Neuromodulation : journal of the International Neuromodulation Society
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For more than a decade, spinal cord stimulation (SCS) has been used as an adjuvant treatment for patients who are unresponsive to conventional therapies for angina pectoris. Many studies showed that SCS has both electro-analgesic and anti-ischemic effects. Nonetheless, the biological substrates by which SCS acts have not yet been unraveled, although recently areas in the brain have been described that show changes in blood flow, following SCS, and during provocation of angina. ⋯ In conclusion, the rat model we developed appears to be suitable for studying potential mechanisms through which SCS may act. In addition, SCS affects c-fos expression in specific parts of the brain known to be involved in regulation of pain and emotions. HSP72-expression is limited to the endothelium of certain parts of the CNS and thereby excludes physical stress effects as a potential mechanism of SCS.
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Epidural spinal cord stimulation (SCS) has gained a secure place in the armamentarium of the surgeon treating chronic pain conditions (1, 2). The complexity of the intraspinal structures and their different susceptibility to electrical signals, however, has made it difficult to characterize the effects of the stimulation, Some important recent work has helped shed light on the electrical properties of the intraspinal structures and on the electrical field potentials generated with epidural spinal cord stimulation. This work, initially pioneered by Sin and Coburn, has successfully been expanded and perfected by Holsheimer and Strujik at the University of Twente, The Netherlands (3-8). ⋯ The model can simulate the effects of epidural stimulation with different electrode geometries and configurations (8). The data generated from the model were then validated by comparing them to a large number of data collected by the author in implanted subjects (9-12). The author also conducted a detailed analysis of the clinical properties of the activation of the intraspinal structures at various electrode positions in the spine (13, 14).
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This article introduces two clinical fields in which stimulation is applied to the nervous system: neuromodulation and functional electrical stimulation. The concepts underlying these fields and their main clinical applications, as well as the methods and techniques used in each field, are described. Concepts and techniques common in one field that might be beneficial to the other are discussed.
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This report details the course of a 77-year-old patient suffering mild pain from operated tongue cancer and excruciating, intractable pain from thoracic (T6-T8) post-herpetic neuralgia (PHN), The mouth pain was treated with nonopioid analgesics, as the patient had personal objections to opioid treatment. All the components of the pain from his PHN (continuous burning pain, intermittent lancinating stabbing pain, and tactile allodynia) were successfully treated with an Intrathecal Infusion of buprenorphine (0.03 mg/ml) and bupivacaine (4.75 mg/ml) administered via an externalized intrathecal catheter with the tip located at T9-T10 intervertebral disc. The treatment started three months after the appearance of the herpetic eruption and lasted 294 days until the patient died of malnutrition and the progression of his tongue cancer. ⋯ The patient could ambulate without support while on 90-100 mg/day of intrathecal bupivacaine. During a series of high-pressure oxygen treatments in a pressure chamber to treat an infection at the site of his tumor, the intrathecal infusion was interrupted. Thus, repeated observation of the intervals of severe pain and of analgesia were possible.
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Objective. In addition to treatment of refractory chronic pain in patients with peripheral vascular disease, dorsal spinal cord stimulation (DCS) increases cutaneous blood flow to the extremities and may have a limb-saving effect. The purpose of this study was to examine the role of the sympathetic nervous system in the cutaneous vasodilation due to DCS. ⋯ Propranolol (5 mg/kg, i.v.), a nonselective beta-adrenergic receptor antagonist, attenuated the DCS response while adrenal demedullation did not. Conclusion. Overall, our results show that DCS-induced vasodilation can occur through mechanisms that are independent of sympathetic outflow.