beta-Endorphin (beta-EP) and cholecystokinin 8 (CCK-8) concentrations in peripheral blood mononuclear cells were measured in 12 drug-free autistic (AU) children, in 10 drug-free children with pervasive developmental disorders (PDD) and in 11 healthy controls. The aim of the study was to see whether or not there was an alteration of beta-EP and CCK-8 concentrations in this peripheral compartment, in which it has been suggested that secretion and regulation of the two peptides mimic those of neurons in the central nervous system. Mean beta-EP values were significantly higher in AU than in PDD and control children, while there were no differences in CCK-8 values of the three groups.

The responses of growth hormone (GH) to administration of growth hormone-releasing hormone (GHRH-1 micrograms/kg b.w.) and of clonidine (clon-2.5 micrograms/kg b.w.) and basal levels of somatomedin C (SmC) were measured in nine peripubertal patients with Major Depressive Disorder (MDD) and in 9 age- and gender-matched controls. Basal GH and SmC levels, and GH response to GHRH did not differ in patients and controls, whereas responses to clonidine were significantly higher in some and lower in other patients than in controls.

The responses of cortisol to acute administration of saline and of clonidine (2.5 mu g/kg B.W.) were examined in 10 children and adolescents with major depressive disorder and in 10 age- and sex-matched controls. Clonidine administration did not inhibit cortisol secretion in controls or in patients, contrary to what has been observed in depressed adults. In controls, but not in patients, clonidine administration induced a transitory increase of the steroid.

Brambilla, F.; Musetti, C.; Tacchini, C.; Petraglia, F.; Guareschi-Cazzullo, A. Author Information

A neuroendocrine study was conducted in eight children and adolescents with dysthymic disorders (three females and five males) and in eight age- and sex-matched psychologically normal controls. The dexamethasone suppression test (DST), TSH and GH responses to TRH stimulation and GH response to clonidine stimulation were studied in parallel in each patient. Depressive symptomatology was monitored with the Poznanski Rating Scale. The DST, TRH and clonidine tests revealed normal responses in each patient. TRH induced abnormal GH rises in five of the eight patients. There were no correlations between neuroendocrine parameters and degree of depression, age, sex or weight of the patients, age of onset, duration and family history of the disease.

The effects of chronic sulpiride therapy on growth hormone (GH) secretion were studied in 11 mentally disturbed children, aged 5 to 13 years, five with personality disorders, three with childhood psychoses, one with hysteria, one with anxiety reactions, and one with neurosis. The basal GH secretion and response to insulin-induced hypoglycemia were studied before the beginning of therapy and after ten days and three months of treatment with sulpiride (8 mg/kg body weight). No modifications in basal levels of GH or in the response to the stimulus were observed after ten days of therapy. After three months of treatment a blunted GH response to the stimulation was observed in three subjects, one of whom showed increased basal levels of GH.

1. Neuroleptic drugs are still widely employed in childhood psychoses, but new experiences on a large number of cases in this field, have shown the usefullness of antidepressive drugs, either alone or associated with neuroleptics, also when depressive symptoms are not clearly evident. 2. This peculiar aspect, still noticed in pathological situations of less gravity, calls again attention to childhood depression and to the difficulty of identifying it. 3. The problem is developed and discussed as follows: a. The psychopathological features regarded from the psychodynamic point of view; b. The neurofunctional background in various ages; c. The pharmacodynamic characteristics of the drugs; d. The good results with lithium treatment in several cases allow the authors to outline some clinical pictures as well as biochemical markers as to recognize endogenous depression in childhood.