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Revista mexicana de neurociencia

versión On-line ISSN 2604-6180versión impresa ISSN 1665-5044

Rev. mex. neurocienc. vol.22 no.5 Ciudad de México sep./oct. 2021  Epub 25-Oct-2021 

Review articles

Eating epilepsy. A narrative review

Epilepsia refleja por alimentación. Una revisión narrativa

Mariana Ruiz-León1 

Marco A. Sánchez-Torres2 

Sonia Luquin-de Anda2 

Mónica E. Salmerón-Mercado3 

José L. Ruiz-Sandoval2  4  * 

1Department of Neurology, Hospital Civil de Guadalajara Fray Antonio Alcalde. Guadalajara, Jalisco, Mexico

2Department of Neurosciences, Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara. Guadalajara, Jalisco, Mexico

3Department of Neurophysiology, Hospital Civil de Guadalajara Fray Antonio Alcalde. Guadalajara, Jalisco, Mexico

4Instituto de Neurociencias Traslacionales. Guadalajara, Jalisco, Mexico


Eating epilepsy (EE) is rare reflex epilepsy in which seizures are triggered by mechanisms related to the eating process. In this narrative review, we analyzed case series and case reports found in the literature and describe sociodemographic, semiological, and radiological characteristics of patients with EE in the general population. Our analysis revealed that this epilepsy is more common in male patients and usually presents with focal onset seizures. There is wide variability in clinical presentation and there is not enough evidence to affirm that there is a specific food or diet that triggers the seizures. Temporolimbic and suprasylvian areas of the frontal and temporal lobes, particularly the insular and opercular cortex, play an important role in the pathophysiology of EE as found in neuroradiological and neurosurgical studies. As for the treatment, there is a high prevalence of pharmacoresistance and clobazam was the most used antiepileptic drug, usually as an add-on therapy.

Key words Eating epilepsy; Eating seizures; Reflex epilepsy; Reflex seizures


La epilepsia por alimentación es un tipo de epilepsia refleja poco frecuente, en donde las crisis epilépticas son detonadas por mecanismos relacionados con el proceso de alimentación. En esta revisión narrativa analizamos reportes y series de casos de este tipo de epilepsia en la población general y detallamos características sociodemográficas, semiológicas y radiológicas. Nuestro análisis reveló que la epilepsia por alimentación es más prevalente en el sexo masculino y generalmente se presenta como crisis convulsivas focales. Existe una alta variabilidad en la presentación clínica y no hay evidencia suficiente para afirmar su asociación con algún tipo de alimento o dieta específica. En los estudios complementarios se encontró relación clínico-radiológica y quirúrgica en áreas temporolímbicas y suprasilvianas de los lóbulos frontal y temporal, particularmente la corteza insular y opercular, recalcando su importante papel en la fisiopatología de esta epilepsia. En cuanto al tratamiento, hay una alta prevalencia de farmacorresistencia y el clobazam fue el antiepiléptico más utilizado, generalmente en conjunto con otros fármacos.

Palabras clave Epilepsia por alimentación; Crisis epilépticas por alimentación; Epilepsia refleja; Crisis epilépticas reflejas


Reflex epilepsy (RE) or reflex seizures refers to epileptic syndromes characterized by focal or generalized seizures elicited by a specific stimulus or activity. These stimuli can be simple (visual, auditive, proprioceptive, or tactile) or complex (while eating, talking, tooth-brushing, bathing, etc.)1,2. RE estimated prevalence represents 4-7% of all epilepsies and 21% of idiopathic generalized type, being photosensitive epilepsy the most common3.

Eating epilepsy (EE) is a rare form of RE with a prevalence of 1:1000-2000 of all patients with epilepsy, although it ranges higher in Asia3-6. EE is more common in males and usually presents as focal seizures with impaired awareness which can occur before, during, and/or after eating3,4,7.

In this critical review, we aimed to answer the following questions: which are the sociodemographic, semiological, and radiological characteristics of EE in the general population?


