In a series of previous papers fairly detailed studies of an individual patient with a precisely timed forty-eight hour periodic psychosis have been presented. Jenner (1963), and Jenner, Gjessing, Cox, Davis-Jones, Hullin and Hanna (1967) have presented the clinical findings. Essentially, for thirteen years the patient regularly suffered from one day of depression alternating with one day of hypomania. The change of state occurred during sleep, usually between 02.00 and 03.00 hours. There were only eight major defects of the cycle in ten years. The timing of the cycle was however influenced by the environment; this was confirmed when the patient lived in an artificial environment in which a day and night totalled twenty-two hours instead of twenty-four. The psychotic cycle then became one of forty-four hours rather than forty-eight (Jenner, Goodwin, Sheridan, Tauber and Lobban (1968)).

No abstract

Summary Blood samples were collected from forty-five patients with depression who had been taking nortriptyline for at least 14 days. At the time of blood collection the observer recorded his opinion of each patient’s response to treatment either as ‘satisfactory’ or ‘unsatisfactory’, together with any change in therapy then decided upon. The patients came from six different hospitals but all plasma nortriptyline estimations were performed at a single laboratory. No statistically significant correlation could be discerned between dose or plasma nortriptyline concentration and therapeutic response or decision to change treatment. Under the conditions of general psychiatric practice, the occasional ‘spot’ estimation of plasma nortriptyline concentrations is unlikely to be a practical guide to the nortriptyline requirements of most patients.

No abstract

Graded doses of propylthiouracil, carbimazole, sulphadiazine, potassium perchlorate and potassium thiocyanate were fed to groups of rats under standardized conditions for 2 months. The rats were given 131I 24 hr. before they were killed, and the thyroid weight, the proportions of labelled iodoaminoacids, and the thyroidal iodine content were determined. All the goitrogens produced increase in thyroid size, reduction of thyroidal iodine content, and an elevation of the monoiodotyrosine : di-iodotyrosine (MIT : DIT) ratio. The tri-iodothyronine : thyroxine (T3 : T4) ratio was usually increased. Irrespective of the antithyroid compound used, there was a close correlation between the decrease in thyroidal iodine content and the rise in the MIT:DIT ratio.In further experiments, either thyroid stimulating hormone (TSH) or thyroxine were injected s.c. twice daily for 5 days. TSH decreased the MIT:DIT ratio and increased the amount of labelled T3. Thyroxine increased the MIT : DIT ratio and decreased the amount of T4.It is suggested that when goitrogens were administered for a prolonged period, the pattern of 131I-labelling of iodoaminoacids was dependent on a balance between inhibition of synthesis caused by the goitrogen and stimulation due to TSH. There was increased production of the physiologically more economical T3 in an attempt to compensate for decreased thyroxine formation.

No abstract

SUMMARY Fresh and dried milk samples obtained during 1960–64 have been examined for antithyroid and goitrogenic activity in rats. In acute experiments milk caused a depression in the uptake of 131I. Samples taken during the spring months were most active in this respect. The iodine content of milk was not responsible for this depression. Calcium and fat in the amounts present in milk caused a decrease in uptake of 131I and the calcium content of milk was highest in the spring. In experiments involving feeding fresh or dried milk for 3 months neither thyroid enlargement nor interference with thyroid hormone synthesis was produced regularly though occasional samples caused some minor changes. There was no consistent evidence for goitrogenic activity in milk.

No abstract