Childhood Occipital Visual Epilepsy: Disease-Characteristics Research Report

Scope and evidence caveat. Childhood occipital visual epilepsy (COVE) is rare, and recent syndrome-specific primary research is sparse. The strongest current source is the 2022 International League Against Epilepsy (ILAE) classification, summarized in a 2024 pediatric update and a 2025 classification review. Much of the quantitative literature predates 2023 and was not available in full text during this retrieval. Consequently, this report distinguishes established COVE findings from broader focal-epilepsy practice and does not assign genes, variants, frequencies, or ontology identifiers without adequate evidence.

Executive summary

COVE is a childhood-onset, self-limited focal epilepsy characterized by brief focal sensory visual seizures arising from occipital networks. Elementary visual hallucinations—often colored, circular forms—and transient visual loss are characteristic; seizures may spread to produce eye/head deviation, impaired awareness, or bilateral tonic–clonic activity, and postictal headache can mimic migraine. The modern name replaces “late-onset benign occipital epilepsy” and “idiopathic childhood occipital epilepsy of Gastaut.” The ILAE places COVE among childhood self-limited focal epilepsies and regards its inheritance as presumed complex rather than established monogenic. Most patients remit by adolescence, although a minority continue to have seizures. EEG and appropriate MRI are central to diagnosis; no disease-specific molecular biomarker, causal gene, precision therapy, or validated COVE-specific animal model is established in the retrieved evidence. (manokaran2024the2022international pages 2-4, manokaran2024the2022international pages 4-5, wirrell2025epilepsysyndromesclassification. pages 6-7)

Table: This table condenses the evidence-supported knowledge base fields for Childhood Occipital Visual Epilepsy using only retrieved context. It highlights what is established, what can be mapped provisionally to ontologies, and where the evidence is currently limited or unavailable.

1. Disease information

Definition and classification

COVE is an electroclinical epilepsy syndrome whose defining cluster comprises childhood onset, focal sensory visual seizures, and occipital epileptiform EEG findings. The 2024 ILAE update places it among four childhood self-limited focal epilepsies and states that its name reflects “occipital semiology and EEG findings.” Childhood-onset syndromes in this framework generally begin from ages 2–12 years. (manokaran2024the2022international pages 4-5)

Current and historical names

• Childhood occipital visual epilepsy (COVE)—current ILAE term.
• Idiopathic childhood occipital epilepsy–Gastaut type.
• Gastaut-type childhood occipital epilepsy.
• Late-onset benign childhood occipital epilepsy.
• Benign occipital epilepsy of childhood, late-onset type.

The authoritative terminology table explicitly maps COVE to “late onset (benign) occipital epilepsy” and “idiopathic childhood occipital epilepsy–Gastaut type.” “Benign” has been replaced by “self-limited,” because spontaneous remission does not guarantee absence of cognitive, behavioral, or psychosocial morbidity. (manokaran2024the2022international pages 2-4, manokaran2024the2022international pages 4-5)

Identifiers

• MONDO: no confidently verified COVE-specific MONDO identifier was found. Do not populate one without direct MONDO confirmation.
• OMIM/Orphanet: no dedicated syndrome-specific entry was verified in the retrieved evidence.
• ICD-10: usually coded under focal/localization-related epilepsy, selected according to intractability and status-epilepticus qualifiers; there is no verified COVE-specific code.
• ICD-11: classified within focal epilepsy/epilepsy syndromes rather than by a unique verified COVE code.
• MeSH: “Epilepsy, Occipital Lobe” is the closest disease concept; a separate COVE-specific heading was not verified.

These are aggregated disease-level findings from classifications and published cohorts—not individual EHR-derived observations.

2. Etiology

Causal and risk factors

COVE is currently best regarded as a presumed genetic epilepsy with complex or multifactorial inheritance, not a single-gene disorder. The 2024 review specifically places COVE and photosensitive occipital lobe epilepsy among focal syndromes with presumed complex inheritance. No gene has sufficient syndrome-specific evidence to be annotated as a definitive COVE causal gene. (manokaran2024the2022international pages 4-5)

A family history of epilepsy or migraine may occur in historical cohorts, but penetrance, recurrence risk, susceptibility loci, founder variants, and carrier frequency remain undefined. Reported GABA-receptor or other epilepsy-gene variants in families with occipital epilepsy should not automatically be equated with classic COVE because structural, familial focal, photosensitive, and neurodevelopmental occipital epilepsies are heterogeneous.

