A Rare Form of Reflex Epilepsy: Eating Epilepsy – A Case Report

Reflex epilepsies (REs) are identified as epileptic seizures that are consistently induced by identifiable and objective-specific triggers, which may be an afferent stimulus or by the patient’s own activity [1]. Eating epilepsy (EE) is a distinct subtype of RE, where seizures are triggered by the act of eating [2]. In 1967, the first-ever case of EE was reported, in which seizures were brought on by meals or even just the sight of food [3]. Typically, seizures occur during or shortly after eating [4].

Since a significant number of EE cases have been documented in South Asia, it is possible that genetic or ethnic factors, such as diet or eating habits, have a pathological connection to EE. Despite this unique ethnic prevalence, cases have been noted across populations and encompass a mixture of symptomatic and idiopathic causes [5].

The types of food associated with the onset of reflex seizures are various. Rice-based meals, spicy foods, hot food, and milk are foods that have been reported to be associated with RE [5].

EE seizures are typically focal onset and most commonly of the focal impaired awareness type. EEG abnormalities are more commonly interictal rather than ictal. Focal epileptiform discharges, particularly localizing to the temporal region, are the most frequent interictal abnormality [5]. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000545067).

A 55-year-old man was admitted to the neurology clinic with a complaint of recurrent loss of consciousness that started a few minutes after meals. He stated that his complaints occur especially after spicy meals. Witnesses said the patient first froze, staring blankly, and then began to make repetitive, purposeless movements of his left hand for about 2 min. The patient did not remember these attacks but described confusion lasting about 30 min after he regained consciousness.

The patient stated that he had his first seizure 2 years ago (when he was 53 years old) and therefore applied to the emergency department, but since he had not had a seizure recurrence until the last year, he did not apply to the neurology clinic. However, the patient had a seizure again approximately 1 year ago and had frequent seizure recurrences after this seizure. For this reason, he applied to the neurology clinic.

The patient did not have any chronic diseases or any neurological disorders in his medical history, and he did not use any medication regularly. He did not have a personal or family history of seizures.

The history given by the patient and his relatives, especially the purposeless movements suggesting automatism observed in the left upper limb and the fact that the patient lost awareness during the event, primarily suggested a focal impaired awareness seizure. Additionally, considering the symptoms, it was thought that the seizure might be caused by a focus originating from the temporal lobe.

His neurological examination and metabolic values were normal. MRI showed nonspecific white matter changes. Interictal EEG showed poly-spike activity in the left temporal-anterior region (Fig. 1). Additionally, bi-frontal high-amplitude 4 Hz transients and the lower amplitude sharp transients in the right temporal lobe were observed (Fig. 2).

Considering the patient’s EEG study and clinical findings, the prominent epileptogenic focus in the patient was interpreted as the left temporal lobe. The patient was started on valproic acid treatment at 1,000 mg/day. Following therapy, the eating-related seizures ceased, and the EEG normalized.

The precise process that underlies EE is still unknown. Thinking about food, the sight and/or smell of food, digestive and autonomic functions like salivation, mastication, swallowing, and gastric distention, and the chemical composition of food such as meals rich in carbohydrates have all been proposed as possible stimuli. These seizures may be triggered by hunger or appetite and could stem from hyperactivation of primary taste areas (anterior insula and frontal operculum) in response to taste, olfaction, and anticipation of food [2, 5, 6].

Some cases are idiopathic, while focal structural changes on imaging, if present, are often confined to the temporal lobe or perisylvian region. On the other hand, some cases support the hypothesis of a genetic etiology [7].

Interictal EEG abnormalities are more common than ictal abnormalities in EE. Focal epileptiform discharges, particularly localizing to the temporal region, are the most frequent interictal abnormality. However, interictal EEG could also be normal [5]. MRI is usually normal. Among the abnormalities found are cortical dysplasia, gliosis, polymicrogyria, and pachygyria [2, 5].

In most cases, polytherapy is necessary to help these patients control their seizures. Despite best management efforts, EE can be drug-resistant in a substantial proportion of patients. Drug-resistant EE patients should be evaluated for epilepsy surgery [2, 8, 9].

The case we presented had characteristic features of EE in many respects. Most cases of EE have been seen in male patients. EE seizures are typically focal onset and most commonly of the focal impaired awareness type [5]. Focal epileptiform discharges, particularly localizing to the temporal region, are the most frequent interictal abnormality. There may be a family history in some cases, but there are also cases without a family history, as in our patient. Our patient had the general characteristics of the EE cases reported in the literature that we listed above.

However, considering the EE cases previously reported in the literature, our patient had few different characteristics. In EE, seizures generally occur after carbohydrate-rich foods, especially rice-based meals. Our patient did not have such a complaint after eating carbohydrate-rich foods. His seizures occurred after spicy meals. Although this condition is rare, a few cases of seizures being triggered after spicy foods have been reported in the literature [5]. EE usually starts in the second or third decades, but our patient’s seizure history started in sixth decade, when he was 53 years old [6]. Another difference in our case is that while seizure control in EE patients is generally achieved with polytherapy, our patient’s seizures were controlled with valproic acid monotherapy [2, 8, 9].

The fact that there was no video EEG recording in our case report and only interictal EEG recording could be considered a limitation of study. However, considering that interictal EEG abnormalities are more commonly detected in EE, we believe that this does not create a major deficiency in the case report.

In conclusion, we described a case of EE and pointed out a few common characteristics of this uncommon condition. If there is a eating-induced seizure in the patient’s history, EE should be kept in mind and the points we emphasized in our case presentation should be taken into consideration during the diagnosis and treatment process.

The patient was compliant with the treatment. He did not report any additional seizures or treatment-related side effects after valproic acid treatment in his follow-up examinations.

Written informed consent was obtained from the patient for the publication of this case report and accompanying images. Ethical approval was not required for this study in accordance with local guidelines.

No potential conflict of interest was reported by the authors.

The authors did not receive support from any organization for the submitted work.

Cem Direybatoğulları: literature review, manuscript drafting, and manuscript review; Mehmet Fevzi Öztekin: supervision, conceptualization, and manuscript review.

The data that support the findings of this study are not publicly available due to privacy reasons but are available from corresponding author (C.D.) upon reasonable request.