Singh, Bansal, More, Bhuyan, and Garg: Eating Epilepsy in North India: Case Series and Its Management


Eating epilepsy is a rare form of reflex epilepsy where seizures are triggered by eating. We describe a case series of 12 such patients presenting to our epilepsy clinic based in North India. Eating epilepsy was noted to have male predominance with focal seizures with impaired awareness. Most of these patients had either temporal or perisylvian localization. Clobazam taken half an hour before meal was found to be an effective add-on therapy in its management.


Reflex epilepsy is a type of epilepsy in which seizures are provoked habitually by external stimulus or uncommonly by internal mental process.1 Eating epilepsy (EE) is a distinct subtype of reflex epilepsy, where seizures are triggered by the act of eating. The first case of EE was described as early as 1967 in which seizures were triggered during meals and even at the mear sight of meal.2 This variant though scantly reported in other parts of world, has been widely reported from Indian subcontinent in last 2–3 decades.3,4 Seizures usually happen during or few minutes after meals.5 Eating is a complex process which starts from thought of food to satisfactory feeling of satiety after eating. It involves many stimuli which may have different pathophysiology in seizure occurrence in patients with EE.
Electroencephalogram (EEG) and functional neuroimaging evidence suggest involvement of complex perisylvian neuronal circuits.6 Many of these patients are not well controlled of seizures despite polytherapy. We describe case reports here to present various characteristics of EE in our patient series from North India.

Case Report

A total of 12 patients out of 1,532 patients presenting to epilepsy clinic were detected to have EE in 18 months (January 2015 to June 2016). Age and duration of seizure onset, seizure semiology and on-going medications, their EEG and magnetic resonance imaging (MRI) brain findings were tabulated as variables (Table 1). A follow up after 6 months was done during their scheduled visit or telephonically for assessing treatment response (Table 2). Categorical variables were summarized using counts and percentages. Quantitative variables were summarized using mean and standard deviation or median and interquartile range (IQR).
Of them, 11 patients (91.7%) were male. Median age at presentation was 24 years (21.5, 27.5) and median age at onset of seizures was 13.5 years (10.5, 23.0). None of them had a family history of seizure disorder. Nine patients (75%) reported ‘eating’ as the only triggering stimuli. Others (three patients, 25%) had an additional trigger such as anxiety, while bathing or spontaneously. Majority of the patients (seven patients, 58.3%) developed seizures either during lunch or dinner. Rest of them (five patients, 41.7%) had no such predilection to any meal. Semiology of seizures was variable and complex in most of them. Four patients (33.3%) had aura preceding the events. Most of them (11 patients, 91.7%) had focal onset seizures. Focal onset impaired awareness seizures were noted in nine of them while focal to bilateral tonic clonic type was present in seven of them. Only one patient (8.3%) had generalized onset tonic seizures (Table 1).
All patients underwent routine EEG recording during meals. Five of them (41.7%) had temporal or centrotemporal interictal epileptiform discharges (IEDs) in form of spikes while one of them (8.3%) had bilateral posterior head region IEDs. Six patients (50%) had normal EEG during eating. Neuroimaging (MRI brain) was abnormal in five patients (41.6%). Two had bilateral lesions and three had unilateral lesions. Three patients had perisylvian gliosis, one had right frontal lesion and one had right temporal lesion. Eight patients (75%) had MRI and/or EEG abnormality confined to perisylvian region (Table 1).
Eleven out of 12 patients were on adequate doses of antiepileptic drugs at presentation. They were started on clobazam, a benzodiazepine antiepileptic in doses of 5 to 10 mg half hour prior to meals. Addition of clobazam, led to reduction in seizure frequency in nine out of 11 patients (81.8 %). Of these nine patients, four became seizure free for many months together. One did not show any response while one had increase in seizure frequency after addition of clobazam. One patient (patient No. 9) improved by optimizing his ongoing antiepileptic drug therapy without addition of clobazam (Table 2).


