Unmasking the role of the occipital lobe in epilepsy with eyelid myoclonia

ABSTRACT

Epilepsy with eyelid myoclonia (EEM) is classified within the spectrum of genetic generalized epilepsies. However, the involvement of the occipital lobe in seizure generation in EEM remains a topic of debate. This study aims to investigate the role of the occipital lobe in the pathophysiology of EEM. We reviewed the medical charts and video–electroencephalography (EEG) recordings of patients diagnosed with EEM at the Danish Epilepsy Centre from 2019 to 2024. We included 21 consecutive patients with clinically and video‐EEG‐confirmed EEM. In addition to visual analysis, EEG recordings were assessed using integrated quantitative methods, including amplitude mapping, power spectrum frequency analysis, and source localization. Interictal and ictal epileptiform discharges with onset in the posterior brain regions were consistently observed. Quantitative EEG analysis documented occipital onset within the network involved in eyelid myoclonia, both with and without absence seizures. Furthermore, a focal‐onset occipital seizure was recorded in one patient. These findings support the involvement of the occipital lobe in initiating seizures in EEM and better define the underlying pathophysiological mechanisms of this condition.

Abbreviations

bi‐CPO

bi‐centroparietoccipital

bi‐F

bifrontal

bi‐FC

bifrontocentral

bi‐O

bioccipital

bi‐PO

biparietoccipital

bi‐TPO

bitemporoparietoccipital

BTCS

bilateral tonic clonic seizure

ETX

ethosuximide

F

female

ID

intellectual disability

M

male

NA

not available

NGS

next generation sequencing

O

occipital

OXC

oxcarbazepine

PER

perampanel

prev

prevalence

TO

temporoccipital

TPM

topiramate

1. INTRODUCTION

Epilepsy with eyelid myoclonia (EEM), also known as Jeavons syndrome, is a genetic generalized epilepsy (GGE) ¹ with childhood onset and a female predominance. Eye‐closure–induced eyelid myoclonia (EM), with or without absences, and/or generalized electroencephalography (EEG) epileptiform discharges (EDs) are the hallmarks of EEM. Other typical features include clinical and/or EEG photosensitivity—which may decrease with age and medical treatment—and occasional recurrence of typical absences, myoclonic, and generalized tonic–clonic seizures (GTCS). ²

According to the International League Against Epilepsy (ILAE) criteria, focal seizures were exclusionary for the diagnosis of EEM, ¹ and an international expert consensus panel recommended reconsidering the diagnosis of EEM if focal seizures co‐occur. ³ However, a recent study of a large cohort of patients with EEM found that some also experienced focal seizures, with anecdotal reports documenting occipital seizures. ⁴ , ⁵ , ⁶

In recent years, there has been extensive discussion about the role of the occipital lobe in the ictogenesis of EEM. Some authors have even suggested an overlap between EEM and photosensitive occipital lobe epilepsy (POLE). ⁶

Therefore, we aimed to further investigate the electroclinical features of EEM by performing an integrated EEG analysis, with a focus on the contribution of the occipital lobe in generating interictal and ictal EDs in patients with EEM.

2. MATERIALS AND METHODS

We retrospectively reviewed the medical charts and the video‐EEG recordings of patients diagnosed with EEM at the Danish Epilepsy Centre in the past 5 years (2019–2024). Inclusion criteria were: (1) fulfillment of the ILAE mandatory diagnostic criteria for EEM ¹ ; (2) at least one video‐EEG showing generalized (poly)spike‐and‐wave (poly‐SW) discharges; (3) availability of both wakefulness and sleep video‐EEG recordings; (4) at least one video‐EEG documenting eyelid myoclonic jerks at eye closure (EM), possibly followed by impaired consciousness (EM‐absences); and (5) good quality EEG recordings including 25 EEG derivations. Exclusion criteria were: (1) presence of atonic and tonic seizures, (2) typical absence or myoclonia in body regions other than the eyelids as the predominant seizures type; (3) genetic variants associated with other neurological syndromes, (4) moderate to severe intellectual disability, and (5) abnormal neuroimaging findings.