Eating is a complex mechanism that includes olfactory, taste, somatosensory, and other interoceptive inputs, which activate brain structures such as the insular cortex, frontal operculum, orbitofrontal cortex, and the amygdala8. The hypothalamus and other components of the autonomic nervous system regulate central and peripheral homeostasis of digestion and metabolism9. These structures are of particular interest in the study of hunger, satiety, obesity, as well as eating and body image disorders such as anorexia and bulimia. Moreover, all of the aforementioned structures are well recognized as trigger zones of EE in various studies8,10.

Although the pathophysiology of EE is not clear, according to case reports and small case series in the literature, plausible mechanisms for its appearance have been proposed. A genetic involvement is shown in subjects with mutations in genes SYNGAP12, MECP211; as well as familial EE5, associated with Rett12, Cri du Chat,13,14 and congenital or acquired bilateral opercular syndromes15,16. Ethnic origin and environmental factors such as chemical composition of food, culinary habits, feeding behavior, and emotional and psychological involvement may be important in EE etiology7,17. EE can present with other epileptic syndromes, structural pathologies (malformations, tumors), and/or brain injury (hypoxic brain damage, gliosis, encephalomalacia, and meningoencephalitis)4,7,17. Therefore, it has been proposed that EE may be a long-term manifestation of an initial precipitating event in the past7,17.

Clinical presentation of EE is diverse. Seizures usually present as focal onset with impaired awareness and less commonly with generalized onset, including atonic, myoclonic, or even autonomic types3,4,7,17. EE occurs more frequently in the context of temporal or frontal lobe epilepsies4 and it usually is symptomatic or associated with imaging abnormalities in these locations (Tables 1 and 2).

Table 1 Clinical characteristics, diagnosis, and treatment of main case report series of patients with eating epilepsy 

