Les études de suivi à long terme des épilepsies généralisées idiopathiques (EGI) indiquent un faible taux de rémission, suggérant leur persistance à un âge avancé. La fréquence des EGI dans cette tranche d’âge reste cependant incertaine.

Les EEG de 700 patients consécutifs de plus de 70 ans à l’hôpital Charles-Foix ont été inspectés à la recherche d’anomalies évocatrices d’EGI ; l’histoire des patients ayant ces anomalies a été revue.

Quatre patientes (âge moyen de 79 ans) furent retenues et présentaient une EGI ancienne : deux une épilepsie myoclonique juvénile et deux une épilepsie avec crises grand mal. Le diagnostic d’EGI n’était pas connu et leur maladie n’était pas ou peu active avant l’hospitalisation. L’événement révélateur fut un épisode plus grave que d’habitude : état d’absence (EA), crises myocloniques subintrantes ou crises généralisées convulsives (CGC). La découverte du diagnostic a permis de guider la prise en charge thérapeutique : arrêt d’une aggravation iatrogène, initiation ou continuation d’un traitement adapté.

Les EGI peuvent se manifester à un âge avancé par une exacerbation des crises, incluant EA, myoclonies subintrantes et CGC répétées, après une longue période quiescente. Elles ne semblent pas rares mais, difficiles à identifier, elles sont vraisemblablement sous-estimées. Leur diagnostic est pourtant un gage de réussite thérapeutique.

Long-term follow-up studies indicate a low remission rate in idiopathic generalised epilepsies (IGE) (Martinez-Juarez et al., 2006), suggesting they may persist to an advanced age. However there are few estimates of IGE frequency in the elderly.

EEGs of 700 patients aged over 70 years, recorded between January 2006 and March 2007, were reviewed for anomalies consistent with IGE. We then examined the clinical history of patients with these anomalies.

A persistent IGE was identified in four female patients (mean age: 79 years); in two cases it was a juvenile myoclonic epilepsy (JME) and in two an epilepsy with grand mal seizures. Seizures in three patients had begun in childhood or adolescence and in one at 40 years. Before hospitalization, few or no seizures were reported and IGE had not been diagnosed. IGE was revealed in each patient by a relatively severe event: an absence status (AS), subcontinuous myoclonic seizures or repeated convulsive generalised seizures (CGS). These events were not situation-related but in one patient the relapse of simple convulsive seizures, may have been related to the withdrawal of anti-epileptic drugs (AED) several months previously. EEG records showed generalised spikes or polyspikes and waves organised in a status epilepticus or in interictal rhythmic discharges. In one case they were evident only from a 24hours recording. Clonazepam injection was used to suppress the AS episode and the subintrant myoclonia. After the AS, interictal generalised epileptic discharges persisted. Two of the four patients had familial history of epilepsy or febrile seizures but in no case was an epileptogenic lesion evident in brain CT scan or MRI. Clinical exams and biologic parameters were normal. All of the patients had worked and were married with children. Appropriate therapies were followed after the diagnosis of IGE. One patient with JME had been treated by Valproate which was discontinued by the general practitioner because of lethargy and replaced by Carbamazepine; seizures were aggravated under both Carbamazepine and then Lamotrigine and until the patient became seizure-free on Levetiracetam. The antiepiletic treatment was also modified in a second patient, while the two others responded well to Valproate.

IGE can exacerbate in the elderly, as different types of seizures including AS, subintrant myoclonia or repeated CGS. Our data suggest persistent IGE are quite frequent in an aged population and may be underestimated due to difficulties in diagnosis. Correctly diagnosed, adjustment of AED may offer substantial clinical improvements in IGE of the elderly.