LESIONAL REFLEX EPILEPSY ASSOCIATED WITH THE THOUGHT OF FOOD

A 44-year-old right-handed woman was walking in the Scottish highlands. Upon unwrapping her lunch, she had a focal seizure with witnessed onset on the right side of the face and secondary generalization. Postictally, she was aphasic with a right hemiparesis. She was airlifted to hospital. Sodium valproate was commenced, increasing to 700 mg twice daily, and she was discharged home. Three weeks later, the smell of food triggered another seizure and she was admitted to the neurology unit where carbamazepine was introduced (200 mg twice daily).

The next morning, the patient had a simple partial seizure after eating a spoonful of porridge and 3 more when eating lunch, a snack, and dinner. Thereafter, most meals triggered seizures, as did other food-related stimuli such as being offered a piece of cake, seeing her visitors pass around food at her bedside, and smelling the hospital dinner trolley. Fifty-four seizures occurred over the next 14 days and 50 were related to food. The episodes typically lasted 80 seconds and were characterized by a tingling sensation in the tongue and right-sided facial and tongue movements. Consciousness was unimpaired.

Thirty-four seizures occurred during the act of eating, always early on in the meal while the patient still felt hungry. Fifteen were precipitated by the sight or smell of food alone, 1 while browsing a recipe book, and 3 when she could smell her pet dog's food. One seizure was provoked by discussing cooking and another was triggered by the mint flavor of toothpaste. A single nocturnal seizure was accompanied by a strong feeling of nausea. The 2 other seizures associated with nonfood stimuli were related to stressful situations such as discussing a call from the doctor. Neither chewing movements nor speaking induced seizures.

Interictal EEG was normal. MRI revealed a nonenhancing lesion in the left premotor strip (figure).

Figure Localization of the tumor and seizure focus

(A) Transverse T2-weighted MRI scan with arrow indicating the lesion in the left frontal cortex (L = left). (B) Three-dimensional reconstruction of the patient's brain with superimposed graphics showing the location of the tumor (yellow) and intraoperative cortical electrodes. The electrodes that recorded epileptiform activity are shown in red. (C) Intraoperative electrocorticography revealed epileptiform activity in the leads indicated by the asterisk.

The seizures were refractory to medical therapy. An awake frontoparietal craniotomy was performed with electrocorticography. Epileptiform activity was identified in the left frontal operculum, anterior and inferior to the lesion (figure). A subtotal resection was performed. Histopathology revealed a WHO grade IV glioblastoma. No reflex seizures occurred after surgery.

Discussion.

We present a case of symptomatic reflex seizures triggered by food-related stimuli, with detailed neuroimaging and electrophysiologic localization of the epileptic focus. Reflex epilepsies are characterized by seizures consistently induced by a specific stimulus. Typically, they are idiopathic and generalized. Recognized stimuli include flashing lights, music, reading, toothbrushing, and eating. Over 200 cases of idiopathic eating epilepsy have been reported, many from South Asia, with a male preponderance and onset typically in the second decade of life.¹ In all cases, the act of eating was required to provoke seizures, which were focal or generalized. Of 128 cases in which treatment response is described, 48 (37.5%) became seizure-free, 64 (50%) achieved partial control of seizures, and 16 (12.5%) showed no benefit.^1,2

There are far fewer reported cases of symptomatic eating epilepsy. The associated pathologies include congenital malformations, vascular abnormalities, postinfective lesions, and 1 neoplasm: an astrocytoma. Lesions involved the opercula, amygdalae, and temporoparietal lobes.^3,4 Most cases were refractory to medical therapy.

Rarer still are cases of reflex epilepsy triggered by the thought of a specific stimulus. One report described a man with temporal lobe seizures induced by thinking of his childhood home.⁵ Another patient with a left temporal focus on EEG had seizures when brushing his teeth but also on thinking of a toothbrush.⁶ To our knowledge, there have been no reports of seizures precipitated by the thought of food or hunger alone.^1,3

Several mechanisms have been postulated for eating epilepsy, from somatosensory and motor stimulation to gastric distension.^2,3 Primary taste areas in the anterior insula and frontal operculum are activated by taste and olfactory stimuli but also the anticipation of food.³ Taste processing is refined in the secondary taste areas of the amygdala and orbitofrontal cortex where a greater number of neurons receive multimodal inputs.³ Functional MRI has demonstrated activation in the primary and secondary taste regions in response to the visual presentation and imagination of food.⁷ Subjective reports of appetite in healthy subjects correlate with activity in the left frontal operculum and insula.⁷

In this case, seizures were specifically triggered by food-related stimuli in the context of hunger. The finding of a seizure focus in the left frontal operculum, adjacent to the tumor, is consistent with the hypothesis that activation of this region by appetite triggered seizure activity that then propagated to the surrounding cortex and was manifest clinically as a motor seizure.

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