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In the past two decades there has been a dramatic increase in fusion surgery in the U.S.: in 2001 over 122,000 lumbar fusions were performed, a 22% increase from 1990 in fusions per 100,000 population, increasing to an estimate of 250,000 in 2003, and 500,000 in 2006.<ref>{{cite journal |author=Deyo RA, Gray DT, Kreuter W, Mirza S, Martin BI |title=United States trends in lumbar fusion surgery for degenerative conditions |journal=Spine |volume=30 |issue=12 |pages=1441–5; discussion 1446–7 |year=2005 |month=Jun |pmid=15959375 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=12&spage=1441 |doi=10.1097/01.brs.0000166503.37969.8a}}</ref><ref name=ease>Abelson, R and Petersen, M. “An operation to ease back pain bolsters the bottom line, too.” New York Times, December 31, 2003.</ref><ref name=invest>Abelson, R. “Surgeons invest in makers of hardware”.  New York Times, December 30, 2006.</ref> In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year.<ref name=ease/> <ref>{{cite journal |author=Guyer RD, Patterson M, Ohnmeiss DD |title=Failed back surgery syndrome: diagnostic evaluation |journal=J Am Acad Orthop Surg |volume=14 |issue=9 |pages=534–43 |year=2006 |month=Sep |pmid=16959891 |url=http://www.jaaos.org/cgi/pmidlookup?view=long&pmid=16959891}}</ref>
In the past two decades there has been a dramatic increase in fusion surgery in the U.S.: in 2001 over 122,000 lumbar fusions were performed, a 22% increase from 1990 in fusions per 100,000 population, increasing to an estimate of 250,000 in 2003, and 500,000 in 2006.<ref>{{cite journal |author=Deyo RA, Gray DT, Kreuter W, Mirza S, Martin BI |title=United States trends in lumbar fusion surgery for degenerative conditions |journal=Spine |volume=30 |issue=12 |pages=1441–5; discussion 1446–7 |year=2005 |month=Jun |pmid=15959375 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=12&spage=1441 |doi=10.1097/01.brs.0000166503.37969.8a}}</ref><ref name=ease>Abelson, R and Petersen, M. “An operation to ease back pain bolsters the bottom line, too.” New York Times, December 31, 2003.</ref><ref name=invest>Abelson, R. “Surgeons invest in makers of hardware”.  New York Times, December 30, 2006.</ref> In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year.<ref name=ease/> <ref>{{cite journal |author=Guyer RD, Patterson M, Ohnmeiss DD |title=Failed back surgery syndrome: diagnostic evaluation |journal=J Am Acad Orthop Surg |volume=14 |issue=9 |pages=534–43 |year=2006 |month=Sep |pmid=16959891 |url=http://www.jaaos.org/cgi/pmidlookup?view=long&pmid=16959891}}</ref>
For patients with continued pain after surgery which is not due to the above complications or conditions, interventional pain physicians speak of the need to identify the "pain generator" i.e. the anatomical structure responsible for the patient's pain. To be effective, the surgeon must operate on the correct anatomic structure; however it is often not possible to determine the source of the pain.<ref name="diagnosis"/><ref name=persistent/> The reason for this is that many patients with [[chronic pain]] often have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain.<ref name=diagnosis/> In addition, [[spinal fusion]] itself, particularly if more than one spinal level is operated on, may result in “adjacent segment degeneration”.<ref name=levin>{{cite journal |author=Levin DA, Hale JJ, Bendo JA |title=Adjacent segment degeneration following spinal fusion for degenerative disc disease |journal=Bull NYU Hosp Jt Dis |volume=65 |issue=1 |pages=29–36 |year=2007 |pmid=17539759 |url=http://www.nyuhjdbulletin.org/Permalink.aspx?permalinkId=e6fb30e7-8841-4258-be97-610c1d8e7b9c}}</ref>  This is thought to occur because the fused segments may result in increased torsional and stress forces being transmitted to the [[intervertebral discs]] located above and below the fused vertebrae.<ref name=levin/> This pathology is one reason behind the development of artificial discs as a possible alternative to fusion surgery.  But the fusion surgeons argue, with some validity, that [[spinal fusion]] is more time-tested, and artificial discs contain metal hardware that is unlikely to last as long as biological material without shattering and leaving metal fragments in the spinal canal. These represent different [[schools of thought]]. (See discussion on disc replacement infra.)
For patients with continued pain after surgery which is not due to the above complications or conditions, interventional pain physicians speak of the need to identify the "pain generator" i.e. the anatomical structure responsible for the patient's pain. To be effective, the surgeon must operate on the correct anatomic structure; however it is often not possible to determine the source of the pain.<ref name="diagnosis"/><ref name=persistent/> The reason for this is that many patients with [[chronic pain]] often have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain.<ref name=diagnosis/> In addition, [[spinal fusion]] itself, particularly if more than one spinal level is operated on, may result in “adjacent segment degeneration”.<ref name=levin>{{cite journal |author=Levin DA, Hale JJ, Bendo JA |title=Adjacent segment degeneration following spinal fusion for degenerative disc disease |journal=Bull NYU Hosp Jt Dis |volume=65 |issue=1 |pages=29–36 |year=2007 |pmid=17539759 |url=http://www.nyuhjdbulletin.org/Permalink.aspx?permalinkId=e6fb30e7-8841-4258-be97-610c1d8e7b9c}}</ref>  This is thought to occur because the fused segments may result in increased torsional and stress forces being transmitted to the [[intervertebral discs]] located above and below the fused vertebrae.<ref name=levin/> This pathology is one reason behind the development of artificial discs as a possible alternative to fusion surgery.  But the fusion surgeons argue, with some validity, that [[spinal fusion]] is more time-tested, and artificial discs contain metal hardware that is unlikely to last as long as biological material without shattering and leaving metal fragments in the spinal canal. These represent different schools of thought.  