Referring physicians filled in a semi‐structured spreadsheet with the clinical findings. Video‐EEG was acquired using digital acquisition systems (NicoletOne Software; Brain Quick Micromed Software), for a minimum of 30 min, with EEG electrodes placed according to the 10–10 Standard International System (open filter setting), electrocardiography (ECG), and at least two electromyography (EMG) derivations. Qualitative video‐EEG analysis was performed independently by two epileptologists with EEG expertise (E.G. and E.R.) and one clinical neurophysiologist, all blinded to the clinical data. In cases of disagreement, consensus was reached through discussion. ED morphology was described according to the 2017 revised glossary ⁷ and the topography was classified as “posterior” (T5/T6, P4/PZ/P3, O1/O2 derivations), “anterior” (Fp1/Fp2, F3/FZ/F4, F7/F8, C3/CZ/C4, T3/T4), “unilateral,” or “bilateral.” The photo‐paroxysmal response (PPR) was classified according to the 2001 criteria. ⁸

For each patient, 10 consecutive artifact‐free EEG epochs with eye closure underwent an integrated quantitative EEG analysis in the first second after eye closure. This included: (1) power spectrum frequency analysis, on occipital and frontal derivations, (2) amplitude map analysis (BrainQuick, Micromed), and (3) EEG source imaging (BESA GmbH). For the power spectrum frequency analysis, the grand average of the median frequency values and relative power for each frequency band (α, β, γ, and δ) was calculated for each patient.

The study was approved by the institutional review board at the Danish Epilepsy Centre (EMN‐2024‐10185). Informed consent for video‐EEG disclosure was obtained from all patients and their legal guardians.

3. RESULTS

3.1. Clinical features

Twenty‐one patients (20 female, 1 male) ages 12–55 years (mean age: 21 years) were included. A positive family history for GGE was reported for 8 of 21 (38%). The mean age at seizure onset was 7.2 years (range: 2–14 years); the follow‐up duration was 14.1 years (range: 5–49 years). All patients exhibited EM, with absences (15/21, 71%) and rare GTCS (12/21, 57%); 19 of 21 (90%) had clinical photosensitivity.

Most patients had normal (15/21, 71%) or borderline (5/21, 24%) intelligence; 1 of 21 (5%) had mild intellectual disability, 4 of 21 (19%) had autism spectrum disorder (ASD) or autistic traits, 4 of 21 (19%) had attention‐deficit/hyperactivity disorder (ADHD), and 3 of 21 (14%) experienced mild psychiatric symptoms (anxiety, functional seizures, and low stress threshold). All but one (95%) were taking 1–3 (mean 1.9) antiseizure medications (ASMs) at the last follow‐up, including levetiracetam (n = 9), ethosuximide (n = 6), zonisamide (n = 6), valproic acid (n = 5), lamotrigine (n = 5), brivaracetam (n = 2), and carbamazepine (n = 1). Eight of 21 patients (38%) underwent genetic testing; two of them harbored pathogenic variants in the CHD2 gene. No pathogenic variants were detected in the remaining six patients (Table 1, Table S1).

TABLE 1.

Main electroclinical features.

