Epilepsy is one of the most common chronic neurological disorders of childhood and represents a major public health challenge worldwide. It is characterized by a persistent predisposition of the brain to generate recurrent unprovoked seizures resulting from abnormal, excessive, and synchronous neuronal discharges within the cerebral cortex [1]. Childhood epilepsy encompasses a heterogeneous group of disorders with diverse etiologies, clinical manifestations, prognoses, and treatment outcomes. The condition contributes substantially to childhood morbidity and may adversely affect cognitive development, academic performance, psychosocial well-being, and quality of life of both affected children and their families [2].

The burden of epilepsy is particularly significant in developing countries, where limited access to specialized neurological services often delays diagnosis and treatment. Epidemiological studies have estimated that approximately 4–10 per 1,000 children are affected by active epilepsy, with the highest incidence occurring during the first decade of life [3]. The developing brain exhibits increased susceptibility to epileptogenic insults, making childhood a critical period for the onset of seizure disorders. Furthermore, epilepsy accounts for a substantial proportion of pediatric neurology outpatient visits and hospital admissions, emphasizing the need for comprehensive understanding of its etiological spectrum and clinical characteristics [4].

The etiology of childhood epilepsy is multifactorial and varies according to age, geographic region, and socioeconomic conditions. Traditionally, etiological factors have been classified as idiopathic, symptomatic, or cryptogenic. Idiopathic epilepsies are presumed to have a genetic basis and occur in the absence of identifiable structural brain abnormalities, whereas symptomatic epilepsies result from recognized cerebral insults or neurological disorders. Cryptogenic epilepsies are presumed symptomatic but lack a demonstrable underlying cause despite extensive investigation [5]. Advances in neuroimaging and molecular genetics have improved the identification of etiological factors; however, a considerable proportion of childhood epilepsies remain of unknown origin.

Perinatal hypoxic-ischemic injury, central nervous system infections, congenital brain malformations, traumatic brain injury, cerebrovascular disorders, metabolic abnormalities, and genetic predisposition are among the most important causes of epilepsy in children [6]. In developing countries, preventable causes such as perinatal complications, neuroinfections, and head trauma continue to account for a substantial proportion of cases [7]. Identification of the underlying etiology is essential because it influences seizure type, prognosis, therapeutic approach, and long-term neurological outcome.

The clinical presentation of epilepsy in children is highly variable and depends on the seizure type, age at onset, underlying etiology, and epileptic syndrome. Seizures may be broadly classified as partial (focal) or generalized. Focal seizures originate within a localized region of the cerebral cortex and may present with motor, sensory, autonomic, or psychic manifestations. Generalized seizures involve both cerebral hemispheres from onset and include tonic-clonic, absence, myoclonic, tonic, clonic, and atonic seizure types [8]. Younger children often present with atypical clinical features, making diagnosis challenging. In addition to seizures, many children with epilepsy exhibit associated neurological and developmental abnormalities such as intellectual disability, behavioral disturbances, learning difficulties, and motor deficits [9].

Age at seizure onset is an important determinant of epilepsy characteristics. Neonatal and infantile epilepsies are frequently associated with structural or metabolic etiologies and generally carry a poorer prognosis. In contrast, several epilepsy syndromes of later childhood, including childhood absence epilepsy and benign childhood epilepsy with centrotemporal spikes, are often idiopathic and associated with favorable outcomes [10]. Accurate characterization of seizure semiology and identification of epilepsy syndromes are therefore critical components of pediatric neurological assessment.

Electroencephalography (EEG) remains the cornerstone of epilepsy evaluation, providing valuable information regarding seizure classification and syndrome identification. Neuroimaging, particularly magnetic resonance imaging (MRI), has become increasingly important for detecting structural abnormalities responsible for symptomatic epilepsy [11]. A detailed understanding of the etiological profile and clinical spectrum of childhood epilepsy attending pediatric neurology clinics can facilitate early diagnosis, appropriate management, and effective preventive strategies.

