PURPOSE: Pharyngeal dysesthetic auras are typically described with centrotemporal and opercular seizure-onset localizations. In this report we describe the fourth case in literature with temporal lobe seizures, apparently secondary to an amygdalar lesion on magnetic resonance imaging (MRI), presenting with prominent pharyngeal dysesthesias as the initial, or only, seizure manifestation. METHODS: Because of diagnostic uncertainty regarding the nature of the pharyngeal sensations, our case underwent prolonged extracranial video-EEG monitoring. RESULTS: Video-EEG information documented the epileptic origin of the dysesthesias and was concordant with the side and location of the amygdalar lesion. CONCLUSIONS: Pharyngeal dysesthetic auras may be produced by epileptic activity originating from the amygdala, and perhaps other mediotemporal structures. The underlying topography of this aura is not known with certainty, and it may reflect seizure spread from the amygdala and adjacent areas to the closely interconnected insular and opercular cortex, whose secondary activation could elicit similar sensations.
PURPOSE: Pharyngeal dysesthetic auras are typically described with centrotemporal and opercular seizure-onset localizations. In this report we describe the fourth case in literature with temporal lobe seizures, apparently secondary to an amygdalar lesion on magnetic resonance imaging (MRI), presenting with prominent pharyngeal dysesthesias as the initial, or only, seizure manifestation. METHODS: Because of diagnostic uncertainty regarding the nature of the pharyngeal sensations, our case underwent prolonged extracranial video-EEG monitoring. RESULTS: Video-EEG information documented the epileptic origin of the dysesthesias and was concordant with the side and location of the amygdalar lesion. CONCLUSIONS: Pharyngeal dysesthetic auras may be produced by epileptic activity originating from the amygdala, and perhaps other mediotemporal structures. The underlying topography of this aura is not known with certainty, and it may reflect seizure spread from the amygdala and adjacent areas to the closely interconnected insular and opercular cortex, whose secondary activation could elicit similar sensations.