Abstracts

Rationale: Epilepsy incidence in gliomas ranges between 30-80%. Low-grade gliomas are more epileptogenic than less benign brain tumours and for this reason epilepsy has been considered a positive prognostic factor. Seizures may represent the symptom carrying out the diagnosis and seem to be more frequent in frontal and parietal lobe gliomas. Epileptogenesis in glioma is multifactorial and it may explain drug resistance that usually occur in more than 30% of patients. Although it is known that the AED are not antiepileptogenic, prophylaxis in gliomas still remains an open question. Methods: Between February 1th 2004 and April 1th 2006 all patients with glioma, who underwent surgical treatment at the Neurosurgery Division of Bolzano were prospectively unrolled on the study (last evaluation in April 1th 2007). At the enrolment time on the study (surgery time) patients were included in a list of progressive numbers. Epileptic patients enrolled with pair number and with impair number were respectively treated with PHT and LVT. However, patients with different therapy were not shifted on PHT or LVT, if seizure-free. Clinical, histological, and MRI features were analyzed. Results: 64 patients (35 male and 29 female) were enrolled on the study. Age at the diagnosis ranged from 30 to 78 yrs (mean: 57 ± 12 yrs). Duration of disease ranged from 50 days to 8.8 yrs (median: 18 mo). Onset seizure type was focal (17), secondarily generalized (10), and epileptic status (2). Epilepsy diagnosis was made in 27 (42%) cases. Ictal semeiology was motor (8), sensitive (3), focal complex (11) and convulsive (5). Histological diagnosis was astrocytoma (3), mixed glioma (3), oligodendroglioma (10), malignant astrocytoma (4), and glioblastoma multiforme (GBM) (44). Surgical resection was total in 34, subtotal in 21 and partial in 9 cases. Adjunctive therapy was chemiotherapy (38) and/or radiotherapy (41). Glioma recurred in 46 pts and epilepsy first appeared in three of them. At the last follow-up 13/27 (48%) patients were seizure-free. Antiepileptic drugs included: PHT (10), LVT (6), CBZ (6), OXC (2), CBZ + PB (2), PB (1). All patients without AED never developed seizures during the follow-up (12 pts) or until death (23 pts). Epilepsy correlated with low-grade glioma (p=0.02), and MRI cystic component (p=0.04). Amongst highest grade gliomas, epilepsy was more frequent in GBM deriving from a low-grade tumour (p=0.02). Conclusions: 1) Seizures in glioma represent a quite exclusive onset symptom, that rarely occurs at the glioma recurrence and never during a “radiologically” stable disease. 2) Radiological and histological features indicating a low malignancy and/or a slow growing are associated to a highest epilepsy incidence. 3) A poor seizure control is associated with: motor and sensitive focal seizures; abnormal neurological examination; radiotherapy; high-grade glioma diagnosis. 4) LVT is more effective compared to old AES. 5) The absence of AED prophylactic role is prospectically confirmed.