Clinical features									Interictal EEG		Ictal EEG
Pt	Sex, age (years)	Family history (GGE)	Seizure onset (years)	Seizure types	Clinical PhS	ASM (current underlined)	Cognition, behavior	MRI/genetics	IED	PPR/EC sensitivity	ED	Spectral analysis
												Occipital		Frontal
												Peak (tot/β)	Power (tot/β)	Peak (tot/β)	Power (tot/β)
1	F,16	+	9	EM +/− Ab, FO	+	ETS, LEV, PER, VPA	Borderline IQ, anxiety	Normal/normal NGS epilepsy panel	Bi‐F, bi‐O, Gen	Grade 5a/+	EM +/− Ab: gen (PO prev) FO: Right O S/SsW	9.8/ 14.4	48.3/ 16.3	1/ 13.2	25.9/ 7.7
2	F,18	−	12	EM +/− Ab	+	ETS, ZNS	Borderline IQ, functional seizures	Normal/ not done	Bi‐FC, bi‐O, Gen	Grade 5a/+	EM: Bi‐O→Gen EM: Gen	7.8/ 14.8	197.5/ 53.6	6.3/ 13.9	62.9/ 34.8
3	F,19	−	6	EM +/− Ab	+	ETS, LTG, VPA, ZNS	Borderline IQ	Normal/ not done	Bi‐PO, Gen	Grade 5b/+	EM +/− Ab: Bi‐O→Gen	12.7/ 13.2	78.8/ 91.3	4.6/ 13.fa	13.2/ 13.8
4	F,18	NA	10	EM +/− Ab, BTCS	+	LEV, LTG, PER, ZNS	Normal IQ, high‐functioning ASD	Normal/ not done	Right‐O, Bi‐O, Gen	Grade 5a/+	EM: Bi‐O→Gen EM: Bi‐O EM: Gen	8.5/ 18.3	69.5/ 35.6	1.5/ 17.3	23.8/ 6.2
5	F,16	+	8	EM+/− Ab, Ab, BTCS	+	AZM, ETS, LEV, VPA, ZNS	Normal IQ, low weight at birth and IUGR.	Normal/normal NGS epilepsy panel and array‐CGH	Right‐F, Right‐O, Bi‐O, Gen	Grade 5a/+	EM: Gen	15.1/ 15.1	39.5/ 97.3	2.45/ 15.8	10.8/ 16
6	F,23	+	14	EM +/− Ab, BTCS	+	LEV, ZNS	Specific learning difficulties	Not done/ not done	Bi‐F, Bi‐PO, Gen	Grade 3/+	EM: Gen	12.7/ 13.2	52.65/ 46.3	1.5/ 13.2	38.4/ 15.5
7	M,55	−	6	EM, BTCS	+	CBZ, LEV, LTG	Normal IQ, high‐functioning ASD	Not done/ not done	LeftF, Gen	No (Grade 2)/+	EM: Gen	6.3/ 16.35	64.95/ 29.3	3.9/ 16.6	40.9/ 18.4
8	F,12	−	2	EM +/− Ab	+	LTG, VPA	Borderline IQ, autistic traits	Normal/CHD2 c.693‐3C>G; p NA	Right FCT, Gen	Grade 5a/+	EM: Bi‐O→Gen	7.55/ 13.2	243.3/ 63.9	1.5/ 14.4	41.25/ 25.75
9	F,15	−	9	EM, BTCS	−	BRV, STM	Borderline IQ, ADHD, autistic traits, migraine	Normal/ normal	Right‐O, Bi‐PO, Gen	Grade 5a/+	EM: Gen	14.2/ 14.2	441.8/ 534.5	5.6/ 14.2	43.4/ 64.4
10	F,14	+	9	EM	−	LEV, VPA	Normal IQ	Not done/ not done	Right PO, Bi‐PO, Gen	Grade 5a/+	EM: Bi‐PO→Gen	6.1/ 15.6	133.3/ 129.7	5.1/ 15.3	25.1/ 16.9
11	F,20	+	5	EM +/− Ab, BTCS	+	LEV, LTG, VPA	Normal IQ; low stress‐threshold	Normal/ not done	Bi‐TPO, Bi‐FT, Gen	Grade 5a/+	EM: Bi‐PO→Gen	8.1/ 17.14	85.34/ 108.88	5.3/ 17	79/ 39.6
12	F,23	+	3	EM +/− Ab, BTCS	+	ACZ, CLB, ETS, LEV	Normal	Normal/ not done	Bi‐O, Right TO, Gen	No (Grade 2)/+	EM: Bi‐PO→Gen	8.5/ 14.5	541.25/ 1053.85	3.25/ 14.25	297.1/ 334.1
13	F,21	NA	4	EM +/− Ab, BTCS	+	LEV, VPA, ZNS	Normal IQ	Normal/ not done	Gen	NA/+	EM: Bi‐PO→Gen	10.9/ 16.1	46.5/ 47.25	6.1/ 16.1	21.7/ 16.5
14	F,18	−	11	EM +/− Ab, BTCS	+	ETX, LEV, VPA	Normal IQ	Normal/ not done	Bi‐O; Gen	Grade 5a/+	EM: Bi‐PO→Gen	13/ 13.5	235.1/ 432.8	2/ 14.25	16.25/ 20.4
15	F, 17	NA	8	EM +/− Ab	+	LEV, TPM	Normal IQ	Not done/ not done	Bi‐F; Bi‐PO; Gen	Grade 5a/+	EM: Bi‐PO→Gen	7.5/ 13.9	17.2/ 31.8	6.3/ 15.6	13.6/ 11.9
16	F, 24	+	9	EM +/− Ab, BTCS	+	ETX, LEV, LTG, OXC, PER, TPM, VPA, ZNS	Normal IQ	Normal/ normal	Bi‐F; Bi‐PO; Gen	Grade 5a/+	EM: Bi‐PO→Gen	13.7/ 13.7	67.9/ 97.8	2/ 13.9	34.7/ 31.25
17	F, 24	−	3	EM +/− Ab	+	ETX, LEV, LTG, VPA	Mild ID	Not done/CHD2 c.2087delT; p.Phe696SerfsTer38	Bi‐TPO; Bi‐FC; Gen	Grade 5a/+	EM: Bi‐PO→Gen EM: Gen	14.85/ 15.1	76.4/ 119.8	14.6/ 14.8	19/ 43.3
18	F, 21	−	NA	EM +/− Ab	+	BRV, ETX, LEV, VPA	Learning difficulties, ADHD	Not done/ normal	Bi‐PO; Gen	Grade 5a/+	EM: Bi‐PO→Gen	13.4/ 14.1	35.4/ 66.6	3.6/ 14.1	8.7/ 12
19	F, 48	+	8	EM, BTCS	+	CLB, LEV, LTG, VPA, ZNS	Normal IQ	Normal/ normal	Gen	Grade 5a/+	EM: Bi‐PO→Gen	12/ 15	37/ 71.9	10.5/ 14.5	5.4/ 13.4
20	F,13	+	3,5	EM, BTCS	+	ESM, LEV, LTG, VPA, ZNS	Normal IQ, ADHD	Normal/ not done	Bi‐PO; Bi‐FC; Gen	Grade 5a/+	EM: Bi‐PO→Gen Ab: Gen	9/ 14.2	133/ 168.5	6.1/ 13.2	33.1/ 29.5
21	F,12	−	4	EM +/− Ab	+	CLB, ESM, LEV, LTG, VPA	Normal IQ	Normal/not done	Bi‐CPO; Bi‐FCP; Gen	Grade 5a/+	EM: Bi‐PO→Gen EM: Gen Ab: Gen	11.2/ 15.6	38.6/ 44.1	4.9/ 14.2	20.2/ 11.7

