1. INTRODUCTION:

Approximately 0.5 to 1% of children worldwide suffer from epilepsy, one of the most prevalent neurological disorders. However, it is characterized by a range of symptoms rather than being a specific medical disorder itself, which may occur alongside various brain morphological and metabolic changes. Epileptic seizures or temporary bioelectrical abnormalities in the brain's nerve cells, are one of the signs of epilepsy¹. Epilepsy is a neurological illness that affects people of all genders, social classes, locations, and races. According to a recent study, there are almost 90% of the world's 70 million epileptics in poor nations. Epilepsy is a brain disorder marked by unpredictability and frequent disturbances of normal functioning. Epileptic seizures are a type of neurological phenomenon. Epilepsy is a neurological condition with multiple causes. It is not one disease entity². The epilepsy Paroxysmal cerebral dysrhythmia is a characteristic of this category of CNS illnesses, which can present as brief episodes (seizures) of loss or disturbance of consciousness, associated or not by distinctive body movements (convulsions), sensory, or mental events. The frequency of these events varies greatly and they are unpredictable. The sites of the focus, the areas into which the discharges develop, and the postictal depression of these regions all influence the symptoms of epilepsy, which has a focal origin in the brain. Known as the “disease of lightning” since the beginning of time³. The International League Against Epilepsy (ILAE) defines an epileptic seizure as the brief manifestation of signs and symptoms caused on by abnormal, excessive, or synchronous neuronal brain activity. Since 2014, the ILAE has suggested including one of the following to the definition of epilepsy due to changes in the topic: 1. Two or more unprovoked (or reflex) seizures that happen more than twenty-four hours apart;

2. Two unprovoked (or reflex) seizures during a ten-year period, followed by a likelihood of further seizures similar to the general risk of recurrence (at least 60%) with clinical, electrical-electroencephalogram (EEG), or neuroimaging abnormalities; 3. Epilepsy syndrome diagnosis⁴. Hyperexcitability and an imbalance between excitation and inhibition are the causes of epilepsy, which results in seizures. The clinical features of epileptic seizures are adverse. Patients’ lives are negatively impacted by these seizures, especially those who suffer them regularly. Patients with epileptic seizures suffer neurological, behavioral, and emotional abnormalities. Different parts of the brain may feel seizures, and the effectiveness of a seizure depends on its characteristics, the type of seizure, and the location of abnormal neuronal activity. Patients with epilepsy suffer social stigma and prejudice; societal misunderstandings and negative opinions about this condition may keep them from getting treatment and living confident lives⁵. The word "epilepsy" refers to a group of different conditions whose main characteristic is a tendency for common, unplanned seizures. While certain seizures can be categorized based on their clinical characteristics (such as generalized tonic-clonic seizures and complex partial seizures), epilepsy conditions can also be categorized based on the type of seizure, the fact that neurological or developmental abnormalities are present, and electroencephalogram (EEG) results. For example, in young people with normal mental abilities, the condition of childhood myoclonic epilepsy is defined by the onset of myoclonic seizures, generalized tonic-clonic seizures, and less commonly absence seizures, along with rapid, widespread high-frequency and polyspike-wave discharges on the EEG⁶.

2. Correlation Between: Epilepsy And Attention Deficit:

Hyperactivity Disorder (ADHD):

A common neurological condition that first develops in childhood, attention deficit hyperactivity disorder (ADHD) is linked to both structural and functional problems in different parts of the brain. Epilepsy and ADHD have been connected since the 1950s. ADHD is commonly seen in children with epilepsy. According to a research by the international League against Epilepsy, 30–40% of children with epilepsy had ADHD (7). Children's social and behavioral development is seriously affected by both epilepsy and attention deficit hyperactivity disorder (ADHD). Behavioral difficulties in epileptic children suggest a high risk for ADHD. It is unknown if ADHD is a general symptom based on by antiepileptic medications (AEDs), non-convulsive epileptic discharges, or adverse long-term seizure effects. It's also not clear when overlapping pathophysiologic pathways link ADHD and epilepsy (8). ADHD development, seriousness, and recurrence into adulthood are linked to childhood trauma. Clinical symptoms of ADHD are present in 20% to 50% of children who suffer from childhood trauma. In the same way, adult patients symptoms of ADHD are positively correlated with recent stress, or stressful events that occurred within the past year. pleasantly, children who suffer stress during pregnancy are more likely to develop ADHD later in life. ADHD is frequently associated with anxiety problems, which increases the illness. Given multiple opinions on the effectiveness of methylphenidate in this population, more study is required to determine the therapeutic implications for ADHD with anxiety comorbidity⁹.

