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Spinal cord stimulation use in patients with failed back surgery syndrome
Practice Points
Nancy Lee* & Sridhar Vasudevan1 Failed back surgery syndrome is a heterogeneous term reserved for back surgery patients who do not
meet the presurgical expectations of the patient and surgeon. The terminology does not specify the patient’s prior diagnosis, the reason for surgery failure or any present symptoms. Randomized controlled studies have demonstrated spinal cord stimulation (SCS) to be most effective in
failed back surgery syndrome with persistent radiculopathy. While SCS was initially inspired by the gate theory, its actual mechanism of action remains elusive. Recent rat models have suggested that the N‑methyl‑d‑aspartate receptor may play a role in the
mechanism of action for SCS. No consensus patient selection criteria exist. However, a successful screening trial, defined as at least
50% pain relief at rest and during provocative physical activity, with concurrent reduced analgesic consumption and patient satisfaction, is required prior to permanent implantation. Psychological assessment from a trained interdisciplinary pain center prior to SCS implantation has
not had evidence establishing predictability of these factors. However, various experts encourage an in-depth psychosocial evaluation early on, as this will likely identify patients who may have a poor SCS outcome.
SUMMARY
The increase in failed back surgery syndrome (FBSS) cases in the USA has been paralleled by an increase in the number of spinal cord stimulation (SCS) treatments performed. Over the last 40 years, SCS technique has improved drastically and has been shown to be efficacious in FBSS patients with radiculopathy and neuropathic pain. This article will focus on the current patient selection process of SCS in the setting of FBSS, with a review of pertinent clinical trials and current evidence-based guidelines. The current working mechanism of SCS, complications surrounding SCS and the definition of FBSS will also be briefly discussed. The societal impact of chronic back pain remains a formidable issue; direct annual costs have been estimated to be between US$12.2 billion
and $90.6 billion [1] . Moreover, the prevalence of back pain has been increasing over the last decade. In 2009, a population-based study noted
Wisconsin Rehabilitation Medicine Professionals, SC PO Box 240860, Milwaukee, WI 53224, USA *Author for correspondence: Medical College of Wisconsin, 8701 West Watertown Plank Road, Milwaukee, WI 53226-3548, USA; [email protected] 1
10.2217/PMT.12.3 © 2012 Future Medicine Ltd
Pain Manage. (2012) 2(2), 135–140
part of
ISSN 1758-1869
135
REVIEW Lee & Vasudevan an increase in the prevalence of chronic low back pain from 3.9% in 1992 to 10.2% in 2006 [2] . The pursuit of back pain management has also steadily increased. Between 1994 and 2001, Medicare spending for lumbrosacral injections for low back pain increased from $24 million to over $175 million [3] . Subsequently, back surgery, in attempts to alleviate back pain, has been on the concurrent rise. From 1992 to 2003, Medicare spending for inpatient back surgery increased from $75 million to $482 million, with 47% of total spending attributable to lumbar fusion [4] . This steady increase in the number of back surgeries, however, is largely a US phenomenon; rates of spine surgery in the USA are reported to be double that of Australia, Canada and Finland, and five-times that of Great Britain [5] . Unfortunately, an estimated 10–40% of patients improve only modestly or not at all after back surgery [6,7] . These patients who fail to improve are labeled with the relatively new term: ‘failed back surgery syndrome’ (FBSS). Naturally, the number of FBSS cases has risen in parallel with the increased number of back surgeries [8,9] , generating a new dimension to the chronic pain patient. In attempts to treat FBSS nonsurgically, spinal cord stimulation (SCS), a technique first developed over 50 years ago, has been growing in popularity. While SCS has strong evidence supporting its ability to reduce pain by at least 50%, it does not guarantee pain relief in all patients, and remains a costly, labor-intensive, invasive procedure [10] . Thus, the patient selection criterion warrants a closer exploration to optimize patient outcome. FBSS: a definition FBSS is a term embracing a heterogeneous collection of conditions that describes persistent or recurring low back pain, with or without sciatica following one or more spine surgeries [11] . A more functional definition proposes that FBSS results when the outcome of lumbar spinal surgery does not meet the presurgical expectations of the patient and surgeon [11] . As such, FBSS remains an umbrella term that does not specify the patient’s prior diagnosis, the reason for surgery failure or any present symptoms. There have been multiple attempts in the literature to classify the vast etiologies of FBSS. Several studies list spinal stenosis, disc disruption or retained disc and epidural fibrosis as the most common causes of FBSS [12–15] . Less
136
Pain Manage. (2012) 2(2)
common etiologies include recurrent disc herniations, iatrogenic instability, facet pain and sacroiliac joint pain. The studies also indicate that neuropathic pain, typically described as a constant, burning or dysesthetic pain in one or two dermatomes, aggravated by activity, accounts only for a minority of FBSS cases at 6–16% [12–14] . The mechanism of SCS The use of neuromodulation in modern pain medicine dates back to 1965 with the publication of Melzack and Wall’s gate theory. The revolutionary theory proposed that stimulation of innocuous neural pathways, carried on large myelinated fibers, could block concurrent noxious information carried on C‑fibers and A‑d fibers. The interference of noxious stimuli would effectively ‘close the gate’ on pain in the CNS [16] . Translating theory into clinical practice, Shealy et al. implanted the first SCS device for the treatment of chronic pain in 1967 [17] . While the inception of SCS was initially based on the gate control theory, the actual neurophysiologic mechanism of action