Eating epilepsy is a rare subtype of reflex epilepsy. Because of unknown reasons it has been widely reported from Indian subcontinent38 and only scarcely reported as small case series9,10 or case reports1113 from other parts of the world. A maximum prevalence of eating epilepsy is 5.6% of all epilepsy cases, which has been reported from Srilanka.5 In our north Indian study, it is noted to be less than 1% (0.78%, 12 in 1,532). The world over prevalence of eating epilepsy is considered to be 0.05 to 0.1% of all epilepsies.11 EE has male predominance3,710 and the usual age of onset of symptoms is 2nd decade.36 In our case series, we also observed similar clinical characteristics.
Various authors have noted significant heterogeneity in triggers for these seizures. Act of mastication while eating,2 oesophageal stimulation,14 satisfactory feeling of having meal,15 timing of the meal,10,16 sight, smell or even thought of food17 have been described in different groups of patients worldwide. Heavy carbohydrate rich meals traditionally consumed in Indian subcontinent particularly during lunch and dinner could be one of the factors contributing to its high prevalence in predisposed individuals.3,8
Since these seizures occur in relation to food, EE is almost exclusively a symptomatic focal epilepsy.11 Multiple case reports and case series have reported focal aetiologies like cortical malformation,13,18 hypoxic brain damage,12 meningoencephalitis19 or space occupying lesions6,9,20 involving temporal lobe8,12,16,20 and perisylvian area.6,9,19 Sometimes they may not have any structural lesions on neuroimaging4,9 In our series majority of the patients had either MRI or EEG abnormality localizing to perisylvian region. Apart from these acquired causes, cases of defined genetic etiology in pediatric population with mutations in SYNGAP1 gene21 and duplication of MECP2 gene22 have been described. Cluster of familial cases with EE have also been reported by Senanayake23 and Yacubian et al.24
The predominant semiology was sudden unresponsiveness, staring look with or without subtle tonic posturing of limbs. Eyelid myoclonia with short absences with tonic, atonic or myoclonic movements of limbs or trunk has been described in intellectually disabled children with SYNGAP1 mutation, especially around meals.21 One third of our patients described nonspecific aura prior to seizures. The aura was described as light or heavy headedness, uneasiness, or epigastric sensation suggesting a temporal lobe onset. The seizures characteristically are focal onset with impaired awareness.7 These focal seizures may generalize to tonic, atonic or myoclonic seizures infrequently.25 Our 11 out of 12 patients had focal onset seizures.
IEDs have diagnostic as well as localization significance in these patients. Most studies have found focal IEDs at temporal and centro-temporal areas of brain3,10,16 in up to 70% of patients.3 Continuous EEG recording during meals increases the frequency of these discharges and could also precipitate ictus. Ictal discharges consist of focal slowing or fast beta activity during these episodes.6 Ictal and interictal EEG in most of these patients showed fronto-central or temporal discharges3,6,911,12 even in MRI negative patients. Our six patients had a similar distribution of IEDs. Children with SYNGAP1 mutation have shown short duration 3/sec irregular high amplitude spike and wave discharges in temporal and occipital areas.21
Positive neuroimaging findings such as gliosis, encephalomalacia or space occupying lesions have been noted either at temporal lobe9,12,16,20 or perisylvian areas6,18,19 in some of the patients irrespective of the side involved. Our neuroimaging positive patients also had gliosis either at perisylvian area or inferior frontal and temporal lobes. These locations represent opercular area which innervates facial, pharyngeal, masticatory, tongue, laryngeal and branchial muscles. Ictal SPECTand EEG may be of help in localization and determining the extent of lesion5,19 specially in MRI negative patients.
The studies suggest eating to be a complex process which leads to activation of opercular cortex and generation of multiple efferent sensory. Investigators have suggested two different type of syndromes. The one with involvement of temporo-limbic region has reflex eating seizures from onset of epilepsy. Triggers usually constitute gustatory, olfactory, autonomic and emotional stimuli. Seizures in this syndrome may occur during any time of meal. The other syndrome involving extralimbic/suprasylvian region (extratemporal) which precipitates reflex eating seizures in previously existing epileptic disorder. Seizures usually precipitate during first few minutes of a meal because of proprioceptive sensory stimuli from complex lingual, buccal and pharyngeal movements.10 These sensory stimuli lead to recruitment of epileptogenic neurons triggering a critical mass of cortex to precipitate seizures.26 Recently it has been suggested that hyperexcitability of perisylvian/opercular region (including insular cortex) leads to EE irrespective of the side of lesion.6,25 Three fourth of patients in our study had perisylvian electrographic or neuroimaging localization.
Available literature suggests variable treatment response ranging from good control3,9 to treatment refractory EE.10 Clobazam was found to be useful in less than 10% of a large Srilankan study.3 We used clobazam in 11 patients. Patients were asked to consume 5 mg or 10 mg of clobazam half hour prior to meal in addition of their pre-existing antiepileptic drugs in adequate doses. On 6 months follow up, nine of 11 patients had responded with decrease in number of seizures. Four of these showed excellent response and became seizure free for months together. Clobazam has also been found effective in patients with another form of reflex seizures known as hot water epilepsy.27 However, none of our patients was on monotherapy with clobazam. Clobazam has GABA-A agonist action similar to many other antiepileptic drugs. The precise mechanism of clobazam for its role in EE is not known. Though good response to clobazam addition was seen, we cannot suggest its efficacy as monotherapy. A bigger study with larger sample size and long term follow up may help to evaluate its efficacy.