3. Classification of Seizures:

A. Focal Seizure:

generally having a unilateral specific origin in the brain, they may spread to the entire brain or to a small or big area. Clinically, focal origin may be obvious, or the EEG may show it¹⁰.

1. Focal Motor Seizure: Motor onset includes automatism, atonic, clonic, epileptic spasms, hyperkinetic, myoclonic and tonic seizures ¹¹.

a. Focal Automatism Seizure: Since automatism seizures are a typical sign of Focal Impaired Awareness Seizure, they are a particularly important type of focal seizure. Automatisms are motions that like those of a robot, like continuously speaking the same sentence, picking at clothing, rubbing, struggling, lip-smacking, or wandering¹².

b. Focal Atonic Seizure: One side of the body or a single limb could suffer rapid seizures with loss of muscular tone that last only a few seconds. Usually awareness is maintained¹³.

c. Focal Tonic Seizure: Clinically, seizures characterized by a prolonged increase in muscular contraction that lasts a few seconds or minutes may occur as tightness in the neck or limb¹³.

d. Focal Clonic Seizure: The following example indicates focal clonic seizures: a baby boy shows rhythmic jerking of one arm. The jerks continue after changing positions, and the EEG shows right frontal cerebral rhythms. The seizure is focal since the EEG shows a localization of the electrical discharge¹⁴.

e. Focal Epileptic Spasms: Children often suffer from sudden, uncontrollable, and sometimes painful muscular contractions. Clinically show with sudden hip flexion and arm and leg flexion or extension; these symptoms might be specific, common, or have an unclear onset. They may also occur in groups¹³.

f. Focal Hyperkinetic Seizure: A hyperkinetic seizure, formerly known as a hypermotor seizure, is characterized by rapid motion, writhing, and kicking. Usually, the frontal lobe is where these seizures start¹².

g. Focal Myoclonic Seizure: Since they are typically short, uncontrolled muscle spasms that happen suddenly and continue for a few seconds or even less than a second, or only an irregular jerking in one portion of the face or body, they could look like clonic seizures. Usually, awareness is maintained¹³.

2. Focal Non-Motor Seizure: Nonmotor onset comprises autonomic, behavior arrest, cognitive, emotional and sensory seizures¹⁴.

a. Focal Non-Motor Automatic Seizure: Autonomic seizures are characterized by changes in blood pressure, heart rate, sweating, skin color, or gastrointestinal upset¹⁵.

b. Focal Non-motor Behavior Arrest Seizures: Behavioral arrest seizures are characterized by stop of movement¹⁵.

c. Focal Non-motor Cognitive Seizures: Cognitive seizures are characterized by abnormal language or thinking, eg, jamais vu, déjà vu, hallucinations, and visualization of illusions¹⁵.

d. Focal Non-motor Emotional Seizures: Emotional changes like dread, anxiety, worry, or pleasure are characteristic of emotional seizures. Gelastic nonmotor seizures are characterized by laughter, while dacrystic seizures are characterized by crying ¹⁵.

e. Focal Non-motor Sensory Seizures: Sensory seizures are characterized by changes in sensation, such as abnormal sensations of vision, tingling, hearing, smell, or pain¹⁵.