Environmental, protective, and gene–environment factors

No toxin, infection, diet, lifestyle, occupational exposure, or immune trigger is established as a cause of COVE. Sleep deprivation, illness, or missed medication can lower seizure threshold in epilepsy generally but are not proven causes of this syndrome. Visually induced seizures instead suggest photosensitive occipital lobe epilepsy, an important separate syndrome. No validated genetic or environmental protective factors or COVE-specific gene–environment interactions were identified.

3. Phenotypes

Core manifestations

1. Elementary visual hallucinations—positive visual phenomena such as small multicolored circles or spots, commonly moving or multiplying in a visual hemifield. These are focal sensory visual seizures, abrupt, stereotyped, and usually brief. Suggested HPO: Visual hallucination, Focal sensory seizure, Abnormality of vision.
2. Transient ictal blindness or visual loss—a negative visual symptom that may involve a field or the whole visual scene. Suggested HPO: Transient visual loss, Blindness, Visual field defect.
3. Eye or head deviation—reflecting spread from visual cortex to adjacent cortical networks. Suggested HPO: Versive seizure, Abnormal eye movement.
4. Impaired awareness, hemiclonic, or focal-to-bilateral tonic–clonic seizure—downstream manifestations when an occipital discharge propagates. Suggested HPO: Focal impaired awareness seizure, Focal to bilateral tonic-clonic seizure.
5. Ictal or postictal headache, nausea, or vomiting—clinically important because visual aura plus headache may be mistaken for migraine. Suggested HPO: Headache, Nausea and vomiting.

Current reviews succinctly characterize COVE seizures as sensory visual symptoms with elementary visual phenomena; occipital seizures can manifest as hallucinations or blindness. (wirrell2025epilepsysyndromesclassification. pages 6-7)

Timing, severity, and progression

Onset is pediatric, typically school age in the historical Gastaut phenotype. Attacks are episodic rather than progressive. Seizure frequency varies substantially: some patients have few attacks, whereas others have frequent seizures requiring treatment. Baseline neurological examination, development, and routine structural imaging are generally expected to be normal in a prototypical self-limited syndrome; developmental regression, persistent neurological deficits, or major MRI abnormalities should prompt reassessment.

Quality of life

Transient blindness, hallucinations, impaired awareness, headache, and tonic–clonic spread can disrupt school, sports, bathing, travel, and other safety-sensitive activities. Anxiety and diagnostic confusion with migraine may add burden. Although “self-limited,” these epilepsies can have cognitive or behavioral comorbidity; no COVE-specific EQ-5D, PedsQL, PROMIS, or neuropsychological prevalence estimates were found. The ILAE deliberately abandoned “benign” because self-limited syndromes can still carry such morbidity. (manokaran2024the2022international pages 4-5)

4. Genetic and molecular information

No definitive causal gene, HGNC locus, pathogenic variant spectrum, chromosomal abnormality, modifier gene, epigenetic signature, allele frequency, or somatic mosaic mechanism is established for classic COVE. Therefore:

• A COVE knowledge-base entry should not list GRIN2A as causal. GRIN2A is strongly associated with epilepsy–aphasia syndromes, particularly speech-language impairment, Landau–Kleffner syndrome, and rolandic-spectrum epilepsy—not specifically COVE. A 2024 GRIN2A MRI study involved only 10 affected individuals from three families and found bilateral occipital cortical-thickness differences, but its phenotype was epilepsy–aphasia syndrome. This is mechanistically adjacent evidence, not validation of a COVE gene. (thompsonlake2024perisylvianandhippocampal pages 1-2, thompsonlake2024perisylvianandhippocampal pages 5-6)
• In that GRIN2A study, pathogenic-variant carriers had greater left pars-opercularis thickness than controls, with partial η²=0.37, and corrected whole-brain analysis retained bilateral lateral-occipital thickness increases. The authors’ abstract states: “Pathogenic variants in GRIN2A are associated with a spectrum of epilepsy-aphasia syndromes.” These data should be stored under GRIN2A-related epilepsy–aphasia, not COVE. Published April 2024; DOI URL: https://doi.org/10.1212/NXG.0000000000200129. (thompsonlake2024perisylvianandhippocampal pages 1-2, thompsonlake2024perisylvianandhippocampal pages 5-6)

Clinical genetic testing is consequently not routine for an otherwise typical, normally developing child with classic COVE. It becomes appropriate when onset or course is atypical, development is impaired, seizures are drug-resistant, MRI is abnormal, examination is abnormal, or there is a strong multigenerational phenotype.

