractography. We further quantify the graph-theoretical properties of individual networks. The Tract-Based Spatial Statistic did identify lower fractional anisotropy as a predictor of cognitive status, although this effect was mostly attributable to the age-related white matter integrity decline. We further observed the effect of age propagating into other levels of analysis. Specifically, in the structural connectivity approach we identified pairs of regions significantly correlated with clinical scales, namely memory, attention, and visuospatial functions. However, none of them persisted after the age correction. Finally, the graph-theoretical measures appeared to be more robust towards the effect of age, but still were not sensitive enough to capture a relationship with clinical scales. In conclusion, the effect of age is a dominant confounder especially in older cohorts, and unless appropriately addressed, may falsely drive the results of the predictive modelling., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Bučková et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

The present study aimed to elucidate the effect of sulforaphane (a natural isothiocyanate) on oxidative stress and mitochondrial dysfunction during and at selected periods following status epilepticus (SE) induced in immature 12-day-old rats by Li-pilocarpine. Dihydroethidium was employed for the detection of superoxide anions, immunoblot analyses for 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE) levels and respiratory chain complex I activity for evaluation of mitochondrial function. Sulforaphane was given i.p. in two doses (5 mg/kg each), at PD 10 and PD 11, respectively. The findings of the present study indicate that both the acute phase of SE and the early period of epileptogenesis (1 week and 3 weeks following SE induction) are associated with oxidative stress (documented by the enhanced superoxide anion production and the increased levels of 3-NT and 4-HNE) and the persisting deficiency of complex I activity. Pretreatment with sulforaphane either completely prevented or significantly reduced markers of both oxidative stress and mitochondrial dysfunction. Since sulforaphane had no direct anti-seizure effect, the findings suggest that the ability of sulforaphane to activate Nrf2 is most likely responsible for the observed protective effect. Nrf2-ARE signaling pathway can be considered a promising target for novel therapies of epilepsy, particularly when new compounds, possessing inhibitory activity against protein-protein interaction between Nrf2 and its repressor protein Keap1, with less "off-target" effects and, importantly, with an optimal permeability and bioavailability properties, become available commercially., (© 2023. The Author(s).)

Status epilepticus (SE) is a common paediatric emergency with the highest incidence in the neonatal period and is a well-known epileptogenic insult. As previously established in various experimental and human studies, SE induces long-term alterations to brain metabolism, alterations that directly contribute to the development of epilepsy. To influence these changes, organic isothiocyanate compound sulforaphane (SFN) has been used in the present study for its known effect of enhancing antioxidative, cytoprotective, and metabolic cellular properties via the Nrf2 pathway. We have explored the effect of SFN in a model of acquired epilepsy induced by Li-Cl pilocarpine in immature rats (12 days old). Energy metabolites PCr, ATP, glucose, glycogen, and lactate were determined by enzymatic fluorimetric methods during the acute phase of SE. Protein expression was evaluated by Western blot (WB) analysis. Neuronal death was scored on the FluoroJadeB stained brain sections harvested 24 h after SE. To assess the effect of SFN on glucose metabolism we have performed a series of 18F-DG μCT/PET recordings 1 h, 1 day, and 3 weeks after the induction of SE. Responses of cerebral blood flow (CBF) to electrical stimulation and their influence by SFN were evaluated by laser Doppler flowmetry (LDF). We have demonstrated that the Nrf2 pathway is upregulated in the CNS of immature rats after SFN treatment. In the animals that had undergone SE, SFN was responsible for lowering glucose uptake in most regions 1 h after the induction of SE. Moreover, SFN partially reversed hypometabolism observed after 24 h and achieved full reversal at approximately 3 weeks after SE. Since no difference in cell death was observed in SFN treated group, these changes cannot be attributed to differences in neurodegeneration. SFN per se did not affect the glucose uptake at any given time point suggesting that SFN improves endogenous CNS ability to adapt to the epileptogenic insult. Furthermore, we had discovered that SFN improves blood flow and accelerates CBF response to electrical stimulation. Our findings suggest that SFN improves metabolic changes induced by SE which have been identified during epileptogenesis in various animal models of acquired epilepsy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Daněk, Danačíková, Kala, Svoboda, Kapoor, Pošusta, Folbergrová, Tauchmannová, Mráček and Otáhal.)

The aim of the present study was to elucidate the effect of resveratrol (natural polyphenol) on seizure activity, production of ROS, brain damage and mitochondrial function in the early phase of status epilepticus (SE), induced in immature 12 day-old rats by substances of a different mechanism of action (Li-pilocarpine, DL-homocysteic acid, 4-amino pyridine, and kainate). Seizure activity, production of superoxide anion, brain damage and mitochondrial function were assessed by EEG recordings, hydroethidium method, FluoroJadeB staining and Complex I activity measurement. A marked decrease of complex I activity associated with the acute phase of SE in immature brain was significantly attenuated by resveratrol, given i.p. in two or three doses (25 mg/kg each), 30 min before, 30 or 30 and 60 min after the induction of SE. Increased O 2 .- production was completely normalized, brain damage partially attenuated. Since resveratrol did not influence seizure activity itself (latency, intensity, frequency), the mechanism of protection is likely due to its antioxidative properties. The findings have a clinical relevance, suggesting that clinically available substances with antioxidant properties might provide a high benefit as an add-on therapy during the acute phase of SE, influencing also mechanisms involved in the development of epilepsy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Folbergrová, Ješina and Otáhal.)

The study examined the morphological and long-term behavioral impacts of neonatal hypoxic-ischemic brain injury in a mouse model. We investigated the modification of different behavioral domains, such as spontaneous climbing, which represents fine motor skills. We also focused on sex-dependent differences during hypoxic-ischemic encephalopathy. The Rice-Vannucci model of hypoxia-ischemia was used, adjusted and adapted to 7-day-old C57BL/6NTac mice. The effects of induced hypoxia and ischemia were also studied separately. At postnatal day 60, mice underwent behavioral testing using the LABORAS apparatus. The perfusion for histological evaluation was performed one day after the behavioral analyses. In groups with separately induced hypoxia or ischemia, the observed alterations in behavior were not accompanied by morphological changes in the cortex or hippocampal formation. Female mice naturally climbed significantly more and hypoxic females reared less than hypoxic males (p<0.05). Male mice postnatally exposed to hypoxia-ischemia exhibited significantly lower vertical activity and higher horizontal activity (p<0.05). Mild hypoxic damage may not be morphologically detectable but may induce substantial behavioral changes in adult mice. There were significant differences between horizontal and vertical activity in reaction to hypoxia-ischemia. Our study indicates that the importance of behavioral testing is irreplaceable and may be reflected in neonatal medicine.

Neonatal hypoxic-ischemic encephalopathy is a disorder with heterogeneous manifestation due to asphyxia during perinatal period. It affects approximately 3-12 children per 1000 live births and cause death of 1 million neonates worldwide per year. Besides, motor disabilities, seizures, impaired muscle tone and epilepsy are few of the consequences of hypoxic-ischemic encephalopathy. Despite an extensive research effort regarding various treatment strategies, therapeutic hypothermia with intensive care unit supportive treatment remains the only approved method for neonates who have suffered from moderate to severe hypoxic-ischemic encephalopathy. However, these protocols are only partially effective given that many infants still suffer from severe brain damage. Thus, further research to systematically test promising neuroprotective treatments in combination with hypothermia is essential. In this review, we discussed the pathophysiology of hypoxic-ischemic encephalopathy and delved into different promising treatment modalities, such as melatonin and erythropoietin. However, preclinical studies and clinical trials are still needed to further elucidate the mechanisms of action of these modalities.