Abbreviations: Ab, absence, ASD, autism spectrum disorder, AZM, acetazolamide, BRV, brivaracetam, CBZ, carbamazepine, CLB, clobazam, CPO, centroparietooccipital, ED, epileptiform discharge, EM, eyelid myoclonia, ETS, ethosuximide, F, frontal, FC, frontocentral, FCP, frontocentroparietal, FCT, frontocentrotemporal, FO, focal occipital, Gen, generalized, GTCS, generalized tonic–clonic seizures, IED, interictal epileptiform discharges, IQ, intelligence quotient, IUGR, intrauterine growth restriction, LEV, levetiracetam, LTG, lamotrigine, O, bioccipital, PhS, photosensitivity, PO, parietoccipital, PPR, photoparoxysmal response; SsW, Spike and slow Wave; STM, sulthiame, tot, total, TPO, temporoparietooccipital, VPA, valproic acid, ZNS, zonisamide.

3.2. Video‐EEG analysis

We analyzed 85 video‐EEG recordings (31 including sleep). The mean number of EEG recordings for each patient was 4 (range: 2–9) and the mean age at recording was 14.4 years (range: 2–52 years).

The interictal EEG showed generalized EDs (g‐EDs) in all patients (51/85 EEG studies), consisting of spike‐and‐waves (SW) in 11 of 21 (52%) (31/51 EEG studies), poly‐spikes (poly‐S) in 8 of 21 (38%) (15/51 EEG studies) and poly‐SW in 8 of 21 (38%) (16/51 EEG studies). g‐EDs were observed during wakefulness and sleep in 11 of 21 patients (52%) patients, only during sleep in 6 of 21 (29%), and only during wakefulness in 4 of 21 (19%).

Nineteen of 21 patients (90%) (51/85 EEG studies) also had focal EDs (f‐EDs), in the posterior regions (9/19, 47%; 31/51 EEG studies), in the anterior regions (2/19, 11%; 8/51 EEG studies), or both anteriorly and posteriorly (8/19, 42%; 12/51 EEG studies). The posterior f‐EDs were bilateral in all patients (22/31 EEGs, in 9/31 EEG studies also unilateral). The anterior f‐EDs were unilateral in five of eight and bilateral in three of eight EEG studies. The morphology of the f‐EDs consisted of spikes (S) in 15 of 19 patients (79%) (36/51 EEG studies), SW in 8 of 19 (42%) (14/51 EEG studies), sharp waves (ShW) in 4 of 19 (21%) (7/51 EEG studies), poly‐S in 4 of 19 (21%) (7/51 EEG studies), and poly‐SW in 2 of 19 (11%) (2/51 EEG studies). Ten of 19 patients (53%) showed f‐EDs during wakefulness and sleep and 9 of 19 (47%) only during wakefulness.

