Recovery from depressive illness after electroconvulsive therapy
Experiment One Plasma concentrations of oxytocin-associated neurophysin and prolactin were measured before and after the first treatment in a course of electro-convulsive therapy (ECT) given to 25 depressed patients. Plasma neurophysin concentration was measured by the radioimmunoassay (RIA) of Robinson (1975)• The percentage peak increase in plasma neurophysin concentration was three times greater (p < 0.001) in the 16 depressed patients who had a good outcome two months after the last ECT compared with the nine who did not. The rise in plasma neurophysin concentration correlated (rho = 0-46, p < 0.05) with improvement in symptoms measured by the Hamilton Rating Scale for Depression (HRSD). There was no difference in the percentage peak increase in plasma prolactin concentration between patients who had a good outcome two months after the last ECT and those who did not. The rise in plasma prolactin concentration did not correlate with improvement in HRSD score. Experiment Two Serum concentrations of the vasopressin- (hNpl) and oxytocin-associated neurophysins (hNpIl) were measured by the RIA of Legros et al. (1969) before and after the first ECT in a course of treatment given to 19 unipolar depressed patients. The percentage peak increase in hNpII was four times greater (p < 0.001) in the six patients who had a good outcome two months after the last ECT than in the patients who had a poor outcome. The rise in serum hNpII correlated with improvement in HRSD score (r = 0.50, p < 0.05) and improvement in score on the Montgomery and Asberg Depression Rating Scale (r = 0.47, p < 0.05). The rise in serum hNpl concentration did not correlate with improvement. There were no significant correlations between spike-wave activity or total seizure activity measured by a six-channel electroencephalogram (EEG) and the rise in either of the neurophysins. Experiment Three Serum concentrations of hNpI and hNpII were measured at the first and last treatments in a course of ECT given to 17 unipolar depressed patients (seven of whom also took part in Experiment Two). There were no significant differences in the average release of either neurophysin between the first and last treatments. There were no significant correlations between alterations in the release of the neurophysins between the first and last treatments and improvement in symptoms of depression. Conclusions Although there is a correlation between the release of MfpII after the first ECT and improvement in symptoms of depressive illness, the correlation is not sufficiently close to be of clinical utility in the prediction of ECT outcome. The reason for the correlation is not known. There was no support for the hypothesis that the release of hNpII was a correlate of cerebral seizure activity. The release of hNpII may be a sensitive measure of electrical stimulation in the midbrain or may occur at the same time as the release of a neurotransmitter with mood-regulating activity.
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