To characterize and classify neonatal seizures, we studied 349 neonates, using a portable, cribside EEG/polygraphic/video monitoring system. We recorded 415 clinical seizures in 71 infants; 11 other infants had electrical seizure activity without clinical accompaniments. Each seizure was analyzed in terms of its clinical character and its relationship to the presence of EEG seizure activity. Focal clonic seizures, some forms of myoclonic seizures, and focal tonic seizures were consistently associated with electrical seizure activity. Most "subtle" seizures, all generalized tonic seizures, and some forms of myoclonic seizures were either not associated with EEG seizure activity or had an inconsistent relationship with such activity. Seizures that were consistently and coherently related to focal EEG seizure activity had a high correlation with focal brain lesions and a favorable short-term outcome. Seizures with no relationship or an inconsistent relationship to EEG seizure activity were correlated with diffuse processes such as hypoxic-ischemic encephalopathy and a poor short-term outcome. The clinical and background EEG features of infants whose seizures were not accompanied by EEG seizure activity suggest that these seizures may not be epileptic in character.

No abstract

With the use of a time-synchronized video and polygraphic recording system, 5,042 infantile spasms were monitored and analyzed in 24 infants aged 1 to 43 months. Of these, 33.9% were flexor, 22.5% extensor, and 42.0% mixed flexor-extensor. Sometimes the spasms were followed by a period of akinesia and diminished responsiveness lasting up to 90 seconds, and rarely (1.0%) this "arrest" effect constituted the entire seizures. More than one type of seizure occurred in 21 of the 24 infants. In the same number, 78.3% of the seizures occurred in clusters, and the intensity and frequency of the spasms in each cluster often increased to a peak, then progressively decreased until they stopped. Predominantly, the clusters occurred soon after arousal from sleep. The number of seizures occurring at night (55.2%) was similar to the diurnal number (44.8%). The electroencephalographic seizure pattern was variable, but a marked generalized attenuation of electrical activity was a feature of 71.7% of the attacks. Attenuation episodes of similar degree and duration occurred with no evidence of a seizure.

Prolonged monitoring studies of patients with infantile spasms have shown that hypsarrhythmia is a highly variable and dynamic electroencephalographic pattern. Variations of the prototypic pattern (modified hypsarrhythmia) include hypsarrhythmia with increased interhemispheric synchronization, asymmetrical hypsarrhythmia, hypsarrhythmia with a consistent focus of abnormal discharge, hypsarrhythmia with episodes of attenuation, and hypsarrhythmia comprising primarily high-voltage slow activity with little sharp-wave or spike activity. Marked changes in the hypsarrhythmic pattern usually occur during sleep, chiefly during rapid eye movement sleep, when there is a marked reduction in, or total disappearance of, the hypsarrhythmic pattern. Relative normalization of the hypsarrhythmic pattern can also be seen immediately on arousal and during clusters of infantile spasms. Thus, the specific EEG features seen in a given patient depend on multiple factors, including the duration of the EEG recording, the clinical state of the patient, and the presence of various structural abnormalities of the brain.

No abstract

There is no experimental model of benign rolandic epilepsy, and the neurophysiologic and molecular mechanisms involved in the generation and elaboration of this type of epilepsy and its unique electroencephalographic features have yet to be determined. These EEG features are constituted by ionic currents generated at a cellular level. They are cortical in origin, and the cortical neurons responsible for their generation must be arranged and interconnected in such a manner as to permit their synchronous or virtually synchronous activation. This capacity for synchronization is inherent in the cellular arrangement and connectivity of the cortical network itself, but also may reflect imposed synaptic influences of thalamic origin.The dominant EEG feature of benign rolandic epilepsy is a focal surface negative spike ( Fig. 1) with specific biophysical characteristics. The average duration is -74 ms (leading some authors to insist that it should be referred to as a sharp wave rather than a spike). The average sharpness or degree of curvature of the peak is 0.022 pV/ms/8 ms, indicating a relatively blunt character. The average amplitude is about 160 FV (I), but some individual spikes may exceed 300 pV.The high amplitude, the relatively prolonged duration, and the bluntness of the spike suggest that it is generated by an extensive neuronal pool, the duration and bluntness of the spike reflecting the disbursement of the firing time of the neurons within the pool. When effective drug treatment results in clinical seizure control, these parameters of the spike change: the amplitude and duration of the spike decrease, and the sharpness increases ( Fig.

Sleep staging was performed on 32 patients with infantile spasms. All patients demonstrated significantly less total sleep time and lower percentage of REM time than the expected normal values for age. Seventeen were treated with ACTH or prednisone. There was no increase in total sleep time in those who received hormone therapy, whether or not it was successful. However, the percentage of REM time increased significantly in patients who responded to therapy; this increase occurred concurrently with clinical and electroencephalographic improvement. There was no significant change in REM-sleep values in patients who did not respond.

Epileptic mechanisms in the brain are subject to long-duration, time-ordered neuromodulatory processes controlled by endogenous oscillators which are responsible for appropriately phased modulation of various normal physiological processes, including the 24-h sleep/wakefulness cycle and the ultradian 100-min cycle of rapid eye movement/non-rapid eye movement sleep. Both focal and generalized types of epileptiform activity in humans are subject to biorhythmic modulation, and the various modulation patterns observed are in accord with a model which explains these patterns as a consequence of the interaction of two endogenous modulatory processes: one with a period of about 24 h, the other with a period of about 100 min. Differences in the phase angle between the two cyclic processes, determined by time of sleep onset, explain the various modulatory patterns observed. The mechanisms involved in the genesis and elaboration of electrical epileptiform activity in animal models are examined in relation to known processes involved in the physiology of sleep, and compared with data derived from long-term studies of the time distribution of epileptic events in humans. In infantile spasms, clinical seizure activity and the ictal and interictal EEG patterns in relationship to the phases of the sleep cycle, the significant defects in the quality and quantity of sleep in this disorder, and the changes that take place in all of these when seizures are abolished by effective treatment, suggest that pontine mechanisms responsible for the sleep cycle may be involved in the elaboration of infantile spasms and hypsarrhythmia.