AIM: To describe the epidemiological, diagnostic, therapeutic, and outcome aspects of pediatric neuromyelitis optica spectrum disorders (NMOSD) in Dakar, Senegal. METHODS: We conducted a multicenter retrospective and pro...AIM: To describe the epidemiological, diagnostic, therapeutic, and outcome aspects of pediatric neuromyelitis optica spectrum disorders (NMOSD) in Dakar, Senegal. METHODS: We conducted a multicenter retrospective and prospective study including patients with pediatric-onset NMOSD (<18 years) diagnosed according to the 2015 Wingerchuk criteria. RESULTS: Over 7 years and 3 months, 8 children (7 females) were included, with a median age at symptom onset of 13.5 years (range 8-17). The main neurological manifestations during the disease course were myelitis (7/8), optic neuritis (5/8), and area postrema syndrome (4/8). Brain magnetic resonance imaging revealed nonspecific white matter abnormalities in 2 patients. Anti-aquaporin 4 antibodies were positive in 6 patients. Cerebrospinal fluid analysis, performed in 4 patients, showed lymphocytic pleocytosis in 2 of them (72 and 17 cells/mm). All patients received prednisone; 7 also received azathioprine. After a median follow-up of 26.5 months, the mean Expanded Disability Status Scale was 4.44. Six patients had a relapsing-remitting course, with a median time to second relapse of 3 months (range 2-6). CONCLUSION: This preliminary study highlights the clinical heterogeneity, female predominance, and frequent AQP4-IgG positivity of pediatric NMOSD in Senegal, broadly comparable to international cohorts. However, diagnostic delays, limited access to intensive therapies, and significant disability were observed, underscoring regional disparities in treatment and prognosis and the need for earlier diagnosis and improved access to effective therapies to optimize outcomes in sub-Saharan Africa.
BACKGROUND: Takenouchi-Kosaki syndrome (TKS), caused by the CDC42 c.191A>G (p.Tyr64Cys; Y64C) variant, characterized by a range of clinical manifestations, including developmental delay with intellectual disability (ID)....BACKGROUND: Takenouchi-Kosaki syndrome (TKS), caused by the CDC42 c.191A>G (p.Tyr64Cys; Y64C) variant, characterized by a range of clinical manifestations, including developmental delay with intellectual disability (ID). While CDC42 is essential for neurogenesis, the mechanisms by which the Y64C mutation contributes to the neurological impairments observed in TKS patients remain unclear. OBJECTIVE: This study aimed to investigate the functional impact of ectopically expressing the Y64C variant on the neurite outgrowth of neuroblastoma cells, Neuro2A. METHODS: Neuro2A cells were transfected with the Y64C variant to assess changes in neurite outgrowth and cellular morphology. The cells were also treated with a lipidation inhibitor, GGTI-298, or CDC42 activity inhibitor, ML141 to evaluate its ability to ameliorate the mutation-induced phenotypes. Whole transcriptome sequencing and differentially expressed gene (DEG) analysis were performed between WT- and Y64C-expressing cells. RESULTS: The overexpression of the Y64C variant impaired neurite outgrowth and changed the cell morphology of Neuro2A cells. Both the neurite outgrowth defect and the enhanced membrane localization induced by Y64C overexpression were restored by GGTI-298 treatment but not by ML141. To explore the molecular basis of these phenotypes, we performed DEG analysis and identified 32 upregulated and 19 downregulated genes, including Smarca1. Consistent with the transcriptomic findings, Smarca1 protein expression was decreased in Y64C-expressing cells in comparison to WT. Treatment with GGTI-298 effectively preserved Smarca1 levels, whereas ML141 reduced its expression in both WT- and Y64C-expressing cells. CONCLUSIONS: The Y64C variant disrupts neurite outgrowth, attributable to altered CDC42 activity and localization. The restoration of neurite outgrowth by GGTI-298 highlights the importance of CDC42 signaling for neurite outgrowth in Neuro2A cells. Our findings raise the possibility that molecular disruptions caused by the Y64C mutation may contribute to the brain malformations and neurodevelopmental features observed in TKS.
