Spinal cord stimulation in patients: Basic anatomical and neurophysiological mechanisms

Abstract

Peripheral vascular diseases of the legs may lead to decrease of nutritional blood flow, ischemia, pain, ulcera, and other changes. These changes may eventually result in amputation of the extremity. Repetitive electrical spinal cord stimulation in these patients may lead to increase of blood flow through skin and deep tissues of the limb (in particular through the microvascular compartment) and of transcutaneous O2-tension, may generate relief of ongoing pain (with increase of walking distance), and may be followed by healing of the ulcera (see Table 1 and contributions to this volume). This therapeutic intervention prevents amputation, at least in some of the patients, and improves quality of life. Interestingly, it does not appear to work in patients with autonomic neuropathy (e.g. in patients with diabetes mellitus) when the post-ganglionic axons are destroyed. Furthermore, the procedure is only successful, first, when the spinal stimulation electrodes are positioned over those spinal segments which contain the sympathetic outflow to the legs (i.e., in humans over the lower thoracic and two upper lumbar spinal segments) and, second, when the spinal cord stimulation generates paresthesias which are projected into the diseased limb.