The intermittent photic stimulation induced a PPR in all but two patients (95%) (47/85 EEG studies): Grade 3 (8 EEG studies), Grade 4a (26 EEG studies), Grade 5a (39 EEG studies), and Grade 5b (3 EEG studies). IPS provoked seizures in 12 of 21 patients (57%; 11 EM, 1 EM‐absences). Hyperpnea induced g‐EDs in 12 of 21 (57%) and absences in 5 of 22 (23%) patients.

All patients showed EM (64/85 EEG studies) on eye closure, with an EEG correlate consisting of g‐EDs (57/85 EEG studies): SW (42/85), poly‐SW (18/85), and/or poly‐S (46/85). A focal posterior discharge preceding the g‐EDs was evident in 16 of 21 patients (76%) (36/57 EEG studies), consisting mainly of S (>13 Hz) or spiky beta activity (15/16, 29/36 EEG studies). In one patient (Patient 4), the EEG correlate remained restricted to the occipital regions. In another patient (Patient 1), during long‐term video‐EEG‐monitoring for EM‐absences quantification, we recorded a focal seizure with a subtle semiology followed by amnesia (Video S1). This seizure had occipital onset with frontal spreading (Figure 1B) and was preceded by a series of eye closure–induced EM. This patient otherwise had a typical EEM phenotype (Data S1).

FIGURE 1.

Integrated quantitative electroencephalography (EEG) analysis. (a) Patient 1 ‐ interictal EEG (with EEG amplitude map and source analysis): Interictal abnormalities are observed in both the occipital (A) and frontal (A') regions. Patient 1 ‐ Eyelid Myoclonia (EM): A posterior‐to‐anterior progression of the epileptiform discharges is observed after eye closure (A‐ > B‐ > C) as shown in the EEG traces, amplitude maps, and source analysis. Patient 2 ‐ EM: Two episodes show a posterior‐to‐anterior spread of epileptic discharges after eye closure (A‐ > B‐ > C; A'‐ > B′‐ > C′), based on EEG traces, amplitude maps, and source analysis. Patient 3 ‐ EM‐Absence: A similar posterior‐to‐anterior progression is observed (A‐ > B‐ > C‐ > D) after eye closure. (b) Patient 1 ‐ EM (detailed above) followed by a right occipital focal onset seizure: The seizure begins with a rhythmic activity in the right occipital region (A), then spreads anteriorly (B), and ends with a rhythmic sequence of high amplitude spikes in the right occipital region (C). Amplitude and source analysis maps confirm a right occipital onset of the focal seizure.

The spectral frequency analysis of the first‐second EEG epoch following eye closure, corresponding to EM, showed in the occipital regions a main peak in the alpha band (mean frequency 10.8 Hz; power 128.6 μV²) and a second peak in the beta band (mean frequency 14.8 Hz; power 159.7 μV²). The same analysis in the frontal regions showed a main peak in the theta‐delta band (mean frequency 4.9 Hz; power 41 μV²) followed by a peak in the beta band (mean frequency 14.7 Hz; power 37.3 μV²).

The amplitude map analysis documented a posterior onset and prevalence of the ictal EDs related to EM in 18 of 21 (86%) patients with subsequent rapid anterior propagation (Figure 1A), whereas in 3 of 21 (18%), a more widespread network was simultaneously involved. The source analysis of averaged generalized S confirmed a predominant occipital representation of the g‐EDs (Figure 1A).

4. DISCUSSION

For the first time, we propose an integrated quantitative EEG evaluation in a homogenous cohort of patients with typical EEM (Jeavons syndrome). ¹ Our data suggest a pivotal role of the occipital lobe in both interictal and ictal discharges.

Over the years, the analysis of EEG interictal/ictal focal abnormalities in EEM has highlighted the key role of the occipital lobe, defined as an “epileptic generator” that spreads to the thalamocortical and transcortical networks. ⁹ Indeed, in more than half of patients with EEM, posterior interictal EDs have been detected, often accompanied by time‐locked PPR, ⁹ and an “alpha squeak” after starting ASMs. ¹⁰ A predominance of posterior EDs, preceding the g‐EDs, has also been described in relation to EM. ¹¹

In one patient with typical electroclinical EEM features, we recorded an occipital seizure with subtle semiology, preceded by a series of eye closure–induced EMs, and followed by amnesia for the episode. Focal seizures are usually considered a criterion for reconsidering the diagnosis of EEM. ¹ , ³ However, another “incidental” occipital seizure and two cases with postictal occipital slowing have been reported previously in patients with EEM. ⁵ , ⁶ A recent large study showed that 8.6% of subjects with EEM have focal seizures, ⁴ suggesting a potential underestimation of focal seizures in EEM.

