Non-Febrile Seizures (Epilepsy)

This section will mainly focus on Paediatric Epilepsy (NOT FEBRILE SEIZURES)

Overview

Seizures are a common occurrence in children. 8% will have at least one seizure by 15 years of age. A seizure is the result of an abnormal paroxysmal discharge by cerebral neurons. Many underlying conditions and neurological challenges may provoke seizures, and in over 50% of children seizures are isolated events associated with either a fever (febrile seizures/convulsions) or minor head injury in early childhood.

Thus, Seizures can be broadly divided based on:

• Fever (febrile seizure)
• Non-febrile seizures

There are many….many causes of non-febrile seizures, one of which is epilepsy.

Aetiology

Structural

• Congenital brain malformation
• Cortical dysplasia
• Perinatal stroke or hypoxic–ischaemic injury
• Traumatic brain injury
• Brain tumour
• Hippocampal sclerosis
• Neurocutaneous disorders, such as tuberous sclerosis

Genetic

• Pathogenic gene variants affecting ion channels or neuronal function
• Examples include Dravet syndrome, often associated with SCN1A, and other genetic generalised epilepsies

Infectious

• Meningitis
• Encephalitis
• Cerebral abscess
• Neurocysticercosis or other central nervous system infections

Metabolic

• Inherited metabolic disorders
• Mitochondrial disease
• Pyridoxine-dependent epilepsy
• GLUT1 deficiency

Immune-mediated

• Autoimmune encephalitis
• Other inflammatory brain disorders

Unknown

• No cause is identified despite appropriate investigation.

Additional risk factors include a family history of epilepsy, developmental delay, previous complicated febrile seizures and previous central nervous system injury or infection.

Pathophysiology

• Epileptic seizures arise from abnormal neuronal excitability and excessive synchronisation within cerebral networks.
• An imbalance may develop between:
  • Excitatory neurotransmission, particularly glutamate
  • Inhibitory neurotransmission, particularly GABA
• Abnormal ion-channel function, neurotransmitter receptors, neuronal connections or cortical structure may lower the seizure threshold.
• Focal seizures originate from a localised cerebral network and may spread to involve both hemispheres.
• Generalised seizures involve bilateral networks from the beginning.
• Recurrent seizures and persistent epileptic activity may interfere with cognition and development, particularly in developmental and epileptic encephalopathies.

Clinical Manifestation

Presentation depends on the seizure type and the brain regions involved.

Classification of Epilepsy

• Partial (Focal) Seizures – Retained consciousness seizure
  • Simple
  • Complex
  • Status epilepticus
• Generalised Seizures – Immediate loss of conciousness
  • Absence
  • Tonic-Clonic
  • Myoclonic
  • Status epilepticus
• Unknown whether focal or generalised: available information cannot determine the seizure origin.
• Unclassified seizures: insufficient information or the seizure does not fit an established category.

SEIZURES TYPES
Partial (focal)	Generalised
Simple	Tonic & Clonic
Complex	Absence
Status Epilepticus	Myoclonic
	Atonic
	Infantile Spasms (West Syndrome)
	Status Epilepticus

Epilepsy – Partial (Focal) Seizure

Partial or Focal seizures is now known as retained consciousness seziures. Partial seizures start in a focus in the brain. The focus may be the site of previous cerebral damage. Partial seizures may be motor, sensory, automatic or psychic. Partial seizures may occur with or without impairment of consciousness and awareness. Partial seziures are divided into simple partial or complex partial.