Another highly relevant consideration is the increasing recognition of the importance of “chemical radiculitis” in the generation of [[back pain]].<ref name=chemical>{{cite journal |author=Peng B, Wu W, Li Z, Guo J, Wang X |title=Chemical radiculitis |journal=Pain |volume=127 |issue=1-2 |pages=11–6 |year=2007 |month=Jan |pmid=16963186 |doi=10.1016/j.pain.2006.06.034 }}</ref>  A primary focus of surgery is to remove “pressure” or reduce mechanical compression on a neural element: either the [[spinal cord]], or a [[nerve root]]. But it is increasingly recognized that back pain, rather than being solely due to compression, may instead entirely be due to chemical inflammation of the nerve root.  It has been known for several decades that disc herniations result in a massive inflammation of the associated nerve root.<ref>{{cite journal |author=Marshall LL, Trethewie ER |title=Chemical irritation of nerve-root in disc prolapse |journal=Lancet |volume=2 |issue=7824 |pages=320 |year=1973 |month=Aug |pmid=4124797 |doi=10.1016/S0140-6736(73)90818-0 }}</ref><ref>{{cite journal |author=McCarron RF, Wimpee MW, Hudkins PG, Laros GS |title=The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain |journal=Spine |volume=12 |issue=8 |pages=760–4 |year=1987 |month=Oct |pmid=2961088 |doi=10.1097/00007632-198710000-00009 }}</ref> <ref>{{cite journal |author=Takahashi H, Suguro T, Okazima Y, Motegi M, Okada Y, Kakiuchi T |title=Inflammatory cytokines in the herniated disc of the lumbar spine |journal=Spine |volume=21 |issue=2 |pages=218–24 |year=1996 |month=Jan |pmid=8720407 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=21&issue=2&spage=218 |doi=10.1097/00007632-199601150-00011}}</ref><ref name=chemical/> In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain.<ref>{{cite journal |author=Igarashi T, Kikuchi S, Shubayev V, Myers RR |title=2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats |journal=Spine |volume=25 |issue=23 |pages=2975–80 |year=2000 |month=Dec |pmid=11145807 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=25&issue=23&spage=2975 |doi=10.1097/00007632-200012010-00003}}</ref><ref>{{cite journal |author=Sommer C, Schafers M |title=Mechanisms of neuropathic pain: the role of cytokines |journal=Drug Discovery Today: Disease Mechanisms |volume=1 |issue=4 |pages=441–8 |month=Dec |year=2004 |doi=10.1016/j.ddmec.2004.11.018 }}</ref>  This inflammatory molecule, called [[tumor necrosis factor-alpha]] ([[TNF]]), is released not only by the herniated or protruding disc, but also in cases of disc tear (annular tear), by facet joints, and in [[spinal stenosis]].<ref name=chemical/><ref>{{cite journal |author=Igarashi A, Kikuchi S, Konno S, Olmarker K |title=Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders |journal=Spine |volume=29 |issue=19 |pages=2091–5 |year=2004 |month=Oct |pmid=15454697 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=19&spage=2091 |doi=10.1097/01.brs.0000141265.55411.30}}</ref><ref>{{cite journal |author=Sakuma Y, Ohtori S, Miyagi M, ''et al'' |title=Up-regulation of p55 TNF alpha-receptor in dorsal root ganglia neurons following lumbar facet joint injury in rats |journal=Eur Spine J |volume=16 |issue=8 |pages=1273–8 |year=2007 |month=Aug |pmid=17468886 |pmc=2200776 |doi=10.1007/s00586-007-0365-3 }}</ref><ref>{{cite journal |author=Sekiguchi M, Kikuchi S, Myers RR |title=Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain |journal=Spine |volume=29 |issue=10 |pages=1105–11 |year=2004 |month=May |pmid=15131438 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=10&spage=1105 |doi=10.1097/00007632-200405150-00011}}</ref> In addition to causing pain and inflammation, [[TNF]] may also contribute to disc degeneration.<ref>{{cite journal |author=Séguin CA, Pilliar RM, Roughley PJ, Kandel RA |title=Tumor necrosis factor-alpha modulates matrix production and catabolism in nucleus pulposus tissue |journal=Spine |volume=30 |issue=17 |pages=1940–8 |year=2005 |month=Sep |pmid=16135983 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=17&spage=1940 |doi=10.1097/01.brs.0000176188.40263.f9}}</ref>    If the cause of the pain is not compression, but rather is inflammation mediated by [[TNF]], then this may well explain why surgery might not relieve the pain, and might even exacerbate it, resulting in FBSS.
