RARE DISEASE
Eating reflex epilepsy
Eating reflex epilepsy
Eating reflex epilepsy
Synonyms: Eating epilepsy, Eating seizures
Synonyms: Eating epilepsy, Eating seizures
Synonyms: Eating epilepsy, Eating seizures
Drug discovery
46
papers
On emerging therapies
Overview
Eating reflex epilepsy is a rare seizure disorder triggered by eating-related stimuli, characterized predominantly by focal impaired-awareness seizures. It exhibits male predominance, onset typically in adolescence, and higher prevalence in South Asia (5.6% in Sri Lanka vs <1% globally). Diagnosis combines clinical history, EEG (often showing temporal or perisylvian epileptiform activity), and MRI to exclude structural causes. First-line therapy involves anti-seizure medications (ASMs) like clobazam or valproate, though 25% show drug resistance.
Population
Affects 0.05–0.1% of epilepsy patients, rising to 5.6% in endemic regions like Sri Lanka [1][5][14]
Male predominance (2:1 ratio), onset peaks in second decade [1][5][14]
Strong regional clustering suggests genetic and dietary influences (e.g., carbohydrate-rich meals, vagal reflex activation) [1][3][7]
Therapies
Clobazam: Prophylactic administration 30 minutes pre-meal reduces seizures in >70% of cases [3][5][11]
ASM combinations: Valproate monotherapy or adjunctive levetiracetam/lamotrigine for temporolimbic foci [1][3][10]
Surgery: Considered for lesional cases (e.g., cortical malformations, perisylvian gliosis) refractory to ≥2 ASMs [5][10][14]
Categories: rare neurological diseases
Research Papers
46 drug discovery papers about Eating reflex epilepsy. Recent publications:
46 drug discovery papers about Eating reflex epilepsy. Recent publications:
categories:
Small molecules
small molecules
2026-01-23 | Unaware and unrestrained: binge-eating behavior in epileptic absence seizures.
Binge-eating disorder (BED) frequently co-occurs with dissociative symptoms and psychiatric comorbidities, yet potential neurological underpinnings remain underexplored. We report an 18-year-old female with BED presenting with frequent binge episodes accompanied by memory lapses and altered consciousness. Initially attributed to dissociation, comprehensive evaluation revealed previously undiagnosed absence epilepsy, confirmed by EEG and neuroimaging. Neuropsychological assessment demonstrated significant impairments in working memory, processing speed, and divided attention. Treatment with lamotrigine (200 mg/day) resulted in complete remission of binges occurring during absence seizures and substantial cognitive improvements across multiple domains. This case highlights the critical importance of neurological evaluation in eating disorder patients presenting with altered consciousness or memory lapses. The temporal relationship between seizures and binge episodes, coupled with treatment response, suggests potential neurobiological mechanisms linking epileptic activity to disinhibited eating behaviors. Clinicians should maintain heightened awareness of possible epilepsy-eating disorder comorbidity and consider integrated treatment approaches addressing both neurological and psychiatric components.
2025-06-26 | Separating Subjective from Objective Food Value in the Human Insula: An Exploratory Study Using Intracranial EEG.
Background/Objectives: The human insula is a key structure implicated in integrating internal states and external food cues, yet its precise role remains unclear, in part due to the temporal limitations of neuroimaging techniques like fMRI. To address this gap, we conducted an exploratory study using an intracranial EEG (iEEG) to investigate how the insula encodes both the subjective and objective properties of food-related stimuli, and how this encoding is modulated by hunger and satiety. Methods: Eight patients with drug-resistant epilepsy undergoing a pre-surgical evaluation between 2017 and 2023 participated in this study. Depth electrodes implanted in the insular cortex recorded event-related potentials (ERPs) in response to visual food cues. The sessions were conducted in two prandial states (hungry and satiated). The subjective ratings (appetite and palatability) and objective nutritional values (e.g., calories, carbohydrates) were collected and analyzed using paired t-tests, MANOVAs, and partial correlations. Results: Hunger increased the ERP amplitudes within the 350-450 ms interval, consistent with the EPIC model and positive alliesthesia, while satiety unexpectedly enhanced the early responses (150-250 ms). Importantly, the neural activity related to nutritional values was largely uncorrelated with the subjective ratings, suggestive of distinct processing streams. The mid- and posterior insula showed greater sensitivity to both subjective and nutritional information than the anterior insula. Conclusions: These findings offer novel electrophysiological insights into how the insula differentiates between implicit and explicit food-related signals, depending on the homeostatic state. This work supports a dual-route model of food cue processing, and may inform interventions targeting insular activity in disordered eating.