B. Generalized Seizures: The principal types of generalized seizures are absence, atypical absence, myoclonic, atonic, tonic, and tonic-clonic¹⁶. There are two types of generalized seizures: motor seizures and nonmotor (absence) seizures. Additional divisions approach those in the 1981 classification, but they also include Myoclonic absence, absence seizures with eyelid myoclonia observed in the condition described by Jeavons and elsewhere, myoclonic-tonic-clonic seizures found in juvenile myoclonic epilepsy, and myoclonic-atonic seizures common in epilepsy with myoclonic-atonic seizures (Doose syndrome). Asymmetrical generalized seizure signs can make it challenging to differentiate them from focal-onset seizures. Because the term "absence" has a common meaning, a "absent stare" is not the same as an absence seizure because other seizure types also involve an arrest of activity¹⁷.

1. Typical and Atypical Absence: Typical absences in school-age children, childhood absence epilepsy, and juvenile absence epilepsy occur during childhood and adolescence, respectively. They happen a lot during the day. The kid cannot hear the teacher during an absence seizure, and because they happen regularly, the child is no longer able to follow the lessons. The teacher will discipline the student for concentration and disinterest if he is unaware of this situation. Hyperventilation, or overbreathing, can easily cause absences. They can be easily identified on an EEG since they have a typical EEG pattern¹⁸.

2. Myoclonic Seizure: Another type of generalized seizure is a myoclonic jerk, which happens when a group of muscles contracts suddenly and rapidly. They might be unilateral or bilateral and impact the head, arms, legs, or entire body¹⁹.

3. Atonic Seizure: A sudden decrease of postural tone in a patient is known as atonic or astatic seizures. Patients may fall unexpectedly, which could be dangerous as they could connect with anything²⁰.

4. Epidemiology of Epilepsy in Children:

Epilepsy is one of the most common neurological disorders with a point incidence ranging from 4–10 per 1,000 people according to earlier research. Up to 8% of people can have at least one seizure in their lifetime, and the incidence rate of epilepsy is believed to be between 50 and 60 per 100,000 person-years. According to studies, almost 80% of epileptics live in low- and middle-income nations, where the treatment gap significantly increases the prevalence of epilepsy globally. Because of things including a lack of healthcare resources, customs of society, social disapproval, and a preference for traditional therapies, up to 90% of epilepsy in these places goes untreated or is treated improperly²¹. There are significant variations in the prevalence of childhood epilepsy between studies and geographical areas. According to a Canadian study, the prevalence was 8.1 per 1,000 live births overall, with considerably greater rates among premature babies and boys²² Men have a comparatively greater incidence and prevalence of epilepsy than women. The variation may be explained by the different incidence of the most prevalent risk factors and the sociocultural reasons for certain regions' women conceal the disease. The prevalence of epilepsy in children peaks during the first year of life and then decreases to adult levels by the end of ten years²³.

5. Etiology:

An imbalance between excitation and inhibition in specific areas of the central nervous system (CNS) causes seizures and epilepsy. Six etiologic categories for epilepsy have been established by the ILAE Task Force: genetic, structural, metabolic, infectious, immunological, and unknown. A patient's epilepsy may fall under more than one etiologic group, and these are not hierarchical²⁴.

1. Structural Etiology: A structural etiology is defined as abnormalities seen on structural neuroimaging where the imaging results and electroclinical evaluation provide a reasonable finding that the patient's seizures are most likely caused by the imaging abnormalities²⁵.

2. Genetic Etiology: According to certain research, there is no link between epilepsy and genetic variables. However, many studies have connected epilepsy to family history and mostly inherited variables. The complex inheritance patterns of the most prevalent human genetic epilepsies are largely unknown, as are their gene relationships²⁶.

3. Infectious Etiology: Bacterial meningitis is a common cause of seizures both in developed and in developing countries. Haemophilus influenzae B (Hib), pneumococcus, and meningococcus are the three most prevalent aetiological agents in around the world. But the rate of meningitis caused on by these organisms has developed in both industrialized and developing nations²⁷.

4. Metabolic Etiology: Seizures are one of the main symptoms of metabolic epilepsy, which is thought to be caused by a known or suspected metabolic disturbance. A person who experiences acute symptomatic seizures due to a temporary metabolic abnormality would not be considered epileptic because their seizures occur²⁴.

