Abstracts

Rationale: Peri-ictal nose-wiping (NW) is a well-known seizure semiology in temporal lobe epilepsy (TLE). There was only one intracranial EEG study which supported the role of an amygdala involvement in the pathophysiology of NW. However, in that study, the insular cortex (IC) was not monitored.  Although IC involves in autonomic and sensory functions which are hypothesized to be the most likely causes of NW, seizures in the IC had never been reported as a cause of NW. In addition, NW had never been reprted during CS by an intracranial electrode. Methods: Four patients ages between 7 and 19 years with medically intractable epilepsy caused by focal cortical dysplasias who developed ictal NW during stereo-electroencephalography (SEEG) at the Children’s Hospital Colorado were studied. All patients had at least 2 depth EEG electrodes implanted in the IC by an oblique (anterior and posterior) approach. One patient (case 1) had an additional EEG electrode implanted by an orthogonal approach. Three out of four patients had simultaneous mesial temporal monitoring. All patients had been seizure free between 1 and 15 months after complete resection of an epileptogenic zone (EZ). NW disappeared in all cases after the surgeries. Results: Case 1: EZ was recorded in the posterior IC (original focus) and left superior temporal gyrus (STG) (immediate spreading). NW occurred during the ictal EEG onset in the left posterior IC. Cortical stimulation (CS) of the left IC did not reveal NW.Case 2: EZ was recorded in the left hippocampus and amygdala. NW occurred during late spreading of ictal discharges (ID) into the left anterior IC. CS of the left IC did not reveal NW.Case 3: EZ was recorded in the right hippocampus and amygdala. NW occurred during late spreading of ID into the right anterior IC. CS of the right IC did not reveal NW.Case 4: EZ was recorded in the left mesial, mid frontal and anterior cingulate gyri. NW occurred during immediate spreading of the ID into the left anterior IC. Resection of EZ in the left mesial mid frontal and anterior cingulate gyri was performed. CS of the left anterior IC without after discharges activated ipsilateral NW. The patient reported simultaneous nasal congestion and itching during NW. Conclusions: This is the first report of ictal NW caused by ictal discharges in the IC and of NW symptom induced by CS during SEEG. This study supports not only the role of the IC rather than the temporal cortex in the pathophysiology of NW but also the ictal rather than postictal nature of the peri-ictal NW. A combination of sensory (itching) and autonomic (nasal congestion) involvements are most likely to be the causes of NW as recorded during the CS in Case 4.  Funding: None