of SCS remains complex and elusive. Postulations include direct inhibition of pain transmission in the dorsal horn of the spinal cord and possible recruitment of endogenous inhibitory pathways through the posterior columns of the spinal cord. Clinically, intermittent SCS may provide several hours of pain relief after cessation of the stimulation, suggesting long-lasting modulation of neural activity at the level of local transmitter systems in the dorsal horns [18] . The current neurophysiologic mechanism of SCS suggests a simultaneous increase in GABA and serotonin with concurrent suppression of glutamate and aspartate [19] . Recent animal models have investigated the role of neuropathic pain medications in conjunction with the use of SCS, expanding our understanding of the receptor systems involved in SCS. In 2011, Truin et al. demonstrated in rat models that subeffective intrathecal ketamine administered to nonresponders of SCS produces an enhanced pain-relieving effect of SCS to tactile hypersensitivity, thereby converting previously SCS nonresponders to SCS responders [20] . The study implicates the N‑methyl‑d‑aspartate receptor as a pivotal player in the induction and maintenance of neuropathic pain. Further research into the use of antidepressant medications showed similar results [21] . In 2011, Song et al. found that
future science group
Spinal cord stimulation use in patients with failed back surgery syndrome intrathecal pretreatment with a subeffective dose of milnacipran or amitriptyline, but not fluoxetine, enhanced the SCS suppressive effect on mechanical hypersensitivity after partial sciatic nerve lesion [21] . For reasons that remain unclear, SCS does not treat nociceptive pain effectively. Studies have shown that SCS is able to �������������������� dampen both continuous and evoked pain (tactile/thermal allodynia), but has had little effect on induced, acute nociceptive pain [22] . This is important to note, as an estimate of only 10–19% of chronic pain is characterized with neuropathic pain [12,13] . Complications of SCS SCS has undergone numerous technical and clinical refinements since its first proposal, striving to decrease invasiveness and apply advancing technology. Today, SCS remains a technically challenging modality. The process involves the careful placement of electrode leads into the epidural space, followed by a trial period to predict outcome. If the trial period proves to be effective, the leads are anchored, a pulse generator or radiofrequency receiver is implanted and connection wires are tunneled and connected [19] . SCS, like any invasive procedure, has its share of complications. A review by Taylor in 2006 revealed that 34% of patients who received a stimulator experienced complications [23] . The incidence of minor complications varies among different centers and models of SCS devices. The most common complications included electrode migration (11%), lead fracture (6%), infection (5%), hardware malfunction (2.5%), discomfort over the generator implant site (2.5%), rotation of the generator (2.5%) and insulation damage (1%) [24] . While rare, major complications with neurological injury do occur. Neurological injury resulting from direct trauma of the epidural vessels may lead to epidural bleeding and hematoma formation, requiring urgent surgical treatment. Neurological injury may also result from an epidural abscess, typically requiring explantation of the device [19] . Epidural electrode placement has also been reported as a rare cause of neurologic damage, requiring immediate SCS expert attention [19] . Patient selection for SCS SCS indications vary from FBSS, complex regional pain syndrome, neuropathic pain or refractory angina pectoris to peripheral ischemic limb pain. This article, however, focuses on SCS
future science group
REVIEW
in relation to FBSS, as it is the most common indication for SCS in the USA [25] . Patients with FBSS have typically had a longstanding history of pain and have attempted a wide variety of prior treatments. In brief, conservative management consists of pharmacotherapy, physical medicine and psychological therapies. Interventional modalities include facet medial branch blocks, sacroiliac joint blocks, epidural steroids and percutaneous epidural adhesiolysis. Surgical treatments include SCS, intrathecal drug-delivery systems and revision surgeries. Several authors have proposed management algorithms for the many available options, and generally consider SCS as a last resort treatment [11,26] . Currently, the selection protocol for SCS implantation requires a successful screening period with temporary percutaneous leads and an external generator [27] . The rationale stems from the finding that the strongest predictor of a negative SCS outcome is associated with
Spinal cord stimulation use in patients with failed back surgery syndrome
Practice Points
Nancy Lee* & Sridhar Vasudevan1 Failed back surgery syndrome is a heterogeneous term reserved for back surgery patients who do not
meet the presurgical expectations of the patient and surgeon. The terminology does not specify the patient’s prior diagnosis, the reason for surgery failure or any present symptoms. Randomized controlled studies have demonstrated spinal cord stimulation (SCS) to be most effective in
failed back surgery syndrome with persistent radiculopathy. While SCS was initially inspired by the gate theory, its actual mechanism of action remains elusive. Recent rat models have suggested that the N‑methyl‑d‑aspartate receptor may play a role in the
mechanism of action for SCS. No consensus patient selection criteria exist. However, a successful screening trial, defined as at least
50% pain relief at rest and during provocative physical activity, with concurrent reduced analgesic consumption and patient satisfaction, is required prior to permanent implantation. Psychological assessment from a trained interdisciplinary pain center prior to SCS implantation has
not had evidence establishing predictability of these factors. However, various experts encourage an in-depth psychosocial evaluation early on, as this will likely identify patients who may have a poor SCS outcome.