2025-04-17 | GABAB Receptor: Structure, Biological Functions, and Therapy for Diseases.
Gamma-aminobutyric acid (GABA) B receptors (GABABRs) that acts slowly and maintains the inhibitory tone are versatile regulators in the complex nervous behaviors and their involvement in various neuropsychiatric disorders, such as anxiety, epilepsy, pain, drug addiction, and Alzheimer's disease. Additional study advances have implied the crucial roles of GABABRs in regulating feeding-related behaviors, yet their therapeutic potential in addressing the neuropsychiatric disorders, binge eating, and feeding-related disorders remains underutilized. This general review summarized the physiological structure and functions of GABABR, explored the regulation in various psychiatric disorders, feeding behaviors, binge eating, and metabolism disorders, and fully discussed the potential of targeting GABABRs and its regulator-binding sites for the treatment of different psychiatric disorders, binge eating and even obesity. While agonists that directly bind to GABABR1 have some negative side effects, positive allosteric modulators (PAMs) that bind to GABABR2 demonstrate excellent therapeutic efficacy and tolerability and have better safety and therapeutic indexes. Moreover, phosphorylation sites of downstream GABABRs regulators may be novel therapeutic targets for psychiatric disorders, binge eating, and obesity. Further studies, clinical trials in particular, will be essential for confirming the therapeutic value of PAMs and other agents targeting the GABABR pathways in a clinical setting.
2025-04-08 | Reflex "toothbrushing" epilepsy: Seizure freedom after focal ablation assisted by ictal fMRI.
A 22-year-old female presented with drug-resistant focal motor seizures with onset at age 14. This manifested as daily episodes of right facial dystonia triggered by toothbrushing, but also by eating, talking, and strenuous exercise. On ictal scalp EEG, there was low-voltage fast activity over the left pericentral area. Structural MRI did not identify a definite lesion. Functional MRI (fMRI) of a reflex seizure, as well as task-based fMRI during toothbrushing, both demonstrated focal activation at the left low pericentral cortex. Stereoelectroencephalography (sEEG) showed recurrent ictal trains of focal spiking concordant with the fMRI activation. Radiofrequency (RF) thermocoagulation was applied at the posterior bank of the left low pre-central gyrus, with post-operative MRI confirming small ablative lesions immediately deep to the ictal fMRI activation, and the patient remains seizure-free more than 3 years after this treatment. Toothbrushing epilepsy is a rare form of reflex epilepsy where seizures are induced by toothbrushing. In this unique case, ictal fMRI assisted targeting of the sEEG implantation, to confirm seizure onset and enable minimally invasive treatment via RF thermocoagulation, resulting in seizure freedom.
2025-03-01 | Eating Epilepsy
Abstract Eating epilepsy (EE) is a rare form of epilepsy, affecting 0.05%–0.1% of epilepsy patients globally, with higher prevalence in South Asia. A high male preponderance and rare familial clustering are reported. Approximately half of EE cases involve seizures exclusively triggered by eating, while others are associated with unprovoked seizures. The etiology is largely unknown, but recent research links EE to SYNGAP1 gene mutations. Around one-third of EE patients exhibit brain lesions, often focal cortical dysplasia and polymicrogyria. Focal epilepsy is prevalent in over half of EE cases, with temporo-insular and perisylvian structures prominently involved. Treatment relies on anti-seizure medications, and dietary changes may be suggested for some patients. Administering clobazam around mealtimes seems to be an effective approach. Resective surgery is considered in refractory cases, but overall seizure outcomes are suboptimal. Advanced electrophysiology and radiological assessments aid in diagnosis and treatment planning for EE patients.
