A Clinical Review of Paediatric Epilepsy
Definition
Epilepsy is a disease of the brain defined by the International League Against Epilepsy (ILAE) as the presence of any of the following conditions: (1) at least two unprovoked (or reflex) seizures occurring more than 24 hours apart; (2) one unprovoked seizure combined with a high probability of further seizures, similar to the recurrence risk after two unprovoked seizures (at least 60%), over the next 10 years; or (3) the diagnosis of a specific epilepsy syndrome (1). This modern, operational definition is a crucial shift from previous classifications. Framing epilepsy as a disease rather than a "disorder" helps to reduce social stigma, validates it as a serious neurological condition for patients and families, and encourages a proactive diagnostic and therapeutic approach. The second criterion is particularly important for clinical practice, as it allows for a diagnosis—and thus, initiation of treatment—after a single seizure if certain risk factors are present, such as a prior brain insult (e.g., stroke or trauma), a significant structural abnormality on neuroimaging, or the presence of unequivocal epileptiform discharges on an EEG (1).
The ILAE framework also provides clarity on when epilepsy can be considered resolved. This applies to individuals who had an age-dependent epilepsy syndrome but are now past the applicable age (e.g., SeLECTS, which resolves by adolescence) or those who have remained seizure-free for the last 10 years, with no anti-seizure medications (ASMs) for at least the last 5 years (1). This concept is vital for counselling families about long-term prognosis and making decisions about discontinuing treatment.
Epidemiology
Epilepsy is one of the most common chronic neurological conditions globally, affecting an estimated 50 million people. A significant portion of this burden, nearly 80%, is shouldered by individuals in low- and middle-income countries, including Malaysia and its Southeast Asian neighbours, where access to diagnostic tools and treatment can be limited, creating a substantial "treatment gap" (11, 14).
In Malaysia, the most robust local data from a 2021 nationwide survey established a lifetime epilepsy prevalence of 7.8 per 1,000 persons and an active epilepsy prevalence (defined as having seizures or requiring treatment within the last 5 years) of 4.2 per 1,000 persons (17). The incidence of epilepsy is not uniform across the lifespan; it follows a bimodal distribution, with the highest peaks in early childhood and in the elderly. The incidence is greatest in the first year of life, underscoring the vulnerability of the developing brain and the importance of paediatric epilepsy as a major public health issue (1). Regional studies have highlighted intriguing ethnic variations, with multiple reports from Singapore consistently showing a lower cumulative incidence of epilepsy among individuals of Malay ethnicity compared to those of Chinese and Indian ethnicity, a finding that persists across different etiological categories (20).
Etiology
Identifying the underlying cause is a cornerstone of modern epilepsy management, as it directly influences treatment choices and prognosis. The ILAE classifies etiologies into six main categories, which are not mutually exclusive; for instance, a genetic cause can lead to a structural brain abnormality (9).
Structural: Epilepsy caused by a visible lesion on neuroimaging. These abnormalities act as a seizure focus.
Acquired: These result from brain injury at any point after development. A key example is hypoxic-ischemic encephalopathy (HIE) at birth, which leads to selective neuronal loss and gliosis (scarring), particularly in the hippocampus, creating a highly epileptogenic zone. Other examples include traumatic brain injury, CNS infections leaving behind scar tissue (e.g., post-meningitic gliosis), and brain tumours (22).
Congenital: These are malformations of cortical development (MCDs) that arise during fetal brain formation. Focal cortical dysplasia (FCD) is a common cause of drug-resistant focal epilepsy in children, characterized by disorganized cortical layers and abnormal, hyperexcitable neurons. Neurocutaneous syndromes like Tuberous Sclerosis Complex (TSC), which causes multiple cortical tubers, are prime examples of a genetic cause leading to a structural etiology (24).
Genetic: Epilepsy that is the direct consequence of a known or presumed disease-causing variant in one or more genes. It is vital to counsel families that "genetic" does not necessarily mean "inherited." Many severe childhood epilepsies, particularly the Developmental and Epileptic Encephalopathies (DEEs), are caused by de novo (new) mutations that occurred spontaneously in the child and are not present in the parents (22).
Examples: Mutations in genes encoding ion channels (channelopathies), such as SCN1A in Dravet Syndrome or KCNQ2 in self-limited neonatal epilepsy (12).
