Introduction the Clinical Features of Nocturnal Frontal Lobe Epilepsy (nfle) Consist of a Spectrum of Paroxysmal Motor Manifestations of Increasing Complexity and Duration1-4 Occurring during Non–rapid-eye- Movement

THE CLINICAL FEATURES OF NOCTURNAL FRONTAL LOBE EPILEPSY (NFLE) CONSIST OF A SPECTRUM OF PAROXYSMAL MOTOR MANIFESTATIONS OF INCREASING COMPLEXITY AND DURATION1-4 OCCURRING DURING NON–RAPID-EYEMOVEMENT (NREM) SLEEP. These include a) minor events,1-5 represented by short-lasting (2-4 seconds) stereotyped movements involving the limbs, the axial musculature and/or the head; b) paroxysmal arousals (PA),2,4 characterized by frequent and recurring abrupt brief arousals lasting about 5 to 10 seconds, accompanied by stereotyped movements (trunk and head elevation) often associated with vocalization and frightened expression; and c) major attacks, previously defined under the term of nocturnal paroxysmal dystonia (NPD),2,4,6,7 which are characterized by stereotyped movements such as asymmetric tonic or dystonic posturing or other bizarre behaviors (choreoathetoid and ballistic movements of the limbs) lasting about 20 to 30 seconds These manifestations may coexist in the same patient,1-5,7 and it has been postulated that the increasing complexity of the ictal motor behavior reflects a different duration and propagation of the discharge within the frontal lobe.4 Unfortunately, this hypothesis has not been corroborated by conventional electrophysiologic data, since, in most of these cases, scalp electroencephalography (EEG) does not show definite ictal abnormalities.1-5 This may be explained by an origin of the discharge in structures whose activity is not easily detectable by EEG surface electrodes, as the mesial frontal cortex. Indeed some NPD attacks seem to originate in the supplementary motor area (SMA) or the cingulate gyrus (CG).8-11 A definite electroclinical correlation of the whole spectrum of nocturnal paroxysmal motor events occurring in NFLE is still lacking. Moreover, the possible ictal origin of minor episodes has not yet been assessed by electrophysiologic investigations. The present report is the first demonstration, by the employment of intracerebral recordings and with the corroboration of the postoperative outcome, that these seizures can be provoked by discharges involving primarily the SMA and the CG.