Abstracts

Rationale: Measurements of electrodermal activity (EDA) provide information about sympathetic dysfunction during seizures and can be used as a biomarker for seizure detection, particularly for secondary generalized tonic-clonic seizures (sGTCS). To date, limited data are available about EDA during other seizure types, such as complex partial (CPS) and primary generalized seizures (GS) to inform potential future studies establishing EDA as biomarker for seizure detection, SUDEP risk and treatment response. Methods: Patients with epilepsy who were admitted to the video EEG monitoring units were prospectively enrolled and underwent continuous EDA monitoring. Patients with vagus nerve stimulator, skin conditions or autonomic disorders were excluded. EDA of captured CPS, GS and sGTCS were analyzed using a MatLab based algorithm and EDA increase after seizure, tonic baseline EDA over 24 hours, area under the curve (AUC) power, AUC duration, AUC from the slope 10% and 90%) was calculated after epileptic seizures. Results: We evaluated 48 patients with a median age of 22.1 years [standard deviation (SD): 18.5; interquartile range (IQR): 7.1 - 36.5] including 18 (37.5%) females. The median of seizure duration was 5.2 years (SD: 14; IQR: 2.8-19.7). Genetic epilepsy etiology was found in 6 (12.5%) patients, structural/metabolic in 22 (45.8%) patients, and unknown in 20 (41.7%) patients. MRIs of 27 (56.3%) patients demonstrated lesions. CPS was captured in 26 patients (54.2%), GS in 11 (22.9%) patients, and sGTCS in 11 (22.9%) patients. Forty-seven patients were using antiepileptic drugs (AED): (i) one AED: 6 (12.8%); two AED: 21 (44.7%); more than 3 AED: 20 (42.5%). EDA increases related to a seizure were observed in 38/48 (79.2%) patients. EDA increase distribution by seizure type was as follows: (i) CPS 19/26 (73%) patients, (ii) GS 8/11 (72.7%), and (iii) SGTCS 11/11 (100%). The median of seizures per patient was 2 (SD: 6.6; range: 1 - 31). A median of one (SD: 2.7; range: 0 - 17) EDA peak was observed per patient; and the median EDA peak percentage per seizure was 67.3% (SD: 41%; IQR: 18.4%-100%). See Table 1. Restricting the analysis to CPS, EDA increases in the first seizure were observed in 11/26 (42.3%) patients and this proportion increased to 19/26 (73%) in subsequent seizures. Younger patients with CPS demonstrated significantly more often an EDA increase after the first seizure (Wilcoxon rank sum test, p=0.018). Additionally, the number of seizures were also higher in these patients in comparison to patients with no EDA change (p=0.041). EDA increases in CPS were significantly more often found in patients with non-lesional MRI (p=0.01), but these results were not significant in patients with GS (p=0.54). Conclusions: In addition to sGTCS, EDA increases are also observed in CPS and may be utilized as a clinical biomarker for seizure detection. This finding may be depending on age and the presence of MRI lesions, as younger patients and patients without MRI lesions more frequently with ictal EDA increases during CPS (Supported by Danny Did Foundation).