Abstract
INTRODUCTION: Epilepsy in cancer patients has a prevalence of 13%, and is especially high in patients with brain tumours, with a higher morbidity and mortality rate compared to non-tumour-related epilepsy. Its physiopathogenic mechanisms are distinct and include distortion of the cortical architecture and alteration of the glutamate-enhancing tumoural and peritumoural molecular microenvironment. Nevertheless, there is scarce and inconsistent scientific evidence on some fundamental aspects, such as primary post-operative prophylaxis, the ideal pharmacological profile or the withdrawal time of antiseizure drugs after their release. DEVELOPMENT: Characteristics such as low tumour grade, number/size of cortical lesions, location (frontal, cortical/subcortical or eloquent area), early seizures and molecular alterations, such as IDH1/2 mutation, are factors that favour the occurrence of seizures. Within the treatment, surgery will provide cytoreduction and seizure control by excision of the epileptogenic area, with 75-90% freedom from disabling seizures. Although still a controversial issue, the post-operative use of antiseizure drugs is contraindicated by the main scientific societies due to the scarce evidence and the wide spectrum of side effects. However, they are frequently used in daily clinical practice. CONCLUSIONS: All this forces us to establish a group of patients at 'high risk' of postoperative seizures, who will need to select the ideal antiseizure drug for primary prevention, with a route of administration that facilitates a rapid action effect and pharmacokinetics that prevents hepatic metabolism and CYP450 induction to achieve a lower number of interactions with chemotherapy, corticosteroids and radiotherapy. Despite this, drug resistance rates of 20-40% and relapse rates of 25-29% have been reported.