
Spinal Cord Stimulation: “Neural Switch” in Complex Regional Pain Syndrome Type I
Author(s) -
Williams Kayode A.,
Korto Kau,
Cohen Steven P.
Publication year - 2009
Publication title -
pain medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.893
H-Index - 97
eISSN - 1526-4637
pISSN - 1526-2375
DOI - 10.1111/j.1526-4637.2009.00630.x
Subject(s) - complex regional pain syndrome , medicine , sudomotor , allodynia , neurostimulation , vasomotor , hyperalgesia , neuropathic pain , anesthesia , spinal cord injury , stimulation , neuroscience , spinal cord , nociception , psychology , psychiatry , receptor
. Complex regional pain syndrome type I (CRPS I) is a neuropathic pain disorder of unclear etiology. It commonly follows a trivial injury and is characterized by spontaneous pain manifesting regionally that is disproportionate to the inciting event. Associated signs and symptoms include allodynia, hyperalgesia, edema, sudomotor, vasomotor abnormalities, and trophic changes. Although multiple modalities exist to treat CRPS I, significant disability, diminution in quality of life, and reduction in overall health often accompany the syndrome. Case. A case of a 57‐year‐old man with CRPS I who was treated with spinal cord stimulation (SCS) after failing conservative therapy is presented. One month following treatment, he experienced complete symptom resolution such that stimulation was subsequently discontinued without recurrence over the 1‐year follow‐up period. Conclusions. To date there is currently no reliably validated “cure” for CRPS. There has only been one recent report where SCS resulted in the complete eradication of the signs and symptoms associated with CRPS. This series involved adolescent girls aged 11–14 years of age, who tend to have a more benign and self‐limited treatment course than that seen in adults. This raises the question as to whether a “neural switch” exists, and if so, where it is located. We postulate that the inter‐neuronal connections between the central and peripheral nervous systems implicated by the current pathophysiological model is the most plausible site of this “neural switch,” and that reorganization of this interface can account for the ability of SCS to effect a complete “cure” in CRPS.