This paper contains a clinical, classical electroencephalographic and computerized electroencephalographic (by original methods) study of 271 cases with vertebro-basilar strokes, all the cases being verified by transcranial Doppler ultrasound investigations and some of the patients by morphopathological studies. In the first part, the standard EEG modifications in relation with the clinical pictures and with the affected arterial field are presented. In the second part, the aspects of the computerized EEG recordings with the carrying out of the cortical EEG mappings which have brought important contributions in setting down the topography of the infarctions are discussed. The third part presents the results of the polysomnographic recordings of the 70 selected cases with ischaemic vertebro-basilar attacks without disorders of consciousness (32 cases), with attacks accompanied by symptomatic hypersomnias (13 cases), with ischaemic attacks accompanied by insomnia (5 cases) and with ischaemic attacks with disorders of consciousness (20 cases). The opinion of the authors on the possible relations between the disturbances of the vigilance, the perturbations of the polysomnographic organization of sleep-wakefulness cycles (with the realisation of some interesting competitive dysfunctions between the three states of vigilance) and the electrographic anomalies are discussed.

The present paper reports biochemical and neurophysiological investigations in ten cases with restless leg syndrome. Other neuropsychiatric affections and factors which could generate the symptomatology of restless legs syndrome were not included. The EEG recordings demonstrated evident reticular neuronal hypersynchrony generated by hyperpnoea (sinusoidal slow waves). The classical EEG investigations pointed out neuromuscular hyperexcitability, but some modifications of the functional parameters of the neuromuscular excitability and conductibility (signs of neuropathy) were also noticed. In all the cases, continuous 8-hour polysomnographic recordings and monitorization on infrared TV screen were performed. Investigations reported: important disorders of sleep organization, agitated sleep with frequent periods of nocturnal awakenings, increase of the durations and percentages of light slow-wave sleep (LSWS) and rapid and frequent changes of various stages of LSWS, a decrease of duration and percentage of DSWS, a decrease of duration and percentage of REM sleep (as in other parasomnias caused by magnesium deficiency) and nocturnal EEG anomalies (long discharges of sinusoidal slow waves, of sharp waves and of sharp slow waves appearing in the LSWS stages with the disappearance in the REM sleep).

The present study has selected 125 cases with psychomotor attacks (sometimes secondarily generalized). Polysomnographic recordings were carried out for a continuous period of eight hours. All this time, the patients have been observed by video-monitorization on a closed infrared circuit screen. The diagnostic procedure was supported by several computerized EEG mappings (CEM) according to a model achieved by us, transcribing the primary data which were obtained by Hjorth's NSD parameters (activity and ability) from the Siemens-Elema Mingograph to a microcomputer. In many cases, we have employed an interface which had been envisaged by us for analog-digital conversion of amplitudes and frequencies from the Mingograph to the microcomputer. Sleep organization anomalies were found: increase of the percentages of light slow-wave sleep (LSWS) and of REM sleep and reduction of the percentages of deep slow-wave sleep (DSWS). The temporal foci appeared with the greatest frequency and with a clear-cut evidence during LSWS, especially in REM sleep and in the transitional states of SWS to REM sleep and from REM sleep to wakefulness. Our researches supplemented with CEM, demonstrate a peculiar activation of the temporal foci during REM sleep, during the states of LSWS and during the transitional states, showing that many psychomotor attacks appear predominantly during these sleep states and that many cases initially clinically misinterpreted as grand mal seizures are, in fact, focal temporal epilepsies secondarily generalized.

Clinical and polysomnographical investigations have been performed in 35 patients with REM narcolepsy (group 1), comparatively with 45 patients suffering from symptomatic hypersomnia in NREM sleep (group 2). The polysomnographical recordings have been made by: a) continuous recording covering 24 h; b) submission of the subjects to the "Maintenance of wakefulness tests" (MWT). In 20 narcoleptics and in 12 normal subjects, computerized EEG mappings were performed in wakefulness and in different sleep stages. In the narcoleptic patients, the association of the sleep attacks with other symptoms of Gélineau's disease has been noticed. The 24 h continuous polysomnographical recordings pointed out relevant differences between the first and the second group: the patients with REM narcolepsy (Gélineau's disease) presented increased quantities and percentages of REM sleep and manifested several periods wish sleep-onset REM. Comparatively, the patients with NREM hypersomnias slept predominantly in NREM sleep, and presented normal percentages of REM sleep and also manifested sleep-onset NREM periods. One found great differences between the two groups by the MWT, that is, in the first group the mean values of REM sleep were greater, the REM latency and the sleep latency were very short and one assisted to many sleep-onset REM. The cortical EEG mappings were ampler and slower on the right posterior temporal and occipital regions (especially during the REM sleep) either in normal or in narcoleptic patients. These results suggest the consistency of some previous data regarding the differentiation of the true REM narcolepsy (as an independent entity) from the various frequent NREM hypersomnias.

One hundred and twelve patients with temporal lobe epilepsy were studied. Continuous polysomnographical recordings were performed for eight hours, the patients being video-monitored all the time. These researches, completed with computerized EEG cortical mappings demonstrated a peculiar activation of the temporal foci during REM phases and during some stages of LSWS.

Twenty seven patients with parasomnias (night terrors, nocturnal motor automatisms, nocturnal verbal automatisms and sometimes with bruxisms) associated with magnesium deficiency were selected. In all of them marked hypomagnesemia, clinical, EEG and EMG signs of spasmophilic syndromes were found. The 8 hours polysomnographical recordings of all cases (monitored in a system with infra-red video-TV cameras) showed severe sleep disorders and EEG nocturnal abnormalities occurring in the SWS (especially in the I b, II and III stages) with disappearance in the REM sleep. The authors suggest that these clinical and polysomnographic anomalies may be the expression of the brain damage caused by magnesium deficiency or of the clinical electrographic manifestations of the reticulate neuronal hypersynchrony exacerbated by sleep.

The authors carried out 8 hours of continuous night polysomnographic recordings in 40 selected cases with various forms of absences. In all these patients, the computerized electroencephalographic mappings were performed according to several methods achieved by the authors. The nocturnal electrographic abnormalities, the morphological patterns of the epileptic discharges during different sleep stages and the cortical computerized cartography were comparatively analysed in the five groups of patients: 1) genuine (pure, classical or simple) petit mal (PM) absences: 8 cases; 2) myoclonic PM absences: 10 cases; 3) amyotonic-akinetic PM absences: 6 cases; 4) "false" temporal epileptic absences: 10 cases; 5) "hybrid" (or "bastard") PM absences in 6 cases with Lennox-Gastaut disease.