Late Onset Idiopathic Generalized Epilepsy: A Clinical Analysis of 33 Cases.
Abstract number :
G.03
Submission category :
Year :
2001
Submission ID :
246
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
M.A. King, MD, Epilepsy Research Institute, Austin and Repatriation Medical Centre, Melbourne, Victoria, Australia; C. Marini, MD, Epilepsy Research Institute, Austin and Repatriation Medical Centre, Melbourne, Victoria, Australia; J. Archer, MD, Brain Re
RATIONALE: Idiopathic generalised epilepsy (IGE) beginning in adult life, is considered rare and in the majority of cases it is thought to be a relapse from a childhood disorder. We studied late onset IGE in a setting of a first seizure clinic in a general hospital.
METHODS: 121 consecutive patients with an electro-clinical diagnosis of IGE were collected from our first seizure clinic. Patients at this clinic undergo an early EEG, ideally within 24 hours of the seizure. If this is not conclusive a sleep deprived study is performed. Late onset IGE was defined as the first seizure ever manifesting after the age of 20 years.
RESULTS: 33/121 (27%) patients were diagnosed as late onset IGE. Tonic clonic seizures (TCS) were the presenting symptom in all, commonly precipitated by alcohol or sleep deprivation. The patients were divided according to seizure types into: TCS + absence (n=3), TCS + myoclonus (n=6) and TCS alone (n=24). Nineteen were treated with valproate, 5 with other antiepileptic drugs and 9 were untreated. Follow-up of 24 months revealed that TCS seizures recurred in 5 patients only with provocative factors or when they discontinued the medication. About half of the older IGE patients, similar to the younger cohort with IGE, had relatives with epilepsy or febrile seizures.
CONCLUSIONS: Late onset IGE is not rare and easily controlled. We suspect that patients are often misdiagnosed as having non-lesional partial epilepsy. Early post-ictal EEG and sleep deprived EEG study may improve the detection of these patients. Our preliminary clinical genetic analysis suggests a common genetic origin with classical IGE.
Support: The National Health & Medical Research Council, Australian Research Council, Bionomics Limited and University of Melbourne Scholarship