Simple

• Asynchronous tonic or clonic movements; most of the face, neck and extremities, average duration 10-20seconds
• +/- aura; no postictal period

Complex 

• Impaired consciousness at some point
• +/- aura
• Automatisms common after loss of consciousness

Epilepsy – Generalized Seizures

Generalized seizures the whole brain is involved characterized by immediate loss of consciousness. It can be defined by a variety of seizures:

• Tonic-clonic seizures (Grand Mal) These fits comprise of  a:
  • Tonic phase (muscle spasm) which may start with a cry – if prolonged to cyanosis THEN
  • Clonic phase (jerking) +/- tongue biting and frothing at the mouth THEN
  • Relaxation and unconsciousness FOLLOWED BY A
  • Period of drowsiness and/or confusion

Flashing lights can be triggers. Seizures can last from less than 1minutes to over 30minutes (status epilepticus)

• Absence Seizures (petit mal) Sudden cessation of motor activity or speech with blank stare and blinking. uncommon <5 years of age. No aura and lasts usually <30seconds with no postictal period.

• Myoclonic Seizure Repetitive seizures – brief, symmetric muscle contraction and loss of body tone with falling over.

• Atonic Seizure Known as drop attacks. Sudden decrease in muscle tone makes a child lose postural control and drop to the floor.

• Infantile Spasms Rare and serious form of seizure occurring usually at age 1-6months. Associated developmental delay is common. The single most common cause is tuberous sclerosis. Treatment: ACTH + Prednisone + anticonvulsants if no response

Diagnosis

Clinical assessment

• Obtain a detailed description from the child and eyewitnesses.
• Ask about:
  • Events before, during and after the episode
  • Duration and recovery
  • Fever, illness, sleep deprivation or trauma
  • Developmental history
  • Family history of epilepsy
  • Medication or toxin exposure
• Video footage recorded by caregivers may be very useful.

Electroencephalography

• Routine EEG supports seizure classification and identification of an epilepsy syndrome.
• Perform EEG as soon as practical after a first seizure, ideally within 72 hours when requested.
• Hyperventilation and photic stimulation may provoke characteristic abnormalities.
• If routine EEG is normal but suspicion remains:
  • Sleep-deprived EEG
  • Ambulatory EEG
  • Video EEG monitoring
• A normal EEG does not exclude epilepsy.

Neuroimaging

• MRI brain using an epilepsy protocol

Additional investigations

• FBC, electrolytes, calcium, magnesium, glucose, renal and liver function where clinically indicated.
• Lumbar puncture if meningitis or encephalitis is suspected, after assessing for contraindications.
• Genetic testing should be considered with:
  • Epilepsy beginning in infancy
  • Developmental delay or autism
  • Dysmorphic or congenital abnormalities
  • Suspected genetic syndrome
  • Unexplained drug-resistant epilepsy
• Metabolic testing may be required with regression, episodic deterioration or other systemic features.
• Autoimmune antibody testing may be considered when autoimmune encephalitis is suspected.

DIFFERENTIATING FEATURES BETWEEN SEIZURE AND SYNCOPE
	Seizures	Syncope
Age	Any	8-15 years
Timing	Whenever	Day
Situation	Commonly during activity	Standing
Prodrome	Brief (twitching, hallucinations)	Long (dizziness, sweats, nausea)
Duration	Variable	Under 5 minutes
Tonic-clonic movement	Common	Rare
Colour change	Maybe be cyanosis	Pallor
Injury	Common	Rare
Incontinent of urine	Common	Rare
Recovery	Drowsiness, confusion or headache	Quick Recovery

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Diagnosis of epilepsy

• Two unprovoked seizures occurring more than 24 hours apart
• One unprovoked seizure with a high predicted recurrence risk
• Diagnosis of a recognised epilepsy syndrome

Treatment

Treatment is individualised according to seizure type, epilepsy syndrome, age, comorbidities, adverse-effect profile and reproductive considerations.

General

• Begin antiseizure medication once epilepsy is confirmed.
• Treatment may be considered after a first unprovoked seizure when there is:
  • An epileptiform EEG
  • Structural brain abnormality
  • Neurological deficit
  • An unacceptable predicted risk of recurrence
• Use monotherapy whenever possible.
• Start at a low dose and titrate gradually.
• If the first medication fails, reconsider the diagnosis and seizure classification before changing treatment.
• Do not stop antiseizure medication suddenly.