Author/year Ahuja, 198023 Nagaraja, 198424 Koul, 198925 Senanayake, 19905 Loreto, 200026 Nakazawa, 200227 Seneviratne, 200328 Labate, 200529 Cukiert, 201022
n 3 13 50 20 3 2 28 2 3
Sex (M/F) 3/0 8/5 ND 13/7 2/1 2/0 13/15 2/0 2/1
Eating epilepsy mean age onset (year) 22 14 15.2 17 22.6 9.5 18.6 8.6 11
Triggers Eating Chewing, drinking (water), eating, snacks Chewing, swallowing ND Eating Chewing, eating, swallowing Eating Eating Eating
Meal of the day ND ND ND Lunch Meals, lunch ND ND ND ND
Moment of eating/meal After, during At the middle, at the end During After (30 min post main meal), during At sight, beginning, during After, before, during After, during Beginning, during During
Quality or quantity of meal ND Bulky meals, conventional Indian meals ND ND ND ND ND ND ND
Aura (focal aware) Numbness ND Forced thinking and memorizing, visual hallucination ND ND ND ND ND ND
Radiological abnormal findings (CT/MRI/PET/SPECT) ND ND NR ND MRI: L ventriculomegaly, R retrotrigonal hyperintensity
SPECT: Me-RT lobe focal hyperperf.
MRI: none
SPECT: R-F hyperperfusion and R-striate body hypoperf.
ND MRI: poor operculum formation with thickened Co MRI: B perisylvian polymicrogyria
Electroencephalographic abnormal findings Interictal EEG:
R-H: diffuse, unilateral Spk and Shw.
Generalized discharges.
L-FT Slw Shw.
R-T Swv bursts.
Generalized Spk.
Interictal EEG: "positive", ED. Interictal EEG:
B-MT, B-PoT Shw and Slw.
vEEG: low voltage slowed background
Ictal vEEG: high voltage Slw + diffuse Slw; R-Po Sh-Slw
Interictal vEEG: R-TF, L-T paroxysm; R-T ED
Ictal vEEG: high amplitude delta or theta
Interictal EEG: R-F Sp and Shw; R-O Sp
ND Ictal EEG: diffuse Spw, ED + diffuse attenuation
Interictal EEG: generalized Spk or poly-Spw; R-T slowing and high amplitude Shw Slw
Ictal EEG: B-T lobe onset Interictal EEG: B-T spiking; L-FC Spk
Treatment CBZ, PB, PHT CBZ, PB, PHT, PMD. Avoidance of bulky meals. CBZ, PB, PHT. Use of left hand and/or spoon. CBZ, CLB, PHT, PMD CBZ, CLB, GBP, GVG, LTG, PB, VPA CBZ, CLB, CLZ, PHT, VPA, ZNS, Fed by another person, reduced attention to the meal CBZ, VPA ACTH, CBZ, CLZ, GVG, NZ, PB, VPA CBZ, CLB, PB, OXC, VPA.
+ Vagus nerve stimulation
Pharmacoresistance ND Present in 10 ND None Present in 1 Present in 1 ND ND Present in three
Surgery None None ND None ND ND None ND R-TO resection; L-F resection
Author/year Bae, 201130 Gujjar, 201221 Patel, 201331 Kokes, 20137 Shirai 201514 Jagtap, 201632 Von Stülpnagel, 20192 Singh, 20194 Atalar, 202033
n 2 5 6 6 2 47 8 12 2
Sex (M/F) 1/1 4/1 3/3 4/2 1/1 41/6 4/4 11/1 1/1
Eating epilepsy mean age onset (year) 39.5 23.6 20.6 20 10.5 16 3 13.5 20
Triggers Eating Eating Eating, though of food Chewing (prolonged), drinking, swallowing, taking food to the mouth Chewing, eating ND Chewing, eating, orofacial stimuli Eating Eating
Meal of the day ND Lunch, midday meal ND Breakfast, dinner, lunch. Particularly Sundays Breakfast, dinner, lunch ND ND Dinner, lunch, no predilection ND
Moment of eating/meal After (immediately), during At the middle, at the end, during Beginning, at the middle Beginning, during Beginning, during After, beginning, at the end ND ND ND
Quality or quantity of meal ND ND Rice made food Overeating, pastry/salty food, solid food ND Rice, wheat-based diet ND ND ND
Aura (focal aware) Blurred vision, jamais-vu, palpitations, unpleasant fear. ND ND Dyscognitive, "experiential" ND Cephalic sensation, déjà vu, epigastric rising sensation, fear, somatosensory, vertigo, visual, ND Cephalic sensation, epigastric sensation, giddiness, uneasiness, Epigastric, visual, vertigo,
Eating reflex seizure type A, FBTC FBTC, FOIA GTC FO FBTC, FOA, FOIA FOA FBTC, FOIA, "HD" Ab, At, EM, GTC, M, Oc, To FBTC, FOIA, GT FBTC, FOIA
Radiological abnormal findings (CT/MRI/PET/SPECT) MRI: none CT: none
L-MeT sclerosis, L-T: atrophy, cortical lesion,
R-T horn dilatation.
MRI: L-FP perisylvian cortical dysplasia, R and L Sylvian and perisylvian gliosis, LF calcified granuloma.
SPECT: F hypoperf.; F, T + P-insular hyperperf.
L-F-EA meningioma, L-H sequel lesions.
L-MeT, L-LaT, O, and multifocal hypo-metabolism.
MRI: pontine and cerebellar hypoplasia MRI: PoTPO polymicrogyria.
Peritrigonal hyperintensities, pachygyria, gliosis. Me-T sclerosis. T cavernoma. F dysplasia.
B perisylvian,
F dilatation of external spaces of CSF.
B: perisylvian gliosis.
L-I-F gliosis.
R-F perisylvian sclerosis, R-T sclerosis.
MIR: "non-specific"
SPECT: L-T, L-I-F, and R-S-F hypoperf.
PET: R-T hypometabolism.
Electroencephalographic abnormal findings Ictal EEG:
L-T onset of generalized rhythmic theta and delta activity.
Interictal vEEG:
B-T: Spk.
Interictal vEEG:
L-MT onset of isolated discharges.
Interictal EEG:
R-FT, R-TP generalized Spk, Shw.
Ictal EEG: L-PT, L-FC, R-FTC slowing. R-FCT beta, theta activity. L-FCT Shw
Interictal EEG:
L-C theta wv, L-FC Shw.
Ictal EEG onset:
Interictal EEG:
L-FT, L-PT, and L-T Spk and slowing, L-H slowing.
R-TO Spk and slowing.
Ictal EEG: Slw (>T); negative-positive potentials (>F, midline)
Interictal EEG: ED (>MT, PoT), Spw
Ictal vEEG
Diffuse, F-C, PoTPO and T ED.
Interictal vEEG:
Lateralized, uncertain, and diffuse ED.
B (>O), B-PO Spw, B-O slowed background activity (theta).
Diffuse Spk and Spw.
PO slowing.
Interictal EEG:
B-Po ED, B perirolandic Spk.
L-FT ED, L-PoT ED with secondary generalization, L-T Spk.
R-CT ED, R-Po Spk.
R-FT slow and Spw
Pharmacoresistance ND Present in 1 ND Present in 5 Present in 2 Present in 16 Present in 6 ND ND
Surgery None L-T lobectomy + amygdalohippocampectomy Lesionectomy None ND Yes (in 2) None ND None