5. Immune Etiology: When there is proof of inflammation in the central nervous system caused by an autoimmune disease, this is known as an immunological etiology. The number of these autoimmune encephalitides being diagnosed is rising quickly, especially as antibody testing becomes more widely available²⁵.

6. Pathophysiology:

Excessive excitement or, in the absence of such stimulation, seizures Attacks resulting from abnormal inhibition of a significant number of cortical neurons. This appears as a strong wave or spike on the EEG. First, A small number of neurons fire abnormally. The typical membrane inhibitory synaptic currents and conductances break down and When excessive excitability spreads, it can cause focal seizures locally or more extensively to cause a seizure that is global. This beginning spreads using physiological pathways to reach nearby or remote areas. The Clinical symptoms vary depending on the focus's location, the extent of irritation of the brain's surrounding region, as well as the severity of the drive. Continuous hyperexcitability may be caused by a variety of mechanisms, such as:¹ changes in the distribution, number, type, and biophysical characteristics of ion channels in the neural membranes; ² biochemical modifications of receptors;³ modulation of gene expression and second messaging systems;⁴ changes in extracellular ion concentrations;⁵ modifications in glial cell uptake and metabolism of neurotransmitters; and ⁶ modifications in the ratio and function of inhibitory circuits. In addition, human research on presurgical patients have not consistently revealed variations in focused epileptogenesis, although local neurotransmitter imbalances may be a plausible explanation. However, in susceptible patients, seizures may be triggered by transient imbalances between the primary neurotransmitters, glutamate (excitatory) and γ-aminobutyric acid (GABA) (inhibitory), as well as neuromodulators (such as acetylcholine, norepinephrine, and serotonin). By increasing the sensitivity of neurons to electrical or chemical stimulation or by preventing the seizure discharge from spreading from its source, AEDs can control abnormal neuronal activity. While inhibiting propagation involves lowering nerve conduction and depressing synaptic transmission, raising the threshold most likely involves stabilizing neuronal membranes. In sensitive neuronal populations, prolonged seizures can cause neuronal damage that leads to permanent changes in the neuronal circuit's wiring and functional deficiencies, mainly in memory. neural death, brain injury, and a persistent susceptibility to seizures could result from the budding and rearrangement of neural projections. Additionally, sustained glutamate exposure may be a factor in neuronal injury. It has been proposed that patients who experience numerous episodes of status epilepticus and a high frequency (greater than 100) of generalized tonic-clonic (GTC) seizures may be at risk for future cognitive declines, even though individual seizures by themselves do not significantly impair intelligence²⁸.

7. Physical Examination:

1. The blood pressure should be measured in the supine and standing positions to assess postural drop in patients with vasovagal syncope.

2. Skin exam is important as the skin and the nervous system have the same embryologic origin (ectoderm). Therefore, developmental CNS disorders may have associated skin signs

3. (neurocutaneous disorders) such as ash leaf spots of tuberous sclerosis, facial angioma of Sturge-Weber syndrome, café-au-lait spots of neurofibromatosis, nevi of the linear nevus syndrome, and swirling hypopigmentation of Ito syndrome.

4. 3.Examination of the skull for shape, fontanel size and tenseness, sutures for premature fusion or wide separation are important²⁹.

8. Diagnosis:

1. Electroencephalography: The simple, readily available and inexpensive method of studying neural dysfunction is electroencephalography (EEG). as well as abnormal cortical excitability in children who have seizures. Using conductive paste, the gold or silver disc (silver chloride) surface EEG electrodes are placed at specific points on the scalp. The 10-20 International System (Electrode placement involves a gap of between 10 and 20%). In newborns and young infants, pediatric EEG typically calls for the implantation of 21 electrodes on the scalp, with fewer electrodes (minimum of 12 electrodes). Sleep EEG records are necessary for infants, young children, and kids with suspected focal epilepsies. For the diagnosis of epileptic encephalopathy, sleep EEG is crucial. CSWS stands for continuous spike waves during slow sleep. When awake, EEG can be used to identify generalized seizures. The activation process consists of intermittent photic stimulation (4-6 Hz generalized epileptiform discharges in juvenile myoclonic epilepsy) and hyperventilation (3 Hz spike wave pattern in absence epilepsies). Fixation of sensitivity (late onset occipital lobe epilepsy), precipitation by trigger (such as watching videos) in reflex epilepsies, and recommendation to precipitate paroxysmal non-epileptic episodes are other activation treatments recommended for particular situations³⁰.