BACKGROUND: EEG abnormalities are frequently reported in children with developmental language disorders, particularly in language-associated regions, though existing data remain inconsistent. AIM: This study investigated...BACKGROUND: EEG abnormalities are frequently reported in children with developmental language disorders, particularly in language-associated regions, though existing data remain inconsistent. AIM: This study investigated the frequency, density, and localization of epileptiform discharges in children with language delays, and the incidence of epilepsy within a 12-month follow-up. METHOD: A total of 132 children with language delay were evaluated. Ten later diagnosed with autism spectrum disorder were excluded, leaving 122 for analysis. Epileptiform discharges were assessed for frequency, localization, and spike-wave index (SWI). Clinical, demographic, neuroimaging, and developmental data were collected. Comparative analyses were performed between children with and without epileptiform discharges, and between those who did and did not develop epilepsy. RESULTS: The mean age at admission was 39.6 months, with boys comprising 73.8% of the cohort. Epileptiform discharges were present in 14 children (11.5%), predominantly in the temporoparietal region (83.3%), mostly right-sided or bilateral. Notably, no patient exhibited unilateral discharges on the left. Epilepsy developed in six children during follow-up, all of whom had epileptiform discharges on initial EEG. None with a normal baseline EEG developed epilepsy. Age, sex, parental consanguinity, or family history of language delay, epilepsy, or febrile seizures showed no significant differences between groups. Although SWI values increased significantly over one year, neither baseline SWI nor its temporal change was associated with the development of epilepsy. CONCLUSION: EEG abnormalities and epilepsy are not rare in children with language delay. Those with epileptiform discharges on initial EEG require careful monitoring, as they carry a higher risk of developing epilepsy.
OBJECTIVE: Tic disorders (TD) are childhood-onset neurodevelopmental conditions marked by sudden, rapid, recurrent motor and/or vocal tics. This study aimed to investigate attentional network functioning in children with...OBJECTIVE: Tic disorders (TD) are childhood-onset neurodevelopmental conditions marked by sudden, rapid, recurrent motor and/or vocal tics. This study aimed to investigate attentional network functioning in children with TD using the Attention Network Test (ANT), which assesses alerting, orienting, and executive control. METHODS: Seventy-eight children with TD and 78 age-matched healthy controls were recruited. TD participants were classified into three subtypes: persistent motor/vocal tic disorder, provisional tic disorder, and Tourette syndrome (TS). All participants completed the ANT, and outcomes were analyzed for alerting, orienting, conflict effects, reaction time, and accuracy. Subgroup comparisons were also conducted based on TD subtype and Yale Global Tic Severity Scale (YGTSS) scores (≥30 vs <30). RESULTS: Compared to controls, children with TD showed significantly reduced orienting effects, longer reaction times, and lower accuracy (all P < 0.05). No group differences were observed in alerting or conflict effects. Subtype analyses revealed significant differences in reaction time and accuracy but not in attentional network effects. No significant ANT performance differences were found between severity subgroups. CONCLUSION: Children with TD exhibit specific impairments in attentional networks, particularly in orienting function, along with slower responses and reduced accuracy. These findings highlight cognitive features of TD and support the use of ANT in neuropsychological assessment.
OBJECTIVE: This study aims to investigate research trends, key contributors, and emerging topics in the field of infantile epileptic spasms syndrome (IESS). METHODS: Publications on IESS from 1954 to 2024 were retrieved...OBJECTIVE: This study aims to investigate research trends, key contributors, and emerging topics in the field of infantile epileptic spasms syndrome (IESS). METHODS: Publications on IESS from 1954 to 2024 were retrieved from the Web of Science Core Collection (WoSCC) database. Bibliometric analysis was performed using Microsoft Excel, VOSviewer, CiteSpace, and R version 4.3.3. RESULTS: A total of 2905 publications were identified, revealing a marked increase in research output from 2000 onward. The USA led with 760 publications. The University of California System was the most productive institution, contributing 420 papers. Epilepsia was the most influential journal, publishing 371 papers with 12,246 citations. Leading authors included Naomichi Matsumoto and Ingrid E. Scheffer. Keywords formed five thematic clusters: (1) genetic foundations and molecular mechanisms (e.g., "mutations"), (2) therapeutic strategies for seizure control (e.g., "ketogenic diet"), (3) epidemiological patterns and seizure classification (e.g., "classification"), (4) clinical practices and treatment outcomes (e.g., "vigabatrin"), and (5) brain structure and diagnostic imaging (e.g., "MRI"). Burst keyword analysis indicated a focus on terms including "encephalopathy", "epileptic spasms", "intellectual disability", "ilae commission", "hypsarrhythmia", "classification", "multicenter", and "management". CONCLUSION: The findings highlight current hotspots spanning genetic mechanisms, therapeutic strategies, epidemiological patterns, clinical practices, and neuroimaging. Future research should optimize treatments, improve diagnostics, and address developmental impacts.
