Photosensitive Occipital Lobe Epilepsy: Disease Characteristics Report

Evidence date: literature searched through 2024, with emphasis on the 2023 syndrome-delineation study and recent supporting literature.
Disease category: complex reflex epilepsy phenotype.
Evidence caveat: photosensitive occipital lobe epilepsy (POLE), historically called idiopathic photosensitive occipital lobe epilepsy (IPOE), is rare. Much of the quantitative literature concerns photosensitive epilepsy generally, not POLE specifically. Such extrapolations are labeled below. PubMed identifiers are omitted where they could not be verified from the retrieved records; DOI links are provided instead.

The following table summarizes the calibration of the evidence used in this report.

Table: This table calibrates what can be concluded specifically for photosensitive occipital lobe epilepsy versus what must be extrapolated from broader photosensitive epilepsy research. It is useful for structuring a cautious, evidence-graded disease report without overstating gene, epidemiology, or treatment claims.

1. Disease information

Definition and scope

POLE is an electroclinical phenotype in which visual stimulation reproducibly provokes seizures with an occipital onset or occipital semiology. It occupies the boundary between reflex focal epilepsy and the wider genetically influenced photosensitivity spectrum. It should not be equated with either (1) an isolated photoparoxysmal response (PPR) in a person without visually induced seizures or (2) generalized photosensitive syndromes such as juvenile myoclonic epilepsy, epilepsy with eyelid myoclonia, Dravet syndrome, or progressive myoclonus epilepsy.

The principal syndrome literature includes Guerrini et al. (1995; DOI), Politi-Elishkevich et al. (2014; DOI), Koutroumanidis et al. (2015; DOI), and the important 2023 long-term reassessment by Cerrahoğlu Şirin et al. (DOI). These reports support recognition of an underdiagnosed reflex focal phenotype, although POLE is not presently among the best-established, separately codified ILAE epilepsy syndromes.

Identifiers and synonyms

• MONDO: no dedicated POLE entry was established in the retrieved evidence. The broader concept photosensitive epilepsy is MONDO:0015643. Open Targets returned no associated targets for that MONDO disease record, underscoring the absence of a validated POLE-specific target set. (OpenTargets Search: photosensitive epilepsy)
• OMIM/Orphanet: no dedicated, verified POLE record was found.
• ICD-10/ICD-11: no unique POLE code was verified; coding generally falls under focal epilepsy/reflex epilepsy according to local coding rules.
• MeSH: use broader concepts such as Epilepsy, Reflex and Epilepsy, Partial/Occipital Lobe Epilepsy; no distinct POLE descriptor was verified.
• Synonyms: photosensitive occipital lobe epilepsy; idiopathic photosensitive occipital lobe epilepsy; idiopathic/possibly genetic photosensitive occipital epilepsy; visually induced occipital epilepsy.

This report synthesizes aggregated disease-level literature, not individual EHR records. Small cohorts and case reports are nevertheless prominent because of the syndrome’s rarity.

2. Etiology

Causal and risk factors

POLE is most plausibly a complex genetically influenced network epilepsy in which visual stimuli recruit an unusually excitable occipital cortex. No single gene, pathogenic variant, infectious agent, toxin, or structural lesion has been proven to cause the syndrome as presently defined.

Broader genetic-photosensitivity data demonstrate marked locus and syndrome heterogeneity. A 2022 cohort selected 35 patients with pathogenic genetic findings and photosensitivity: SCN1A variants occurred in 7, CHD2 in 6, TPP1 in 3, SYNGAP1 in 3, and GABRA1 in 2; other findings included GABRG2, KCTD7, MFSD8, KCNC1, GBA, CACNA1A, KCNMA1, FLNA, SZT2, SLC2A1, a 5q33.2–q34 deletion, and mitochondrial variants. Ion-channel genes represented 46.7% of cases. This cohort chiefly comprised progressive myoclonus epilepsy, Dravet syndrome, and developmental/epileptic encephalopathies—not POLE—so these genes are differential-diagnostic or susceptibility candidates, not established POLE genes. (niu2022geneticandphenotypic pages 6-8, niu2022geneticandphenotypic pages 12-13, niu2022geneticandphenotypic pages 1-3)

An exact abstract statement from that study is: “The most common genes for epilepsy with genetic photosensitivity are SCN1A and CHD2, and the most common syndromes are PME and Dravet syndrome.” The authors also proposed MFSD8, KCNMA1, SZT2, FLNA, and SLC2A1 as candidates, which should not be interpreted as validated POLE associations. (Published August 2022) (niu2022geneticandphenotypic pages 1-3, niu2022geneticandphenotypic pages 13-14)