2. Neuroimaging: The diagnosis and treatment of brain disorders have been greatly impacted by modern structural and functional imaging techniques of seizures. More understanding of the pathophysiology behind symptomatic epilepsies has been made possible by the combination of suitable new imaging techniques.³¹

3. Genetic Testing:

About 70% of instances of epilepsy are influenced by genetics, either in the form of a single genetic variant (rare forms) or many genetic variants mixed with environmental influences (common forms). Next-generation sequencing (NGS) technologies, such as targeted gene panels, whole-exome sequencing (WES), and whole-genome sequencing (WGS), have enabled the analysis of hundreds of genes associated with various epilepsy syndromes. To date, approximately 265 genes have been identified in epilepsy; of these, several genes, including STXBP1, ARX, SLC25A22, KCNQ2, CDKL5, SCN1A, and PCDH19, have been associated with early-onset EEs. Clinical testing using gene panels, exomes, and genomes has revolutionized the diagnosis of genetic epilepsy³².

9. Treatment of Pediatric Epilepsy:

1. Antiepileptic Drugs:

A. Carbamazepine:

It was first used to treat trigeminal neuralgia in the 1960s and is chemically linked to imipramine. It is currently a first-line antiepileptic medication. The pharmacological activities are similar to those of phenytoin, however experimental research has shown some significant distinctions. Carbamazepine increases the risk for PTZ and electroshock seizures and alters maximum electroshock seizures. It prevents burning as well. Although it acts similarly to phenytoin on Na+ channels (prolongation of inactivated state), its profile of action on the brain's neural systems differs.

Pharmacokinetics: Due to its weak water solubility, carbamazepine has a slow and variable oral absorption rate. 75% of it is bonded to plasma. proteins and broken down in the liver by hydroxylation, conjugation to inactive metabolites, and oxidation to an active metabolite (10-11 epoxy carbamazepine).

Adverse effects: Carbamazepine produces dose-related neurotoxicity—sedation, dizziness,

vertigo, diplopia and ataxia. Vomiting, diarrhoea, worsening of seizures are also seen with higher doses.

Use: The most popular medication for Generalized tonic-clonic seizure and Stiff persone syndrome, as well as the most effective medication for CPS, is carbamazepine.³³

B. Ethosuximide (ETS):

ETS was approved in the USA in 1970 as first-line and adjunctive therapy for treatment of generalized absence seizures, which only included four studies, showed uncertain results when comparing ETS, VPA or LTG in the treatment of absence seizures. In a recent double-blind, randomized, controlled trial comparing the efficacy, tolerability, and neuropsychological effects of ETS, VPA and LTG in 453 children with newly diagnosed childhood absence epilepsy, ETS was similar to VPA and both were more effective than LTG in terms of freedomfrom-failure rates after 16 weeks of therapy (OR 1.26,95 % CI 0.80–1.98). However, ETS is considered to be the agent of choice for childhood absence epilepsy without GTCS because of a lower risk of attention dysfunction compared with VPA (33 vs. 49 %)³⁴.

C. Levetiracetam:

Since one month of age, levetiracetam has been approved as an adjuvant treatment for people with focal epilepsy. Information on the effectiveness and safety Results from a double-blind, randomized, placebo-controlled study of levetiracetam in children under 4 years old include 12 children under 12 months, 20 children between 12 and 24months, and 28 children between 24 and 48months. Using a 48-hour video electroencephalogram, this trial showed that levetiracetam treatment increased the daily seizure reduction over the starting point frequency as well as a higher than 50% response rate in comparison to the placebo. Levetiracetam seemed to be well tolerated; the levetiracetam group experienced a higher incidence of the two adverse events (AEs) of irritation and somnolence than the placebo group. Both adverse events were temporary and related to levetiracetam's quick up-titration. For this age range, pharmacokinetic data are also provided. As anticipated, levetiracetam given as a 10% oral solution had a somewhat shorter total elimination half-life than that recorded for children aged 6 to 12³⁵.