BACKGROUND: Perinatal arterial ischemic stroke (PAIS) is a major cause of long-term neurological impairments. Understanding its etiologic and prognostic factors is essential for improving outcomes. METHODS: A retrospecti...BACKGROUND: Perinatal arterial ischemic stroke (PAIS) is a major cause of long-term neurological impairments. Understanding its etiologic and prognostic factors is essential for improving outcomes. METHODS: A retrospective single-center study was conducted on children diagnosed with PAIS between 2008 and 2024. Clinical, imaging, and EEG data were analyzed to identify predictors of epilepsy and poor outcomes based on modified Rankin Scale (mRS) scores. RESULTS: A total of 44 patients (9 neonatal arterial ischemic stroke [NAIS], 35 Presumed perinatal arterial ischemic stroke [PPAIS]) with a mean follow-up of 6.49 years were included. Seizure was the first symptom in 45.5%, and focal motor deficit in 54.5%. The most affected artery was the middle cerebral artery (92%), particularly the M1 branch (36.4%). Cortical involvement was noted in 59.1%. Fourteen patients developed epilepsy; 14.2% were drug-resistant. Focal EEG slowing (odds ratio [OR] = 8.484, p = 0.019) and cortical involvement (OR = 6.857, p = 0.023) significantly predicted epilepsy. Poor mRS outcomes (≥3) were seen in 44.2%, and were associated with epilepsy (OR = 5.556, p = 0.016), EEG slowing (OR = 5.353, p = 0.035), and cortical involvement (OR = 7.467, p = 0.008). CONCLUSIONS: Early EEG and MRI findings are crucial in predicting long-term prognosis in PAIS. Further multicenter studies are needed to validate and enhance outcomes.
BACKGROUND: MRI-based classification of hypoxic-ischemic encephalopathy (HIE), particularly using diffusion-weighted imaging (DWI), remains susceptible to subjective bias in determining the presence or absence of diffusi...BACKGROUND: MRI-based classification of hypoxic-ischemic encephalopathy (HIE), particularly using diffusion-weighted imaging (DWI), remains susceptible to subjective bias in determining the presence or absence of diffusion restriction. Quantitative measures such as apparent diffusion coefficient (ADC) values may provide a more objective assessment of injury severity. PURPOSE: To evaluate the depth and distribution of brain injury in neonatal HIE by quantitatively assessing regional ADC values across MRI pattern classifications, independent of subjective visual interpretation of DWI signal changes. MATERIALS AND METHODS: Seventy-three consecutively enrolled full-term infants with HIE underwent brain MRI, and ADC values were measured at five predefined brain regions. Correlations between regional ADC values and MRI pattern groups were analyzed. RESULTS: Five MRI patterns were identified: normal, white matter injury (WMI), watershed (WS), basal ganglia/thalamus injury (BGT), and near total brain injury (nTBI). ADC distribution analysis demonstrated two principal findings: (1) no significant differences among the normal, WMI, and WS pattern groups; and (2) significantly lower ADC values in the nTBI group compared with the BGT group at all brain regions during the first week of life, and at the centrum semiovale during the second week. CONCLUSION: Quantitative analysis revealed distinct ADC distribution differences between the BGT and nTBI patterns during the first and second weeks of life, indicating substantially more severe and widespread brain injury in the nTBI pattern.
BACKGROUND: Epilepsy is a genetically heterogeneous disorder with a high burden in the pediatric population. Advances in next-generation sequencing (NGS) have enhanced molecular diagnosis, enabling more accurate subclass...BACKGROUND: Epilepsy is a genetically heterogeneous disorder with a high burden in the pediatric population. Advances in next-generation sequencing (NGS) have enhanced molecular diagnosis, enabling more accurate subclassification and targeted interventions. OBJECTIVE: This study aimed to evaluate the diagnostic utility of epilepsy gene panel testing in a large pediatric cohort and to characterize the clinical and genetic features of molecularly diagnosed cases. METHODS: A retrospective analysis was conducted on 516 pediatric epilepsy patients who underwent targeted gene panel testing between 2021 and 2025 at a tertiary medical center. Only pathogenic and likely pathogenic variants were considered diagnostic. RESULTS: A molecular diagnosis was established in 81 patients (15.7 %). The most frequently implicated genes were KCNQ2, SCN1A, CACNA1A, SLC2A1, and SCN2A, collectively accounting for 43.2 % of all diagnoses. Despite this concentration, pathogenic variants were distributed across 37 different genes, emphasizing the high genetic heterogeneity. Most diagnosed patients had seizure onset in infancy, particularly within the first year of life. Notably, two-thirds of neonates with seizures had pathogenic KCNQ2 variants. Additionally, 23 of the diagnostic variants (29.9 %) were novel, underscoring the evolving spectrum of epilepsy-associated mutations. CONCLUSION: Epilepsy gene panel testing is a valuable diagnostic tool in pediatric clinical practice. The identification of pathogenic variants across a wide range of genes - including a high proportion of novel mutations - supports the integration of genetic testing into the routine evaluation of pediatric epilepsy for improved etiological clarification and long-term management.
