Consistent EEG Focalities Detected in Subjects with Primary Generalized Epilepsies Monitored for Two Decades

Abstract

Summary:Purpose: To describe the evolution of interictal findings in serial EEGs from patients with primary generalized epilepsy.Methods: A cohort of 89 subjects with various primary generalized epilepsies were reviewed. Thirty-one did not meet a priori criteria. Of the 58 patients analyzed, 12 had only absence seizures, 28 had absence seizures followed by one or more generalized tonic-clonic seizures, 9 had generalized tonicclonic seizures followed by absence and/or myoclonic seizures, and 9 had juvenile myoclonic epilepsy. Patients were followed for a mean of 16 years. An average of 39 EEGs were obtained on each patient.Results: Thirty-two patients (56%) had focal features present in up to 65% of the EEGs in each of the patients. Accepted focalities were only those that were consistent in lateralization, location and, often, morphology across the span of the study. Focal findings were most often temporal or frontal.Conclusions: Patients with typical primary generalized epilepsies show a high incidence of focal EEG features that cannot be explainea on the basis of structural lesions, coincidental factors, or to artifacts of the selection criteria. Although the data do not allow a definitive explanation, possible mechanisms include associated focal cortical pathology such as microdysgenesis, and development over time of localized, self-sustaining hyperexcitability in low-threshold cortical structures subjected to repeated generalized spike-wave activity. Either hypothesis implies the participation and interaction of genetic, ontogenic, and environmental factors. Key Words: Focal electroencephalograms-Idiopathic generalized epilepsy-Longterm follow-up.The classification of epilepsies and epileptic syndromes proposed in 1989 (1) defines the idiopathic (primary) generalized epilepsies (ICE) as those whose seizure phenotypes indicate the involvement of -both hemispheres from the onset, both clinically and electrographically. By definition, the IGE show no evidence of structural brain lesions, in contrast to the secondarily generalized group of epilepsies, and no known or suspected etiology other than the contributions of polygenic factors. Their EEG expression (ictally or interictally) consists of initially generalized, bilaterally symmetrical discharges, whereas the background patterns are normal for age.Despite many efforts made in the past half century by both clinicians and neuroscientists, the pathophysiology of IGE remains unsettled. Among still-controversial issues are the predicated complete lack of structural brain lesions and the precise role played by the cortex.A long-term follow-up in a population of subjects with ICE shows that their EEGs often contain focal abnormalities that are persistent and consistent in location-an

Epileptiform Asymetries and Treatment Response in Juvenile Myoclonic Epilepsy

“…Lombroso 13 described the evolution of interictal findings in serial EEGs from patients with primary generalized epilepsy and found 56% of patients with consistent EEG asymmetries. He proposed two possible explanations: focal cortical pathology such as microdysgenesis or development of localized, selfsustaining hyperexcitability in low-threshold cortical structures subjected to repeated generalized epileptiform activity.…”

Auras Are Frequent in Patients with Generalized Epilepsy

“…The clinical semiology of generalized from onset seizures commonly includes focal features such as version or asymmetric myoclonus (5). Surface EEG frequently contains shifting focal as well as generalized spike wave discharges (6). Dense array EEG shows a more focal ictal onset in some presumed generalized seizures (7), and fMRI and MEG studies identify specific cortical involvement in spike wave discharges (8,9).…”

Auras in generalized epilepsy

“…These findings tend to be intermittent and shifting in laterality. 15,[23][24][25] Densearray EEG analysis of patients with absence epilepsy demonstrated ictal onsets, often unilateral, arising from the dorsolateral frontal or orbital frontal lobe followed by stereotyped evolution to involve both mesial frontal and orbital frontal structures. 26 Auras and other "focal" features in patients with GE can lead to the misdiagnosis of FE.…”