SUMMARY
The increase in failed back surgery syndrome (FBSS) cases in the USA has been paralleled by an increase in the number of spinal cord stimulation (SCS) treatments performed. Over the last 40 years, SCS technique has improved drastically and has been shown to be efficacious in FBSS patients with radiculopathy and neuropathic pain. This article will focus on the current patient selection process of SCS in the setting of FBSS, with a review of pertinent clinical trials and current evidence-based guidelines. The current working mechanism of SCS, complications surrounding SCS and the definition of FBSS will also be briefly discussed. The societal impact of chronic back pain remains a formidable issue; direct annual costs have been estimated to be between US$12.2 billion
and $90.6 billion [1] . Moreover, the prevalence of back pain has been increasing over the last decade. In 2009, a population-based study noted
Wisconsin Rehabilitation Medicine Professionals, SC PO Box 240860, Milwaukee, WI 53224, USA *Author for correspondence: Medical College of Wisconsin, 8701 West Watertown Plank Road, Milwaukee, WI 53226-3548, USA; [email protected] 1
10.2217/PMT.12.3 © 2012 Future Medicine Ltd
Pain Manage. (2012) 2(2), 135–140
part of
ISSN 1758-1869
135
REVIEW Lee & Vasudevan an increase in the prevalence of chronic low back pain from 3.9% in 1992 to 10.2% in 2006 [2] . The pursuit of back pain management has also steadily increased. Between 1994 and 2001, Medicare spending for lumbrosacral injections for low back pain increased from $24 million to over $175 million [3] . Subsequently, back surgery, in attempts to alleviate back pain, has been on the concurrent rise. From 1992 to 2003, Medicare spending for inpatient back surgery increased from $75 million to $482 million, with 47% of total spending attributable to lumbar fusion [4] . This steady increase in the number of back surgeries, however, is largely a US phenomenon; rates of spine surgery in the USA are reported to be double that of Australia, Canada and Finland, and five-times that of Great Britain [5] . Unfortunately, an estimated 10–40% of patients improve only modestly or not at all after back surgery [6,7] . These patients who fail to improve are labeled with the relatively new term: ‘failed back surgery syndrome’ (FBSS). Naturally, the number of FBSS cases has risen in parallel with the increased number of back surgeries [8,9] , generating a new dimension to the chronic pain patient. In attempts to treat FBSS nonsurgically, spinal cord stimulation (SCS), a technique first developed over 50 years ago, has been growing in popularity. While SCS has strong evidence supporting its ability to reduce pain by at least 50%, it does not guarantee pain relief in all patients, and remains a costly, labor-intensive, invasive procedure [10] . Thus, the patient selection criterion warrants a closer exploration to optimize patient outcome. FBSS: a definition FBSS is a term embracing a heterogeneous collection of conditions that describes persistent or recurring low back pain, with or without sciatica following one or more spine surgeries [11] . A more functional definition proposes that FBSS results when the outcome of lumbar spinal surgery does not meet the presurgical expectations of the patient and surgeon [11] . As such, FBSS remains an umbrella term that does not specify the patient’s prior diagnosis, the reason for surgery failure or any present symptoms. There have been multiple attempts in the literature to classify the vast etiologies of FBSS. Several studies list spinal stenosis, disc disruption or retained disc and epidural fibrosis as the most common causes of FBSS [12–15] . Less
136
Pain Manage. (2012) 2(2)
common etiologies include recurrent disc herniations, iatrogenic instability, facet pain and sacroiliac joint pain. The studies also indicate that neuropathic pain, typically described as a constant, burning or dysesthetic pain in one or two dermatomes, aggravated by activity, accounts only for a minority of FBSS cases at 6–16% [12–14] . The mechanism of SCS The use of neuromodulation in modern pain medicine dates back to 1965 with the publication of Melzack and Wall’s gate theory. The revolutionary theory proposed that stimulation of innocuous neural pathways, carried on large myelinated fibers, could block concurrent noxious information carried on C‑fibers and A‑d fibers. The interference of noxious stimuli would effectively ‘close the gate’ on pain in the CNS [16] . Translating theory into clinical practice, Shealy et al. implanted the first SCS device for the treatment of chronic pain in 1967 [17] . While the inception of SCS was initially based on the gate control theory, the actual neurophysiologic mechanism of action of SCS remains complex and