5. Environmental information

No COVE-specific association with pollution, radiation, heavy metals, smoking, alcohol, diet, exercise, infection, autoimmunity, or occupational exposure was identified. Photosensitivity is not a defining environmental cause of COVE: consistent precipitation by patterned light, television, or video games favors POLE. General seizure-safety measures—adequate sleep, adherence to medication, avoiding individual triggers—reduce provoked attacks but do not prevent the syndrome from arising.

6. Mechanism and pathophysiology

Syndrome-level causal chain

Upstream predisposition of uncertain polygenic basis → age-dependent hyperexcitability/synchronization in occipital cortical networks → focal ictal discharge in primary or associative visual cortex → positive visual phenomena or transient blindness → propagation to parietal, temporal, frontal, or bilateral networks → eye/head deviation, impaired awareness, motor seizure, or bilateral tonic–clonic activity → postictal headache/nausea.

The relevant organ is brain; tissue is cerebral cortex; principal cell classes are glutamatergic cortical projection neurons and GABAergic interneurons. This is an electroclinical model rather than a proven COVE-specific molecular pathway. No direct evidence establishes mTOR, PI3K–AKT, Wnt, MAPK, immune, oxidative-stress, mitochondrial, or metabolic pathology in classic COVE.

Suggested ontology mappings

• GO biological process: regulation of membrane potential; neuronal action potential; chemical synaptic transmission; visual perception; regulation of synaptic transmission.
• GO cellular component: neuron projection; synapse; postsynaptic membrane; axon initial segment.
• CL: neuron; glutamatergic neuron; GABAergic neuron; cortical pyramidal neuron.

No disease-specific transcriptomic, proteomic, metabolomic, lipidomic, methylomic, single-cell, spatial-transcriptomic, CRISPR-screen, or integrated multi-omic study was found. Generic chemically induced epilepsy models are insufficiently specific: one retrieved rat penicillin model used cortical epileptiform induction, but it does not reproduce the age dependence, visual semiology, EEG signature, or spontaneous remission of COVE. (rubio2024classificationofcurrent pages 1-2)

7. Anatomical structures affected

• Organ/system: brain and central nervous system.
• Primary site: occipital lobe and visual cortex; suggested UBERON: brain, cerebral cortex, occipital lobe, primary visual cortex.
• Networks: extrastriate visual association cortex and propagation pathways into parietal, temporal, and frontal regions.
• Cells: cortical excitatory projection neurons and inhibitory interneurons; these are inferred network participants rather than histologically demonstrated targets.
• Subcellular structures: neuronal membrane, ion channels, synapses, and axons are generic electrophysiological compartments; no COVE-specific protein defect is established.
• Lateralization: seizures may begin in either occipital hemisphere. Visual symptoms can be lateralized to a hemifield; EEG abnormalities may be unilateral, bilateral, or shift in predominance. Fixed unilateral deficits are atypical and raise concern for structural disease.

8. Temporal development

COVE starts in childhood, usually with sudden, brief, recurrent visual seizures. It is episodic and nondegenerative. Current expert review states that most cases remit in adolescence, although a small subset has persistent seizures. (wirrell2025epilepsysyndromesclassification. pages 6-7)

There are no accepted early/intermediate/advanced stages. A practical temporal framework is: onset and diagnostic characterization; active seizure period; treatment-controlled or spontaneous remission; and, rarely, persistent epilepsy. Developmental regression or an increasingly diffuse sleep-activated EEG pattern is not expected and warrants evaluation for developmental/epileptic encephalopathy with spike-wave activation in sleep or another diagnosis.

9. Inheritance and population

Reliable population-based incidence and prevalence per 100,000 are not available from the retrieved evidence. COVE is substantially less common than self-limited epilepsy with centrotemporal spikes and self-limited epilepsy with autonomic seizures. Published samples are generally small referral-center cohorts, which limits precise sex ratios, ethnic comparisons, geographic variation, and outcome estimates.

Inheritance is presumed complex/polygenic, with incomplete and unquantified penetrance and variable expression. Anticipation, founder effects, consanguinity effects, carrier frequency, and germline mosaic recurrence have not been established. No robust sex predilection or ancestry-specific enrichment should be entered without direct cohort evidence.