Another highly relevant consideration is the increasing recognition of the importance of “chemical radiculitis” in the generation of [[back pain]].<ref name=chemical>{{cite journal |author=Peng B, Wu W, Li Z, Guo J, Wang X |title=Chemical radiculitis |journal=Pain |volume=127 |issue=1-2 |pages=11–6 |year=2007 |month=Jan |pmid=16963186 |doi=10.1016/j.pain.2006.06.034 }}</ref>  A primary focus of surgery is to remove “pressure” or reduce mechanical compression on a neural element: either the [[spinal cord]], or a [[nerve root]]. But it is increasingly recognized that back pain, rather than being solely due to compression, may instead entirely be due to chemical inflammation of the nerve root.  It has been known for several decades that disc herniations result in a massive inflammation of the associated nerve root.<ref>{{cite journal |author=Marshall LL, Trethewie ER |title=Chemical irritation of nerve-root in disc prolapse |journal=Lancet |volume=2 |issue=7824 |pages=320 |year=1973 |month=Aug |pmid=4124797 |doi=10.1016/S0140-6736(73)90818-0 }}</ref><ref>{{cite journal |author=McCarron RF, Wimpee MW, Hudkins PG, Laros GS |title=The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain |journal=Spine |volume=12 |issue=8 |pages=760–4 |year=1987 |month=Oct |pmid=2961088 |doi=10.1097/00007632-198710000-00009 }}</ref> <ref>{{cite journal |author=Takahashi H, Suguro T, Okazima Y, Motegi M, Okada Y, Kakiuchi T |title=Inflammatory cytokines in the herniated disc of the lumbar spine |journal=Spine |volume=21 |issue=2 |pages=218–24 |year=1996 |month=Jan |pmid=8720407 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=21&issue=2&spage=218 |doi=10.1097/00007632-199601150-00011}}</ref><ref name=chemical/> In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain.<ref>{{cite journal |author=Igarashi T, Kikuchi S, Shubayev V, Myers RR |title=2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats |journal=Spine |volume=25 |issue=23 |pages=2975–80 |year=2000 |month=Dec |pmid=11145807 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=25&issue=23&spage=2975 |doi=10.1097/00007632-200012010-00003}}</ref><ref>{{cite journal |author=Sommer C, Schafers M |title=Mechanisms of neuropathic pain: the role of cytokines |journal=Drug Discovery Today: Disease Mechanisms |volume=1 |issue=4 |pages=441–8 |month=Dec |year=2004 |doi=10.1016/j.ddmec.2004.11.018 }}</ref>  This inflammatory molecule, called [[tumor necrosis factor-alpha]] ([[TNF]]), is released not only by the herniated or protruding disc, but also in cases of disc tear (annular tear), by facet joints, and in [[spinal stenosis]].<ref name=chemical/><ref>{{cite journal |author=Igarashi A, Kikuchi S, Konno S, Olmarker K |title=Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders |journal=Spine |volume=29 |issue=19 |pages=2091–5 |year=2004 |month=Oct |pmid=15454697 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=19&spage=2091 |doi=10.1097/01.brs.0000141265.55411.30}}</ref><ref>{{cite journal |author=Sakuma Y, Ohtori S, Miyagi M, ''et al'' |title=Up-regulation of p55 TNF alpha-receptor in dorsal root ganglia neurons following lumbar facet joint injury in rats |journal=Eur Spine J |volume=16 |issue=8 |pages=1273–8 |year=2007 |month=Aug |pmid=17468886 |pmc=2200776 |doi=10.1007/s00586-007-0365-3 }}</ref><ref>{{cite journal |author=Sekiguchi M, Kikuchi S, Myers RR |title=Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain |journal=Spine |volume=29 |issue=10 |pages=1105–11 |year=2004 |month=May |pmid=15131438 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=10&spage=1105 |doi=10.1097/00007632-200405150-00011}}</ref> In addition to causing pain and inflammation, [[TNF]] may also contribute to disc degeneration.<ref>{{cite journal |author=Séguin CA, Pilliar RM, Roughley PJ, Kandel RA |title=Tumor necrosis factor-alpha modulates matrix production and catabolism in nucleus pulposus tissue |journal=Spine |volume=30 |issue=17 |pages=1940–8 |year=2005 |month=Sep |pmid=16135983 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=17&spage=1940 |doi=10.1097/01.brs.0000176188.40263.f9}}</ref>    If the cause of the pain is not compression, but rather is inflammation mediated by [[TNF]], then this may well explain why surgery might not relieve the pain, and might even exacerbate it, resulting in FBSS.

