Thalamic relay nucleus stimulation for relief of intractable pain. Clinical results and β-endorphin immunoreactivity in the cerebrospinal fluid

Abstract

Deep brain stimulation (thalamic relay nucleus, periaqueductal gray and internal capsule) was applied to various cases of intractable pain, and the resulting degree of pain reduction and alteration in .beta.-endorphin immunoreactivity in the CSF were compared. The studies on intractable pain revealed that the levels of .beta.-endorphin immunoreactivity in the CSF were lower than those in the control group. Thalamic relay nucleus stimulation proved effective not only for deafferentation pain, but also for somatogenic pain. No relationship was noted between pain reduction and the rate of increase of .beta.-endorphin immunoreactivity in the CSF. The incidence of stimulation tolerance following prolonged stimulation of the thalamic relay nucleus can be reduced to a minimum by administration of L-dopa. The increase in .beta.-endorphin in the CSF is not the direct and major cause of pain reduction during treatment by thalamic relay nucleus stimulation. It may be assumed that neuronal facilitation on the monoaminergic descending pain inhibitory system plays a role in reducing pain.