Animal experimental studies conducted at the turn of the century resulted in the use of magnesium sulphate as an anticonvulsant in humans. In U.S. clinics, parenteral administration of magnesium sulphate became a routine procedure in the treatment of eclampsia and pre-eclampsia. This treatment has proved very effective in treating convulsions in pregnancy provided an adequate dosage was given amounting to up to 60 g daily. Mother and infant mortality were largely eliminated. Numerous clinical studies showed a negligible side effect rate. Side effects in the foetus: These are due to penetration of magnesium into the foetal blood circulation. Reports on an inhibition of cardiac rate fluctuation and changes in calcium levels have been contradictory, and hence not generally accepted. It is claimed that the parathormone level may drop slightly. Isolated reports on foetal magnesium intoxications associated with depression of breathing, slackness and hyporeflexia often prompt the conclusion that this disease pattern had been due to immaturity and asphyxia. Generally, foetal magnesium blood levels do not correlate well with signs of magnesium intoxication. Urine excretion is greatly slowed down in foetal immaturity. Side effects in the mother: Short-term relaxing action on the uterus has been described frequently. High dosages have been successfully used in arresting labour if there is a tendency to premature birth. Increase in uterine blood flow was seen after administration of magnesium sulphate in animal experiments. Magnesium is said to reduce blood coagulation by influencing fibrinolysis and thrombocyte resistance. However, a somewhat enhanced loss of blood during birth is said to be more likely due to relaxation of the uterus than to a disturbance of blood coagulation. Rapid intravenous injection causes short-term flushing, nausea and vomiting. Short-acting drops in blood pressure are possible. The cardiac output is said to increase at the conventional dosage level whereas the peripheral resistance drops due to vasodilation. Increases and decreases in heart rate have been reported, but in most cases no changes were seen. Changes in ventricular action time occur with toxic doses only, which can lead to cardiac arrest in the diastole. Other toxic signs are hyporeflexia, depressed breathing and CNS depressions which may result in coma. Hyporeflexia always occurs before the other toxic signs appear, so that it can be used as a clinical control criterion. Calcium gluconate, given via the IV route, is a good and rapid-acting antidote.(ABSTRACT TRUNCATED AT 400 WORDS)