Table 1
Demographics, seizure semiology, EEG and neuroimaging of patients with eating epilepsy
No. Age (years) Sex Age of onset (years) Trigger stimuli Triggering meal Seizure semiology Type of seizures Seizure frequency before clobazam (per week) Family history EEG Neuroimaging (MRI brain)
1 24 M 15 Eating L, D Aura-Vague uneasiness; Ictus-Sudden onset staring followed by manual automatisms and ictal speech. Focal onset impaired awareness 7–14 None Frequent left posterior temporal IEDs with secondary generalization Normal
2 28 M 21 Eating L, D Aura-None; Ictus-Sudden unresponsiveness for few seconds associated oromandibular automatisms sometimes is followed by posturing of all limbs Focal onset impaired awareness, focal to bilateral tonic clonic 7–14 None Normal Right temporal sclerosis
3 22 M 10 Eating L, D Aura-None; Ictus-Behavioral arrest followed by eyes to one side and posturing of both upper limbs (right>left). Sometimes clonic movement in fingers. Focal to bilateral tonic clonic 5–7 None Normal Bilateral perisylvian gliosis
4 19 M 8 Eating Any Aura-Giddiness; Ictus-Fall, tonic posturing of limbs with salivation. Followed by prolonged sleepiness. Generalized tonic 14–21 None Left centro-temporal IEDs Left inferior frontal gliosis
5 14 M Birth Eating, anxiety Any meal, Fluids Aura-None; Ictus-Sudden onset stare with behavior arrest followed by subtle tonic posturing of limbs with neck deviation for few seconds. Focal to bilateral tonic clonic 21–28 None Bilateral peri-rolandic spike Bilateral perisylvian gliosis (left>right)
6 31 M 27 Eating, spontaneous Any Aura-None; Ictus-Sudden onset unresponsiveness, stare, not able to talk for 1–2 minutes. Focal onset impaired awareness 1 None Right posterior head region and left temporal spikes Normal
7 27 F 12 Eating L, D Aura-Epigastric rising sensation, heaviness in head; Ictus-Behavioral arrest wit spontaneous recovery in lass than a minute, sometimes develops tonic clonic movements of right UL/LL followed by all 4 limbs; post ictal weakness of right UL for about 5–10 minutes. Focal onset impaired awareness, focal to bilateral tonic clonic 1 None Normal Normal
8 22 M 12 Eating Any Aura-None; Ictus-Sudden staring look. Oro-mandibular automatisms for about few seconds followed by headache and sleep. Occasionally progresses to generalized seizures with tonic clonic movements. Focal onset impaired awareness, focal to bilateral tonic clonic 0.5–1 None Normal Normal
9 51 M 31 Eating Any Aura-Cephalic sensation; Ictus-Behavioral arrest, stare, spontaneously recovers to normal in 30–40 seconds. No post ictal confusion. Focal onset impaired awareness 2–3 None Normal Normal
10 25 M 25 Eating, bathing L, D Aura-None; Sudden ill-defined uneasiness, some involuntary movements over the jaw region with restlessness for few seconds followed by loss of consciousness for 1–2 minutes. Sleeps thereafter. Focal onset impaired awareness 0.5 None Normal Right frontal perisylvian sclerosis
11 24 M 11 Eating L, D Aura-None. Will complain of sudden sleepiness during later part of meals and will doze off for one minute. Rare episodes of GTCS in past. Focal onset impaired awareness, Focal to bilateral tonic clonic 3–4 None Right centro-temporal IEDs Normal
12 21 M 18 Eating L, D Aura-None. Suddenly feels headache, uneasiness followed by staring look lasting for 40–50 seconds. Sometimes induces vomiting for relief from uneasiness. Rare episodes progressing to bilateral tonic clonic movements with post ictal confusion. Focal onset impaired awareness, focal to bilateral tonic clonic 4–7 None Rare bilateral post head region IEDs Normal