Infectious: Epilepsy that is a direct consequence of a CNS infection, where the infection itself is the cause of the enduring predisposition to seizures. This is a leading cause of preventable epilepsy worldwide and is particularly relevant in the Malaysian and Southeast Asian context (16).
Examples: Viral encephalitis (especially Herpes Simplex Virus), bacterial meningitis, neurocysticercosis (from the tapeworm Taenia solium), cerebral malaria, tuberculosis (tuberculomas), and congenital infections like Cytomegalovirus (CMV), toxoplasmosis, and Zika virus (14).
Metabolic: Epilepsy resulting from a known or presumed metabolic disorder where seizures are a core symptom. Many are inborn errors of metabolism with an underlying genetic basis.
Examples: Pyridoxine (Vitamin B6)-dependent epilepsy is a classic example of a treatable epilepsy, where seizures are refractory to standard ASMs but respond dramatically to pyridoxine supplementation. Glucose transporter 1 (GLUT1) deficiency syndrome impairs glucose transport into the brain, causing seizures that respond specifically to the ketogenic diet, which provides an alternative fuel source (ketones) (22).
Immune: Epilepsy caused by an autoimmune-mediated process targeting the CNS. This is an increasingly recognized cause of new-onset refractory status epilepticus (NORSE).
Examples: Anti-NMDA receptor encephalitis, which often presents with a combination of psychiatric symptoms, movement disorders, and seizures. Rasmussen's encephalitis is a rare but devastating paediatric example, characterized by chronic inflammation of one cerebral hemisphere, leading to intractable focal seizures and progressive neurological decline (22).
Unknown: Despite a thorough evaluation including advanced imaging and genetic testing, the underlying cause remains unidentified in a significant portion of cases. This category acknowledges the current limits of our diagnostic capabilities (14).
Pathophysiology
At its most fundamental level, an epileptic seizure is the clinical manifestation of abnormal, excessive, or synchronous neuronal activity in the brain (1). This phenomenon arises from a critical imbalance between excitatory and inhibitory forces within neural networks. The developing brain is particularly susceptible to this imbalance due to ongoing synaptogenesis, pruning, and myelination, making it inherently more prone to seizures than the adult brain (8).
The primary excitatory neurotransmitter in the brain is glutamate, while the primary inhibitory neurotransmitter is gamma-aminobutyric acid (GABA). Seizures can be triggered by mechanisms that either enhance glutamatergic excitation or reduce GABAergic inhibition. This disruption is often rooted in the dysfunction of ion channels embedded in neuronal membranes, a concept known as a "channelopathy."
Voltage-Gated Sodium Channels (NaV): These channels are crucial for initiating action potentials. Gain-of-function mutations can cause them to open too easily or fail to inactivate, leading to a persistent influx of sodium ions and a state of intrinsic neuronal hyperexcitability. In Dravet Syndrome, a loss-of-function mutation in the SCN1A gene specifically impairs the function of inhibitory interneurons, leading to disinhibition of the network and a net state of hyperexcitation (8).
Voltage-Gated Potassium Channels (KV): These channels are responsible for repolarizing the neuron after an action potential. Dysfunction impairs this "braking" mechanism, resulting in prolonged or repetitive neuronal firing (8).
Beyond single channels, complex intracellular signaling pathways are critical. A prime example is the PI3K-AKT-mTOR pathway, a master regulator of cell growth and proliferation. Genetic mutations in this pathway, such as in TSC, cause its hyperactivation. This leads to the formation of structural brain lesions (cortical tubers) filled with dysmorphic, hyperexcitable neurons that become seizure foci. Furthermore, mTOR hyperactivation also disrupts normal neuronal migration and synapse formation, contributing directly to cognitive impairment. This provides a clear molecular link for the concept of a Developmental and Epileptic Encephalopathy (DEE), where the epileptic activity itself contributes to developmental slowing or regression, beyond the impact of the underlying structural lesion alone (8).
Clinical Presentation
The diagnosis of epilepsy is fundamentally clinical, relying on a meticulous description of the seizure event (semiology) obtained from the patient and, crucially, from eyewitnesses.
Diagnostic Clues: How to Take a Seizure History
A structured approach to history-taking is essential. The clinician should systematically inquire about the three phases of the event:
Pre-ictal Phase: Was there a warning or "aura"? An aura is itself a focal seizure with subjective symptoms. Its character can provide clues to the seizure's origin (e.g., a rising epigastric sensation is classic for temporal lobe epilepsy; flashing lights suggest an occipital lobe onset).