ACTH: adrenocorticotropic hormone; At: atonic; Ab: abscense; B: bilateral; C: centro; CBZ: carbamazepine; CES: cluster of epileptic spasms; CLB: clobazam; CLZ: clonazepam; Co: cortex; CSF: cerebrospinal fluid; CT: computerized tomography; DA: drop attacks; EA: extra-axial; ED: epileptiform discharges; EEG: electroencephalogram; EM: eyelid myoclonia; ESM: ethosuximide; F: frontal; FOA: focal onset aware; FOAI: focal onset impaired awareness; FBTC: focal to bilateral tonic-clonic; FC: fronto-central; fRMI: functional magnetic resonance imaging; GBP: gabapentin; GT: generalized tonic; GTC: generalized tonic-clonic; GVG: vigabatrin; H: hemisphere; HD: head drops; I: inferior; L: left; La: lateral; LCM: lacosamide; LEV: levetiracetam; LTG: lamotrigine; Me: mesial; M: myoclonic; MRI: magnetic resonance imaging; MT: mid-temporal; ND: no data; NR: no realized; NZ: nitrazepam; O: occipital; Oc: oculocephalics; OXC: oxcarbazepine; P: parietal; PB: phenobarbital; PET: position emission tomography; PHT: phenytoin; PNET: primitive neuroectodermal tumor; Po: posterior; PRM: primidone; R: right; sEEG: stereoelectroencephalography; Shw: sharp wave; Slw: slow wave; SPECT: single photon emission tomography; Sp: spikes; Spw: spike wave; S: superior; T: temporal; To: tonic; TPM: topiramate; vEEG: videoelectroencephalogram; VPA: valproate; wv: wave; ZNS: zonisamide.

Table 2 Clinical characteristics, diagnosis, and treatment of main case reports of patients with eating epilepsy 