Environmental and modifying risks

Relevant provocations include binocular flicker, high-contrast striped patterns, television/video games, flashing lamps, discotheque lighting, sunlight flickering through trees, escalators, blinds, and patterned fabrics. Sensitivity generally spans approximately 8–50 Hz, peaking near 15–20 Hz; long-wavelength red and alternating red-blue stimuli are particularly provocative. Sleep deprivation, stress, and alcohol can lower seizure threshold. (silva2017photosensitivityandepilepsy pages 10-12, covanis2004treatmentofphotosensitivity pages 1-2, silva2017photosensitivityandepilepsy pages 9-10)

Female sex, adolescence, and family history are established correlates of broader photosensitivity, but POLE-specific risk ratios are unavailable. Broader photosensitive epilepsy is approximately twice as common in females and often begins around puberty. (silva2017photosensitivityandepilepsy pages 1-3, silva2017photosensitivityandepilepsy pages 4-6)

Protective factors and gene–environment interaction

No validated protective allele is known. Environmental protection comprises reducing stimulus contrast, frequency, duration, and visual-field exposure; increasing screen distance; avoiding sleep deprivation; and using monocular occlusion or tested tinted lenses. The causal interaction is best expressed as:

Inherited/developmental cortical susceptibility → excessive visual-cortical synchronization during provocative stimulation → occipital epileptiform discharge → propagation through parietal, temporal, motor, and thalamocortical networks → focal visual seizure, impaired awareness, motor manifestations, or bilateral tonic-clonic seizure. (silva2017photosensitivityandepilepsy pages 1-3, covanis2004treatmentofphotosensitivity pages 1-2, silva2017photosensitivityandepilepsy pages 12-13)

3. Phenotypes

Severity is variable: some patients have only avoidable reflex focal seizures; others also have spontaneous seizures or focal-to-bilateral convulsions. The course is episodic rather than continuously progressive. Disease-specific frequencies and validated POLE quality-of-life scores were not retrieved. Likely burdens include screen avoidance, educational/work limitations, driving restrictions, anxiety around public lighting, injury risk, and medication adverse effects. A lens study explicitly included six-month satisfaction and quality-of-life assessment, illustrating current real-world attention to these outcomes. (NCT04076410 chunk 2)

4. Genetic and molecular information

• Established POLE-causal genes: none.
• Established POLE pathogenic variants/HGNC IDs: none; therefore no defensible POLE-specific allele frequencies, somatic/germline classification, or variant-level ACMG assertions can be supplied.
• Potential broader-photosensitivity genes: CHD2, SCN1A, GABRA1, GABRG2, SYNGAP1 and genes causing progressive myoclonus epilepsy or developmental encephalopathy. Their presence usually argues for a broader syndromic diagnosis rather than isolated POLE. (niu2022geneticandphenotypic pages 6-8, niu2022geneticandphenotypic pages 12-13)
• Chromosomal findings: a 5q33.2–q34 deletion occurred in one heterogeneous genetic-photosensitivity cohort; it is not a recurrent POLE lesion. (niu2022geneticandphenotypic pages 1-3)
• Modifier genes, anticipation, founder effects, germline mosaicism, protective alleles: not established for POLE.
• Epigenetics: no POLE-specific methylation, histone, or chromatin signature was found.

Consequently, POLE should not currently be represented in a knowledge base as a Mendelian disorder with a fixed gene–disease relationship.

5. Environmental information

Visual stimulation is a trigger, not generally the underlying cause. Television was reported as a trigger in 41% and patterns in 39.7% of a broader photosensitive cohort. PPR-positive patients reported visually induced seizures much more often than PPR-negative patients (63% versus 2.3%). These figures are not POLE-specific. (silva2017photosensitivityandepilepsy pages 3-4, silva2017photosensitivityandepilepsy pages 4-6)

No association with smoking, diet, exercise, occupational toxins, ionizing radiation, pollution, bacteria, viruses, fungi, or parasites is established. Alcohol, fatigue, and sleep deprivation are clinically relevant threshold modifiers. (covanis2004treatmentofphotosensitivity pages 1-2)

