The distinction between absence petit mal and psychomotor seizures

Abstract

A brief discussion of the manifestations of limbic lobe discharge as opposed to discharge in neocortical temporal lobe structures is given. The opinion is expressed that, apart from certain characteristic limbic auras, the manifestations of psychomotor epilepsy are those of inactivation of brain stem mechanisms subserving consciousness. A brief discussion of other manifestations of inactivation of brain stem mechanisms subserving various other functions, as seen in other clinical patterns of epileptic discharge, follows. Hippocampal sclerosis is put forth as the cause rather than the result of seizures in both the juvenile and the adult age groups. It is proposed that limbic lobe structures have a low threshold for initiating epileptic discharge when injured, are predisposed to injury and give rise to discharge which has preferential access to brain stem structures. It is stated that petit mal absences and psychomotor attacks are clinically indistinguishable. The further opinion is expressed that the 3 per second wave and spike EEG pattern associated with petit mal is an epiphenomenon dependent upon the maturational stage of development of the brain at the time when the causative lesion responsible for epilepsy is acquired. The view that the 3 per second wave and spike pattern is a direct correlate of the clinical manifestations of epilepsy, in those patients who show this pattern, is challenged. It is concluded that the pattern is the result of rostral brain stem discharge acting upon the cortex. The view is offered that two factors are necessary for the development of epilepsy: (1) an adequate pathological basis in the form of a cerebral lesion and (2) a greater or lesser predisposition toward inadequate biochemical mechanisms tending to check or control the spread of seizure discharge, the latter being in all probability at least partially genetically determined. It is concluded that triggering cortical foci exist in nearly all cases of epilepsy, though the participation of brain stem structures is essential to explain many of the clinical and EEG manifestations of the attack.