antibodies
2023-04-28 | Eating reflex epilepsy of presumed autoimmune etiology after SARS-CoV-2 vaccination
Dear Sirs,Eating epilepsy is an uncommon type of reflex epilepsy in which seizure are often, or even always, triggered by eatingrelated stimuli [1].Seizures related to eating most commonly originate from temporo-limbic structures and they are often of unknown etiology because no focal lesion is identified [1].Herein we describe the case of an adult patient developing new-onset eating epilepsy with refractory seizures shortly after SARS-CoV-2 vaccination in whom no structural, infectious, or metabolic etiologies were found.A possible immune-mediated etiology was suspected and a complete control of seizures was achieved with periodic intravenous immunoglobulin (IVIg) therapy.A 40-year-old woman was admitted to our Department for a first unprovoked seizure.She has no previous personal or family history of neurological disorders, seizures, head trauma or central nervous system (CNS) infection.She received two Pfizer-BioNTech COVID-19 vaccine doses between June and July 2021 (first and second dose given 21 days apart), with no associated flu-like symptoms.Four days after the second injection, she started experiencing episodes of loss of contact, impaired speech, face flushing, mydriasis, and diaphoresis.The episodes were very frequent since the beginning (multiple daily), lasted only few minutes with complete recovery, and were almost always associated with the beginning of a meal (breakfast, lunch, or dinner).Twenty days after the second injection she experienced a probable tonic-clonic seizure with unknown onset: she was alone having breakfast and suddenly she woke up with signs of head trauma, vomit, and tongue biting, without recollection of the events.She was admitted to the Emergency Department, where she underwent a head computed tomography (CT) scan, showing no sign of acute brain damage, and an electroencephalogram (EEG), demonstrating a bilateral temporal theta slowing with rare epileptic abnormalities (spikes and sharp waves), predominantly over the left temporal lobe.A brain magnetic resonance imaging (MRI) was performed, which showed only mild nonspecific gliosis of the white matter.No hippocampal abnormalities were noted (Fig. 1).As suggested, she started keeping record of seizures in a diary.The dose of anti-seizure medication (ASM) was not enough to control the seizures, even though the frequency was lower.Seizures continued to be related to the beginning of meals (Fig. 2).Considering the persistency of seizures, levetiracetam was increased up to 2500 mg daily, without achieving complete resolution of the episodes.She was therefore admitted to the Epilepsy Monitoring Unit in November 2021.Metabolic screening showed no abnormalities.CSF samples were analyzed, including testing for oligoclonal bands, antibodies against neuronal cell surface and onconeuronal antigens, as well as anti-MOG and anti-aquaporin-4 antibodies.A low-title positivity for anti-AMPA1-R/AMPA2-R Ab was detected on serum
small molecules
2026-01-23 | Unaware and unrestrained: binge-eating behavior in epileptic absence seizures.
Binge-eating disorder (BED) frequently co-occurs with dissociative symptoms and psychiatric comorbidities, yet potential neurological underpinnings remain underexplored. We report an 18-year-old female with BED presenting with frequent binge episodes accompanied by memory lapses and altered consciousness. Initially attributed to dissociation, comprehensive evaluation revealed previously undiagnosed absence epilepsy, confirmed by EEG and neuroimaging. Neuropsychological assessment demonstrated significant impairments in working memory, processing speed, and divided attention. Treatment with lamotrigine (200 mg/day) resulted in complete remission of binges occurring during absence seizures and substantial cognitive improvements across multiple domains. This case highlights the critical importance of neurological evaluation in eating disorder patients presenting with altered consciousness or memory lapses. The temporal relationship between seizures and binge episodes, coupled with treatment response, suggests potential neurobiological mechanisms linking epileptic activity to disinhibited eating behaviors. Clinicians should maintain heightened awareness of possible epilepsy-eating disorder comorbidity and consider integrated treatment approaches addressing both neurological and psychiatric components.
