Abstracts

The pathophysiologic mechanisms of seizures induced by eating are unknown and controversy remains as the whether eating epilepsy is evoked by anticipation of the stimulus or proprioceptive or somatosensory afferent inputs. We report a case with seizures induced by eating in whom MRI localized the epileptogenic lesion and ictal SPECT suggested the insular cortex was the ictal onset zone.
A 53 year-old woman had a generalized tonic-clonic seizure at age 19 and over the years had several more. Her medically refractory focal seizures began at age 29. The focal seizures consisted of preservation of consciousness, abdominal discomfort, mouth [quot]numbness,[quot] alteration of taste, involuntary orolingual movements, drooling, spitting, and swallowing. She also experienced anxiety and tachycardia. Seizures sometimes occurred 8 to 10 times a day and lasted 30 seconds to 3 minutes. She reported eating could provoke seizures. A brain MRI scan detected a lesion thought to be a cavernous angioma immediately adjacent to and involving her right insular cortex. She had continuous EEG/video recordings over several days. On two occasions seizures were induced by putting food in her mouth and asking her to chew. A baseline ictal SPECT scan was obtained along with three ictal SPECT scans on separate days using Tc 99m neurolite. The baseline and ictal SPECT scans were coregistered, subtracted and the result coregistered with a high resolution MRI scan.
She had eight recorded seizures, several of which were triggered by placing food in her mouth and asking her to chew. Interictal EEG documented right temporal spikes however no EEG ictal pattern was seen during the events. Ictal SPECT scans demonstrated hyperperfusion in the right insular cortex adjacent to the MRI lesion.
Our patient clearly has eating epilepsy which was documented during EEG/video monitoring. MRI scan localized an epileptogenic lesion involving her right insular cortex and ictal SPECT scans documented right insular hyperperfusion during seizures. This well studied case provides evidence that the insular cortex is involved in the pathogenesis of eating epilepsy.