Given the diversity of causes and clinical manifestations, studies evaluating the etiology and clinical characteristics of epilepsy in children are essential for understanding local disease patterns and healthcare needs. Such investigations contribute to improved diagnostic accuracy, optimized treatment planning, and better long-term outcomes. Therefore, the present study aims to evaluate the etiological factors and clinical characteristics of epilepsy among children attending a pediatric neurology clinic, thereby providing insights into the epidemiological and clinical profile of this important neurological disorder.

Study Design and Setting This hospital-based observational cross-sectional study was conducted in the Department of Neurology, Government Medical College, Amritsar, Punjab, India. The study aimed to evaluate the etiological profile and clinical characteristics of epilepsy among pediatric patients attending the pediatric neurology services. Data were collected over a period of 18 months from children presenting with epilepsy to the outpatient and inpatient facilities of the department. Study Population The study population comprised children aged 1 month to 18 years diagnosed with epilepsy according to the criteria of the International League Against Epilepsy (ILAE). A total of 80 consecutive eligible patients were enrolled during the study period using a consecutive sampling technique. Sample Size The sample size was fixed at 80 pediatric patients fulfilling the eligibility criteria and presenting to the Department of Neurology during the study period. All eligible participants encountered during the recruitment period were included until the required sample size was achieved. Inclusion Criteria 1. Children aged between 1 month and 18 years. 2. Patients diagnosed with epilepsy, defined as the occurrence of at least two unprovoked seizures occurring more than 24 hours apart, or one unprovoked seizure with a high probability of further seizures according to ILAE recommendations. 3. Children whose parents or legal guardians provided written informed consent for participation. 4. Children willing to undergo the required clinical and diagnostic evaluations. Exclusion Criteria 1. Children with acute symptomatic seizures secondary to fever, metabolic disturbances, electrolyte abnormalities, intoxication, or acute central nervous system infections. 2. Patients with isolated febrile seizures. 3. Neonates younger than one month of age. 4. Children with incomplete clinical records or insufficient diagnostic information. 5. Guardians declining consent for participation. Data Collection Procedure After obtaining informed consent from parents or guardians, detailed demographic and clinical information was collected using a structured and pre-validated case record form. Information recorded included age, sex, residence, socioeconomic status, age at seizure onset, duration of illness, family history of epilepsy, prenatal and perinatal history, developmental milestones, history of central nervous system infections, head trauma, and other relevant medical conditions. A comprehensive neurological examination was performed for each participant by a consultant neurologist. Developmental assessment was conducted using age-appropriate clinical evaluation methods. Anthropometric measurements including weight, height, and head circumference were recorded wherever applicable. Clinical Assessment Seizures were classified according to the International League Against Epilepsy (ILAE) classification. Clinical variables assessed included: • Age at onset of epilepsy • Type of seizure • Frequency of seizures • Duration of epilepsy • Presence of status epilepticus • Developmental delay • Intellectual disability • Neurological deficits • Associated comorbidities • Family history of epilepsy Patients were categorized into focal epilepsy, generalized epilepsy, combined generalized and focal epilepsy, or unclassified epilepsy based on clinical features and electroencephalographic findings. Electroencephalographic Evaluation All participants underwent standard electroencephalography (EEG) using a digital EEG system. Recordings were obtained according to the international 10–20 electrode placement system. Activation procedures including hyperventilation and intermittent photic stimulation were employed whenever feasible. EEG findings were classified as normal or abnormal and further categorized into focal epileptiform discharges, generalized epileptiform discharges, multifocal discharges, hypsarrhythmia, or other abnormalities. Neuroimaging Evaluation Neuroimaging studies were performed whenever clinically indicated. Magnetic resonance imaging (MRI) of the brain was the preferred modality. Computed tomography (CT) scans were performed in cases where MRI was contraindicated or unavailable. Imaging findings were evaluated for structural abnormalities including: • Cortical malformations • Perinatal hypoxic-ischemic injury • Cerebral atrophy • Hydrocephalus • Neurocysticercosis • Mesial temporal sclerosis • Post-infectious sequelae • Vascular lesions • Tumors Etiological Classification The etiology of epilepsy was determined based on clinical history, neurological examination, EEG findings, neuroimaging results, and relevant laboratory investigations. Patients were classified according to ILAE etiological categories as: • Structural • Genetic • Infectious • Metabolic • Immune • Unknown etiology For comparative analysis, etiologies were also grouped into symptomatic (structural/metabolic/infectious), idiopathic (presumed genetic), and cryptogenic categories where applicable. Laboratory Investigations Relevant laboratory investigations were performed as clinically indicated and included: • Complete blood count • Blood glucose • Serum electrolytes • Liver function tests • Renal function tests • Serum calcium and magnesium • Metabolic screening • Cerebrospinal fluid examination (when indicated) Outcome Measures The primary outcome measures included: 1. Distribution of etiological factors causing epilepsy. 2. Clinical characteristics and seizure patterns among affected children. Secondary outcome measures included: 1. Association between etiology and seizure type. 2. Correlation of EEG abnormalities with clinical presentation. 3. Relationship between neuroimaging findings and epilepsy characteristics. Statistical Analysis Data were entered into Microsoft Excel and analyzed using Statistical Package for Social Sciences (SPSS) software version 26.0 (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean ± standard deviation (SD) or median with interquartile range (IQR), depending on data distribution. Categorical variables were presented as frequencies and percentages. Associations between categorical variables were assessed using the Chi-square test or Fisher's exact test as appropriate. Continuous variables were compared using Student's t-test or Mann–Whitney U test. A p-value <0.05 was considered statistically significant. Results were presented using tables and figures to facilitate interpretation.