6. Mechanism and pathophysiology

Causal network

1. Upstream trigger: rhythmic luminance/color contrast or spatial pattern activates binocularly innervated neurons in primary and extrastriate visual cortex.
2. Local susceptibility: deficient inhibition and/or excessive excitation permits hypersynchronous activity in occipital networks. At lower stimulation frequencies PPR may remain occipital; increasing frequency facilitates parietal and central spread. (silva2017photosensitivityandepilepsy pages 1-3, silva2017photosensitivityandepilepsy pages 3-4)
3. Network propagation: abnormal occipital–parietal, occipital–supplementary-motor, prefrontal, and thalamocortical connectivity transforms a visual response into an epileptic discharge. Increased occipital–supplementary motor connectivity is one proposed route to motor manifestations. (silva2017photosensitivityandepilepsy pages 1-3, silva2017photosensitivityandepilepsy pages 12-13)
4. Clinical output: local occipital discharge produces visual hallucination or blindness; spread produces eye/head deviation, altered awareness, myoclonus, or focal-to-bilateral tonic-clonic seizure.

Molecular/cellular interpretation

Broader genetic findings implicate voltage-gated sodium/calcium/potassium channels, GABA receptors, synaptic regulation, chromatin remodeling, and lysosomal/mitochondrial disease. These converge on excitation–inhibition imbalance but do not define a unique POLE biochemical pathway. No consistent inflammation, autoimmunity, neurodegeneration, oxidative injury, metabolic signature, protein aggregation, or tissue destruction has been demonstrated in isolated POLE.

Suggested GO biological processes: GO:0050804 modulation of chemical synaptic transmission; GO:0099536 synaptic signaling; GO:0007214 gamma-aminobutyric acid signaling pathway; GO:0007268 chemical synaptic transmission; GO:0007601 visual perception; GO:0007610 behavior; GO:0019228 neuronal action potential.
Suggested cellular components: GO:0045202 synapse; GO:0098794 postsynapse; GO:0030425 dendrite; GO:0030424 axon; GO:0005886 plasma membrane; GO:0034702 ion-channel complex.
Suggested cell types: CL:0000540 neuron; CL:0000099 interneuron; CL:0000617 GABAergic neuron; CL:0000679 glutamatergic neuron; retinal photoreceptors are stimulus sensors, not proven diseased cells.

No POLE-specific transcriptomic, proteomic, metabolomic, lipidomic, single-cell, spatial-transcriptomic, multi-omic, or CRISPR-screen study was identified.

7. Anatomical structures affected

The primary system is the central nervous system, particularly bilateral or unilateral occipital visual cortex. Relevant structures include primary visual cortex, extrastriate cortex, parieto-occipital junction, posterior parietal association cortex, and propagation pathways to temporal, frontal/motor, and thalamic networks. Broader imaging research supports abnormal visual-cortex structure/connectivity but not destructive occipital pathology. (silva2017photosensitivityandepilepsy pages 1-3, silva2017photosensitivityandepilepsy pages 12-13)

Suggested UBERON terms: UBERON:0000955 brain; UBERON:0002021 occipital lobe; UBERON:0000411 visual cortex; UBERON:0001897 dorsal thalamus; UBERON:0001871 temporal lobe; UBERON:0001870 frontal cortex. The disease can be left-sided, right-sided, bilateral, or rapidly bilateral; no fixed lateralization is defining. Routine MRI is usually expected to be normal in an idiopathic/possibly genetic phenotype. A structural occipital lesion should prompt classification as structural focal epilepsy rather than uncomplicated POLE.

8. Temporal development

Onset is most often pediatric or adolescent, but adult-onset photosensitivity and POLE-like presentations are documented. Onset is episodic and stimulus-linked rather than anatomically progressive. Broader photosensitive epilepsy incidence is about fivefold higher at ages 7–19 years. (silva2017photosensitivityandepilepsy pages 4-6)

The course may include:

• reflex seizures only;
• reflex plus spontaneous focal seizures;
• focal-to-bilateral convulsions;
• decreasing photosensitivity after adolescence; or
• persistent photosensitivity into adulthood.

