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Approximately 60% of all patients with epilepsy suffer from focal epilepsy syndromes. In approximately 15% of these patients, the seizures are not adequately controlled with anticonvulsive drugs, and such patients are potential candidates for surgical treatment and majority are children. Epilepsy surgery in children, who have been carefully chosen, can result in either seizure freedom or a marked (>90%) reduction in seizures in approximately two-third of children with intractable seizures. In the multimodality presurgical evaluation approach, sufficient concordance should be established among various independent investigations, thus identifying the location and extent of the epileptogenic zone with a high degree of confidence. Early surgery improves the quality of life and cognitive and developmental outcome of the child. Surgically remediable epilepsies in children should be identified early and include temporal lobe epilepsy with focal lesions, lesional extratemporal epilepsies, hemispherical epilepsies, and gelastic epilepsy with hypothalamic hamartoma, and can be treated by resective or disconnection surgery. Palliative procedures include corpus callosotomy and vagal nerve stimulation for children with diffuse and multifocal epilepsies, who are not candidates for resective surgery. Deep brain stimulation in patients with epilepsy is still under evaluation. For children with \"surgically remedial epilepsy,\" surgery should be offered as a procedure of choice rather than as a treatment of last resort.

Background: Epilepsy is a chronic disorder with recurrent unprovoked seizures which can affect children at any age. A child's quality of life (QOL) is significantly impacted by an epilepsy diagnosis throughout their formative years. Adjustment and QOL for the child and family are highly correlated with parental knowledge, attitudes, and practices (KAP) regarding epilepsy. Objectives: Determining the association between parental KAP and the QOL of children with epilepsy (CWE) and to study the association between them. Materials and Methods: Using convenience sampling procedure, 30 CWE between the ages of 6 and 14-of either sex-and their 30 parents made up the sample. The knowledge, attitude, and practice (KAP) tool, which was given to parents, and the Quality of Life in Childhood Epilepsy Questionnaire-55 (QOLCE-55), which was given to CWE, were used to gather the data. Frequency distribution, percentage, and correlation coefficient tests were used to assess the measures. Results: There were statistically significant relationships between the QOL and KAP domains and parental education, domicile, and socioeconomic position. The cognitive, emotional, and social domains of QOL were adversely connected with the knowledge domain in KAP, but the physical domain was positively correlated. Parents' behavior and physical QOL were found to be negatively correlated. Conclusion: Although educated parents had sufficient information and a positive outlook, there was a discrepancy between recommended and actual practice, and KAP has an impact on the QOL of CWE. Parental education initiatives may significantly improve understanding and promote healthy behaviors.

Background/Objectives: Sleep problems affect the quality of life (QoL) and treatment prognosis of children with epilepsy (CWE). We analyzed sleep problems and QoL in CWE but without neurodevelopmental disorders, which affect sleep and QoL. We also examined discrepancies between child self-reports and parent proxy reports in QoL assessments. Methods: Thirty-two CWE in grades 2–6 (aged 7–12 years) in regular classes who attended Osaka Metropolitan University Hospital and PL General Hospital between January 2022 and August 2023 were compared with 21 children who had attended the hospitals for acute non-neurological disorders and had recovered (control group). Children with neurodevelopmental disorders, those unable to answer questionnaires, and those taking sleeping pills were excluded. Children in both groups completed the Kinder Lebensqualität Fragebogen (KINDL-R); their parents completed the KINDL-R and Japanese Sleep Questionnaire for Elementary Schoolers (JSQ-ES). Results: There were no significant differences in mean (±SD) JSQ-ES total scores between the epilepsy and control groups (71.6 ± 21.4 vs. 63.2 ± 15.2, respectively; p = 0.16). In the epilepsy group, there were no significant differences in total or subscale KINDL-R scores between children with (JSQ-ES ≥ 80) and without (JSQ-ES < 80) sleep problems. Correlation coefficients between child self-reports and parent proxy reports for KINDL-R total scores were 0.171 (p = 0.348) and 0.656 (p = 0.001) for the epilepsy and control groups, respectively. There was a significant difference between the total scores of children’s self-reports and parents’ proxy reports in the control (p = 0.008) group, but not in the epilepsy group (p = 0.837). Conclusions: Sleep problems may not have significant impacts on the QoL of CWE without neurodevelopmental disorders. Parents of CWE do not always correctly assess their children’s QoL, so it is important to ask both children and their parents to obtain a comprehensive picture of their QoL.

Epilepsy is a chronic neurological disorder affecting 50 million patients worldwide, in need of continuous treatment, while 30% of them are refractory to treatment. Despite multiple antiepileptic drugs are available for the treatment of epilepsy, still refractory epilepsy especially in children represents a social burden in developing countries. Low-dose naltrexone (LDN) has been proposed as an immune modulator in multiple diseases and proved benefit especially in diseases with immune dysregulation. The purpose of this study is to demonstrate the effect of LDN in the treatment of children with intractable epilepsy and discuss its potential role in epileptogenesis process.

Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death in intractable epilepsies, but physiological mechanisms that lead to SUDEP are unknown. Dravet syndrome (DS) is an infantile-onset intractable epilepsy caused by heterozygous loss-of-function mutations in the SCN1A gene, which encodes brain type-I voltage-gated sodium channel NaV1.1. We studied the mechanism of premature death in Scn1a heterozygous KO mice and conditional brain- and cardiac-specific KOs. Video monitoring demonstrated that SUDEP occurred immediately following generalized tonic-clonic seizures. A history of multiple seizures was a strong risk factor for SUDEP. Combined video-electroencephalography-electrocardiography revealed suppressed interictal resting heart-rate variability and episodes of ictal bradycardia associated with the tonic phases of generalized tonic-clonic seizures. Prolonged atropine-sensitive ictal bradycardia preceded SUDEP. Similar studies in conditional KO mice demonstrated that brain, but not cardiac, KO of Scn1a produced cardiac and SUDEP phenotypes similar to those found in DS mice. Atropine or N-methyl scopolamine treatment reduced the incidence of ictal bradycardia and SUDEP in DS mice. These findings suggest that SUDEP is caused by apparent parasympathetic hyperactivity immediately following tonic-clonic seizures in DS mice, which leads to lethal bradycardia and electrical dysfunction of the ventricle. These results have important implications for prevention of SUDEP in DS patients.

Background Epilepsy contributes to a significant disease burden in children and adolescents worldwide. The incidence of childhood epilepsy is threefold higher in low and middle income countries compared in high-income countries. Epilepsy is a serious neurological condition associated with stigma and discrimination, an impaired quality of life, and other mental health related problems. Objective This study is aimed to synthesize existing evidence and estimate the pooled prevalence and incidence of epilepsy in children and adolescents in Africa. Methods A comprehensive and systematic search of relevant databases was conducted. The quality of each study was assessed using the Newcastle-Ottawa Quality Assessment Scale adapted for meta-analysis. Two reviewers screened retrieved articles, conducted critical appraisals, and extracted the data. Heterogeneity between studies was assessed by visual inspection of forest plots and statistically using Cochran’s Q statistics and the I 2 test. Publication bias was checked by visual inspection of funnel plots as well as statistically using Egger’s correlation and Begg’s regression tests. Finally, the pooled prevalence and incidence of childhood epilepsy were computed with 95% confidence intervals. Result In this review and meta-analysis 42 studies with 56 findings were included to compute the pooled prevalence of childhood epilepsy. On the other hand, 6 studies were included to estimate the combined incidence. The pooled prevalence of cumulative epilepsy was 17.3 per 1000 children. Whereas the pooled prevalence of active and lifetime epilepsy was 6.8 and 18.6 per 1000 children respectively. The pooled incidence of childhood epilepsy was 2.5 per 1000 children. Conclusion Nearly 1 in 50 children are suffering from epilepsy in Africa. However, little attention has been paid to the prevention and treatment of childhood epilepsy. Mass epilepsy screening, scaling up treatment coverage, and designing strict treatment follow up and monitoring mechanisms are recommended.

Background Intractable epilepsy in children poses significant clinical challenges due to limited efficacy of conventional anti-epileptic drugs (AEDs), leading to persistent neurodevelopmental impairments. This study investigated the therapeutic effects of ketogenic diet (KD), lacosamide (LCM), and their combination on refractory epilepsy, with comprehensive assessment of seizure control, EEG dynamics (including epileptiform patterns and spectral characteristics), cognitive function, lipid metabolism, and endothelial health. Methods Ninety children with refractory epilepsy were divided into three treatment groups: KD ( n  = 30), LCM ( n  = 30), and KD + LCM ( n  = 30). Assessments included detailed EEG characterization (seizure types, interictal discharges, spectral bands), cognitive testing (attention/memory), lipid profiles, and endothelial markers at baseline, 3-, and 6-months post-treatment. Results The KD + LCM group showed superior seizure reduction at 3/6 months (t = 2.171, P  = 0.035; t = 3.177, P  = 0.003), with 76.7% achieving ≥ 50% interictal discharge reduction ( P  = 0.008) and 63.3% seizure type simplification ( P  = 0.003) at 6 months. Cognitive performance significantly improved (attention: Δ=-10.8 ± 2.0; memory: Δ=-9.4 ± 1.8; both P  < 0.001), strongly correlating with frontal θ-band modulation (|r|>0.68). Combination therapy also enhanced α/β/δ/θ spectral power ( P  ≤ 0.019), improved lipid profiles, and restored endothelial function versus monotherapies (all P  < 0.05). Conclusions KD and LCM combination therapy provides comprehensive benefits—superior seizure control, EEG normalization, cognitive enhancement, metabolic optimization, and vascular protection—making it a promising multimodal approach for refractory epilepsy management.