A total of 80 children diagnosed with epilepsy were included in the study. The mean age of the study population was 8.7 ± 4.3 years (range: 6 months–18 years). Males constituted 47 (58.8%) participants, while females accounted for 33 (41.2%), resulting in a male-to-female ratio of 1.42:1.

The majority of patients belonged to the 6–10 years age group (32.5%), followed by the 11–15 years age group (27.5%). Developmental delay was observed in 21 (26.3%) children, while a positive family history of epilepsy was documented in 14 (17.5%) patients.

Table 1. Demographic Characteristics of Study Participants (n = 80)

Table 1 presents the demographic profile of the 80 children diagnosed with epilepsy. The majority of patients belonged to the 6–10 years age group (32.5%), followed by the 11–15 years age group (27.5%). Children aged 1–5 years constituted 22.5% of the study population, while infants younger than one year represented only 6.3% of cases. Male children predominated, accounting for 58.8% of participants, whereas females comprised 41.2%, yielding a male-to-female ratio of approximately 1.4:1. Most patients were from rural areas (61.3%), while 38.7% resided in urban regions.

Table 2. Clinical Characteristics of Epilepsy (n = 80)

Table 2 summarizes the clinical characteristics of epilepsy among the enrolled children. The age of seizure onset was most frequently observed between 6 and 10 years (31.3%), followed by 1–5 years (27.5%). Generalized tonic-clonic seizures were the most common seizure type, occurring in 53.8% of patients. Focal seizures accounted for 30.0% of cases, while absence and myoclonic seizures represented smaller proportions of 6.2% and 5.0%, respectively. A history of status epilepticus was documented in 13.8% of children. Developmental delay was identified in 26.3% of patients, whereas a positive family history of epilepsy was reported in 17.5% of cases.

Table 3. Electroencephalographic Findings (n = 80)

Table 3 depicts the electroencephalographic findings observed among study participants. EEG abnormalities were detected in 76.3% of children, highlighting the important diagnostic role of EEG in childhood epilepsy. Generalized epileptiform discharges constituted the most common abnormality, present in 36.3% of patients. Focal epileptiform discharges were observed in 26.2% of cases, while multifocal discharges were noted in 7.5%. Hypsarrhythmia was identified in 2.5% of patients, primarily among younger children with severe epileptic syndromes. Normal EEG recordings were found in 23.7% of participants despite clinical evidence of epilepsy.