Ictal Phase (The Event):
Level of Awareness: Was the child aware and able to respond? This is the key feature distinguishing focal aware from focal impaired awareness seizures.
Motor Features: Describe the movements precisely. Was there stiffening (tonic), rhythmic jerking (clonic), or brief, irregular, shock-like jerks (myoclonic)? Were movements on one side or both? Were there repetitive, purposeless movements (automatisms) like lip-smacking, chewing, or fumbling with clothes?
Non-Motor Features: Did the child just stare blankly with behavioural arrest (absence seizure)? Were there autonomic changes like pallor, cyanosis, drooling, or incontinence?
Post-ictal Phase: Was the child confused, sleepy, or did they have a headache? The presence of a distinct post-ictal phase is a strong indicator of an epileptic seizure. Focal weakness on one side of the body after a seizure (Todd's paresis) is a highly localizing sign, pointing to a seizure onset in the contralateral motor cortex.
Common Paediatric Epilepsy Syndromes
Recognizing specific epilepsy syndromes is the pinnacle of diagnostic skill in paediatric epilepsy, as it provides a wealth of information on prognosis, comorbidities, and optimal treatment.
Infantile Onset (Birth - 2 years)
Infantile Epileptic Spasms Syndrome (IESS / West Syndrome): A neurological emergency defined by a classic triad.
Features: 1) Epileptic spasms: Sudden, brief (1-2 seconds) flexor, extensor, or mixed movements of the trunk and limbs, often occurring in clusters, particularly upon awakening or falling asleep. They are often subtle and can be mistaken for colic or a normal startle reflex. 2) Developmental arrest or regression: A previously developing child stops gaining new skills or loses existing ones. 3) A pathognomonic EEG pattern called hypsarrhythmia, which appears as chaotic, high-voltage slow waves and multifocal spikes between spasms (26).
⚠️ Red Flag: This is a time-critical diagnosis. Prompt and aggressive treatment with hormonal therapy (high-dose prednisolone or ACTH) or vigabatrin is essential to stop the spasms and improve the long-term developmental outcome.
Dravet Syndrome: A severe DEE.
Features: Typically begins in the first year of life in a previously healthy infant with prolonged, fever-triggered (febrile) seizures, which are often hemiclonic (affecting one side of the body). A key feature is sensitivity to temperature changes (e.g., seizures triggered by a warm bath). As the child ages, multiple other seizure types emerge (myoclonic, atypical absence), and developmental progress slows, leading to significant intellectual disability. The majority have a mutation in the SCN1A gene (26).
⚠️ Red Flag: It is critical to avoid sodium channel blockers (e.g., Carbamazepine, Lamotrigine) as they can paradoxically worsen seizures and precipitate status epilepticus.
Childhood Onset (2 - 12 years)
Self-Limited Epilepsy with Centrotemporal Spikes (SeLECTS / formerly Benign Rolandic Epilepsy): One of the most common and benign childhood epilepsies.
Features: Characteristically nocturnal focal seizures involving unilateral facial twitching, gurgling or grunting sounds, profuse drooling, and speech arrest. The child often remains fully conscious and may run to their parents' room for help. Seizures are typically brief but can secondarily generalize to a tonic-clonic convulsion (28).
Prognosis: Excellent. Seizures are often infrequent and nearly always remit by adolescence. Many children do not require daily ASM treatment.
Childhood Absence Epilepsy (CAE):
Features: The hallmark is frequent (often dozens to hundreds per day), brief (<10 seconds) absence seizures. These are characterized by sudden behavioural arrest, staring, and impaired consciousness with an abrupt onset and offset. Minor automatisms like eyelid fluttering or lip-smacking are common. Seizures are characteristically provoked by hyperventilation, a key diagnostic manoeuvre during EEG (32).
Lennox-Gastaut Syndrome (LGS): A severe DEE that can arise de novo or evolve from an earlier syndrome like IESS.
Features: Defined by a triad: 1) Multiple seizure types, with tonic seizures (especially nocturnal) and atonic seizures ("drop attacks") being characteristic and leading to frequent injuries. 2) Cognitive impairment. 3) A characteristic EEG pattern of slow (<2.5 Hz) spike-and-wave discharges (26).
