The hypothesis that ECT produces selective effects on hypothalamic–pituitary activity was investigated by determining the effect of ECT on pituitary hormone release in nine depressed patients. After ECT there were massive and rapid increases in the plasma concentrations of nicotine-and oestrogen-stimulated neurophysin (NSN and ESN), prolactin (PRL) and adrenocorticotropin (ACTH), smaller increases in plasma luteinizing hormone (LH) and cortisol, a significant decrease in plasma growth hormone (GH) concentration but no change in plasma thyrotropin (TSH). There was significant attenuation of PRL responses with repeated ECT. The hormonal responses to ECT cannot simply be attributed to stress, since a similar pattern of increases in plasma hormone concentrations did not occur in psychologically normal patients in whom plasma hormone concentrations were measured during induction of anaesthesia and abdominal incision for cholecystectomy. Analysis of these hormonal responses in terms of the knowledge available on the neurotransmitter control of pituitary hormone release suggests that some of these hormonal responses to ECT may be mediated by the activation of serotonergic neurones, while others are probadly due to direct stimulation of the neuroendocrine neurones themselves.

Seventy-three patients who had been continuously receiving lithium carbonate for 6 months or more had their thyroid function evaluated clinically and biochemically. Goitre was found in 37 %, exophthalmos in 23 %, positive thyroid auto-antibodies in 24 % and abnormal TRH tests in 49 %. It would appear that thyroid failure due to lithium is usually dependent on antibody mediated damage. It is unlikely that lithium has a direct effect on the hypothalamic–pituitary axis.