Author/year Lavizzari, 196718 Cirignotta, 197719 Robertson, 197834 Fiol, 198635 Mateos, 199515 Kishi, 199916
Sex M F M F M M
Eating epilepsy age onset (yr) 12 16 14 12 11 8
Triggers At sight, chewing, eating Eating Chewing, eating Eating Eating Eating
Meal of the day ND Meals *more frequent at breakfast ND More at breakfast Meals ND
Moment of eating/meal ND Beginning, during ND Beginning ND ND
Quality or quantity of meal ND ND ND None ND ND
Aura (Focal Aware) ND ND Left upper limb numbness and left facial paresthesia. ND ND ND
Eating reflex seizure type FOA FOIA, HD FOA FOIA, GTC FO, FTBC FOIA
Radiological abnormal findings (CT/MRI/PET/SPECT) NR NR CT: R astrocytoma of basal ganglia. CT: none. CT/MRI: B rolandic opercula atrophy. MRI: B perisylvian malformations, polymicrogyria.
Electroencephalographic abnormal findings EEG: B-F sharp transients, positive spikes.
Interictal EEG: generalized slow waves.
EEG: infrequent diffuse spike-wave discharges. Brief low-voltage fast activity and diffuse polyspike-wave discharges during sleep.
Ictal EEG: diffuse sharp wave. B: low voltage fast activity. R-T: rapid activity medium voltage.
R-FT focal slowing. R-F delta focus, spikes, sharp waves.
Ictal vEEG: generalized low-voltage fast frequencies. L -T or R-T onset spikes.
Interictal EEG:
Generalized polyspike wave.
R-Po, R-MT, L-Po, L-MT spikes, and sharp waves.
Interictal EEG: R-CT slow Spk, Slw. Ictal vEEG: generalized low-voltage attenuation.
Interictal EEG: B-CP synchronous Shw.
Pharmacoresistance No Yes ND Yes No Yes
Surgery No No Frontal craniotomy + subtotal resection of low-grade astrocytoma. No ND ND
Author/year Domizio, 200620 D'Orsi, 200736 El Bouzidi, 201037 Manyam, 201038 Martínez, 201112 De Palma, 201211
Sex M M F F F M
Eating epilepsy age onset (yr) < 1 25 44 23 16 6
Triggers Breastfeeding Chewing, eating, swallowing At sight, discussing cooking, eating, hunger thought or smell of food. Eating ND Eating, smell, taste, * especially spicy food.
Meal of the day ND Lunch, breakfast, dinner Dinner, lunch, meals, snacks Meals ND ND
Moment of eating/meal After drinking milk ND Beginning, during ND Beginning ND
Quality or quantity of meal Milk ND ND ND ND ND
Aura (Focal Aware) ND ND ND ND ND ND
Eating reflex seizure type Desaturation, cyanosis, increase in muscular tone. At (generalized) FBTC, FOA FOIA FOA CES
Radiological abnormal findings (CT/MRI/PET/SPECT) MRI/CT: none MRI: B opercular dysplasia + corpus callosum hypoplasia. MRI: L-F (precentral) hyperintensity. MRI: post-surgical. RMI: none RMI: none
Electroencephalographic abnormal findings EEG: R-MeT abnormal waves Ictal EEG: B-An diffuse Slw
Interictal EEG: diffuse alpha-like background + L-TPO theta activity and Spw.
Interictal EEG: none
*Electrocorticography: L-F operculum epileptiform activity (anterior-inferior. to the MRI lesion)
Ictal EEG: delta activity (>F)
Interictal EEG: L-H slowing, theta and delta activity. L-T Shw.
Interictal EEG: F, C ED. Ictal EEG: diffuse slow-wave complex, > B-FC, followed by voltage attenuation.
Treatment PB, antiacid therapy (GER) CBZ, CLB, CLZ, LEV, LTG, OXC, VPA CBZ, VPA LTG, VPA ESM, LEV, VPA CLB, VPA, avoidance of spicy food.
Pharmacoresistance No Yes Yes No No Yes
Surgery No ND -Subtotal resection of L-F operculum: Grade IV glioblastoma. Post-resection left opercular PNET. No No
Author/year Sandhya, 201339 Koul, 201340 Sillanpää, 201441 Lodi, 201513 Blauwblomme, 201542 Kobayashi, 201643
Sex M F F M F F
Eating epilepsy age onset (yr) 8 <1 <1 27 28 8
Triggers Sight or smell of food Breast feeding Breast feeding Eating Eating Eating
Meal of the day ND ND ND ND ND ND
Moment of eating/meal At sight, before Beginning, after Beginning ND ND Beginning, during
Quality or quantity of meal ND ND ND ND Especially strawberry syrup ND
Aura (Focal Aware) ND ND Crying and coughing ND ND ND
Eating reflex seizure type ND FO, GT FBTC CES FOIA CES
Radiological abnormal findings (CT/MRI/PET/SPECT) MRI: none
Interictal SPECT: L-FPO perfusion changes.
Ictal SPECT: B-FTPO perfusion changes.
MRI: none MRI: none MRI: none MRI: post-surgery cavity
fMRI: activation of B insula, R-dorsolateral-F-Co and dorsolateral-P-Co.
MRI: corpus callosum dysgenesis, cerebellar hypogenesis, cerebral asymmetry, polymicrogyria, periventricular heterotopia, closed lip schizencephaly.
Electroencephalographic abnormal findings Interictal vEEG: L-FT ED
EEG-fMRI: ED, activation of L-FT lobes, B-P region, Me-structures (paracentral lobule, caudate, cingulate and medial frontal, lingual and medial occipital gyrus.
Interictal EEG: none
EEG: R-PoT slowing
Interictal EEG:
R asymmetric background activity of lower amplitude and repeated slow-wave discharges
Interictal EEG: slow background activity, poor organization
Ictal EEG:
F-C (>LH) diffuse irregular spike and slow-wave complex, some followed by delta rhythmic activity from L-FC and An vertex.
vEEG: An hippocampus spikes. An insular infrequent asynchronous spikes.
sEEG: AnI insula high-amplitude spike followed by low-voltage high-frequency discharge with secondary spreading to hippocampus and TCo.
Interictal EEG: slow background activity with multifocal spikes L-H, R-CT region.
Ictal EEG: diffuse large triphasic potentials >R-CTP region.
Pharmacoresistance ND No No Yes Yes ND
Surgery No No No No -9 years before EE: Opercular-insular R- cavernoma resection -Epilepsy surgery: An insula resection. ND
Author/year Lee, 201644 Mimura, 201745 Kisli, 201817 Aldosari, 202046 Ruiz-León, 2020 (present case)
Sex F F F M M
Eating epilepsy age onset (yr) 60 20 19 30 20
Triggers Eating At sight, eating Eating Eating Eating
Meal of the day ND ND ND ND No preference
Moment of eating/meal ND Before, during Mostly at the beginning Mostly at the beginning Middle
Quality or quantity of meal ND Specially minced meat Only while eating bread ND Only with solid food
Aura (Focal Aware) Dizziness, impaired speech ND ND ND Dizziness
Eating reflex seizure type FOA FBTC, FOA FOA FBTC, FOIA FOIA
Radiological abnormal findings (CT/MRI/PET/SPECT) MRI: none
PET: bitemporal hypometabolism (>L)
ND MRI: B-PCo encephalomalacia area MRI/PET: none MRI: none
Electroencephalographic abnormal findings ND Ictal vEEG:
L-F to MT: rhythmic theta activity followed by generalized seizure pattern.
Ictal EEG: R-FT sharp wave activity
Interictal EEG: none.
Ictal vEEG: R-T rhythmic activity with perisylvian spreading
R-AnMeT, insula, amygdala, hippocampus.
vEEG: Intermittent R-H slowing waves, predominantly F-C and with no epileptiform abnormality.
Treatment ND ND LEV ND OXC
Pharmacoresistance ND ND ND Yes No
Surgery ND ND ND R-An-T lobectomy including Me structures (amygdala, uncus, hippocampus) + partial inferior insulectomy. No