Table 4. Neuroimaging Findings (n = 80)

Table 4 illustrates the neuroimaging characteristics of the study population. Neuroimaging was normal in 56.2% of patients. Among abnormal findings, perinatal hypoxic-ischemic injury was the most frequently identified lesion, accounting for 12.5% of cases. Cerebral atrophy was detected in 8.8% of children, followed by neurocysticercosis in 6.3%. Cortical malformations and post-infectious sequelae each contributed 5.0% of cases. Mesial temporal sclerosis was observed in 3.7%, while intracranial tumors were identified in 2.5% of patients. These findings underscore the significant contribution of structural brain abnormalities to childhood epilepsy.

Table 5. Etiological Classification of Epilepsy (n = 80)

Table 5 presents the etiological spectrum of epilepsy in the study population. Structural etiologies constituted the largest category, accounting for 35.0% of all cases. Genetic or idiopathic epilepsy represented 27.5% of patients, making it the second most common etiological group. Infectious causes were identified in 12.5% of children, while metabolic and immune-mediated etiologies contributed 5.0% and 2.5% of cases, respectively. Despite comprehensive clinical and diagnostic evaluation, the etiology remained unknown in 17.5% of patients. These findings indicate that structural brain abnormalities remain a major cause of pediatric epilepsy in the studied population.

Table 6. Association BetweenEtiology and Seizure Type

Table 6 demonstrates the relationship between epilepsy etiology and seizure type. Among children with structural epilepsy, focal seizures predominated, occurring in 60.7% of cases, whereas generalized seizures accounted for 39.3%. In contrast, generalized seizures were significantly more frequent among patients with genetic or idiopathic epilepsy (81.8%). Infectious, metabolic, immune, and unknown etiologies also showed a predominance of generalized seizure patterns. Statistical analysis revealed a significant association between epilepsy etiology and seizure type (Chi-square test, p = 0.003), indicating that structural causes were more likely to present with focal seizures compared with other etiological categories.

Figure 1. Age Distribution of Children with Epilepsy

Figure 1 illustrates the age-wise distribution of the 80 children diagnosed with epilepsy included in the study. The highest proportion of patients belonged to the 6–10 years age group, comprising 26 children (32.5%), followed by the 11–15 years age group with 22 children (27.5%). Children aged 1–5 years accounted for 18 cases (22.5%), while those older than 15 years represented 9 cases (11.2%). Infants younger than one year constituted the smallest group, with 5 cases (6.3%). The findings indicate that epilepsy was most frequently diagnosed among school-aged children, particularly between 6 and 10 years of age, suggesting a greater clinical presentation and detection of epilepsy during this developmental period. The overall distribution demonstrates that nearly 60% of the study population was between 6 and 15 years of age.

Figure 2. Electroencephalographic Findings Among Children with Epilepsy

Figure 2 illustrates the distribution of electroencephalographic (EEG) findings among the 80 children with epilepsy included in the study. Abnormal EEG findings were observed in 61 patients (76.3%), whereas 19 children (23.7%) had normal EEG recordings despite clinical evidence of epilepsy. The most common EEG abnormality was generalized epileptiform discharges, detected in 29 patients (36.3%), followed by focal epileptiform discharges in 21 patients (26.2%). Multifocal discharges were identified in 6 children (7.5%). Hypsarrhythmia, a characteristic pattern associated with infantile epileptic spasms, was observed in 2 patients (2.5%). Diffuse slowing and other nonspecific abnormalities were present in 3 children (3.8%). These findings indicate that generalized epileptiform activity was the predominant EEG pattern in the study population and highlight the substantial diagnostic utility of EEG in the evaluation and classification of childhood epilepsy. The high proportion of abnormal EEG recordings further supports its role as an essential investigation for identifying seizure type, determining epilepsy syndrome, and guiding therapeutic decision-making.