10. Diagnostics

Clinical and EEG diagnosis

Diagnosis requires a stereotyped occipital seizure phenotype and supportive EEG. The ILAE framework distinguishes:

• Mandatory features: features that must be present.
• Alerts: unusual findings that require diagnostic reconsideration and further investigation but do not alone exclude the syndrome.
• Exclusionary features: findings incompatible with the syndrome. (manokaran2024the2022international pages 2-4)

For COVE, practical mandatory elements are childhood-onset focal sensory visual seizures and an EEG compatible with occipital epilepsy. EEG should include wakefulness, eye opening/closure, sleep or sleep deprivation, and intermittent photic stimulation. Interictal recordings commonly show posterior/occipital spikes or spike-wave discharges, often enhanced by eye closure or elimination of fixation; ictal EEG begins in an occipital region. A normal short routine EEG does not exclude epilepsy, so prolonged or video EEG can be useful.

Imaging and other testing

Brain MRI with an epilepsy protocol is appropriate, particularly at first presentation or where the phenotype is incomplete, to exclude occipital cortical dysplasia, tumor, vascular lesion, injury, or other structural cause. A causal structural lesion argues for structural occipital lobe epilepsy rather than classic COVE. Routine blood, urine, CSF, biopsy, PET, SPECT, or metabolic testing is not diagnostic in typical COVE and should be driven by clinical red flags.

Differential diagnosis

• Migraine with visual aura: usually gradual evolution over minutes, zig-zag/scintillating or achromatic patterns, longer duration, and migraine sequence; COVE phenomena are sudden, brief, stereotyped, often colored and circular.
• SeLEAS/Panayiotopoulos syndrome: prominent autonomic features, especially vomiting, pallor, cardiorespiratory change, and often prolonged nocturnal seizures; EEG is often multifocal without consistent localization. (wirrell2025epilepsysyndromesclassification. pages 6-7)
• POLE: visual seizures consistently induced by visual stimuli or photic stimulation. The ILAE explicitly distinguishes POLE by photic-induced focal sensory visual seizures. (manokaran2024the2022international pages 4-5, wirrell2025epilepsysyndromesclassification. pages 6-7)
• Structural occipital epilepsy, posterior reversible encephalopathy, stroke, tumor, malformation, infection, and metabolic disease.
• Syncope, psychogenic nonepileptic events, retinal/ophthalmologic disease, and visual release phenomena.

Genetic and omics testing

WES/WGS, epilepsy panels, CMA, mtDNA sequencing, karyotyping, FISH, and repeat-expansion testing are not first-line tests for a classic presentation. Consider trio WES/WGS or a broad epilepsy panel in atypical or severe cases rather than a COVE-specific panel, because no validated COVE gene set exists. No omics diagnostic has demonstrated clinical utility.

Population, newborn, carrier, or prenatal screening is not recommended. Cascade testing is relevant only if a separate pathogenic familial epilepsy variant is established.

11. Outcome and prognosis

The seizure prognosis is generally favorable: most cases remit in adolescence, but a minority persist. (wirrell2025epilepsysyndromesclassification. pages 6-7) No COVE-specific five- or ten-year survival decrement, mortality rate, life-expectancy reduction, or disease-attributable mortality estimate was found. Severe injury, status epilepticus, and sudden unexpected death in epilepsy are general epilepsy risks, but available evidence does not establish elevated syndrome-specific rates.

Normal long-term neurological function is expected in prototypical cases. Morbidity is chiefly recurrent seizures, temporary visual incapacity, headaches, medication adverse effects, psychosocial restriction, and occasional cognitive/behavioral concerns. Poorer-outcome signals include atypical onset, frequent generalized convulsions, drug resistance, developmental impairment, abnormal examination, persistent background slowing, multifocal/diffuse EEG abnormalities, or a causal MRI lesion—features that may indicate misclassification rather than severe COVE.

12. Treatment

Strategy

Whether to start daily therapy is individualized. Observation can be reasonable after rare, brief seizures when diagnosis is secure, MRI and development are reassuring, and family risk tolerance permits. Treatment is more compelling for recurrent/frequent seizures, focal-to-bilateral tonic–clonic events, injury risk, prolonged attacks, substantial school/QoL effects, or family preference.