Juvenile Onset (12 - 18 years)
Juvenile Myoclonic Epilepsy (JME): The most common idiopathic generalized epilepsy syndrome.
Features: The classic triad of seizure types includes: 1) Myoclonic jerks: Sudden, brief, shock-like jerks, predominantly affecting the upper limbs, occurring shortly after awakening. Patients often describe themselves as "clumsy" or report dropping their toothbrush or phone in the morning. 2) Generalized tonic-clonic seizures (GTCS): Occur in over 90% of patients, often preceded by a flurry of myoclonic jerks. 3) Absence seizures: Occur in about one-third of patients. Seizures are often precipitated by classic triggers: sleep deprivation, alcohol consumption, and sometimes photosensitivity (38).
Complications
The impact of epilepsy extends far beyond the seizures themselves.
Developmental and Cognitive: Developmental delay, learning disabilities, and intellectual disability are common, especially in the DEEs, where ongoing epileptic activity can disrupt normal brain development.
Psychiatric: There is a high rate of comorbidity with conditions like ADHD, anxiety, depression, and autism spectrum disorder. This relationship is often bidirectional, meaning the underlying brain dysfunction can predispose to both epilepsy and psychiatric conditions.
Physical Injury: Trauma, burns, and drowning are significant risks, particularly for patients with convulsive or atonic ("drop") seizures.
Status Epilepticus: A seizure lasting longer than 5 minutes, or two or more seizures without a return to full consciousness in between. This is a medical emergency that can lead to permanent neuronal injury and has high morbidity and mortality (1).
Sudden Unexpected Death in Epilepsy (SUDEP): A rare but devastating complication, defined as the sudden, unexpected death of someone with epilepsy, who was otherwise healthy. The greatest risk factor is the presence of frequent, uncontrolled generalized tonic-clonic seizures, especially those occurring during sleep. Risk mitigation focuses on achieving the best possible seizure control and considering nocturnal monitoring for high-risk individuals.
Prognosis
The expected outcome of paediatric epilepsy exists on a wide spectrum and is almost entirely dependent on the specific epilepsy syndrome.
Excellent: Syndromes like SeLECTS and CAE are termed "self-limited" and are not associated with cognitive decline. There is a high likelihood of spontaneous remission in adolescence, and many children can eventually discontinue medication (28, 32).
Good with Treatment: JME is a classic example of a "pharmacoresponsive" epilepsy. While it typically requires lifelong medication, seizures can be very well-controlled, allowing for a normal quality of life and intellectual development (38).
Poor: The severe DEEs like West Syndrome, Dravet Syndrome, and LGS carry a poor prognosis. They are characterized by drug-resistant seizures and are almost universally associated with significant lifelong intellectual, behavioural, and motor impairments (26).
Differential Diagnosis
Differentiating true epileptic seizures from the wide array of Paroxysmal Non-Epileptic Events (PNEs) is one of the most common and challenging diagnostic dilemmas in paediatrics. Misdiagnosis can lead to unnecessary medication and significant psychosocial burden.
Convulsive Syncope: This is the most important differential for a generalized tonic-clonic seizure. It is fainting (syncope) followed by brief stiffening and myoclonic jerks due to transient cerebral hypoxia. The key distinguishing feature is the prodrome: syncope is typically preceded by a clear trigger (e.g., prolonged standing, pain, sight of blood) and pre-syncopal symptoms like light-headedness, blurred vision, and muffled hearing. The convulsive phase is brief, and recovery is rapid, without a prolonged post-ictal confusion (3).
Breath-Holding Spells: These occur in young children (6 months to 2 years) and are always triggered by anger, frustration, or a painful stimulus. The typical sequence is a cry, followed by holding the breath in expiration, leading to cyanosis or pallor, loss of consciousness, and sometimes brief convulsive movements. The clear emotional trigger and preceding cry are diagnostic (3).
Parasomnias (e.g., Night Terrors, Sleepwalking): These are arousal disorders that occur out of deep, non-REM sleep, typically in the first third of the night. A child with night terrors may sit up, scream, and appear terrified with wide eyes and a rapid heart rate, but they are not truly awake and are unresponsive to their environment. Unlike a nocturnal frontal lobe seizure, they are difficult to rouse, and there is no memory of the event and no post-ictal state (10).