2025-06-26 | Separating Subjective from Objective Food Value in the Human Insula: An Exploratory Study Using Intracranial EEG.
Background/Objectives: The human insula is a key structure implicated in integrating internal states and external food cues, yet its precise role remains unclear, in part due to the temporal limitations of neuroimaging techniques like fMRI. To address this gap, we conducted an exploratory study using an intracranial EEG (iEEG) to investigate how the insula encodes both the subjective and objective properties of food-related stimuli, and how this encoding is modulated by hunger and satiety. Methods: Eight patients with drug-resistant epilepsy undergoing a pre-surgical evaluation between 2017 and 2023 participated in this study. Depth electrodes implanted in the insular cortex recorded event-related potentials (ERPs) in response to visual food cues. The sessions were conducted in two prandial states (hungry and satiated). The subjective ratings (appetite and palatability) and objective nutritional values (e.g., calories, carbohydrates) were collected and analyzed using paired t-tests, MANOVAs, and partial correlations. Results: Hunger increased the ERP amplitudes within the 350-450 ms interval, consistent with the EPIC model and positive alliesthesia, while satiety unexpectedly enhanced the early responses (150-250 ms). Importantly, the neural activity related to nutritional values was largely uncorrelated with the subjective ratings, suggestive of distinct processing streams. The mid- and posterior insula showed greater sensitivity to both subjective and nutritional information than the anterior insula. Conclusions: These findings offer novel electrophysiological insights into how the insula differentiates between implicit and explicit food-related signals, depending on the homeostatic state. This work supports a dual-route model of food cue processing, and may inform interventions targeting insular activity in disordered eating.
2025-04-17 | GABAB Receptor: Structure, Biological Functions, and Therapy for Diseases.
Gamma-aminobutyric acid (GABA) B receptors (GABABRs) that acts slowly and maintains the inhibitory tone are versatile regulators in the complex nervous behaviors and their involvement in various neuropsychiatric disorders, such as anxiety, epilepsy, pain, drug addiction, and Alzheimer's disease. Additional study advances have implied the crucial roles of GABABRs in regulating feeding-related behaviors, yet their therapeutic potential in addressing the neuropsychiatric disorders, binge eating, and feeding-related disorders remains underutilized. This general review summarized the physiological structure and functions of GABABR, explored the regulation in various psychiatric disorders, feeding behaviors, binge eating, and metabolism disorders, and fully discussed the potential of targeting GABABRs and its regulator-binding sites for the treatment of different psychiatric disorders, binge eating and even obesity. While agonists that directly bind to GABABR1 have some negative side effects, positive allosteric modulators (PAMs) that bind to GABABR2 demonstrate excellent therapeutic efficacy and tolerability and have better safety and therapeutic indexes. Moreover, phosphorylation sites of downstream GABABRs regulators may be novel therapeutic targets for psychiatric disorders, binge eating, and obesity. Further studies, clinical trials in particular, will be essential for confirming the therapeutic value of PAMs and other agents targeting the GABABR pathways in a clinical setting.
2025-04-08 | Reflex "toothbrushing" epilepsy: Seizure freedom after focal ablation assisted by ictal fMRI.
A 22-year-old female presented with drug-resistant focal motor seizures with onset at age 14. This manifested as daily episodes of right facial dystonia triggered by toothbrushing, but also by eating, talking, and strenuous exercise. On ictal scalp EEG, there was low-voltage fast activity over the left pericentral area. Structural MRI did not identify a definite lesion. Functional MRI (fMRI) of a reflex seizure, as well as task-based fMRI during toothbrushing, both demonstrated focal activation at the left low pericentral cortex. Stereoelectroencephalography (sEEG) showed recurrent ictal trains of focal spiking concordant with the fMRI activation. Radiofrequency (RF) thermocoagulation was applied at the posterior bank of the left low pre-central gyrus, with post-operative MRI confirming small ablative lesions immediately deep to the ictal fMRI activation, and the patient remains seizure-free more than 3 years after this treatment. Toothbrushing epilepsy is a rare form of reflex epilepsy where seizures are induced by toothbrushing. In this unique case, ictal fMRI assisted targeting of the sEEG implantation, to confirm seizure onset and enable minimally invasive treatment via RF thermocoagulation, resulting in seizure freedom.