Commonly used focal-seizure antiseizure medicines include carbamazepine or oxcarbazepine, levetiracetam, and lamotrigine; valproate may be used when generalized seizure susceptibility is a concern. Historical evidence includes a small levetiracetam-monotherapy study, but no modern COVE-specific randomized comparative trial was retrieved. Therefore no single drug can be labeled evidence-based first-line specifically for COVE.

• Sodium-channel blockers: reduce high-frequency neuronal firing; adverse effects include dizziness, diplopia, rash, hyponatremia, and hematologic/hepatic reactions depending on agent.
• Levetiracetam: binds SV2A; behavioral irritability and somnolence are important pediatric adverse effects.
• Lamotrigine: sodium-channel modulation; requires slow titration because of serious rash risk.
• Valproate: broad-spectrum effects; weight gain, tremor, hepatic/pancreatic toxicity, thrombocytopenia, and major teratogenic risk require careful selection.

Suggested NCIT intervention concepts: Anticonvulsant Therapy, Carbamazepine, Oxcarbazepine, Levetiracetam, Lamotrigine, Valproic Acid, Electroencephalography, and Magnetic Resonance Imaging; exact NCIT codes should be validated in the terminology service.

A written rescue plan and benzodiazepine rescue medication may be indicated for a child with prolonged convulsive seizures. Education should cover water/heights safety, sleep, adherence, first aid, and school planning.

Surgery and advanced therapeutics

Resective surgery is not a treatment for classic self-limited COVE. Drug-resistant “COVE” should trigger repeat video EEG and high-resolution MRI to seek a structural occipital focus; surgery may then apply to the structural epilepsy, not COVE itself. No gene therapy, cell therapy, ASO/siRNA, immune therapy, or syndrome-specific targeted drug is available.

The clinical-trial search found no COVE-specific interventional study. A generic wireless pediatric/adult EEG validation study, NCT05123469, does not constitute a COVE treatment trial.

13. Prevention

There is no established primary prevention because the causal predisposition is unknown and cannot currently be modified. Vaccination, antimicrobial prophylaxis, or environmental remediation has no COVE-specific role.

Secondary/tertiary prevention consists of prompt recognition, exclusion of structural disease, seizure treatment when indicated, adherence, adequate sleep, individualized avoidance of triggers, water/heights precautions, helmets only for selected injury risks, school rescue plans, and counseling about driving when age relevant. Routine newborn, population, carrier, prenatal, or preimplantation screening is not supported. Genetic counseling should explain that inheritance appears complex and that a precise recurrence percentage is unavailable unless another molecular diagnosis is found.

14. Other species and natural disease

No naturally occurring animal disorder has been validated as an orthologous COVE syndrome. Dogs and other mammals can develop focal visual/occipital seizures, but equivalence to the human age-dependent, self-limited electroclinical syndrome is unproven. Thus no NCBI Taxon, breed/VBO, orthologous causal gene, zoonotic transmission, or cross-species susceptibility annotation is warranted. COVE is noninfectious and nonzoonotic.

15. Model organisms

No dedicated mouse, rat, zebrafish, Drosophila, organoid, iPSC, knock-in, knockout, conditional, or humanized model recapitulates all defining COVE features. Generic cortical seizure models can study excitation/inhibition, occipital propagation, and antiseizure pharmacology but lack syndrome specificity. For example, the retrieved penicillin rat model produced dose-dependent cortical epileptiform activity but did not model childhood onset, elementary visual hallucinations, spontaneous adolescent remission, or complex inheritance. (rubio2024classificationofcurrent pages 1-2)

A useful future model would need: age-restricted occipital seizures; visual behavioral correlates; posterior EEG discharges modulated by fixation/eye closure; normal baseline development and anatomy; polygenic susceptibility; and spontaneous remission at maturation.

Recent developments and expert assessment

1. Nosology is the major recent advance. The ILAE replaced the ambiguous “benign/Gastaut-type” terminology with the descriptive COVE label and separated it from autonomic and photosensitive occipital syndromes. The pediatric update was published February 2024; DOI: https://doi.org/10.1007/s13312-024-3115-2. (manokaran2024the2022international pages 2-4, manokaran2024the2022international pages 4-5)
2. Current expert framing emphasizes syndrome utility. A 2025 review states that syndrome identification guides high-yield investigation, treatment selection, and prognosis. Its exact abstract wording is: epilepsy syndromes are associated with “a characteristic cluster of clinical and EEG features, often supported by specific etiologic findings.” DOI: https://doi.org/10.1002/epi4.70026. For COVE, that utility is mainly electroclinical because a specific etiology has not been established. (wirrell2025epilepsysyndromesclassification. pages 6-7)
3. Molecular precision remains an unmet need. Recent GRIN2A imaging and broad pediatric-genetics work should not be overgeneralized to COVE. The available evidence supports careful phenotyping before sequencing and strict gene–disease validity standards. (thompsonlake2024perisylvianandhippocampal pages 1-2, thompsonlake2024perisylvianandhippocampal pages 5-6)