Gastroesophageal Reflux (Sandifer Syndrome): Seen in infants, this involves episodic arching of the back (opisthotonus) and dystonic posturing of the head and neck, which can be mistaken for tonic seizures. The key is that these episodes are temporally linked to feeding and are a behavioural response to painful reflux.
Investigations
Immediate & Bedside Tests
Blood Glucose: A finger-prick glucose test is mandatory in any child presenting with an altered level of consciousness or seizure to immediately rule out hypoglycemia as a reversible cause.
Basic Blood Tests: In the setting of a first afebrile seizure, a full blood count, renal profile with electrolytes, calcium, magnesium, and phosphate are essential to rule out acute metabolic disturbances or systemic infection that may have provoked the seizure (42).
Diagnostic Workup
First-Line Investigation (Electroencephalogram - EEG):
Purpose: The EEG is the single most important investigation to support the diagnosis of epilepsy and to classify the epilepsy type (focal vs. generalized). It records the brain's electrical activity and can detect interictal epileptiform discharges (e.g., spikes, sharp waves) which are the electrical signature of an irritable cortex. Specific patterns can be diagnostic for certain syndromes (e.g., 3Hz spike-and-wave for absence epilepsy) (43).
Action: A routine EEG may be normal. The diagnostic yield is significantly increased by performing a sleep-deprived EEG, as sleep deprivation and the state of sleep itself can activate epileptiform abnormalities.
Gold Standard (Video-EEG Monitoring - VEEG):
Purpose: This is the definitive test to characterize paroxysmal events when the diagnosis is uncertain. It involves continuous, time-locked video and EEG recording, typically over several days in a hospital. The goal is to capture a typical event on camera while simultaneously recording the brain's electrical activity (43).
Action: VEEG is the gold standard for differentiating epileptic seizures from PNEs. It is also a cornerstone of the pre-surgical evaluation to precisely localize the seizure onset zone.
Neuroimaging (Brain MRI):
Purpose: MRI of the brain with an epilepsy protocol (using thin slices and specific sequences like FLAIR) is the neuroimaging modality of choice. It provides superior anatomical detail to identify subtle structural etiologies like focal cortical dysplasia, mesial temporal sclerosis (scarring in the temporal lobe), or small tumours that would be missed on a standard MRI or CT scan (42).
Action: An MRI is indicated for all children with focal seizures, any child with an abnormal neurological exam, cases of drug-resistant epilepsy, or any child with seizure onset before the age of two. A CT scan is generally reserved for emergency situations to rapidly exclude acute, life-threatening conditions such as intracranial haemorrhage, large tumours, or hydrocephalus (44).
Management
Management Principles
The overarching goals of management are to achieve the best possible seizure control with the fewest adverse effects, thereby maximizing the child's quality of life and allowing them to reach their full developmental potential (13). Treatment should only be initiated after a secure diagnosis of epilepsy is made. Management is a collaborative process based on shared decision-making between the clinician, the child, and their family, balancing the risks of recurrent seizures against the potential side effects of treatment.
Acute Stabilisation (The First Hour of Status Epilepticus)
Status epilepticus is a medical emergency requiring a rapid, stepwise approach.
Airway/Breathing: Position the patient in the lateral recovery position to avoid aspiration. Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% to prevent secondary hypoxic brain injury.
Circulation: Secure intravenous (IV) access. Check capillary blood glucose and send bloods for electrolytes and a full blood count.
Disability (Stop the Seizure): Follow a time-critical algorithm.
First-Line (Benzodiazepines): Administer a benzodiazepine as soon as possible. These drugs are positive allosteric modulators of the GABA-A receptor, enhancing GABAergic inhibition to terminate the seizure. The preferred routes are IV Lorazepam (0.1 mg/kg) or Buccal Midazolam (0.2-0.3 mg/kg) (4).
Second-Line (ASM Loading Dose): If seizures persist 5 minutes after a second dose of benzodiazepines, the seizure is now established status epilepticus. Administer a loading dose of a non-sedating IV anti-seizure medication. IV Levetiracetam (40-60 mg/kg) is often preferred due to its favourable safety profile. IV Phenytoin (20 mg/kg) is another effective option but requires cardiac monitoring during infusion due to risk of arrhythmia and hypotension (4).
Definitive Therapy
The choice of long-term therapy is guided by the specific epilepsy syndrome.