EEG, electroencephalogram; MRI, magnetic resonance imaging; M, male; L, lunch; D, dinner; IEDs, interictal epileptiform discharges; F, female; GTCS, generalized tonic-clonic seizures.

Table 2
Treatment response on change of therapy
No. Seizure frequency before clobazam (per week) Ongoing medications New medications added to old treatment Seizure frequency after clobazam (per week) Clobazam benefit
1 7–14 LVT, OXC CLB 7–14 No
2 7–14 VPA, LCM CLB 3–4 Yes
3 5–7 CBZ, LVT CLB 1–2 Yes
4 14–21 OXC, LVT, PHB CLB 7 Yes
5 21–28 OXC, LVT CLB 0 Yes
6 1 OXC, LCM CLB 1–2 No
7 1 OXC, LVT CLB 0.06 (1/3–4 months) Yes
8 0.5–1 CBZ CLB 0.25 Yes
9 2–3 VPA, TPM (inadequate dose) TPM (dose increases) 0 (none since 20 months) Not on clobazam
10 0.5 LVT, LCM CLB 0 (none since 5 months) Yes
11 3–4 PHT CLB 0.25–0.75 Yes
12 4–7 VPA CLB 0.25 Yes

LVT, levetiracetam; OXC, oxcarbazepine; CLB, clobazam; VPA, valproate; LCM, lacosamide; CBZ, carbamazepine; PHB, phenobarbitone; TPM, topiramate.


