Uzyskanie remisji napadów padaczkowych w zależności od przyczyny epilepsji: badanie kohortowe retrospektywne
Seizure remission according to epilepsy etiology: A retrospective cohort study
W skrócie
Badanie wykazało, że przyczyna epilepsji ma duży wpływ na to, czy leki zmniejszą lub zatrzymają napady padaczkowe. Pacjenci z genetyczną przyczyną epilepsji i ci, których epilepsja pojawiła się po udarze mózgu, mieli lepsze szanse na wyleczenie, podczas gdy pacjenci z wadami rozwojowymi kory mózgowej mieli gorszą prognozę. Ogółem prawie połowa zbadanych pacjentów uzyskała trwałą remisję napadów (przez co najmniej rok bez napadów).
Oryginalny abstract (angielski)
OBJECTIVE: To evaluate whether seizure outcomes of pharmacological treatment are associated with clinical characteristics, epilepsy type, and underlying etiology. METHODS: We retrospectively analyzed demographic and clinical data of 815 patients with epilepsy. Etiologies were classified using the ILAE framework. Seizure remission was defined as seizure freedom for at least 12 months. Clinical variables, treatment patterns, and etiological distributions were compared between seizure-free and non-seizure-free patients. RESULTS: The study population included 485 women (59.5%). The median age at last follow-up was 35.0 years. Structural etiology was identified in 31.7% of patients, genetic/presumed genetic etiology in 27.4%, infectious etiology in 4.5%, and unknown etiology in 36.1%. Overall, 372 patients (45.6%) achieved seizure remission. Age and sex did not differ between groups. Seizure-free patients had shorter epilepsy duration and were more often treated with monotherapy. Genetic/presumed genetic etiologies, especially idiopathic generalized epilepsy (IGE), were more frequent among seizure-free patients. Within structural etiologies, post-ischemic stroke epilepsy was associated with remission, whereas malformations of cortical development predicted persistent seizures. After adjustment for age, sex, epilepsy duration, and treatment regimen, IGE remained independently associated with a higher likelihood of remission (OR 1.72, 95% CI 1.17-2.53, p = 0.006), as did post-ischemic stroke epilepsy (OR 3.91, 95% CI 1.09-14.05, p = 0.037), while malformations of cortical development predicted lower remission probability (OR 0.33, 95% CI 0.14-0.78, p = 0.012). CONCLUSIONS: Seizure outcomes are strongly associated with epilepsy etiology. IGE and post-ischemic stroke epilepsy are associated with favorable outcomes, whereas malformations of cortical development are linked to poorer prognosis, underscoring the clinical value of etiological classification.