Mechanism of neuroadenolysis of the pituitary for cancer pain control.

Several theories have been advanced to explain how neuroadenolysis of the pituitary (NALP) relieves cancer pain. Interference with hormonal regulation, interruption of pain pathways and a compensatory overproduction of brain endorphins have been proposed. The purpose of the present experimental study is to determine whether neuronal activity of the pituitary gland, as related to the primary somatosensory cortex (PSC), may be involved in the pain perception pathway influenced by NALP, using EEG and tooth pulp evoked potentials (TPEPs). Pituitary activity showed a high voltage slow activity which slowed after alcohol injection into the sella turcica. When naloxone was injected after NALP, a rhythmic high voltage activity appeared in the pituitary gland. After NALP, the TPEP recorded from the PSC disappeared, while NALP induced an increase in the amplitude of the TPEP in the pituitary gland. An injection of naloxone severely decreased this response in the pituitary gland, in contrast to changes in the PSC where the original response reappeared after an injection of naloxone. Our hypothesis is that an increase of TPEPs (hyperactivity) in the pituitary gland is produced after alcohol wounding (wounding effect), leading to a decrease of pain response in the sensory cortex (decrease of TPEPs). This wound effect may be influenced by endorphins, because naloxone, a specific antagonist of opiate receptors, reversed the changes in TPEPs in both places.