elusive. Postulations include direct inhibition of pain transmission in the dorsal horn of the spinal cord and possible recruitment of endogenous inhibitory pathways through the posterior columns of the spinal cord. Clinically, intermittent SCS may provide several hours of pain relief after cessation of the stimulation, suggesting long-lasting modulation of neural activity at the level of local transmitter systems in the dorsal horns [18] . The current neurophysiologic mechanism of SCS suggests a simultaneous increase in GABA and serotonin with concurrent suppression of glutamate and aspartate [19] . Recent animal models have investigated the role of neuropathic pain medications in conjunction with the use of SCS, expanding our understanding of the receptor systems involved in SCS. In 2011, Truin et al. demonstrated in rat models that subeffective intrathecal ketamine administered to nonresponders of SCS produces an enhanced pain-relieving effect of SCS to tactile hypersensitivity, thereby converting previously SCS nonresponders to SCS responders [20] . The study implicates the N‑methyl‑d‑aspartate receptor as a pivotal player in the induction and maintenance of neuropathic pain. Further research into the use of antidepressant medications showed similar results [21] . In 2011, Song et al. found that
future science group
Spinal cord stimulation use in patients with failed back surgery syndrome intrathecal pretreatment with a subeffective dose of milnacipran or amitriptyline, but not fluoxetine, enhanced the SCS suppressive effect on mechanical hypersensitivity after partial sciatic nerve lesion [21] . For reasons that remain unclear, SCS does not treat nociceptive pain effectively. Studies have shown that SCS is able to �������������������� dampen both continuous and evoked pain (tactile/thermal allodynia), but has had little effect on induced, acute nociceptive pain [22] . This is important to note, as an estimate of only 10–19% of chronic pain is characterized with neuropathic pain [12,13] . Complications of SCS SCS has undergone numerous technical and clinical refinements since its first proposal, striving to decrease invasiveness and apply advancing technology. Today, SCS remains a technically challenging modality. The process involves the careful placement of electrode leads into the epidural space, followed by a trial period to predict outcome. If the trial period proves to be effective, the leads are anchored, a pulse generator or radiofrequency receiver is implanted and connection wires are tunneled and connected [19] . SCS, like any invasive procedure, has its share of complications. A review by Taylor in 2006 revealed that 34% of patients who received a stimulator experienced complications [23] . The incidence of minor complications varies among different centers and models of SCS devices. The most common complications included electrode migration (11%), lead fracture (6%), infection (5%), hardware malfunction (2.5%), discomfort over the generator implant site (2.5%), rotation of the generator (2.5%) and insulation damage (1%) [24] . While rare, major complications with neurological injury do occur. Neurological injury resulting from direct trauma of the epidural vessels may lead to epidural bleeding and hematoma formation, requiring urgent surgical treatment. Neurological injury may also result from an epidural abscess, typically requiring explantation of the device [19] . Epidural electrode placement has also been reported as a rare cause of neurologic damage, requiring immediate SCS expert attention [19] . Patient selection for SCS SCS indications vary from FBSS, complex regional pain syndrome, neuropathic pain or refractory angina pectoris to peripheral ischemic limb pain. This article, however, focuses on SCS
future science group
REVIEW
in relation to FBSS, as it is the most common indication for SCS in the USA [25] . Patients with FBSS have typically had a longstanding history of pain and have attempted a wide variety of prior treatments. In brief, conservative management consists of pharmacotherapy, physical medicine and psychological therapies. Interventional modalities include facet medial branch blocks, sacroiliac joint blocks, epidural steroids and percutaneous epidural adhesiolysis. Surgical treatments include SCS, intrathecal drug-delivery systems and revision surgeries. Several authors have proposed management algorithms for the many available options, and generally consider SCS as a last resort treatment [11,26] . Currently, the selection protocol for SCS implantation requires a successful screening period with temporary percutaneous leads and an external generator [27] . The rationale stems from the finding that the strongest predictor of a negative SCS outcome is associated with
