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Abdominal epilepsy (AE) has long been reported as a rare phenomenon in children with various episodic gastrointestinal sensory and painful symptoms suspected to be due to epileptic seizures. Originally, AE was diagnosed when abdominal sensory or painful symptoms were associated with pain, temporal lobe origin, an epileptiform or paroxysmal EEG pattern, and a clinical response to antiseizure medication. AE has also been associated with non-epileptic etiologies such as migraine. Reports of abdominal epilepsy based on an abnormal EEG or clinical response to antiseizure medication without diagnosis confirmation by video-EEG are at best speculative, and at worst, misdiagnoses. We describe three adult patients with focal aware motor seizures manifesting as recurrent, isolated prolonged painless rhythmic clonic jerking of the abdominal musculature including epilepsia partialis continua. All patients had a contralateral structural lesion on high-resolution brain MRI in the abdominal region of the motor homunculus. Standard EEG was unrevealing and only after extra EEG electrodes and video-EEG monitoring was the ictal origin confirmed. Historically, AE has been described as a disorder involving subjective sensory symptoms including vague abdominal pain, instead of epileptic motor signs of abdominal clonic jerking. We recommend replacing the use of vague terms such as AE with International League Against Epilepsy terminology along with diagnostic confirmation validated by video-EEG monitoring. [Published with video sequence].

Objective Evidence suggests disordered breathing is critically involved in Sudden Unexpected Death in Epilepsy (SUDEP). To that end, evaluating structures that are activated by seizures and can activate brain regions that produce cardiorespiratory changes can further our understanding of the pathophysiology of SUDEP. Prior preclinical studies have shown that electrical stimulation of the human amygdala induces apnea, suggesting a role for the amygdala in controlling respiration. In this study, we aimed to both confirm these findings in a larger group of patients with intractable temporal lobe epilepsy (TLE) and also further explore the anatomical and cognitive properties of this effect.