Spinal Cord Stimulation Mechanisms and Indications Douglas Dobecki, M.D. San Diego Pain Institute

Gate Control Theory of SCS Originally derived from gate control theory by Melzack and Wall Peripheral stimulation of Aβ fibers leads to activation of inhibitory interneurons and subsequent inhibition of second order nociceptive neurons in the dorsal horn Expanded to electrical stimulation of the dorsal column with production of paresthesia Melzack et al, Science, 1965, Vol 150 Shealy, et al, Anesthesia and Analgesia, 1967, Vol 46

Neurophysiologic Mechanisms of SCS SCS increases dorsal horn inhibitory neurotransmitter GABAB, while decreasing excitatory amino acids Glutamate and Aspartate Activation of descending somatosensory control pathways through release of Serotonin, Norepinephrine, Adenosine Suppression of sympathetic activation by modulation of α-adrenoreceptors and antidromic release of calcitonin gene-related peptide (CGRP) and Substance P Modulation of WDR neurons Meyerson et al, Journal of Pain and Symptom Management, April 2006, Vol 31, No 4S

Electrophysiologic Mechanisms of SCS Current flows from Cathode (-) to Anode (+) resulting in neuronal depolarization at Cathode (-) and hyperpolarization at Anode (+) Electrical parameters are adjusted during programming including electrode polarity, Frequency (Hz), Amplitude (V or ma), and Pulse Width (μs) Potential segmental conductance blockade of spinothalamic tracts

SCS Mechanism Summary Many theories on the mechanisms of action of spinal cord stimulation have been suggested, including gate inhibition, activation or release of purported neuromodulators, conductance blockade of spinothalamic tracts, blockade of sympathetic mechanisms, and activation of supraspinal mechanisms The mechanism of spinal cord stimulation cannot completely explained by one model It is likely that multiple mechanisms and neurophysiologic pathways operate sequentially or simultaneously

SCS Indications Indicated for the management of chronic and intractable pain of the trunk or extremities Patients have failed adequate trial of conservative and conventional therapies Patients have passed psychological screening Common conditions include Failed Back Surgery Syndrome/Post-Laminectomy Syndrome Complex Regional Pain Syndrome (CRPS) Arachnoiditis Chronic Radiculopathy Epidural Scarring or Fibrosis Chronic Neuropathy or Neuralgia Post-Thoracotomy Pain

Failed Back Surgery Syndrome Defined as persistent or recurrent complaints of low back and/or leg pain in patients who have undergone operative procedures intended to relieve those complaints Can occur in up to 10-40% of spine surgeries $20B annually in direct health care costs 5th most common reason for MD visit Important to identify and treat other etiologies of FBSS that are not neuropathic and not candidates for SCS Foraminal stenonsis, discogenic pain, recurrent disc herniation, pseudoarthrosis, facetogenic pain, sacroiliac syndrome Common psychological disorders in FBSS Depression, anxiety, personality disorders, and secondary gain issues North et al, Neurosurgery, 2005, Vol 56, No 1 Follet et al, Neurosurgery Quarterly, March 1993, Vol 3, Issue 1

Failed Back Surgery Syndrome Etiology Genesis is multifactorial Improper patient selection Inadequate operations Operative complications Epidural scarring, fibrosis, arachnoiditis, Pseudoarthrosis Hardware malposition or failure Progression of degenerative processes Onset of new pathology Altered joint mobility Spondylolisthesis Adjacent segment disease Follet et al, Neurosurgery Quarterly, March 1993, Vol 3, Issue 1 Park et al, Spine, September 2004, Vol 29, Issue 17

Clinical Effectiveness of SCS in FBSS SCS was more successful than re-operation in giving selected FBSS patients at least 50% pain relief Minimally invasive therapeutic trial is an important advantage versus reoperation In most cases, SCS eliminated the need for further spine surgery in patients identified as reoperation candidates by standard criteria Battery life is a major SCS cost driver. Lifetime savings of rechargeable SCS systems can exceed $300,000 for average patient. 24 month outcomes demonstrate significant improvements of SCS patients compared to conventional medical management (CMM) group. Significantly more SCS (47%) patients versus CMM (7%) achieved the primary outcome of greater than 50% pain relief (P=0.02). North et al, Neurosurgery, January 2005, Vol 56, No 1 North et al, Neuromodulation, 2004, Vol 7 North et al, Neurosurgery, August 2007, Vol 61, Issue 2 Kumar et al, Neurosurgery, October 2008, Vol 63, No 4

Complex Regional Pain Syndrome Describes a myriad of pain symptoms which bridge neuropathic and vasculopathic pain conditions Symptoms are typically regional and out of proportion to the clinical course of the inciting event CRPS Type 1- pain symptom development without evidence of nerve injury CRPS Type 2- pain symptom development in setting of obvious nerve injury Sympathetically Maintained Pain (SMP) Sympathetically Independent Pain (SIP) Bennett et al, Neuromodulation, July 1999, Vol 2, Issue 3

Complex Regional Pain Syndrome Diagnosis based on history and physical exam Report 1 symptom in 3 of 4 categories: * Sensory- hyperesthesia and/or allodynia * Vasomotor- temperature asymmetry and/or skin color changes * Sudomotor /Edema- edema and/or sweating changes * Motor/Trophic- decrease ROM and/or motor dysfunction and/or trophic changes Must display at least 1 sign in 2 or more categories: * Sensory- hyperesthesia (pin prick) and/or allodynia (mechanical, Temperature) and/or deep somatic pressure/joint movement * Vasomotor- temperature asymmetry (>1 C) and/or skin color changes * Motor/Trophic - decrease ROM and/or motor dysfunction (weakness, tremor, dystonia, and/or trophic changes) Hayek et al, The Physician and Sports Medicine, May 2004, Vol 32, No. 5

Evidence Supporting SCS for CRPS Reference Type of Study (Level of Evidence) N Outcome Kemler et al. 2000 RCT (level 2) 36 pts. Improved pain and quality of life Successful in 56% of patients at 6 months Kemler et al. 1999 Retrospective (level 3) 23 pts. Successful in 57% of patients Kemler et al. 2004 Successful in 63% of pts; 2 yr follow-up of Kemler et al. 2000 Bennett et al. 1999 101 pts. 70% pt satisfaction for 1 lead 91% pt satisfaction for 2 leads Kumar et al. 1997 Nonrandomized (level 3) 12 pts. Good relief in 4 pts. Excellent relief in 8 pts. *RCT = randomized controlled trial

Summary of Mechanisms and Indications An understanding of the mechanisms of spinal cord stimulation continues to evolve SCS has been proven to be sustainably effective in the treatment of chronic neuropathic pain in several modern randomized clinical trials versus conventional therapies or reoperation Routine trial stimulation and an improved understanding of appropriate indications are associated with increased patient satisfaction, functional capacity and quality of life Rational use of SCS will continue to expand and continuing technological advancements will continue shape treatment algorithms