The effect of electrical stimulation of the internal capsule (IC) or sensory thalamic nucleus (VPM) on neuronal activity in the subnucleus caudalis of the spinal trigeminal nucleus (STNcd) was examined electrophysiologically in the cat. The nociceptive neuronal firing in the STNcd was suppressed by the facilitation of the non-opiate pain inhibitory system, such as electrical stimulation of the IC or VPM of either side.
High amplitude spontaneous and continous neuronal hyperactivity (deafferentation hyperactivity: DH), which was provoked in the left STNcd after complete ablation of the left Gasserian ganglion, was conspicuously suppressed by electrical stimulation of the IC of either side (rt. IC stimulation: 30/60; It. IC stimulation: 13/33), as well as by VPM stimulation of either side (rt. VPM stimulation: 5/13; It. VPM stimulation: 5/9). DH, similar to that provoked in the left STNcd after ganglionectomy, was found to spread to the right sensory thalamic nucleus. Twelve neurons with DH were identified in right VPM and nucleus centralis medialis. As many as nine of these twelve neurons were distributed in the marginal area of the VPM. DH in the right thalamus was also suppressed by the stimulation of the IC on either side, however, the suppressive effect was predominant with ipsilateral IC stimulation.
These results are compatible with the clinical experience of relief of deafferented (deafferentation) pain by electrical stimulation of the IC or sensory thalamic nucleus (VPM, VPL). After detailed analysis and considerations, it was supposed that this experiment supports the postulated theory that not only deafferented pain but also afferent pain is relieved by the facilitation of the non-opiate pain inhibitory system including the IC and/or the sensory thalamic nucleus.
deep brain stimulation