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Clinical and psychological characteristics of 33 patients with low back pain were correlated with prolactin and cortisol concentrations in cerebrospinal fluid (CSF). A significant sex difference was found in CSF prolactin levels: women secreted more prolactin into the CSF than did men. High CSF cortisol levels were associated with a rhizographically-demonstrable abnormality, suggesting a relationship between cortisol and an 'organic' origin of pain symptoms. Impairment-disability indices also were associated with CSF hormone levels. Moreover, the two hormones had dissociated psychological correlates. Prolactin was related to depression and anxiety, whereas cortisol was related to somatization. Sex differences were observed in the cortisol response to the symptoms of chronic low back pain, especially in the presence of anxiety and somatization. The sex differences in psychoneuroendocrine and emotional responses suggest that male and female pain patients have different coping mechanisms.

Baseline concentrations of prolactin (PRL) was determined in the CSF of 28 lobotomized and 28 non-lobotomized patients with chronic schizophrenia. The mean PRL level of the female patients was significantly higher than that of the male patients (p < 0.001). In addition, non-lobotomized patients had significantly higher concentrations of CSF PRL than patients of the lobotomized group (p < 0.05). On the other hand, patients belonging to the latter group exhibited significantly more central as well as cortical brain atrophy than the patients on whom no psychosurgery had been performed (0.05 > p < 0.001). The significance of cerebrospinal PRL as an index of central dopamine metabolism is discussed.

In order to elucidate the interplay of prolactin and dopamine in schizophrenia, base-line levels of prolactin were assayed in the cerebrospinal fluid (CSF) of chronic schizophrenic patients with or without lobotomy. Cental and cortical atrophy and significantly lowered CSF prolactin levels were found in lobotomized patients in comparison to equally neuroleptic-treated non-lobotomized patients. The mean CSF prolactin level in the female patients was significantly higher than in the male patients. This study did not support the 'dopamine hypothesis' of schizophrenia, since CSF prolactin levels did not correlate with schizophrenic symptoms. The brain atrophy blocked completely the expected elevation of CSF prolactin levels induced by neuroleptics.

Concentrations of prolactin in cerebrospinal fluid (CSF) and in serum were determined from 26 neurological patients with or without minor central cerebral atrophy. Neuropsychological memory tests also were performed on these patients. Twenty-eight neurological patients with peripheral nervous lesions and without endocrine dysfunctions served as controls for prolactin levels. Patients with central cerebral atrophy had significant loss of recall capacity, though they did not differ significantly from the normal population in their intellectual performances. CSF and serum prolactin levels in the patients with central cerebral atrophy and/or memory defects did not differ from the values obtained in the patients without cerebral atrophy. Thus, prolactin levels do not appear to reflect either central cerebral atrophy or memory dysfunctions, most likely due to the minor degree of neuronal atrophy around the third ventricle that occurs in patients with these findings.

Bromocriptine was used for Parkinson's disease in 15 patients for 20 weeks. Immunoreactive plasma lutrophin (LH), follitrophin (FSH), prolactin, and somatotrophin (GH, growth hormone) concentrations were analysed before and during the treatment. Plasma prolactin levels were very markedly reduced during treatment. Plasma lutrophin levels were increased significantly in female patients, but not in male patients. No changes were noticed in follitrophin levels, but plasma somatotrophin levels were reduced during treatment. No correlations were found between the degree of clinical response and changes in plasma gonadotrophin and somatotrophin. This suggests that the effects of bromocriptine on extrapyramidal and neuroendocrine dopaminergic neurones are unrelated. We suggest careful and frequent controls of neuroendocrine secretion patterns in patients with Parkinson's disease who are treated with high doses of dopamine receptor stimulators, since the response of some pituitary hormones to bromocriptine are very marked.