Revision as of 07:19, 25 January 2009

Failed back syndrome

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Overview

Failed back syndrome or post-laminectomy syndrome is a condition characterized by persistent pain following back surgeries.

Failed back syndrome (FBS), also called "failed back surgery syndrome" (FBSS), refers to chronic back and/or leg pain that occurs after back (spinal) surgery.[1][2] It is characterized as a chronic pain syndrome. Multiple factors can contribute to the onset or development of FBS. Contributing factors include but are not limited to residual or recurrent disc herniation, persistent post-operative pressure on a spinal nerve, altered joint mobility, joint hypermobility with instability, scar tissue (fibrosis), depression, anxiety, sleeplessness and spinal muscular deconditioning. An individual may be predisposed to the development of FBS due to systemic disorders such as diabetes, autoimmune disease and peripheral blood vessels (vascular) disease. Smoking is a risk for poor recovery.

Common symptoms associated with FBS include diffuse, dull and aching pain involving the back and/or legs. Abnormal sensibility may include sharp, pricking, and stabbing pain in the extremities. The term “post-laminectomy syndrome” is used by some doctors to indicate the same condition as failed back syndrome.

The treatments of post-laminectomy syndrome include physical therapy, minor nerve blocks, transcutaneous electrical nerve stimulation (TENS), behavioral medicine, non-steroidal anti-inflammatory (NSAID) medications, membrane stabilizers, antidepressants, spinal cord stimulation, and intracathecal morphine pump. Use of epidural steroid injections may be minimally helpful in some cases. The targeted anatomic use of a potent anti-inflammatory anti-TNF therapeutics is being investigated.

