The current status of analgesic brain stimulation.
This paper reviews the author's nine years of experience in analgesic brain stimulation. During this time, of 22 patients with pain of peripheral origin who were treated with periaqueductal gray (PAG), stimulation 16 achieved successful control of pain. Of 40 patients who presented with deafferentation pain, 16 were able to control their dysesthesia by brain stimulation of the subcortical somatosensory region alone; follow-up was over a long period. The mechanism of deafferentation pain is poorly understood and the effectiveness of subcortical somatosensory electrical stimulation to relieve such pain is based on empirical observation. The analgesia produced by PAG stimulation appears to be mediated by the release of beta-endorphin from the anterior hypothalamus. The released beta-endorphin binds to the opiate receptors in the PAG and activates the descending pain-inhibitory pathway. However, the repetitive stimulation of this serotonergic system produces tolerance to its analgesic effect, due to a decreased rate of serotonin turnover. Loading of the serotonin precursor by dietary supplementation of the essential amino acid L-tryptophan reverses this tolerance.
D000698:Analgesia / Q000379:methods; D003342:Corpus Striatum; D004599:Electric Stimulation Therapy; D004723:Endorphins / Q000134:cerebrospinal fluid; D005500:Follow-Up Studies; D006801:Humans; D006897:Hydroxyindoleacetic Acid / Q000134:cerebrospinal fluid; D008526:Medulla Oblongata; D008636:Mesencephalon; D009434:Neural Pathways; D010146:Pain / Q000134:cerebrospinal fluid; D010148:Intractable Pain / Q000628:therapy*; D013787:Thalamic Nuclei
D004723:Endorphins; D006897:Hydroxyindoleacetic Acid