Figure 3. Etiological Spectrum of Childhood Epilepsy

Figure 3 illustrates the etiological distribution of epilepsy among the 80 children included in the study. Structural etiologies constituted the largest category, accounting for 28 cases (35.0%), indicating that brain abnormalities such as perinatal hypoxic-ischemic injury, cortical malformations, cerebral atrophy, and other structural lesions were major contributors to epilepsy in the study population. Genetic or idiopathic epilepsy represented the second most common etiological group, comprising 22 patients (27.5%). Infectious causes were identified in 10 children (12.5%), reflecting the continued role of central nervous system infections and their sequelae in the development of epilepsy.

Figure 4. Relationship Between Etiological Categories and Seizure Types

Figure 4 illustrates the distribution of generalized and focal seizures across different etiological categories of childhood epilepsy. Structural epilepsy demonstrated a predominance of focal seizures, with 17 of 28 patients (60.7%) presenting with focal seizure manifestations, whereas generalized seizures were observed in 11 patients (39.3%). In contrast, generalized seizures were markedly more common among children with genetic/idiopathic epilepsy, accounting for 18 of 22 cases (81.8%), while focal seizures occurred in only 4 patients (18.2%).

Epilepsy remains one of the most prevalent neurological disorders in childhood and constitutes a significant cause of morbidity worldwide. The present study evaluated the etiological profile and clinical characteristics of epilepsy among children attending a tertiary care neurology clinic in North India. The findings provide important insights into the demographic distribution, seizure characteristics, electroencephalographic abnormalities, neuroimaging findings, and etiological spectrum of pediatric epilepsy in a hospital-based population. In the present study, the majority of children were between 6 and 10 years of age, accounting for 32.5% of cases, with a mean age of 8.7 years. Similar age distributions have been reported in several pediatric epilepsy studies, where school-aged children constituted the largest proportion of patients seeking neurological care [12,13]. This observation may reflect increased recognition of seizure disorders during school years when academic and behavioral difficulties become more apparent. Male predominance was observed in our cohort, with males constituting 58.8% of participants. Comparable findings have been reported by Sidenvall et al. and Camfield et al., who demonstrated a slight male preponderance in childhood epilepsy populations [14,15]. The reasons for this gender difference remain uncertain but may involve biological susceptibility, sociocultural factors, and healthcare-seeking behaviors. Generalized tonic-clonic seizures were the most common seizure type, accounting for 53.8% of cases, followed by focal seizures (30.0%). These findings are consistent with previous reports from developing countries where generalized seizures frequently predominate in pediatric populations [16]. However, studies conducted in regions with widespread access to advanced neuroimaging have increasingly identified higher proportions of focal epilepsy due to improved recognition of structural brain abnormalities [17]. The predominance of generalized seizures observed in the present study may therefore reflect both genuine epidemiological patterns and referral characteristics of the study population. Developmental delay was identified in 26.3% of patients, highlighting the close association between epilepsy and neurodevelopmental impairment. Previous studies have demonstrated that children with epilepsy are at increased risk of cognitive dysfunction, learning disabilities, and behavioral disorders compared with the general pediatric population [18]. Berg et al. reported that developmental and cognitive impairments are particularly common among children with symptomatic epilepsy and those with early-onset seizures [19]. The relatively high prevalence of developmental delay in our cohort may be explained by the substantial proportion of children with structural and symptomatic epilepsies. A positive family history of epilepsy was present in 17.5% of participants. This finding supports the contribution of genetic factors to epilepsy susceptibility and is consistent with previous epidemiological studies demonstrating familial aggregation of seizure disorders [20]. Genetic predisposition is particularly evident in idiopathic generalized epilepsies, where heritability plays a significant role in disease pathogenesis. Electroencephalography remains a cornerstone in the diagnosis and classification of epilepsy. In the present study, EEG abnormalities were detected in 76.3% of patients. Generalized epileptiform discharges were the most common abnormality, followed by focal epileptiform discharges. Similar EEG yields have been reported by King et al. and Shinnar et al., who demonstrated