Evidence gaps for knowledge-base curation

High-priority gaps are: a verified MONDO/Orphanet mapping; contemporary population-based incidence and prevalence; prospective cohorts using 2022 ILAE criteria; standardized seizure-frequency and QoL outcomes; controlled medication comparisons; well-powered genomic studies restricted to rigorously phenotyped COVE; and COVE-specific network, single-cell, and developmental models. Until those data exist, the safest curation is syndrome-level electroclinical disease; presumed complex inheritance; no definitive causal gene; no molecular biomarker; favorable but not universally remitting course.

References

1. (manokaran2024the2022international pages 2-4): Ranjith Kumar Manokaran, Suvasini Sharma, and Rajesh Ramachandrannair. The 2022 international league against epilepsy classification and definition of childhood epilepsy syndromes: an update for pediatricians. Indian Pediatrics, 61:179-183, Feb 2024. URL: https://doi.org/10.1007/s13312-024-3115-2, doi:10.1007/s13312-024-3115-2. This article has 25 citations and is from a peer-reviewed journal.

2. (manokaran2024the2022international pages 4-5): Ranjith Kumar Manokaran, Suvasini Sharma, and Rajesh Ramachandrannair. The 2022 international league against epilepsy classification and definition of childhood epilepsy syndromes: an update for pediatricians. Indian Pediatrics, 61:179-183, Feb 2024. URL: https://doi.org/10.1007/s13312-024-3115-2, doi:10.1007/s13312-024-3115-2. This article has 25 citations and is from a peer-reviewed journal.

3. (wirrell2025epilepsysyndromesclassification. pages 6-7): Elaine C. Wirrell, Nicola Specchio, Rima Nabbout, Phillip L. Pearl, and Kate Riney. Epilepsy syndromes classification. Epilepsia open, Mar 2025. URL: https://doi.org/10.1002/epi4.70026, doi:10.1002/epi4.70026. This article has 6 citations and is from a peer-reviewed journal.

4. (thompsonlake2024perisylvianandhippocampal pages 1-2): Daisy G.Y. Thompson-Lake, Frederique J. Liegeois, Ruth O. Braden, Graeme D. Jackson, Samantha J. Turner, Lottie Morison, Michael Hildebrand, Ingrid E. Scheffer, and Angela T. Morgan. Perisylvian and hippocampal anomalies in individuals with pathogenic grin2a variants. Neurology Genetics, Apr 2024. URL: https://doi.org/10.1212/nxg.0000000000200129, doi:10.1212/nxg.0000000000200129. This article has 2 citations.

5. (thompsonlake2024perisylvianandhippocampal pages 5-6): Daisy G.Y. Thompson-Lake, Frederique J. Liegeois, Ruth O. Braden, Graeme D. Jackson, Samantha J. Turner, Lottie Morison, Michael Hildebrand, Ingrid E. Scheffer, and Angela T. Morgan. Perisylvian and hippocampal anomalies in individuals with pathogenic grin2a variants. Neurology Genetics, Apr 2024. URL: https://doi.org/10.1212/nxg.0000000000200129, doi:10.1212/nxg.0000000000200129. This article has 2 citations.

6. (wirrell2025epilepsysyndromesclassification. pages 5-6): Elaine C. Wirrell, Nicola Specchio, Rima Nabbout, Phillip L. Pearl, and Kate Riney. Epilepsy syndromes classification. Epilepsia open, Mar 2025. URL: https://doi.org/10.1002/epi4.70026, doi:10.1002/epi4.70026. This article has 6 citations and is from a peer-reviewed journal.

7. (rubio2024classificationofcurrent pages 1-2): Carmen Rubio, Héctor Romo-Parra, Alejandro López-Landa, and Moisés Rubio-Osornio. Classification of current experimental models of epilepsy. Brain Sciences, 14:1024, Oct 2024. URL: https://doi.org/10.3390/brainsci14101024, doi:10.3390/brainsci14101024. This article has 14 citations.

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