1. Striano S, Coppola A, del Gaudio L, Striano P. Reflex seizures and reflex epilepsies: old models for understanding mechanisms of epileptogenesis. Epilepsy Res. 2012;100:1–11.
crossref pmid
2. Scollo-Lavizzari G, Hess R. Sensory precipitation of epileptic seizures. Report on two unusual cases. Epilepsia. 1967;8:157–61.
crossref pmid
3. Senanayake N. ‘Eating epilepsy’--a reappraisal. Epilepsy Res. 1990;5:74–9.
crossref pmid
4. Jagtap S, Menon R, Cherian A, Baheti N, Ashalatha R, Thomas SV. “Eating” epilepsy revisited- an electro-clinico-radiological study”. J Clin Neurosci. 2016;30:44–8.
crossref pmid
5. Seneviratne U, Seetha T, Pathirana R, Rajapakse P. High prevalence of eating epilepsy in Sri Lanka. Seizure. 2003;12:604–5.
crossref pmid
6. Patel M, Satishchandra P, Saini J, Bharath RD, Sinha S. Eating epilepsy: phenotype, MRI, SPECT and video-EEG observations. Epilepsy Res. 2013;107:115–20.
crossref pmid
7. Ahuja GK, Pauranik A, Behari M, Prasad K. Eating epilepsy. J Neurol. 1988;235:444–7.
crossref pmid
8. Mandal DK, Bandyopadhyay S, Tarafdar J, et al. Eating epilepsy: a study of twenty cases. J Indian Med Assoc. 1992;90:9–11.
9. Gujjar AR, Jacob PC, Ramanchandiran N, Al-Asmi A. Eating epilepsy in Oman: a case series and report on the efficacy of temporal lobectomy. Sultan Qaboos Univ Med J. 2013;13:156–61.
crossref pmid pmc
10. Kokes U, Baykan B, Bebek N, Gurses C, Gokyigit A. Eating epilepsy is associated with initial precipitating events and therapy resistance. Clin EEG Neurosci. 2013;44:161–6.
crossref pmid
11. Rémillard GM, Zifkin BG, Andermann F. Seizures induced by eating. Adv Neurol. 1998;75:227–40.
12. Loreto V, Nocerino C, Striano P, D’ Aulos F, Boccella P, Striano S. Eating epilepsy. Heterogeneity of ictal semiology: the role of video-EEG monitoring. Epileptic Disord. 2000;2:93–8.
13. Verdú A, Ruiz-Falco ML. Eating seizures associated with focal cortical dysplasia. Brain Dev. 1991;13:352–4.
crossref pmid
14. Forster FM. Epilepsy associated with eating. Trans Am Neurol Assoc. 1971;96:106–9.
15. Cirignotta F, Marcacci G, Lugaresi E. Epileptic seizures precipitated by eating. Epilepsia. 1977;18:445–9.
crossref pmid
16. Nagaraja D, Chand RP. Eating epilepsy. Clin Neurol Neurosurg. 1984;86:95–9.
crossref pmid
17. El Bouzidi K, Duncan S, Whittle IR, Butler CR. Lesional reflex epilepsy associated with the thought of food. Neurology. 2010;74:610–2.
crossref pmid pmc
18. Kishi T, Moriya M, Kimoto Y, Nishio Y, Tanaka T. Congenital bilateral perisylvian syndrome and eating epilepsy. Eur Neurol. 1999;42:241–3.
crossref pmid
19. Mateos V, Salas-Puig J, Campos DM, Carrero V, Andermann F. Acquired bilateral opercular lesions or Foix-Chavany-Marie syndrome and eating epilepsy. J Neurol Neurosurg Psychiatry. 1995;59:559–60.
20. Manyam SC, Kung DH, Rhodes LB, Newmark ME, Friedman DE. Unilateral opercular lesion and eating-induced seizures. Epileptic Disord. 2010;12:309–13.
21. von Stülpnagel C, Hartlieb T, Borggräfe I, et al. Chewing-induced reflex seizures (“eating epilepsy”) and eye closure sensitivity as a common feature in pediatric patients with SYNGAP1 mutations: review of literature and report of 8 cases. Seizure. 2019;65:131–7.
crossref pmid
22. de Palma L, Boniver C, Cassina M, et al. Eating-induced epileptic spasms in a boy with MECP2 duplication syndrome: insights into pathogenesis of genetic epilepsies. Epileptic Disord. 2012;14:414–7.
crossref pmid
23. Senanayake N. Familial eating epilepsy. J Neurol. 1990;237:388–91.
crossref pmid
24. Yacubian EMT, Skaff R, Garzon E, et al. Seizures induced by eating in a family. Wolf P, Inoue Y, Zifkin B, editors. Reflex epilepsies: progress in understanding. Montrouge: John Libbey Eurotext; 2004. p. 123–33.

25. Narayan S, Nair P, Murgai A, Sharma P, Wadwekar V. Eating epilepsy, redefining the semiology (P07.173). Neurology. 2013;80:7 Supplement. P07.173.

26. Wieser HG. Seizure induction in reflex seizures and reflex epilepsy. Adv Neurol. 1998;75:69–85.
27. Satishchandra P, Sinha S. Hot-water epilepsy: from bench to bedside. Ann Indian Acad Neurol. 2013;16:137–43.
crossref pmid pmc