Forty-two cases of craniopharyngioma in children are reviewed. Only 9.5% had sought medical attention because of symptoms, suggesting hormonal deficit; however, growth retardation was present in 53% and growth hormone deficiency was documented in 72% before treatment. Multiple hypothalamic-pituitary hormone deficiencies were present in all patients after treatment. Eleven percent had normal skull radiographs at presentation; pneumoencephalograms and computed tomographic brain scans were abnormal on every occasion on which they were performed. Recurrence and mortality rates as well as the neurologic outcome of survivors were similar in children treated by radical excision and those treated by limited excision plus radiotherapy. The neurologic prognosis was poorest in those children who had limited excision or drainage without radiotherapy. Additional hypothalamic-pituitary dysfunction following treatment was less common in children who had limited excision plus radiotherapy than in children who had either limited excision or attempted total removal. Unless gross total tumor excision can be readily achieved, limited excision by transsphenoidal microsurgery or craniotomy plus radiotherapy appears to be the treatment of choice for craniopharyngioma in childhood.

Forty-two cases of craniopharyngioma in children reviewed. Only 9.5% had sought medical attention because of symptoms suggesting hormonal deficit; however, growth retardation was present in 53% and growth hormone deficiency was documented in 72% before treatment. Multiple hypothalamic-pituitary hormone deficiencies were present in all patients after treatment. Eleven percent had normal skull radiographs at presentation; pneumonencephalograms and computed tomographic brain scans were abnormal on every occasion on which they were performed. Recurrence and mortality rates as well as the neurologic outcome of survivors were similar in children treated by radical excision and those treated by limited excision plus radiotherapy. The neurologic prognosis was poorest in those children who had limited excision or drainage without radiotherapy. Additional hypothalamic-pituitary dysfunction following treatment was less common in children who had limited excision plus radiotherapy than in children who had either limited excision or attempted total removal. Unless gross total tumor excision can be readily achieved, limited excision by transsphenoidal microsurgery or craniotomy plus radiotherapy appears to be the treatment of choice for craniopharyngioma in childhood.

As part of studies on the ontogeny of PRL secretion and regulation, the effect of TRF on PRL release was studied in the chronically catheterized ovine fetus and neonate. After a 2-h control period, 250 μg TRF were given by rapid iv injection to seven fetuses between 88—133 days gestation (term, 147 days) and five lambs between 4—17 days old. All animals exhibited a prompt increase in the concentration of plasma PRL. In three fetuses with basal PRL concentrations less than 10 ng/ml (88, 89, and 111 days old), PRL rose from a mean value of 3.1 ± 2.0 to 11.5 ± 5.6 (SE) ng/ml 15 min after TRF and was 10.7 ± 5.0 ng/ml at 90 min. In four fetuses with basal PRL concentrations greater than 10 ng/ml (112, 121, 124, and 133 days old), significantly (P ≪ 0.05) more PRL was secreted; the mean concentration of PRL increased from 36.9 ± 12.1 to 88.2 ± 21.7 ng/ml at 15 min and was 77.8 ± 22.8 ng/ml at 90 min. In five neonates (5, 6, 10, 10, and 17 days old), PRL rose from 13.1 ± 2.3 to 81.6 ± 20.1 ng/ml at 15 min and fell to 38.2 ± 4.5 ng/ml at 90 min. The plasma GH concentration did not increase after TRF administration. TRF evokes PRL secretion as early as 88 days gestation and the response increases with advancing gestational age; late gestation fetuses have peak PRL levels similar to those in neonates. However, neonates have lower basal levels and a less sustained (P ≪ 0.05) PRL response to TRF than late gestation fetuses. These differences reflect changes in PRL reserve and may be modulated by changing estrogen levels which rise in late pregnancy and fall after birth. The differences in the pattern of the PRL response to TRF in neonates may also reflect increased dopaminergic activity in the neonate compared to the late gestation fetus. (Endocrinology106: 1074, 1980)

The concentration of plasma PRL in the ovine fetus is low in midgestation, rises to high concentrations in late gestation, and remains elevated in the early neonatal period. To investigate the development of the dopaminergic regulation of PRL secretion in the ovine fetus and neonate, we infused, after a 2-h control period, the dopaminergic agonist apomorphine (40 or 100 μg/kg, iv over 1 h) or bromergocryptine (1-mg iv bolus) into chronically catheterized ovine fetuses (term gestation, 147 days) and neonatal lambs. Apomorphine at both dosages caused significant (P < 0.01) suppression of PRL concentrations in both the fetuses (118–136 days of age) (40 μg/kg, n = 3; 100 μg/kg, n = 4) and neonatal lambs (40 μg/kg, n = 4; 100 μg/kg, n = 4). The degree of suppression in the neonatal lamb was greater (P < 0.01) than that in the fetus. Similarly, bromergocryptine lowered PRL concentrations in three fetuses (122, 126, and 127 days of age) and one neonate. To assess the presence of tonic dopaminergic regulation of PRL secretion, we administered haloperidol (1-mg iv bolus) to 11 fetuses (92–140 days of age) and 5 neonates. In all but the youngest fetus, haloperidol caused an elevation of plasma PRL concentration. In fetuses with low basal concentrations (n = 4, 106–122 days of age), PRL rose from less than 2 to 4.6 ± 0.6 ng/ ml (P < 0.01) after haloperidol; in fetuses with basal PRL greater than 10 ng/ml (n = 6,113–140 days of age), the mean concentration of PRL increased (P < 0.05) from 32.8 ± 5.9 to 88.2 ± 18.6 ng/ml, and in 5 neonates it increased from 20.1 ± 6.1 to 175.5 ± 26.7 ng/ml (P < 0.005). The response to haloperidol in the neonate was greater (P < 0.05) that that in the late gestation fetus. These observations provide evidence for dopaminergic inhibition of PRL release by 106 days. This mechanism is operative before the rapid rise in PRL concentration in fetal plasma between 110–120 days gestation, suggesting that the high perinatal concentration of PRL is not due to the lack of maturation of dopaminergic control.