The intrinsic hyperexcitability of the occipital lobe has been recognized as central in the pathophysiology of EEM, alongside alterations of the alpha rhythm generator system observed in photosensitive epilepsies. ⁶ , ¹² The brainstem and its close connection with the occipital lobe have also been considered crucial in the genesis of EM. ¹⁰

EEG correlated functional magnetic resonance imaging (EEG‐fMRI) studies in EEM showed that eye closure activates a network involving the visual cortex, the thalamic pulvinar (implicated in alpha rhythm generation), and cortical areas involved in gaze and eye closure control (intraparietal sulcus and premotor cortex). ¹² The thalamus activation has been associated primarily with generalized SW discharges ¹³ (Figure 2).

FIGURE 2.

Schematic representation of the extended pathophysiological network in epilepsy with eyelid myoclonia (EEM). The occipital lobe plays a central role in EEM. Eye closure and intermittent photic stimulation synchronize neuronal activity in the occipital visual cortex and the thalamic pulvinar, both involved in alpha rhythm generation. This activity spreads to the brainstem, intraparietal sulcus, and premotor cortex—regions implicated in eye closure control—contributing to the ictal transformation that leads to the photo‐myoclonic response. Thalamocortical interactions are essential for the generation of generalized spike‐and‐wave discharges underlying absence seizures (Liu et al., 2008 ¹³ ; Striano et al., 2009 ¹⁰ ; Vaudano et al., 2014 ¹² ). Created in BioRender https://BioRender.com/u0hi451.

EM are not pathognomonic of any specific epilepsy syndrome. Rather, they reflect the involvement of a shared pathophysiological network originating in the occipital lobe, underlying photosensitivity in idiopathic generalized epilepsies (IGEs)/GGEs, in certain developmental epileptic encephalopathies (DEEs) as well as in some focal occipital epilepsies, ¹⁴ through distinct etiopathogenetic mechanisms. Recently some authors have proposed considering POLE as a subtype of EEM ⁶ ; however, a similar argument could apply to POLE and other GGEs/IGEs with photosensitivity. It is not uncommon for pediatric patients to experience multiple types of epilepsy, both self‐limited and generalized, either concurrently or sequentially.

In line with the ILAE classification, we believe that POLE and EEM should be considered two distinct epilepsy syndromes, each with unique electroclinical features, cognitive/behavioral profiles, and prognoses. We propose that POLE and EEM may be considered different expressions of the same phenotypic spectrum, affecting a shared neural network, consistent with the concept of system epilepsy. ¹⁵

From a practical perspective, it is important to highlight the potential coexistence of focal occipital and generalized seizures in EEM, particularly given their likely underestimation due to subtle ictal clinical manifestations. Further studies with prolonged video‐EEG monitoring could help better estimate the true incidence of focal seizures in EEM, and a reconsideration of the exclusion criteria for EEM may be warranted. Such considerations are essential for optimizing EEM diagnosis, follow‐up, and treatment strategies.

AUTHOR CONTRIBUTIONS

Emilia Ricci collected and analyzed data and wrote the manuscript. Tomasz Stanislaw Mieszczanek, Monica Zilmer, Katarzyna Cebula, Stefan Juhl, Marina Nikanorova, Katarzyna Maria Mieszczanek, Marianne Sondergaard Khinchi, Britta Inga Ulfsdotter Hesslow, Kristin Siølie Thygesen, Charlotte Reinhardt Pedersen, Kern Olofsson, and Stephan Wüstenhagen collected data. Rikke S Møller collected data and revised the manuscript. Guido Rubboli collected data and revised the manuscript. Sándor Beniczky analyzed data and revised the manuscript. Elena Gardella conceived and designed the study, supervised all the study development, and revised the manuscript.

CONFLICT OF INTEREST STATEMENT

The authors don't have any conflict of interest to disclose. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

Supporting information

Data S1.

Figure S1.

Table S1.

Video S1.

Ricci E, Mieszczanek TS, Zilmer M, Cebula K, Juhl S, Nikanorova M, et al. Unmasking the role of the occipital lobe in epilepsy with eyelid myoclonia. Epilepsia. 2025;66:e194–e201. 10.1111/epi.18477

DATA AVAILABILITY STATEMENT

Anonymized data supporting the clinical report are available from the corresponding author on reasonable request. Sensitive data containing information that can compromise patients’ privacy will not be publicly available.