Abstracts

Rationale: The signal study of Sillanpaa (Sillanpää Engl J Med. 2010) suggested that at the onset of epilepsy children had a 7% lifetime risk of SUDEP, mainly in their adult years. Our goal was to confirm or refute this assertion using the much larger Nova Scotia childhood onset, population-based epilepsy study.  Methods: All children in Nova Scotia with new onset epilepsy (incidence cases) between 1977-85 form the Nova Scotia cohort. Patients with normal intelligence and any type of epilepsy except Childhood Absence Epilepsy were selected. Patients were followed up by personal telephone interviews with parents and/or patients by the authors.  Results: 421 patients met the entry criteria. For the 412 survivors, age at epilepsy onset averaged 6.8±4 years (range 1month-16 years) with a follow up averaging 23.9±8.6 years (range 1-42 years). Quartiles for follow up were 25% 20 years, 50% 27 years, 75% 31 years, 100% 42 years. On average at the end of follow up patients were in mid adulthood (30.5±10.5 years). The cause of epilepsy was unknown in 50% and considered “remote symptomatic’ in 59 (14%). Considering risk factors for SUDEP,  at the end of follow up, 122 (29%) were still receiving AEDs and 18% had active epilepsy (≥1 seizure of any type in the last year of follow up) and 9% had ≥1 generalized tonic clonic seizure (GTC) (primary GTC or evolving from focal onset) in the last year. Throughout the clinical course, 313 (75%) had ≥1 generalized tonic clonic seizure with 103 (25%) having >20. We do not know how often these GTCs occurred during sleep.  A total of 42 patients had intractable epilepsy at the end of follow up. During the clinical course 21 had epilepsy surgery (Engle outcome class 1&2, n=15). During follow up 9 patients died at an average age of 29 years ±13.5 years (range 5-40 years). Causes of death were directly related to epilepsy in 2 cases (status epilepticus and drowning during a witnessed seizure) and from non epilepsy causes in 6 (suicide, homicide, accident, colonic cancer, cardiomyopathy, myocardial infarction, aspiration pneumonia not related to a seizure). There was not a single case of definite or probable SUDEP during a total of 10,015 person years of follow up. Conclusions: Children with normal intelligence who develop epilepsy appear to have an extremely low risk of SUDEP during childhood and up to mid-adulthood, even if their epilepsy persists. The cohort described in this abstract is population-based and includes only incidence cases with normal intelligence. The lower rate of remote symptomatic epilepsy (14%) than the Turku, Finland cohort (50%) may explain our different, but very reassuring results.  Funding: none