Watanabe C, Miyauchi A, Aoki S
… +18 more, Watanabe M, Jimbo EF, Miyama Y, Kitayama H, Uno Y, Watanabe K, Hattori Y, Yotsumoto Y, Onuki T, Sugiyama Y, Ichimoto K, Yatsuka Y, Okazaki Y, Imasawa T, Murayama K, Ohtake A, Yamagata T, Osaka H
BACKGROUND: Primary coenzyme Q (CoQ) deficiency is a group of mitochondrial disorders caused by pathogenic variants of genes involved in CoQ biosynthesis. Although some patients respond to oral CoQ supplementation, the p...BACKGROUND: Primary coenzyme Q (CoQ) deficiency is a group of mitochondrial disorders caused by pathogenic variants of genes involved in CoQ biosynthesis. Although some patients respond to oral CoQ supplementation, the pathophysiology remains poorly understood. Ferroptosis, a form of iron-dependent cell death driven by lipid peroxidation, is suppressed by reduced CoQvia ferroptosis suppressor protein 1 (FSP1). However, its involvement in primary CoQ deficiency has not yet been studied using patient-derived cells. CASES AND RESULTS: We reported six patients from three families and investigated ferroptosis susceptibility in fibroblasts from three representative patients: one with COQ2 variants and two with COQ4 variants. Fibroblasts with COQ2 variants showed increased vulnerability to ferroptosis inducers, plasma membrane lipid peroxidation. In contrast, fibroblasts with COQ4 variants exhibited only mild changes. Notably, susceptibility to ferroptosis remained unchanged after increasing intracellular CoQ levels. Despite this persistent ferroptosis sensitivity in vitro, the COQ2 patient exhibited significant clinical improvement following CoQ supplementation. These findings suggest that ferroptosis may contribute to cellular vulnerability in primary CoQ deficiency but may not be the primary driver of renal and neurological symptoms. CONCLUSIONS: Our results highlight a complex interplay between CoQ biosynthesis, ferroptosis defense, and therapeutic response, warranting further investigation of subcellular CoQ distribution and ferroptosis-related mechanisms.
Paediatric neurology has evolved significantly since its early recognition as a subspecialty in the mid-20th century, though interest in childhood neurological conditions dates back centuries. In Sub-Saharan Africa (SSA)...Paediatric neurology has evolved significantly since its early recognition as a subspecialty in the mid-20th century, though interest in childhood neurological conditions dates back centuries. In Sub-Saharan Africa (SSA), however, the field remains underdeveloped, despite a rising burden of neurological disorders such as epilepsy, cerebral palsy, cerebral malaria, autism spectrum disorder, and paediatric brain tumours. These conditions represent a significant proportion of paediatric morbidity and mortality in the region, yet limited epidemiological data, underdiagnosis, and health system constraints continue to obscure their true impact. Aetiological factors in SSA are diverse and include infectious diseases, perinatal complications, genetic disorders and environmental exposures. While countries such as South Africa, have made strides in diagnosis and care, progress remains uneven across the region. Structured training programmes like the African Paediatric Fellowship Programme and public engagement initiatives have contributed to capacity building, but most countries in the region still lack adequate specialist care, essential diagnostic tools such as electroencephalography and magnetic resonance imaging, and sustained investment in paediatric neurology infrastructure and epidemiological research. To address these gaps, this narrative review recommends expanding local training programmes, integrating task-shifting approaches to empower general practitioners and community health workers, and investing in clinical and epidemiological research. Equally critical is the need to strengthen health systems, improve access to diagnostic services, and promote inclusive, stigma reducing advocacy. Only through coordinated efforts can paediatric neurological care in SSA be advanced to meaningfully improve child health outcomes across the region. Thus, this narrative review explores the evident burdens of paediatric neurology care in SSA and proposes potential strategies to address these challenges.
