Chapter 26 - Seizure control in brain tumors

Abstract

Epilepsy is common in brain tumors, 30–70% of all patients develop symptomatic epilepsy which considerably influences the daily life of this patient group. Low-grade tumors and a cortical location are the most important factors predicting the development of epilepsy in brain tumor. Low-grade brain tumors present with seizures in 60–85%, malignant gliomas in 20–40%, and both groups experience seizures in 10–30% later in the course of the illness. Epileptogenesis in brain tumors is multifactorial, and includes the influence of tumor type, peritumoral changes in the microenvironment, and genetic changes. Refractory epilepsy is common in patients with brain tumors. The multidrug resistance pathway affecting the transport of antiepileptic drugs (AEDs) into the brain parenchyma probably explains why seizures are often difficult to control in patients with brain tumors. There are few hard data regarding the best medical treatment. Special considerations such as the potential of interactions of AEDs with chemotherapeutic agents and a greater likelihood of side-effects probably require a particular approach to the appropriate epileptic treatment in patients with brain tumors. Meta-analysis does not support the prophylactic use of AEDs in patients with brain tumors. A consensus statement has recommended that AEDs should not be used, and that they should be withdrawn in the first week after surgery if given preoperatively, in patients with brain tumors who never have experienced a seizure. The treatment of epilepsy in brain tumor is similar to that of other conditions associated with symptomatic localization-dependent epilepsy, apart from specific conditions associated with brain tumors including prevention of common interactions with concomitantly administered chemotherapy or corticosteroids. Because of potential inefficacy of chemotherapy, the use of enzyme-inducing antiepileptic drugs (EIAEDs) in patients with a brain tumor is discouraged. As first- or second-line anticonvulsants, lamotrigine, valproic acid, or topiramate may be chosen, and, if insufficient, add-on therapy with either levetiracetam or gabapentin can be recommended as these latter two anticonvulsants have no apparent interactions with other drugs, including chemotherapeutic agents. Based on practical considerations and clinical studies, it is the authors’ preference to start with valproic acid and, if insufficient, to use it in combination with levetiracetam.