Since the senior author's (J.E.A.) first report in 1972 of the use of deep brain stimulation (DBS) to control chronic pain, electrodes for DBS have been implanted in 141 patients. Of reported series, this one has the largest number of patients and the longest period of follow-up. The mean age of patients in this study was 51.2 years. The mean length of follow-up was 80 months. Patients had experienced pain for a mean period of 65 months before DBS was attempted; all patients had exhausted other medical and surgical therapies. For the purposes of this study, pain states were characterized as being either nociceptive or deafferentation in nature. Nociceptive pain was treated primarily by stimulation of the periaqueductal or periventricular gray, and deafferentation pain was treated primarily by stimulation of the sensory thalamus. Eighty-four patients were treated for deafferentation pain, which included the thalamic pain syndrome (25 cases), peripheral neuropathic pain (16 cases), anesthesia dolorosa (12 cases), paraplegia pain (11 cases), postcordotomy dyesthesia (5 cases), phantom limb pain (5 cases), thoracic neuralgia (4 cases), and miscellaneous pain states (6 cases). We treated 57 patients with nociceptive pain states, 51 for low back and skeletal pain and 6 for pain from the invasion of cancer. Initial relief of pain was obtained by 83 patients (59%). After the mean follow-up period of 80 months, 42 patients (31%) continued to obtain significant pain relief with DBS. Some pain states, particularly anesthesia dolorosa and paraplegia pain, did not seem to respond to DBS. Major complications of therapy included wound infection (12%) and intracranial hemorrhage (3.5%); there was one death in the series (0.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

SYNOPSISRay and Wolff in a landmark study of human patients under local anesthesia, concluded that the brain was not sensitive to pain; however, at the time of their study, the anatomy and physiology of pain transmission and modulation were largely unknown and their stimulating electrodes were not implanted in the brainstem or thalamic cells or projections now known to be important to pain perception. We now report 15 patients, previously headache-free, who underwent electrode implantation in the periaqueductal gray between 1977 and 1982 who immediately at implantation or in the few days subsequent to implantation reported severe continuous head pain usually with florid "migrainous" feature that persisted for 2 months to 10 years. Ten of these patients were treated with reserpine and all were dramatically responsive to it, but 8 patients rapidly became tolerant. Seven patients who were treated with dihydroergotamine rapidly became headache-free; 2 of the 7 became tolerant quickly. One patient developed the "cough headache" syndrome after implantation, was responsive to indomethacin, the syndrome abating in 6 months. These data suggest that perturbation of brain may generate head pain. (Headache 27:416-420, 1987) Studies performed 45 years ago concluded that the brain is a pain-insensitive structure; 1,2 however, the anatomy and physiology of pain transmission and modulation was not understood at that time, and stimuli were not applied to central nervous system (CNS) sites now known to be important to the perception of pain. Whereas evidence is emerging that migraine and other benign headache disorders are generated by dysfunction of the CNS 3,4 the source(s) of pain has remained unclear. The dogma, based on incomplete data, that the brain is pain-insensitive has stultified hypothesis-testing of CNS mechanisms that might produce head pain.We now report our experience with 15 patients previously headache-free, who underwent electrode implantation in the periaqueductal gray region (PAG) and/or the somatosensory region of the thalamus and immediately or soon thereafter developed headache syndromes that simulated headache disorders that usually arise de novo.

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