abnormal EEG findings in approximately 60–80% of children with epilepsy [21,22]. The predominance of generalized epileptiform activity observed in our study parallels the high proportion of generalized seizure types identified clinically. Importantly, nearly one-quarter of patients had normal EEG recordings despite established epilepsy, emphasizing that a normal EEG does not exclude the diagnosis of epilepsy and should always be interpreted in conjunction with clinical findings. Neuroimaging revealed abnormalities in 43.8% of patients, while 56.2% had normal imaging studies. Perinatal hypoxic-ischemic injury was the most common structural abnormality identified, followed by cerebral atrophy and neurocysticercosis. Similar observations have been reported from developing countries where perinatal insults continue to represent major contributors to childhood neurological morbidity [23]. The substantial burden of hypoxic-ischemic injury highlights the importance of improving perinatal healthcare services, obstetric management, and neonatal intensive care facilities. Neurocysticercosis accounted for 6.3% of cases in the present study. This finding is consistent with reports from India and other endemic regions where neurocysticercosis remains an important preventable cause of epilepsy [24]. Del Brutto et al. demonstrated that neurocysticercosis contributes significantly to the burden of epilepsy in developing countries and remains one of the most common parasitic diseases affecting the central nervous system [25]. The persistence of neurocysticercosis in our cohort underscores the need for improved sanitation, public health interventions, and early diagnosis. Regarding etiology, structural causes constituted the largest category (35.0%), followed by genetic or idiopathic epilepsy (27.5%). Infectious etiologies accounted for 12.5% of cases, while the etiology remained unknown in 17.5% of children. These findings are broadly consistent with reports from tertiary care centers where symptomatic epilepsies frequently predominate because of referral bias toward more complex neurological disorders [26]. Advances in neuroimaging have substantially improved the detection of structural causes of epilepsy, thereby reducing the proportion of cases classified as cryptogenic or unknown [27]. The predominance of structural etiologies in our study is clinically significant because structural epilepsy is often associated with greater seizure severity, neurological deficits, developmental impairment, and poorer long-term outcomes [28]. Identification of an underlying structural lesion may also facilitate targeted therapeutic interventions, including epilepsy surgery in selected cases. One of the most important findings of the present study was the significant association between epilepsy etiology and seizure type (p = 0.003). Structural etiologies were predominantly associated with focal seizures, whereas generalized seizures were more common among genetic, infectious, metabolic, immune, and unknown etiological groups. These findings are biologically plausible because focal structural abnormalities generate localized epileptogenic zones that typically produce focal seizure manifestations [29]. In contrast, many genetic epilepsies involve widespread neuronal network dysfunction resulting in generalized seizure activity [30]. The observed relationship between structural lesions and focal epilepsy is supported by previous studies demonstrating strong correlations between focal cortical abnormalities and focal seizure semiology [31]. Such associations have important clinical implications because seizure type may provide valuable clues regarding the underlying etiology and guide further diagnostic evaluation. Children presenting with focal seizures should therefore undergo comprehensive neuroimaging assessment to identify potentially treatable structural abnormalities. Overall, the findings of the present study emphasize the heterogeneous nature of childhood epilepsy and reinforce the importance of comprehensive diagnostic evaluation incorporating clinical assessment, EEG, and neuroimaging. Early identification of etiological factors can improve prognostication, optimize treatment strategies, and facilitate preventive interventions aimed at reducing the burden of epilepsy in children.

Childhood epilepsy remains a heterogeneous neurological disorder with diverse clinical presentations and etiological determinants. The present study demonstrated that epilepsy predominantly affected school-aged children, with a slight male predominance. Generalized tonic-clonic seizures constituted the most common seizure type, while developmental delay and positive family history were observed in a considerable proportion of patients. Electroencephalography proved to be a valuable diagnostic tool, revealing abnormalities in more than three-fourths of the study population, with generalized epileptiform discharges being the most frequent finding.

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