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The history of stereotactic neurosurgery in the United Kingdom of Great Britain and Northern Ireland is reviewed. Horsley and Clarke's primate stereotaxy at the turn of the 20th century and events surrounding it are described, including Mussen's development of a human version of the apparatus. Stereotactic surgery after the Second World War is reviewed, with an emphasis on the pioneering work of Gillingham, Hitchcock, Knight, and Watkins and the contributions from Bennett, Gleave, Hughes, Johnson, McKissock, McCaul, and Dutton after the influences of Dott, Cairns, and Jefferson. Forster's introduction of gamma knife radiosurgery is summarized, as is the application of computed tomography by Hounsfield and Ambrose. Contemporary contributions to the present day from Bartlett, Richardson, Miles, Thomas, Gill, Aziz, Hariz, and others are summarized. The current status of British stereotactic neurosurgery is discussed.

BACKGROUND:: Deep brain stimulation (DBS) has shown considerable promise for relieving nociceptive and neuropathic symptoms of refractory chronic pain. Nevertheless, for some patients, standard DBS for pain remains poorly efficacious. Pain is a multi-dimensional experience with an affective component: the unpleasantness. The anterior cingulate cortex (ACC) is a structure involved in this affective component and targeting it may relieve patients.OBJECTIVE:: To describe the first case series of ACC DBS to relieve the affective component of chronic neuropathic pain.METHODS:: 16 patients (13 males and 3 females) with neuropathic pain underwent bilateral ACC DBS. Mean age at surgery was 48.7 [33-63] years. Patient reported outcome measures were collected before and after surgery, using a Visual Analogue Scale (VAS), Short Form 36 quality of life survey (SF-36), McGill pain questionnaire (MPQ) and EuroQol-5D questionnaires (EQ-5D; Health state).RESULTS:: 15 patients (93.3 %) transitioned from externalized to fully internalized systems. 11 patients had data to be analyzed with a mean follow-up of 13.2 months. Post-surgery, VAS dropped below 4 for 5 of the patients, with one patient freed from pain. Highly significant improvement of EQ-5D was observed (mean +20.3%, range +0% to +83%, p=0.008). Moreover, statistically significant improvements were observed for the PF (physical functioning) and BP (bodily pain) domains of the SF-36 quality of life survey: mean +64.7% (range -8.9% to +276%, p=0.015) and mean +39.0% (range -33.8% to +159%, p=0.050), respectively.CONCLUSION:: Affective ACC DBS can relieve chronic neuropathic pain refractory to pharmacotherapy and restore quality of life.

BACKGROUND: Deep brain stimulation (DBS) to treat neuropathic pain refractory to pharmacotherapy has reported variable outcomes and has gained United Kingdom but not USA regulatory approval. OBJECTIVE: To prospectively assess long-term efficacy of DBS for chronic neuropathic pain in a single-center case series. METHODS: Patient reported outcome measures were collated before and after surgery, using a visual analog score, short-form 36-question quality-of-life survey, McGill pain questionnaire, and EuroQol-5D questionnaires (EQ-5D and health state). RESULTS: One hundred ninety-seven patients were referred over 12 years, of whom 85 received DBS for various etiologies: 9 amputees, 7 brachial plexus injuries, 31 after stroke, 13 with spinal pathology, 15 with head and face pain, and 10 miscellaneous. Mean age at surgery was 52 years, and mean follow-up was 19.6 months. Contralateral DBS targeted the periventricular gray area (n = 33), the ventral posterior nuclei of the thalamus (n = 15), or both targets (n = 37). Almost 70% (69.4%) of patients retained implants 6 months after surgery. Thirty-nine of 59 (66%) of those implanted gained benefit and efficacy varied by etiology, improving outcomes in 89% after amputation and 70% after stroke. In this cohort, >30% improvements sustained in visual analog score, McGill pain questionnaire, short-form 36-question quality-of-life survey, and EuroQol-5D questionnaire were observed in 15 patients with >42 months of follow-up, with several outcome measures improving from those assessed at 1 year. CONCLUSION: DBS for pain has long-term efficacy for select etiologies. Clinical trials retaining patients in long-term follow-up are desirable to confirm findings from prospectively assessed case series.

OBJECTIVE: Electrical stimulation of the midbrain is known to influence blood pressure in animals. In humans, it is used for the treatment of chronic neuropathic pain. Our aim was to assess whether orthostatic hypotension can be successfully treated with deep brain stimulation of the periventricular/periaqueductal gray areas in humans. METHODS: We recruited 11 patients who had chronic neuropathic pain and who had undergone implantation of a deep brain stimulator in the periventricular/periaqueductal gray areas. Patients were divided into three groups depending on whether they had orthostatic hypotension (one patient), mild orthostatic intolerance (five patients), or no orthostatic intolerance (five patients). Postoperatively, we continuously recorded blood pressure and heart rate with stimulation off and on and in both sitting and standing positions. From these values, we derived the blood pressure changing rate. Using autoregressive modeling techniques, we calculated changes in low- and high-frequency power spectra of heart rate and baroreflex sensitivity. RESULTS: Electrical stimulation reduced the decrease in systolic blood pressure on standing from 28.2 to 11.1% in one patient with orthostatic hypotension (P < 0.001). In the mild orthostatic intolerance group, an initial drop in systolic blood pressure of 15.4% was completely reversed (P < 0.001). There were no side effects in the remaining group. These changes were accompanied by increases in the blood pressure changing rate, the baroreflex sensitivity, and the baseline (sitting) low-frequency power of the RR interval, but not the high-frequency power. CONCLUSION: Electrical stimulation of the human periventricular/periaqueductal gray areas can reverse orthostatic hypotension. The cause seems to be an increase in sympathetic outflow and in baroreflex sensitivity. This has important implications for future therapies.