The amount of spinal surgery varies around the world. The most is performed in the United States and Holland. The least in the United Kingdom and Sweden. Recently, there have been calls for more aggressive surgical treatment in Europe (see infra). Success rates of spinal surgery vary for many reasons. [3] [4]

Etiology

Spinal surgeons operating on a back.

Patients who have undergone one or more operations on the lumbar spine, and continue to experience and report pain afterward can be divided into two groups. The first group are those in whom surgery was never indicated, or the surgery performed was never likely to achieve the desired result; and those in whom the surgery was indicated, but which technically did not achieve the intended result. [5] It has been observed that patients who have a predominant painful presentation in a radicular pattern will have a better result than those who have predominant complaints of back pain. Litigation tends to decrease the successful results of all spinal surgery. This includes personal injury cases (tort) and worker’s compensation cases. [6] [7]

The second group includes patients who had incomplete or inadequate operations. Lumbar spinal stenosis may be overlooked, especially when it is associated with disc protrusion or herniation. Removal of a disc, while not addressing the underlying presence of stenosis can lead to disappointing results. [8] Occasionally operating on the wrong level occurs, as does failure to recognize an extruded or sequestered disc fragment. Inadequate or inappropriate surgical exposure can lead to other problems in not getting to the underlying pathology. Hakelius reported a 3% incidence of serious nerve root damage. [9]

In 1992, Turner et al. [10] published a survey of 74 articles on the results after decompression for spinal stenosis. Good to excellent results were on average reported by 64% of the patients. There was, however, a wide variation in outcomes reported. There was a better result in patients who had a degenerative spondylolishesis. A similarly desigined study by Mardjekto et al. [11] found that a concomitant spinal arthrodesis (fusion) had a greater success rate. Herron and Trippi [12] evaluated 24 patients, all with degenerative spondylolisthesis treated with laminectomy alone. At follow-up varying between 18 to 71 months after surgery, 20 out of 24 (83%) patients reported a good result. Epstein [13] reported on 290 patients treated over a 25 year period. Excellent results were obtained in 69% and good results in 13%. However, these optimistic reports do not correlate with "return to competitive employment" rates, which for the most part are dismal in post spinal surgery series. To be honest, most articles surverying surgical success do not report on return to work.

In the past two decades there has been a dramatic increase in fusion surgery in the U.S.: in 2001 over 122,000 lumbar fusions were performed, a 22% increase from 1990 in fusions per 100,000 population, increasing to an estimate of 250,000 in 2003, and 500,000 in 2006.[14][15][16] In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year.[15] [17] For patients with continued pain after surgery which is not due to the above complications or conditions, interventional pain physicians speak of the need to identify the "pain generator" i.e. the anatomical structure responsible for the patient's pain. To be effective, the surgeon must operate on the correct anatomic structure; however it is often not possible to determine the source of the pain.[18][19] The reason for this is that many patients with chronic pain often have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain.[18] In addition, spinal fusion itself, particularly if more than one spinal level is operated on, may result in “adjacent segment degeneration”.[20] This is thought to occur because the fused segments may result in increased torsional and stress forces being transmitted to the intervertebral discs located above and below the fused vertebrae.[20] This pathology is one reason behind the development of artificial discs as a possible alternative to fusion surgery. But the fusion surgeons argue, with some validity, that spinal fusion is more time-tested, and artificial discs contain metal hardware that is unlikely to last as long as biological material without shattering and leaving metal fragments in the spinal canal. These represent different schools of thought.

Another highly relevant consideration is the increasing recognition of the importance of “chemical radiculitis” in the generation of back pain.[21] A primary focus of surgery is to remove “pressure” or reduce mechanical compression on a neural element: either the spinal cord, or a nerve root. But it is increasingly recognized that back pain, rather than being solely due to compression, may instead entirely be due to chemical inflammation of the nerve root. It has been known for several decades that disc herniations result in a massive inflammation of the associated nerve root.[22][23] [24][21] In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain.[25][26] This inflammatory molecule, called tumor necrosis factor-alpha (TNF), is released not only by the herniated or protruding disc, but also in cases of disc tear (annular tear), by facet joints, and in spinal stenosis.[21][27][28][29] In addition to causing pain and inflammation, TNF may also contribute to disc degeneration.[30] If the cause of the pain is not compression, but rather is inflammation mediated by TNF, then this may well explain why surgery might not relieve the pain, and might even exacerbate it, resulting in FBSS.