2025-03-01 | Eating Epilepsy
Abstract Eating epilepsy (EE) is a rare form of epilepsy, affecting 0.05%–0.1% of epilepsy patients globally, with higher prevalence in South Asia. A high male preponderance and rare familial clustering are reported. Approximately half of EE cases involve seizures exclusively triggered by eating, while others are associated with unprovoked seizures. The etiology is largely unknown, but recent research links EE to SYNGAP1 gene mutations. Around one-third of EE patients exhibit brain lesions, often focal cortical dysplasia and polymicrogyria. Focal epilepsy is prevalent in over half of EE cases, with temporo-insular and perisylvian structures prominently involved. Treatment relies on anti-seizure medications, and dietary changes may be suggested for some patients. Administering clobazam around mealtimes seems to be an effective approach. Resective surgery is considered in refractory cases, but overall seizure outcomes are suboptimal. Advanced electrophysiology and radiological assessments aid in diagnosis and treatment planning for EE patients.
antibodies
2023-04-28 | Eating reflex epilepsy of presumed autoimmune etiology after SARS-CoV-2 vaccination
Dear Sirs,Eating epilepsy is an uncommon type of reflex epilepsy in which seizure are often, or even always, triggered by eatingrelated stimuli [1].Seizures related to eating most commonly originate from temporo-limbic structures and they are often of unknown etiology because no focal lesion is identified [1].Herein we describe the case of an adult patient developing new-onset eating epilepsy with refractory seizures shortly after SARS-CoV-2 vaccination in whom no structural, infectious, or metabolic etiologies were found.A possible immune-mediated etiology was suspected and a complete control of seizures was achieved with periodic intravenous immunoglobulin (IVIg) therapy.A 40-year-old woman was admitted to our Department for a first unprovoked seizure.She has no previous personal or family history of neurological disorders, seizures, head trauma or central nervous system (CNS) infection.She received two Pfizer-BioNTech COVID-19 vaccine doses between June and July 2021 (first and second dose given 21 days apart), with no associated flu-like symptoms.Four days after the second injection, she started experiencing episodes of loss of contact, impaired speech, face flushing, mydriasis, and diaphoresis.The episodes were very frequent since the beginning (multiple daily), lasted only few minutes with complete recovery, and were almost always associated with the beginning of a meal (breakfast, lunch, or dinner).Twenty days after the second injection she experienced a probable tonic-clonic seizure with unknown onset: she was alone having breakfast and suddenly she woke up with signs of head trauma, vomit, and tongue biting, without recollection of the events.She was admitted to the Emergency Department, where she underwent a head computed tomography (CT) scan, showing no sign of acute brain damage, and an electroencephalogram (EEG), demonstrating a bilateral temporal theta slowing with rare epileptic abnormalities (spikes and sharp waves), predominantly over the left temporal lobe.A brain magnetic resonance imaging (MRI) was performed, which showed only mild nonspecific gliosis of the white matter.No hippocampal abnormalities were noted (Fig. 1).As suggested, she started keeping record of seizures in a diary.The dose of anti-seizure medication (ASM) was not enough to control the seizures, even though the frequency was lower.Seizures continued to be related to the beginning of meals (Fig. 2).Considering the persistency of seizures, levetiracetam was increased up to 2500 mg daily, without achieving complete resolution of the episodes.She was therefore admitted to the Epilepsy Monitoring Unit in November 2021.Metabolic screening showed no abnormalities.CSF samples were analyzed, including testing for oligoclonal bands, antibodies against neuronal cell surface and onconeuronal antigens, as well as anti-MOG and anti-aquaporin-4 antibodies.A low-title positivity for anti-AMPA1-R/AMPA2-R Ab was detected on serum
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