2. Dietary Treatments:

The fundamental mechanism of KD activity is still unknown, although studies using animal models of epilepsy indicate that it is far more intricate. compared to that which has already been documented, and includes changes in mitochondrial activity, ketone body effects on neuronal function and neurotransmitter release, fatty acid antiepileptic actions, and/or glucose stabilization. Ketone bodies may inhibit the release of glutamate, norepinephrine, or adenosine while increasing membrane potential hyperpolarization and γ-aminobutyric acid production. Additionally, the KD might be involved in the suppression of the mammalian target of rapamycin (mTOR). The classic KD is calculated in a ratio of grams of fat to grams of carbohydrate plus protein. The most common ratio is 3:1 or 4:1, which means that 90% of the energy comes from fat and 10% from carbohydrate and protein combined. Calories are typically restricted to 80‒90% of the daily recommendations for age. Fluid restriction to 90% is based on historical use of the diet rather than on scientific evidence³⁶.

CONCLUSION:

Recurrent, spontaneous seizures brought on by aberrant neural activity are the hallmark of epilepsy, a prevalent, complex neurological condition. It affects people of all ages, genders, and geographical locations, but it is disproportionately more common in low-income nations. The disorder is a spectrum of disorders impacted by several structural, metabolic, and genetic factors rather than a single disease. The location and kind of brain hyperexcitability determine the type, frequency, and clinical manifestation of seizures. Neurological, behavioral, and emotional functioning are all greatly impacted by epilepsy, which frequently results in social stigma and care difficulties. While classification is based on the type of seizure, underlying problems, and EEG patterns, diagnosis is based on clinical evaluation, EEG, and neuroimaging. In order to lessen the physical, psychological, and social difficulties associated with epilepsy, complete understanding and care are necessary. ADHD and epilepsy often co-occur, especially in children, and have an impact on social, behavioral, and cognitive development. Stress and childhood trauma can raise an epileptic patient's risk of developing ADHD. Depending on the area of the brain affected, seizures can be either focal or generalized, with a variety of motor and non-motor symptoms. Whereas generalized seizures, such as absence, myoclonic, and atonic kinds, affect both hemispheres, focal seizures start in certain regions. Accurate diagnosis and successful treatment depend on an understanding of seizure types and related comorbidities like ADHD. Due to restricted access to healthcare, childhood epilepsy is a prevalent neurological condition that is more common in low-and middle-income nations. Genetic, structural, metabolic, infectious, immunological, and unknown reasons are some of its various etiologies. Seizures are pathophysiologically caused by an imbalance between neuronal excitation and inhibition, which frequently involves neurotransmitter dysfunction. Neuronal damage and cognitive impairments can result from prolonged or frequent seizures. Effective diagnosis and treatment are guided by the identification of related syndromes and underlying causes through a thorough physical examination that includes skin, skull, and neurological evaluation. EEG, neuroimaging, and genetic tests are used to diagnose pediatric epilepsy in order to determine the type of seizure, underlying etiology, and syndromic correlations. Antiepileptic medications such as carbamazepine, ethosuximide, and levetiracetam are used in treatment; these medications are selected based on the kind of seizure and the patient's age, and side effects are monitored. Through metabolic and neurotransmitter modulation, dietary therapies—especially the ketogenic diet—offer an alternate method of seizure control.

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Received on 30.04.2026 Revised on 21.05.2026

Accepted on 08.06.2026 Published on 10.07.2026

Available online from July 14, 2026

Res.J. Pharmacology and Pharmacodynamics.2026;18(3):325-331.

DOI: 10.52711/2321-5836.2026.00044

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.