ACTH: adrenocorticotropic hormone; At: atonic; Ab: abscense; B: bilateral; C: centro; CBZ: carbamazepine; CES: cluster of epileptic spasms; CLB: clobazam; CLZ: clonazepam; Co: cortex; CSF: cerebrospinal fluid; CT: computarized tomography; DA: drop attacks; EA: extra-axtial; ED: epileptiform discharges; EEG: electroencephalogram; EM: eyelid myoclonia; ESM: ethosuximide; F: frontal; FOA: focal onset aware; FOAI: focal onset impaired awareness; FBTC: focal to bilateral tonic-clonic; FC: fronto-central; fRMI: functional magnetic resonance imaging; GBP: gabapentin; GT: generalized tonic; GTC: generalized tonic-clonic; GVG: vigabatrin; H: hemisphere; HD: head drops; I: inferior; L: left; La: lateral; LCM: lacosamide; LEV: levetiracetam; LTG: lamotrigine; Me: mesial; M: myoclonic; MRI: magnetic resonance imaging; MT: mid-temporal; ND: no data; NR: no realized; NZ: nitrazepam; O: occipital; Oc: oculocephalogyres; OXC: oxcarbazepine; P: parietal; PB: phenobarbital; PET: position emission tomography; PHT: phenytoin; PNET: primitive neuroectodermal tumor; Po: posterior; PRM: primidone; R: right; sEEG: stereoelectroencephalography; Shw: sharp wave; Slw: slow wave; SPECT: single photon emission tomography; Sp: spikes; Spw: spike wave; S: superior; T: temporal; To: tonic; TPM: topiramate; vEEG: videoelectroencephalogram; VPA: valproate; wv: wave; ZNS: zonisamide.