Broader literature reports second-decade remission in approximately two-thirds of valproate-treated and over half of untreated patients, whereas 77.7% of a severely affected genetic cohort retained photosensitivity after one year. These discrepant figures demonstrate that prognosis depends strongly on the underlying syndrome and must not be transferred uncritically to POLE. (niu2022geneticandphenotypic pages 1-3, silva2017photosensitivityandepilepsy pages 1-3)

9. Inheritance and population

No reliable POLE-specific prevalence, incidence, sex ratio, penetrance, carrier frequency, or population distribution was found. Broader photosensitive epilepsy estimates are approximately 1 in 4,000 population and 1.1 new cases per 100,000/year, with typical onset near puberty and an approximately twofold female excess. Clinic PPR prevalence is about 5.6%, rising to 7.3% at ages 10–20 in cited datasets. (silva2017photosensitivityandepilepsy pages 3-4, silva2017photosensitivityandepilepsy pages 4-6)

Familial clustering supports complex/polygenic inheritance with incomplete, age-dependent penetrance and variable expressivity. Autosomal-dominant CHD2-related photosensitivity is relevant to differential diagnosis, but a monogenic POLE inheritance pattern is unproven. No anticipation, consanguinity effect, founder mutation, or geographic variant distribution has been established. (silva2017photosensitivityandepilepsy pages 9-10)

10. Diagnostics

Core evaluation

1. Detailed history/video: characterize elementary visual symptoms, duration, visual-field location, awareness, eye/head deviation, headache, and exact visual triggers.
2. Routine video-EEG with standardized intermittent photic stimulation (IPS): test eyes-open, eye-closure, and eyes-closed conditions, stopping stimulation promptly if a generalized or escalating discharge occurs. IPS around 15–20 flashes/s is generally most sensitive; broader protocols survey approximately 2–60 Hz. (silva2017photosensitivityandepilepsy pages 10-12, silva2017photosensitivityandepilepsy pages 9-10, NCT03603639 chunk 2)
3. Pattern stimulation where appropriate, performed in a controlled neurophysiology setting.
4. Brain MRI using an epilepsy protocol: exclude occipital tumor, malformation, vascular lesion, gliosis, or other structural cause.
5. Formal ophthalmologic assessment when persistent field loss or retinal disease is possible.

A PPR is an EEG biomarker, not sufficient alone for POLE. Diagnosis requires concordant clinical seizures or compelling occipital electroclinical evidence. PPR can occur in otherwise healthy individuals; broader estimates include 7.6% in healthy children in one cited dataset. (silva2017photosensitivityandepilepsy pages 3-4)

Differential diagnosis

• migraine with visual aura—typically slower evolution and longer visual symptoms;
• childhood occipital visual epilepsy/Gastaut-type epilepsy without a photosensitive requirement;
• epilepsy with eyelid myoclonia, juvenile myoclonic epilepsy, and other generalized photosensitive epilepsies;
• pattern-sensitive epilepsy;
• structural occipital epilepsy;
• syncope or psychogenic nonepileptic events;
• retinal/optic-nerve disease;
• Dravet syndrome, CHD2 encephalopathy, progressive myoclonus epilepsy, GLUT1 deficiency, and mitochondrial/lysosomal disease when development, neurologic examination, MRI, or EEG background is abnormal. A genetic cohort showed abnormal background and MRI principally in progressive myoclonus epilepsy, which is useful diagnostically. (niu2022geneticandphenotypic pages 6-8, niu2022geneticandphenotypic pages 1-3)

Genetic testing

Routine single-gene testing is not indicated for a developmentally normal, MRI-negative, otherwise typical POLE presentation. Use an epilepsy panel or WES/WGS when there is developmental delay, drug resistance, early onset, abnormal neurologic examination/MRI, generalized/myoclonic features, or a strong family history. Panels should include CHD2, SCN1A, GABRA1, GABRG2, SYNGAP1 and phenotype-directed PME/metabolic genes. CMA is reasonable for syndromic developmental epilepsy; karyotype, FISH, mitochondrial DNA, and repeat-expansion testing are phenotype-driven. No POLE-specific omics diagnostic or population-screening program exists.

11. Outcome and prognosis

POLE itself is not known to shorten life expectancy, and no syndrome-specific survival or mortality rate is available. Morbidity arises from convulsive injury, impaired awareness, driving limitations, educational/occupational restrictions, anxiety, and treatment toxicity. General epilepsy risks, including status epilepticus and sudden unexpected death in epilepsy, depend more on uncontrolled convulsive-seizure burden than on photosensitivity alone.