First-Line Treatment (Anti-Seizure Medications - ASMs)
The guiding principle is to start with a single, appropriate drug (monotherapy) and titrate the dose slowly to achieve a balance between efficacy and tolerability. In Malaysia, older, broad-spectrum ASMs remain commonly used and effective first-line agents (49).
Focal Seizures: Carbamazepine (a sodium channel blocker) or Levetiracetam (mechanism not fully understood, but affects SV2A protein).
Generalized Tonic-Clonic Seizures: Sodium Valproate is the most effective broad-spectrum agent, acting via multiple mechanisms including sodium channel blockade and increasing GABA levels. However, it is a major human teratogen and should be avoided in female adolescents if effective alternatives exist. Levetiracetam is an excellent alternative (52).
Absence Seizures: Ethosuximide (a T-type calcium channel blocker) is first-line for pure Childhood Absence Epilepsy due to its superior efficacy and better cognitive profile. If the child also has or is at high risk for GTCS, Sodium Valproate is preferred (37).
Infantile Spasms: This is a specific emergency requiring targeted therapy. High-dose prednisolone or ACTH is the first-line treatment. Vigabatrin (a GABA transaminase inhibitor) is the first-line choice specifically for infants whose spasms are caused by Tuberous Sclerosis Complex (4).
Second-Line/Escalation (For Drug-Resistant Epilepsy)
Drug-resistant epilepsy (DRE) is defined as the failure of two appropriately chosen and tolerated ASM trials. At this point, referral to a tertiary epilepsy centre is mandatory.
Medical Nutrition Therapy (Ketogenic Diet): This is a high-fat, adequate-protein, low-carbohydrate medical therapy that alters brain metabolism. It is the treatment of choice for two specific metabolic disorders: GLUT1 deficiency syndrome and pyruvate dehydrogenase deficiency. It is also highly effective and should be considered early in other DRE syndromes like infantile spasms, Dravet syndrome, and epilepsy with myoclonic-atonic seizures (53).
Epilepsy Surgery: For a well-selected group of children with focal DRE, epilepsy surgery offers the best chance for a cure. The ideal candidate is a child whose seizures originate from a single, well-defined, and safely removable area of the brain (the epileptogenic zone). Resective surgery can result in seizure freedom in 60-70% of cases and can lead to significant improvements in development and quality of life (58).
Key Nursing & Monitoring Instructions
Implement seizure precautions (e.g., padded bed rails, suction available).
Maintain a strict seizure chart, documenting the time, duration, triggers, and detailed semiology of every event.
For a patient in status epilepticus, perform and document neurological observations (GCS, pupil size and reactivity) at least hourly.
Inform medical staff immediately if: a seizure lasts longer than 5 minutes, if there is a change in the patient's typical seizure pattern, or if there is any new neurological deficit (like a Todd's paresis) post-seizure.
Long-Term Plan & Patient Education
Adherence: Educate the family on the critical importance of consistent medication adherence, as missed doses are a common trigger for breakthrough seizures.
Rescue Medication: Provide and train parents on how and when to administer rescue medication (e.g., buccal midazolam) for a prolonged seizure at home. This is a key part of the emergency care plan.
SUDEP: Discuss the risk of SUDEP in an open and sensitive manner. Emphasize that the most effective mitigation strategy is achieving optimal seizure control, particularly of nocturnal generalized tonic-clonic seizures.
Comorbidities: Proactively screen for and manage learning, behavioural, and psychiatric issues. This often requires a multidisciplinary team approach involving psychologists, therapists, and educational support services.
When to Escalate
Call Your Senior (Medical Officer/Specialist) if:
A patient is in status epilepticus and fails to respond to second-line IV medication. The patient needs to be escalated to the Paediatric Intensive Care Unit (PICU) for anaesthetic induction.
A child with known epilepsy presents with a significant increase in seizure frequency, a new seizure type, or developmental regression.
You suspect a diagnosis of Infantile Spasms (West Syndrome) – this is a paediatric neurology emergency that requires urgent specialist review and treatment initiation.
Referral Criteria:
Refer to a Paediatric Neurologist after the failure of two appropriately chosen and tolerated ASMs. This meets the formal definition of drug-resistant epilepsy, and these children must be evaluated for advanced therapies like the ketogenic diet and epilepsy surgery. Early referral is crucial to improve long-term outcomes.
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