Abstract
Clinical investigations were carried out to elucidate the mechanism through which pituitary neuroadenolysis (NALP) relieved intractable cancer pain. When investigating hypothalamopituitary interaction, continuous elevation of TRH and arginine vasopressin were observed in the cerebrospinal fluid (CSF) following NALP. ACTH1-39 in the CSF abruptly increased after NALP in cases with complete pain relief, in contrast with the far less elevation in cases without complete relief. There was no significant increase of endorphins in the CSF. The sufficient inactivation of the anterior and posterior pituitary functions indicated the success of the procedure, but had no exact correlation with the obtainability of complete relief of cancer pain, though cancer pain was more frequently alleviated in hormone-dependent carcinomas than in non-dependent.
Valuation of pain responsiveness showed the duration of tourniquet tolerance in cases with complete relief of cancer pain following NALP was twice as long as before NALP, while it was unchanged in cases without complete pain relief. Radiant heat dolorimetry revealed no significant differences between cases with complete pain relief and those without. Sensory decision theory analysis denoted increased pain threshold and improved discriminability in cases with complete relief. Pain threshold determination thus indicated increased C-fiber thresholds, which mainly mediate cancer pain, and excluded the placebo effect of NALP. Observations indicated that the increase of peptides in the CSF, which are mainly synthesized in the hypothalamopituitary axis, would exert a suppressive effect on the mediation and perception of cancer pain through the C-fibers and the central nervous system.
