Abstracts

Rationale: Tumor-associated seizures and epilepsy in patients with primary malignant brain tumors constitute a major healthcare challenge not only to patients, but also to the providers who are responsible for treatment of both the primary disease and these comorbidities. Over 80% of glioma patients report at least 1 seizure during the course of their disease and up to 35% of them develop tumor-associated epilepsy [1]. Seizures and antiepileptic drugs (AEDs) used in their management significantly impact patients' quality of life. Furthermore, despite this profound impact, there is a dearth of information regarding the actual effects of AEDs on cortical irritability as measured by electroencephalograms (EEGs). Herein, we investigated the effects of various AEDs on the presence or absence of epileptiform discharges (EDs) in patients with primary brain tumors. Methods: We identified 210 patients who had a pathologically confirmed diagnosis of a primary glioma and who had undergone at least 1 EEG at our institution from 01/01/2009 to 12/31/2013. Exclusion criteria included prior diagnosis of epilepsy, absence of tissue confirming diagnosis, and inability to obtain EEG for review. All EEGs were independently reviewed and scored for the presence and frequency of EDs (abundant, frequent, occasional, and rare). AEDs taken by the patient at the time of EEG were also recorded. Results: "Last available" EEGs were reviewed on 149 patients (M=75, F=74, mean age at time of EEG=51 SD-14.2). Eighty-five percent of patients had high-grade glioma (HGG); 81 GBM, 22 Anaplastic Astrocytoma, 13 Anaplastic Oligodendroglioma, 9 Mixed Oligoastrocytoma, 1 Gliosarcoma. Fifteen percent had low-grade glioma (LGG); 7 Astrocytoma WHO grade II, 9 Oligoastrocytoma WHO grade II, 1 Ganglioglioma, 5 Mixed Glioma WHO grade II, 1 Pleomorphic Xanthroastrocytoma. EDs were identified in 34.2% of all patients; in 27.3% of those with LGG and in 35.8% of those with HGG. We noted that patients with HGG had a higher incidence of EDs in the EEG than those with LGG, however this difference was not significant (35.8% vs. 27.3%, p=0.44). Further, we did not observe a specific effect of any of the AEDs used on the presence/absence of EDs (p>0.05 for levetiracetam, valproate, lacosamide, zonisamide, or topiramate). Other AEDs, including phenytoin, were used infrequently (in less than 30 patients per AED). Conclusions: Our retrospective data indicate that there is no correlation between AED(s) used and cortical irritability as measured by EEG in patients with gliomas who are currently being treated with AEDs. This is an interesting and important observation. Prospective clinical trials are needed to assess the role of EEG in guiding treatment decisions, as related to AED therapy and choice, in this specialized population. Further, the value of pre-treatment EEG as a possible biomarker for the development of tumor-related epilepsy needs to be further evaluated. 1. Hildebrand, J., et al., Epileptic seizures during follow-up of patients treated for primary brain tumors. Neurology, 2005. 65(2): p. 212-5.