The neurophysiological mechanisms of action of<unk> <unk>  stimulation are not completely understood but may involve masking pain sensation with tingling by altering the pain processing of the central nervous system. The mechanism of analgesia when<unk>  is applied in neuropathic pain states may be very different from that involved in analgesia due to limb ischemia. In neuropathic pain states, experimental evidence shows that<unk>  alters the local neurochemistry in dorsal horn, suppressing the hyperexcitability of the neurons. Specifically, there is some evidence for increased levels of GABA release, serotonin, and perhaps suppression of levels of some excitatory amino acids, including glutamate and aspartate. In the case of ischemic pain, analgesia seems to derive from restoration of the oxygen demand supply. This effect could be mediated by inhibition of the sympathetic system, although vasodilation is another possibility. It is also probable that a combination of the two above mentioned mechanisms is involved.
Spinal cord stimulator
Thalamic stimulator
Non-invasive cerebellar stimulation
Baroreflex activation therapy
Cortical stimulation mapping
Retrobulbar block
Neuroreflexotherapy
Brain mapping