Favorable factors probably include reflex-only seizures, reliable trigger avoidance, normal development/MRI/background EEG, and medication responsiveness. Unfavorable indicators include spontaneous seizures, generalized convulsions, broad PPR frequency range, developmental impairment, abnormal MRI/background EEG, and an underlying encephalopathy or PME. In broader pattern-sensitive epilepsy, 80% in one series were seizure-free for over two years, but a POLE-specific rate remains unavailable. (silva2017photosensitivityandepilepsy pages 4-6)

12. Treatment

Practical strategy

1. Educate the patient and family about triggers and immediate countermeasures.
2. If exposure occurs, cover one eye completely and turn away; simply closing both eyes may retain binocular stimulation through the lids.
3. Increase screen distance—historically at least three screen widths—use well-lit rooms and modern high-refresh/low-flicker displays, reduce contrast/brightness, avoid provocative patterns, and maintain sleep. (covanis2004treatmentofphotosensitivity pages 1-2, covanis2004treatmentofphotosensitivity pages 2-3)
4. Consider individually EEG-tested colored or polarized lenses. Broader evidence found PPR disappearance in 77% and reduction in 19% with colored filters; a 28-participant study tested Z1 and four experimental lenses with EEG and quality-of-life endpoints (NCT04076410). (silva2017photosensitivityandepilepsy pages 10-12, NCT04076410 chunk 2)
5. Prescribe antiseizure medication when avoidance is impractical, spontaneous seizures occur, or events are severe.

Pharmacotherapy

Valproate has the strongest historical evidence across generalized/visually sensitive epilepsies, with reported seizure freedom of 81% in 67 IPS-sensitive patients and 85% in another visually sensitive series. It requires major caution in people who could become pregnant. Levetiracetam is commonly used and is often preferable where pregnancy-related valproate risk is important. Lamotrigine or other focal-seizure agents may be considered according to the complete electroclinical syndrome, but some sodium-channel agents can aggravate particular generalized/myoclonic epilepsies. (covanis2004treatmentofphotosensitivity pages 2-3)

The human photosensitivity model demonstrates rapid PPR suppression by SV2A ligands. In a randomized crossover study of nine completers, intravenous brivaracetam eliminated PPR at a median 2 minutes, versus 7.5 minutes for levetiracetam; combined analyses estimated 61% faster elimination, but the authors cautioned that clinical-outcome comparisons remain necessary. Exact abstract wording: “Outcome studies directly comparing LEV and BRV are needed to define the clinical utility of the response with BRV.” (Published September 2020)

Suggested NCIt intervention concepts: Anticonvulsant Therapy; Valproic Acid; Levetiracetam; Brivaracetam; Benzodiazepine; Patient Education; Avoidance Intervention; Protective Eyewear. No POLE-specific pharmacogenomic rule, surgery series, gene therapy, cell therapy, RNA therapy, or immunotherapy was identified. Surgery is reserved for a demonstrable, concordant structural occipital epileptogenic lesion, not the typical bilateral reflex phenotype.

Experimental trials

The field uses reproducible IPS-induced PPR suppression as a small, efficient Phase IIa pharmacodynamic platform rather than as proof of long-term seizure control. Examples include brivaracetam NCT00401648 (n=20), JNJ-26489112 NCT00579384 (n=12), the AMPA/kainate antagonist BGG492 NCT00784212 (n=13), ACT-709478 NCT03239691 (n=5), and E2730 NCT03603639 (n=6). BGG492 showed dose-dependent PPR suppression; ICA-105665 NCT00979004 was terminated after a serious adverse event at 600 mg. None was POLE-specific. (NCT00579384 chunk 1, NCT00979004 chunk 1, NCT03603639 chunk 1, NCT00401648 chunk 1, NCT00784212 chunk 1, NCT03239691 chunk 1)

13. Prevention

• Primary prevention: no method prevents the inherited/developmental susceptibility. Public-facing media standards that limit flash rate, red saturation, luminance transitions, and high-contrast patterns reduce population exposure.
• Secondary prevention: there is no population or newborn screening. Targeted EEG/IPS is reasonable after visually induced events or in selected high-risk epilepsy syndromes; routine testing of asymptomatic people is unsupported.
• Tertiary prevention: trigger education, sleep hygiene, medication adherence, rescue planning, injury precautions, individualized lens testing, and control of spontaneous convulsions.
• Genetic counseling: recurrence risk is generally empirical unless testing establishes another defined genetic syndrome. Prenatal or preimplantation testing is not available for nonsyndromic POLE without a familial pathogenic variant.
• Vaccination/infectious prophylaxis: not applicable.