Common medication choices
Seizure type	Common first-line options
Focal seizures	Lamotrigine or levetiracetam
Generalised tonic–clonic seizures	Lamotrigine, levetiracetam or sodium valproate
Typical absence seizures only	Ethosuximide
Absence with other seizure types	Lamotrigine, levetiracetam or sodium valproate
Myoclonic seizures	Levetiracetam or sodium valproate
Self-limited epilepsy with centrotemporal spikes	Observation may be reasonable; lamotrigine or levetiracetam if treatment is required
Infantile spasms without tuberous sclerosis	High-dose prednisolone plus vigabatrin
Infantile spasms due to tuberous sclerosis	Vigabatrin
Dravet syndrome	Specialist treatment, commonly sodium valproate followed by syndrome-specific add-on therapy

Acute convulsive seizure and status epilepticus

Seizure first aid

• Protect the child from injury.
• Place the child on their side when possible.
• Loosen restrictive clothing.
• Do not restrain the child.
• Do not place anything in the mouth.
• Time the seizure.
• Call emergency services for a first seizure, injury, breathing difficulty, repeated seizures or a seizure lasting 5 minutes or longer.

Convulsive status epilepticus

• ABC resuscitation, oxygen and cardiorespiratory monitoring.
• Check bedside glucose and treat hypoglycaemia.
• Follow the child’s emergency management plan where available.
• First-line:
  • Buccal or intranasal midazolam, or rectal diazepam in the community
  • IV lorazepam where IV access and resuscitation facilities are available
• Repeat the benzodiazepine once if the seizure continues after 5–10 minutes.
• If seizure activity persists after two benzodiazepine doses, use IV:
  • Levetiracetam
  • Phenytoin
  • Sodium valproate
• Refractory status epilepticus requires intensive-care management, additional antiseizure treatment and possibly general anaesthesia.

Complications and Prognosis

Complications

• Status epilepticus
• Falls, fractures, burns and head injuries
• Aspiration or hypoxic injury
• Drowning
• Developmental delay or regression
• Learning and memory difficulties
• Behavioural problems
• ADHD, autism, anxiety and depression
• Social isolation and stigma
• Reduced school attendance
• Medication-resistant epilepsy
• Sudden unexpected death in epilepsy—SUDEP

The risk of SUDEP is greatest with uncontrolled generalised tonic–clonic or focal-to-bilateral tonic–clonic seizures, nocturnal seizures and poor medication adherence.

Prognosis

• Prognosis depends on the epilepsy syndrome, underlying cause, developmental status, EEG findings and response to treatment.
• Up to approximately 70% of people with epilepsy may become seizure-free with appropriate antiseizure medication.
• Self-limited childhood epilepsies often resolve by adolescence.
• Structural, genetic and developmental epileptic encephalopathies are more likely to remain drug resistant and affect cognition or development.
• Failure of two appropriate antiseizure medications predicts a lower chance of seizure freedom with further medication alone and should prompt tertiary referral.
• Medication withdrawal may be considered after approximately 2 years of seizure freedom, following an individualised specialist assessment of recurrence risk.
• Children with controlled seizures and normal development often have good long-term educational and functional outcomes.

References

1. National Institute for Health and Care Excellence. Epilepsies in children, young people and adults. NICE guideline NG217. London: NICE; 2022. Updated 2025.
2. Beniczky S, Trinka E, Wirrell E, et al. Updated classification of epileptic seizures: position paper of the International League Against Epilepsy. Epilepsia. 2025.
3. Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014;55(4):475–482. doi:10.1111/epi.12550.
4. Specchio N, Wirrell EC, Scheffer IE, et al. International League Against Epilepsy classification and definition of epilepsy syndromes with onset in childhood: position paper by the ILAE Task Force on Nosology and Definitions. Epilepsia. 2022;63(6):1398–1442. doi:10.1111/epi.17241.
5. World Health Organization. Epilepsy [Internet]. Geneva: World Health Organization; 2024.