This study aimed to describe the clinical characteristics and treatment patterns of children with focal and generalized epilepsy and to identify factors associated with seizure control at a tertiary hospital in Tanzania. We conducted a hospital-based cross-sectional secondary analysis of 427 children and adolescents (aged 0–17 years) with a clinical diagnosis of epilepsy whose caregivers were enrolled in a primary study between June and October 2023 at the pediatric neurology clinic of a national referral hospital in Dar es Salaam. Primary outcomes included epilepsy type distribution, treatment patterns (monotherapy vs. polytherapy and specific antiseizure medications), and level of seizure control. The secondary outcome was the identification of factors associated with seizure control, analyzed using ordinal logistic regression and reported as adjusted odds ratios (aORs). Focal epilepsy was the predominant type (52.5%). Most children (65.8%) had infantile seizure onset (<1 year) and were receiving monotherapy (74.9%). Treatment patterns were consistent with guideline recommendations: carbamazepine was prescribed to 94.6% of children with focal epilepsy, while sodium valproate was used in 96.4% of those with generalized epilepsy (both p < 0.001). Seizure freedom in the preceding month was higher among children with focal epilepsy (73.7%) compared with generalized epilepsy (59.5%, p = 0.003). In multivariable analysis, generalized epilepsy was independently associated with worse seizure control (aOR=1.93, 95% CI: 1.28–2.92, p = 0.002). Focal epilepsy was the most common type in this tertiary referral cohort, and treatment largely aligned with international guidelines. Children with generalized epilepsy were more likely to have poorer seizure control. Further prospective studies incorporating detailed syndromic and etiologic classification are needed to better define predictors of seizure control and inform service planning.

Dravet syndrome (DS), an intractable childhood epileptic encephalopathy with a high fatality rate, is typically caused by loss-of-function mutations in one allele of SCN1A, which encodes [Na.sub.V]1.1, a 250-kDa voltage-gated sodium channel. In contrast to other epilepsies, pharmaceutical treatment for DS is limited. Here, we demonstrate that viral vector-mediated delivery of a codon-modified SCN1A open reading frame into the brain improves DS comorbidities in juvenile and adolescent DS mice ([Scn1a.sup.A1783V/WT]). Notably, bilateral vector injections into the hippocampus and/or the thalamus of DS mice increased survival, reduced the occurrence of epileptic spikes, provided protection from thermally induced seizures, corrected background electrocorticographic activity and behavioral deficits, and restored hippocampal inhibition. Together, our results provide a proof of concept for the potential of SCN1A delivery as a therapeutic approach for infants and adolescents with DS-associated comorbidities.

Key Points Working memory and processing speed are often impaired in children with epilepsy, even in those with intact general cognitive abilities, and can adversely affect learning and problem-solving Attention deficit–hyperactivity disorder, primarily of the inattentive type, is seen in 28–70% of people with epilepsy and is common among children with epilepsy; the diagnosis is often delayed in individuals with epilepsy Despite favourable seizure outcomes, people with genetic generalized epilepsy have cognitive and behavioural comorbidities suggestive of frontal lobe dysfunction, which have an adverse effect on long-term psychosocial outcome In individuals with focal epilepsy arising from a single focus, the spectrum of neurocognitive disability is broad, owing to dysfunction of the epileptogenic zone as well as the more-extensive networks connecting with this zone The underlying aetiology of seizures has a substantial causative role in the development of comorbidities, and frequent seizures and/or interictal epileptiform discharges may further exacerbate neurocognitive dysfunction Neuropsychological testing is the gold standard for evaluation of cognitive comorbidities; in addition, formal screening questionnaires completed by parents and/or children are feasible and well received, and enable widespread screening Cognitive and behavioural comorbidities are common in children with epilepsy, and correlate with worse quality of life, increased behavioural and language problems and worse social skills, all of which adversely affect long-term psychosocial functioning. This review outlines the most common cognitive comorbidities in different types of epilepsy, and outlines the current understanding of the pathophysiology of epilepsy-associated cognitive and neurodevelopmental problems in children with epilepsy. Moreover, the authors provide suggestions for screening for cognitive comorbidity in this patient group. Cognitive and behavioural comorbidities are often seen in children with epilepsy, and are more common and severe in refractory epilepsy. These comorbidities are associated with worse quality of life, increased behavioural and language problems and worse social skills, all of which adversely affect long-term psychosocial functioning. To enable early intervention and therapy, children and teens with epilepsy should be periodically screened for cognitive comorbidities. The location of the epileptic focus can, to a certain degree, predict the type(s) of comorbidity; however, the spectrum of disability is often broad, presumably because focal perturbations can cause network dysfunction. Comorbidities often result from underlying structural or functional pathology that has led to seizures. In selected cases, therapy targeting the underlying cause, such as the ketogenic diet for GLUT1 deficiency syndromes, may be remarkably effective in ameliorating both seizures and cognitive concerns. In many cases, however, cognitive impairment persists despite seizure control. In epileptic encephalopathies, frequent seizures and/or interictal epileptiform abnormalities exacerbate neurocognitive dysfunction, owing to synaptic reorganization or impaired neurogenesis, or to other effects on developing neural circuits, and prompt initiation of effective antiepileptic therapy is essential to limit cognitive comorbidities.