Nonpharmacologic management alone may suffice when seizures are exclusively visual, rare, and reliably avoidable. (covanis2004treatmentofphotosensitivity pages 1-2, covanis2004treatmentofphotosensitivity pages 2-3)

14. Other species and natural disease

The principal natural comparative model is the Senegalese baboon, Papio hamadryas papio (NCBI Taxonomy identification should be verified against the current taxonomy record before database ingestion). It naturally develops myoclonic, absence, and generalized tonic-clonic seizures with photosensitivity. This is a model of genetic generalized epilepsy, not a homologous focal POLE disease.

Among 671 baboons, 49% displayed 4–6-Hz generalized spike-wave discharges; photoepileptic responses occurred in 23% of epileptic animals and were maximal at 20–25-Hz stimulation. Pedigree estimates were h²=0.33 for spontaneous seizures and h²=0.19 for interictal discharges; RBFOX1 was a candidate association. (szabo2022neuroimaginginthe pages 1-2, szabo2021thebaboonin pages 1-2)

There is no zoonotic transmission. No companion-animal breed with a validated natural POLE equivalent was identified.

15. Model organisms

Baboon model

Intracranial EEG, PET, MRI/fMRI, and MEG in photosensitive baboons implicate occipital, parietal, orbitofrontal, motor, insular, and thalamic networks. Myoclonic and generalized tonic-clonic seizures can occur spontaneously or after intermittent light stimulation. The model’s gyrencephalic brain, visual-system similarity, and pedigreed colonies confer high translational value for network mapping and antiseizure-drug proof of principle. (szabo2012baboonmodelof pages 1-2, szabo2022neuroimaginginthe pages 1-2, szabo2021thebaboonin pages 2-3, szabo2011functionalpetevaluation pages 1-2)

Limitations include expense, limited availability, subspecies differences, imperfect seizure provocation, electrode displacement/injury, effects of anesthesia and medication, and its generalized rather than focal-occipital electroclinical phenotype. Maximal photic sensitivity also differs—approximately 20–25 Hz in baboons versus roughly 12–20 Hz in humans. (szabo2021thebaboonin pages 1-2, szabo2012baboonmodelof pages 8-10)

No validated POLE-specific mouse, rat, zebrafish, Drosophila, organoid, iPSC, knock-in, or conditional model was identified. Generic ion-channel and CHD2 models may illuminate photosensitivity but cannot presently be claimed to recapitulate POLE.

Overall assessment

POLE is best represented as a rare, under-recognized reflex focal epilepsy phenotype characterized by visually induced occipital seizures and supportive occipital EEG/PPR findings. Its most defensible mechanistic model is visual-cortical hyperexcitability with network propagation, rather than a single-gene or structural disorder. The 2023 syndrome reassessment is the most recent directly relevant publication located, but recent molecular and interventional advances largely concern broader photosensitive epilepsy. Priority research needs are a consensus case definition, multinational registry, POLE-specific prevalence and natural-history estimates, harmonized IPS/video-EEG phenotyping, genomic case-control studies, and prospective comparative treatment studies.

References

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15. (NCT03603639 chunk 1): A Study to Evaluate the Pharmacodynamic Activity of E2730 in Adult Participants With Photosensitive Epilepsy. Eisai Inc.. 2018. ClinicalTrials.gov Identifier: NCT03603639

16. (NCT00401648 chunk 1): Effect of Brivaracetam in Photosensitive Epileptic Subjects. UCB Pharma. 2002. ClinicalTrials.gov Identifier: NCT00401648

17. (NCT00784212 chunk 1): Effect of BGG492 on EEG in Patients With Photosensitive Epilepsy. Novartis Pharmaceuticals. 2008. ClinicalTrials.gov Identifier: NCT00784212

18. (NCT03239691 chunk 1): A Study to Evaluate the Effect of ACT-709478 in Photosensitive Epilepsy Patients. Idorsia Pharmaceuticals Ltd.. 2017. ClinicalTrials.gov Identifier: NCT03239691

19. (NCT04076410 chunk 2): Ana Checa-Ros, MD, PhD. Efficacy of Lenses in Abolishing Photoparoxysmal Responses. Aston University. 2021. ClinicalTrials.gov Identifier: NCT04076410

20. (NCT03603639 chunk 2): A Study to Evaluate the Pharmacodynamic Activity of E2730 in Adult Participants With Photosensitive Epilepsy. Eisai Inc.. 2018. ClinicalTrials.gov Identifier: NCT03603639

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Artifacts

• Edison artifact artifact-00