Idiopathic generalized epilepsy

Abstract

Successful treatment of idiopathic generalized epilepsy begins with accurate seizure classification. Seizure types, such as absence, myoclonic, and primary generalized tonic-clonic seizures (PGTCS), often can be classified based on a detailed history and inter-ictal electroencephalogram (EEG). Ideally, patients can be classified into specific epilepsy syndromes, such as childhood absence epilepsy, juvenile myoclonic epilepsy (JME), or generalized tonic-clonic seizures on awakening. Idiopathic generalized epilepsy should be distinguished from focal epilepsy with rapid secondary generalization. If this distinction is not clear after history, physical examination, and routine inter-ictal EEG, then ambulatory EEG, video EEG monitoring, or neuroimaging studies may be needed. Ethosuximide, valproate, or lamotrigine are all appropriate first-line choices in the treatment of childhood absence epilepsy. The specific medication should be chosen based on the side effect profiles, dosing formulations, and titration schedules of the medications. The available evidence best supports valproate as the first-line choice in the treatment of JME, although lamotrigine and topiramate may be appropriate choices in this setting. More data specific to JME are needed to clarify the role of medications such as levetiracetam and zonisamide in the treatment of JME. The available evidence to guide the treatment of PGTCS is limited, because most trials did not rigorously exclude patients with focal epilepsy with rapid secondary generalization. Available evidence suggests that valproate is an appropriate first-line choice for PGTCE. Lamotrigine or topiramate also may be appropriate choices. More data are needed to clarify the role of levetiracetam and zonisamide in the treatment of PGCTS. If it is unclear whether a patient has idiopathic generalized epilepsy or focal epilepsy with secondary generalization, then a broad-spectrum anticonvulsant, including valproate, lamotrigine, or topiramate, should be considered. More data are needed to support the broad-spectrum efficacy of levetiracetam and zonisamide.

Effects of levetiracetam on EEG abnormalities in juvenile myoclonic epilepsy

“…It is generally agreed that valproate is the current treatment for JME and it is effective in as many as 80–85% of patients (Gelisse et al, 2001). Among newer AEDs, lamotrigine and topiramate have been proposed in the treatment of JME, but controlled trials are lacking and the results are not focused on EEG abnormalities (Panayiotopoulos 2001; Sullivan & Dlugos, 2004; Sousa Pda et al, 2005).…”

“…Among newer antiepileptic drugs (AEDs), lamotrigine, topiramate, and zonisamide have been controversially reported to be effective in JME on the basis of uncontrolled studies in small groups of patients (Carrazana & Wheeler, 2001; Panayiotopoulos, 2001; Sousa Pda et al, 2005; Sullivan & Dlugos, 2004; Kothare et al, 2004). In these studies no electrographic results were reported.…”

Thalamofrontal neurodevelopment in new-onset pediatric idiopathic generalized epilepsy

“…33 We did not find differences in volumes between those not treated with valproate and those treated with valproate, commonly the first-line treatment of choice in IGE. 34 In addition, no volume differences were evident between children whose first medication was valproate and children whose first medication was not valproate. If AED effects were present, they were uniform across subjects and not dependent upon drug type.…”

Defining the clinical role of pharmacogenetics in antiepileptic drug therapy

“…Based on clinical trial data, mechanisms of action, and clinical experience, certain AEDs are generally preferred for focal epilepsy (CBZ, OXC, PHT) and other AEDs are preferred for generalized epilepsy (VPA, ETX, LTG, TPM). 1,2 With rare exceptions, such as VGB as the preferred AED for infantile spasms due to tuberous sclerosis, 3 etiology of epilepsy plays little or no role in AED selection. Similarly, since studies have not yet begun to address genetic determinants of drug efficacy, pharmacogenetics also currently plays no role.…”