Abstracts

Rationale: Based upon four cases of SUDEP we suggested in 2007 a possible association between SUDEP in females and the use of lamotrigine (Aurlien et al, Acta Neurol Scand, 2007;115:199-203). Recently, we presented the preliminary findings from our study in Rogaland county, Norway where we identified 26 cases of SUDEP; 16 definite, 3 probable and 7 possible; 15 females and 11 males (Aurlien et al., AES 2010 (Abst. 3.136)). Here we present a nested case control study in which the clinical data from the 26 SUDEP cases were compared with corresponding data from a control group. Since the exact number of individuals in our county with a prescription of each AED is available from the years 2004 and 2005 (The Norwegian Prescription Database: www.reseptregisteret.no) we also estimated a corrected incidence of SUDEP in patients that were treated with lamotrigine (LTG), carbamazepine (CBZ) and valproate (VPA). Methods: For each SUDEP victim we randomly selected at least 3 living controls that had been registered in the database of Stavanger University Hospital with a diagnosis of epilepsy in the same year as the SUDEP case occurred. First: to investigate whether age or gender could be risk factors for SUDEP a primary unmatched control group was selected. Second: for the remaining analyses a new secondary control group was selected, matched with the deceased by age and gender. The estimated number of individuals at risk on LTG, VPA and CBZ through the 10-year period was corrected for the ratio between the exact number in 2005 and the originally estimated number, based on the market share in defined daily doses. A corrected incidence of SUDEP on each AED was calculated. As 58 % of the individuals on LTG in 2005 were females we also corrected the incidence in females on LTG, assuming the same proportion of female users through the whole 10-year period.Results: 7/12 (58.3 %) of females with definite and probable SUDEP and 10/41 (24.4 %) of controls were on LTG (p = 0.038). In females, the corrected incidence of definite and probable SUDEP on LTG was estimated as 2.5 per 1000 patient-years and 0.5 per 1000 patient-years in women not on LTG (p = 0.007). At the group level (males and females) the difference between cases and controls did not reach statistical significance (p = 0.111). For VPA and CBZ the difference between cases and controls was statistically insignificant as were the difference between the incidence of SUDEP in those that were treated with VPA or CBZ compared with the incidence in patients that were not on these drugs. Age and gender did not differ significantly between cases and unmatched controls. We could not identify risk factors that could represent alternative explanations for the deaths in the deceased that were treated with LTG. Conclusions: The risk of SUDEP was significantly increased in females being treated with LTG. No differences were found for the other investigated drugs or in males. Our findings may have implications for the treatment of epilepsy in females.