In patients with EE, seizures can be caused by diverse and heterogeneous stimuli; nevertheless, all of them are related to the feeding process, either just before, during, or after it. These triggers may involve visual and olfactory stimuli (sight and smell), digestive and autonomic functions (salivating, chewing, swallowing, gastric distention, and gastric acid secretion), proprioceptive stimuli, thinking about food, bulky meals rich in carbohydrates, and gastroesophageal reflux2,12,17-20. Moreover, association of EE to vasovagal syncope attacks has been reported, suggesting a vagal mechanism7.

Electroencephalographic (EEG) findings can be normal or present focal or diffuse epileptiform abnormalities3. Magnetic resonance imaging (MRI) can also be normal or present structural abnormalities specifically in temporolimbic or suprasylvian areas, particularly in the insular and opercular cortex3,4,7,12. A clinical neurotopographic correlation can be made with EEG finding and/or imaging findings.

Although identification and avoidance of stimulus in some patients could aid in seizure control, in EE, this is not always possible, except in very specific associated situations3. Some patients respond and benefit from antiepileptic drugs. Although management of choice has not yet been established, intake of clobazam before meals may be effective as add-on therapy in the management of EE3,4. Kokes et al. suggest that seizures that originate from the left temporal region may be more resistant to antiepileptic management7. Some patients with therapy resistance may benefit with surgical treatment21 or vagus nerve stimulation22, especially those with imaging abnormalities21.


This article is based on unsystematic research in Google Scholar and PubMed for original manuscripts about "Eating epilepsy," "Eating reflex seizures," "Eating seizures," "Reflex eating epilepsy," and "Reflex eating seizures;" followed by a discretionary selection of publications. We included observational studies (such as case reports and case series) published between 1967 and 2020. Editorial notes, literature systematic reviews and clinical images were excluded from the study.


In this review, we analyzed 18 case series and 23 case reports (Tables 1 and 2) and we included the case of a 40-year-old male patient with EE evaluated in our epilepsy clinic (Table 2).


Due to the inherent limitations of the case report and case series, result heterogeneity is obvious, with the consequent weakness of the conclusions. Despite these limitations from the data not reported or specified, the following information is relevant. We found that out of 237 patients, 126 were male and 61 were female (the sex of 50 patients was not specified by the author) with a resulting 2:1 ratio, highlighting the predominance among men. The reason why there is a clear predominance in males is unknown; we wonder if it has to do with the diagnosis approach, or if women are underdiagnosed or if there is a more complex pathophysiological explanation.

