Abstracts

Rationale: Hypermotor seizures are defined by complex movements involving the proximal segments of the limbs and trunk.Even though there is no conclusive proof on the location of the symptomatogenic zone,it has been postulated that it is most likely located in the frontal lobes.We report two cases of hypermotor seizures with no evidence of ictal activity in the depth electrodes covering the frontal lobes.Methods: Case reportResults: Case1A 39-year-old man presented with medically refractory focal epilepsy.His typical seizures occurred out of sleep and were characterized by violent and random proximal extremity movements accompanied by nonsensical vocalizations,followed by oral automatisms with postictal confusion.Occasionally his seizures progressed into a left versive seizure with subsequent secondarily generalized tonic-clonic seizures.Epilepsy protocol MRI was unremarkable.Given the intractable nature of his epilepsy,he underwent depth electrode implantation covering the right frontal lobe,temporal pole,amygdala,hippocampal body and head, anterior and posterior insula, posterior temporal lobe,and the cingulate gyrus.3 typical seizures were recorded all originating in the hippocampal head and body.There was no frontal lobe involvement during all phases of these typical hypermotor seizures.A right temporal lobectomy was performed and the pathology revealed a focal cortical dysplasia,Palmini grade 1A.Case2A 15-year-old girl with medically refractory seizures,whose seizures started with an aura of vibration in the left hemibody,followed by laughing, limb flailing and side-to-side truncal movements with preserved awareness.Brain MRI was unrevealing.She underwent depth electrode implantation,sampling the premotor frontal lobe in a 3x3 grid from the parasagittal to the lateral cortex with 2 additional electrodes in the anterior and the posterior insula given the aura.All of her 9 hypermotor seizures originated in the posterior insular depth electrode with no involvement of the frontal electrodes at any time during her typical hypermotor seizures.These 2 cases illustrate hypermotor seizure semiology with no evidence of ictal activity on stereotactic evaluation of the frontal lobes.Conclusions: Hypermotor seizures are usually thought to originate in the frontal lobes.However,the exact location of the symptomatogenic zone of these seizures is under debate.Both of our cases had extensive stereotactic coverage of the frontal lobes in addition to the hippocampus in case 1 and insula in case 2.The extra frontal coverage was guided by the automatisms and vibration aura in these 2 cases respectively.The findings of the invasive study strongly suggests that hypermotor seizures may originate from an area outside of the frontal lobes.In some cases where clear frontal lobe ictal activity is not seen, the depth electrode coverage should be expanded to sample other regions of the brain.In addition, this observation also supports Williamson and Jobst1 conclusion that hypermotor seizures may not be the expression of an activation of a specific brain region but a release phenomenon of subcortical motor centers from their cortical control.