OBJECTIVE: To develop a multimodal artificial intelligence (AI) fusion model predicting abnormal fetal brain development from magnetic resonance imaging (MRI). METHODS: Using fetal brain MRI data and clinical indicators...OBJECTIVE: To develop a multimodal artificial intelligence (AI) fusion model predicting abnormal fetal brain development from magnetic resonance imaging (MRI). METHODS: Using fetal brain MRI data and clinical indicators from pregnant women (from January 2021 to December 2023), who were split 7:3 into training and validation sets. In the training set, key predictors were identified via univariate analysis and multivariate logistic regression, including both clinical indicators and continuous MRI biometric parameters. Three multimodal AI fusion models，including Convolutional Neural Network-Recurrent Neural Network (CNN-RNN) model, attention mechanism-based model, and feature concatenation model were developed. Performance was assessed by accuracy, precision, recall, F1-score, and the area under the receiver operating characteristic curve (AUC). RESULTS: Among the total 806 participants, 108 cases (19.15 %) had fetal brain abnormalities in the training set (n = 564), 45 cases (18.59 %) in the validation set (n = 242). Multivariate logistic regression analysis showed that gestational age, gestational diabetes mellitus, alpha-fetoprotein, lateral ventricular width, and sulcation development score were independent risk factors for fetal brain abnormalities. The attention mechanism fusion model achieved the highest AUC in both the training set (0.876) and the validation set (0.869), significantly outperforming the CNN-RNN fusion model (AUC in training set: 0.776; AUC in validation set: 0.718) and the feature concatenation fusion model (AUC in training set: 0.754; AUC in validation set: 0.720). CONCLUSION: The multimodal AI fusion model, particularly using attention mechanisms, effectively identifies high-risk fetal brain abnormalities, offering potential for early clinical intervention and improved prenatal counseling to enhance detection and prognosis of neurological disorders.
BACKGROUND: There is a large body of literature on brain health, usually focusing on brain health in adulthood in relation to neurodegenerative diseases. Over the past ten years, brain health has also emerged as a concep...BACKGROUND: There is a large body of literature on brain health, usually focusing on brain health in adulthood in relation to neurodegenerative diseases. Over the past ten years, brain health has also emerged as a concept in studies conducted in youth. But what is brain health in youth and how can we measure this? METHODS: We summarized the literature on brain health in youth and inventoried operationalizations of brain health and research themes. We searched Medline for studies reporting on brain health in youth (from neonates to late adolescent stage). RESULTS: We identified 49 eligible studies: 26 operationalized brain health in youth, 13 measured outcomes which they related to brain health and 10 were reviews about youth brain health. Operationalizations of brain health varied widely and included multimodal measures involving questionnaires, cognitive tests, neuroimaging and blood biomarkers. Identified research themes were obesity/fitness/lifestyle as determinants of youth brain health, neonatal brain health, traumatic brain injury and brain health, technological options for measuring brain health, and childhood determinants of brain health. CONCLUSION: This review offers a comprehensive overview of possibilities for measuring brain health in youth, which could serve as a valuable foundation for a commonly accepted definition, framework and operationalization of brain health in youth.
BACKGROUND: Antiseizure medications (ASM) are essential for patients with epilepsy. Though prenatal exposure to ASMs is associated with increased risk for malformations and neurocognitive problems, whether prenatal ASM e...BACKGROUND: Antiseizure medications (ASM) are essential for patients with epilepsy. Though prenatal exposure to ASMs is associated with increased risk for malformations and neurocognitive problems, whether prenatal ASM exposure modifies offsprings' natural developmental trajectory has not yet been studied. METHODS: This prospective study explores the effect of prenatal ASM exposure on the trajectory of cognitive development of children by studying the association of Bayley Scales III scores at 2 years with WISC-IV scores at 6 years of age and by comparing the results against those of unexposed children. Neurocognitive performance of 30 children with prenatal ASM exposure and 37 unexposed control children were evaluated. Correlations and separate ANCOVAs across these ages were compared between ASM exposed and unexposed controls. Results were controlled for maternal education, type of maternal epilepsy, child sex and child age at the assessment. RESULTS: In unexposed participants, cognitive scores at the age of two years associated positively with working memory and processing speed at six years of age and receptive language scores at the age of two years associated with working memory at six years old. Conversely, with exposed children, there were no significant associations between two- and six-year test scores, and coefficients between receptive language and six-year-old working memory or processing speed differed significantly from unexposed children's coefficients. However, small sample size restricts the stability of the results, and the observed group differences in coefficients were not significant after removal of outlier. CONCLUSION: ASM exposure in utero may affect the trajectory of neurocognitive development, but the findings were impacted by an outlier and should be confirmed in larger cohort.
