A group of 57 women, who had been hospitalised for puerperal psychiatric disorders from 1958 to 1977, were reexamined in 1982. The aim of the study was to determine the proportion of patients who had suffered from nonpuerperal psychotic relapses or other subsequent psychopathology, to define the sample diagnostically, taking into account progress in classification, to characterize the so far relatively neglected later course of illness, and to establish criteria related to relapse and global clinical outcome. Of these patients 65% had at least one nonpuerperal relapse, only 25% remained free of later psychopathology, but the global outcome was favorable or relatively favorable in many cases. Of the patients who had had nonpuerperal relapses 43% were classified as suffering from affective psychosis, as many as 38% from schizoaffective psychosis, and only 19% from schizophrenia. Schizoaffective psychosis seems to be particularly liable to be provoked by childbirth. No major evidence was found that endogenous psychoses with puerperal onset and nonpuerperal relapses have a course of illness different from that of the corresponding diagnostic category in general. Cases with exclusively puerperal decompensations seem to be nosologically independent from the traditionally recognized endogenous psychoses. Characteristics strongly related to nonpuerperal relapses were a family history of psychosis and the occurrence of psychotic episodes before the index episode. Puerperal relapses occurred at a much higher rate in patients who also had nonpuerperal relapses than in patients without.

Desipramine (DMI), like many antidepressant drugs, inhibit the production of paradoxical sleep (PS). In the present experiment, we have investigated the relationships between brain level of DMI and PS inhibition. Groups of rats had their sleep monitored after 1, 2 or 4 mg/kg of DMI. In other animals, the brain concentration of DMI was assayed at various times after the same treatments. The results indicate that a critical threshold concentration of 300 ng/g DMI in the brain is necessary for complete PS inhibition. This stage reappears only when the DMI level falls below this value, and its production resumes at a normal rate, provided the DMI level reached initially was not largely in excess of the threshold concentration. The results are discussed with regard to the present knowledge of specific binding of tricyclics in brain and their "ex vivo" action on norepinephrine uptake resulting in enhancement of collateral inhibiton of noradrenergic cells.

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The ratio of integrated EEG amplitude from left and right temporal areas was analyzed during sleep in normal subjects for two consecutive nights. The results showed that the differences between the subjects were similar in both nights and were much larger than the differences between the stages of sleep. No significant variation was found between stages, although stage 1 tended to show greater relative right activation in night 1. Also, the relative right activation was greater in wakefulness in night 2 as compared to night 1. The classification of the correlation coefficients between stages corresponded to the physiological transitions between stages, suggesting that the small source of variance due to sleep stage contains relevant information.

The effect of chlorpromazine (CPZ) was studied at four different doses in a group of 10 normal subjects. Blood levels of CPZ were assayed by gas chromatography and showed wide interindividual variations. Spontaneous brain electrical activity (EEG) was recorded from 8 leads and submitted to spectral analysis. Evoked responses (ER) to flashes, pattern reversals and clicks were averaged, and measured by their amplitude and variability. Several subjects presented marked side-effects (responders, R) and showed differences in many EEG parameters with respect to subjects without side-effects (non-responders, NR). A cluster analysis permitted to distinguish very clearly these two groups of subjects. The differences in the effects of CPZ between the R and NR groups involved mainly EEG, and appeared with a systematic topography over the scalp. Within the R group, many differences were observed as a function of the dose of CPZ; they consisted mainly in a decrease of alpha and an increase of theta activity in the EEG, decrease of amplitude and increase of variability in the ER measures. These modifications had also a typical topography over the scalp. Finally, many variables of EEG (relative power only) were correlated with plasma level of CPZ, while no such correlation appeared for ER. These results are discussed in terms of individual sensitivity to drugs, relationships between EEG parameters and plasma level, and topographical differences in the effect of CPZ.