As for the type of seizures, the most frequently reported were the focal type with or without impaired awareness (Tables 1 and 2).

In both the case series and the case reports, the most common and constant trigger was by definition the act of eating itself2,4,11,13-19,21-24,26-31,33-38,42-46 but in some cases other stimuli were detailed such as chewing2,7,14,18,24,25,27,34,36, swallowing7,25,27,36, drinking7,24, seeing18,37,39,45, smelling11,37,39, and even thinking31,37 or talking37 about food. Orofacial stimuli2, taking food to the mouth7, hunger alone37, eating snacks24, and tasting food11 were also described.

In the case report series, other specific triggers to EE related to the type of food have also been described, including bulky meals, conventional Indian meals24, wheat-based diet, and on a rice-based diet31,32. Only 4 patients had a preference for a specific type of food (spicy food11, bread17, strawberry syrup42, and minced meat45). Furthermore, just a few authors specified the patient's diet, so it remains unclear if EE has a relation to specific diet type.

MRI and CT findings were variable. Some abnormalities were encephalomalacia, sclerosis, pachygyria, polymicrogyria, dysplasia, glioma, ventriculomegaly, meningioma, cavernoma, astrocytoma, and other lesions2,4,7,14-16,21,22,26,29,31,32,34,36,37,43. Four authors reported positron emission tomography; three presented hypometabolism7,33,44, and one was normal46. Five authors reported single-photon emission computed tomography that showed perfusion changes26,27,31,33,39. Two authors reported functional MRI showing activation of both insula and dorsolateral frontal and parietal cortex42 and the other showing left temporal, bilateral parietal, paracentral lobule, cingulate, medial frontal gyrus, and lingual and medial occipital gyrus abnormalities39. EEG findings were highly variable and different in each patient (Tables 1 and 2). Two authors detailed stereoelectroencephalography, finding affectation of the insula, hippocampus, and temporal cortex and/or amigdala42,48]. One patient underwent electrocorticography with operculum activity37. Surgery was performed on 10 patients, consisting of left-temporal lobectomy and amygdalohippocampectomy21, right-temporo-occipital resection, left-frontal resection22, lesionectomy31, subtotal resection of low grade astrocytoma34, subtotal resection of left-frontal operculum (grade IV glioblastoma)37, anterior insula resection42, right-anterior-temporal lobectomy including mesial structures and partial inferior insulectomy46, and non-specified in two patients. Only three patients underwent vagus nerve stimulation22.

Furthermore, the presence or absence of pharmacoresistance was specified in 131 patients (55% of the reviewed patients), of which 45 (41%) presented pharmacoresistance although sex, age, or type of seizure predominance was not clear.


EE is not the most frequent type of RE and because it can coexist with other epileptic syndromes, we speculate that EE may be under-diagnosed, so RE should be investigated in all patients with known epilepsy. It is our belief that semiology and specific activities during the eating process should be specified in order to identify the possible physiological-etiological mechanism, which until the present day is unknown. Finally, EE can be a therapeutic challenge since each patient presents variability in age of onset, type of stimuli and seizure, clinical course, findings in complementary studies, and response to management.

Supplementary data

Supplementary data are available at Revista Mexicana de Neurociencia online ( These data are provided by the corresponding author and published online for the benefit of the reader. The contents of supplementary data are the sole responsibility of the authors.


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Ethical disclosures

Protection of human and animal subjects. The authors declare that no experiments were performed on humans or animals for this study.

Confidentiality of data. The authors declare that they have followed the protocols of their work center on the publication of patient data.

Right to privacy and informed consent. The authors have obtained the written informed consent of the patients or subjects mentioned in the article. The corresponding author is in possession of this document.

Received: January 25, 2021; Accepted: March 16, 2021

* Correspondence: José L. Ruiz-Sandoval E-mail:

Conflicts of interest


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