BACKGROUND: We aimed to analyze the prevalence, clinico-radiological and genetic features, and outcomes in children with Alexander disease (AD) with special emphasis on atypical presentations. METHODS: This cross-section...BACKGROUND: We aimed to analyze the prevalence, clinico-radiological and genetic features, and outcomes in children with Alexander disease (AD) with special emphasis on atypical presentations. METHODS: This cross-sectional study evaluated children with AD seen over the past 10 years. Neuroimaging was evaluated by a trained neuroradiologist. In-silico tools were used to predict the pathogenicity of the novel variants detected by whole-exome sequencing. RESULTS: N = 12 children (males 58.3 %) with genetically-confirmed AD were evaluated. Disease subtypes were infantile (n = 7, 58.3 %), juvenile (n = 3, 25 %), and neonatal (n = 2, 16.7 %) AD. The clinic-based prevalence of AD was 0.34 cases per 1000 pediatric neurology patients per year, or an average of 1.2 cases per year. Clinical features were developmental delay (n = 9, 75 %), macrocephaly (n = 9, 75 %), spasticity (n = 6, 50 %), and epilepsy (n = 8, 66.7 %); two children with juvenile-onset disease had atypical visual and bulbar manifestations. Pathogenic variations were most common in exons 1 (n = 5, 42 %), and exon 4 (n = 4, 33.3 %). These were missense type (n = 11, 91.6 %) or deletion (n = 1, 8.3 %). Three novel variants were detected: c.251T>G (p.Ile84Ser) in exon 1, c.810_818 deletion (p.Asn271_Glu273del) in exon 5, and c.292G>C (p.Ala98Pro) in exon 1 in the GFAP gene (NM_002055). Majority of children developed spastic paresis (n = 9, 83 %) and mortality rate was 33.3 % (n = 4/12). CONCLUSION: AD is a rare leukodystrophy with high mortality and progressive spastic paraparesis. Neonatal and juvenile types may present atypically and delay correct diagnosis. Deletions may account for a minor proportion of pathogenic variants. Our study expands the clinico-radiological spectrum of AD in children.
INTRODUCTION: Epilepsy is a chronic brain disorder characterized by recurrent seizures. Limited data on childhood epilepsy in Cameroon prompted this study. METHODS: We conducted a cross-sectional study with retrospective...INTRODUCTION: Epilepsy is a chronic brain disorder characterized by recurrent seizures. Limited data on childhood epilepsy in Cameroon prompted this study. METHODS: We conducted a cross-sectional study with retrospective data collection over six months (December 2023-May 2024). Medical records of children aged 3 months to 15 years, diagnosed with epilepsy and followed at Douala General Hospital between January 2020 and December 2023, were analyzed. Statistical analysis used SPSS 26.0, with Fisher's exact and chi-square tests for associations, and logistic regression for predictive factors (p < 0.05). RESULTS: 142 patients were included (male-to-female ratio = 1.21). Epilepsy prevalence was 2.4 %. Generalized seizures predominated (65.7 %) with focal epileptic abnormalities in 50.7 % of cases. Idiopathic generalized epilepsy represented 57.7 % of cases. Sodium valproate was used in 52.8 % of cases. Main etiological factors included: neonatal convulsions (61; 43 %), febrile seizures (49; 34.5 %) and neonatal asphyxia (35; 24.6 %). Seizures persisted in 35 patients (24.6 %) under treatment. Predictive factors for poor seizure control included unknown seizure type (OR 14.25 [1.10-183.97]; p = 0.04), cryptogenic focal epilepsy (OR 12.55 [1.58-99.71]; p = 0.02), and use of prayers or traditional medicines (OR 7.45 [1.01-55.13]; p = 0.05). Memory disorders significantly impacted school performance (OR 4.95 [1.80-13.59]; p = 0.002), along with lack of concentration (OR 3.04 [1.04-8.84]; p = 0.04). CONCLUSION: This study identified specific predictive factors for poor epileptic control and confirms cognitive impact on schooling, providing intervention targets to optimize neurological and educational management in Cameroon.