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  1. ↑ Long DM (1991). "Failed back surgery syndrome". Neurosurg Clin N Am. 2 (4): 899–919. PMID 1840393. Unknown parameter |month= ignored (help)
  2. ↑ Fritsch EW, Heisel J, Rupp S (1996). "The failed back surgery syndrome: reasons, intraoperative findings, and long-term results: a report of 182 operative treatments". Spine. 21 (5): 626–33. doi:10.1097/00007632-199603010-00017. PMID 8852320. Unknown parameter |month= ignored (help)
  3. ↑ Slipman CW, Shin CH, Patel RK; et al. (2002). "Etiologies of failed back surgery syndrome". Pain Med. 3 (3): 200–14, discussion 214–7. doi:10.1046/j.1526-4637.2002.02033.x. PMID 15099254. Unknown parameter |month= ignored (help)
  4. ↑ Taylor VM, Deyo RA, Cherkin DC, Kreuter W (1994). "Low back pain hospitalization. Recent United States trends and regional variations". Spine. 19 (11): 1207–12, discussion 13. PMID 8073311. Unknown parameter |month= ignored (help)
  5. ↑ Fager, C. A., Freiberg, S. R., Spine, 5:87-94; 1980
  6. ↑ Spengler, D. M., et. al. Spine 5:356-60; 1980
  7. ↑ Wiltse, l. L., Rocchio, P. D., J. Bone Joint Surg.; 57 A:478-83, 1957
  8. ↑ Burton, C. V., et. al., Clin. Orthop. 157:191-99; 1981
  9. ↑ Hakelius, A., Acta. Orthop. Scand., Suppl:129-76; 1970
  10. ↑ Turner, J., et al., Spine 1992; 17:1-8
  11. ↑ Mardjetko, S. M., et al., Spine 1994; 20S:2256S-2265S
  12. ↑ Herron, L. D., and Trippi, A. C., Spine 1989; 14:534-538
  13. ↑ Epstein, N. E., J. Spinal Disorder. 1998; 11(2): 116-122
  14. ↑ Deyo RA, Gray DT, Kreuter W, Mirza S, Martin BI (2005). "United States trends in lumbar fusion surgery for degenerative conditions". Spine. 30 (12): 1441–5, discussion 1446–7. doi:10.1097/01.brs.0000166503.37969.8a. PMID 15959375. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 Abelson, R and Petersen, M. “An operation to ease back pain bolsters the bottom line, too.” New York Times, December 31, 2003.
  16. ↑ Abelson, R. “Surgeons invest in makers of hardware”. New York Times, December 30, 2006.
  17. ↑ Guyer RD, Patterson M, Ohnmeiss DD (2006). "Failed back surgery syndrome: diagnostic evaluation". J Am Acad Orthop Surg. 14 (9): 534–43. PMID 16959891. Unknown parameter |month= ignored (help)
  18. ↑ 18.0 18.1
  19. ↑
  20. ↑ 20.0 20.1 Levin DA, Hale JJ, Bendo JA (2007). "Adjacent segment degeneration following spinal fusion for degenerative disc disease". Bull NYU Hosp Jt Dis. 65 (1): 29–36. PMID 17539759.
  21. ↑ 21.0 21.1 21.2 Peng B, Wu W, Li Z, Guo J, Wang X (2007). "Chemical radiculitis". Pain. 127 (1–2): 11–6. doi:10.1016/j.pain.2006.06.034. PMID 16963186. Unknown parameter |month= ignored (help)
  22. ↑ Marshall LL, Trethewie ER (1973). "Chemical irritation of nerve-root in disc prolapse". Lancet. 2 (7824): 320. doi:10.1016/S0140-6736(73)90818-0. PMID 4124797. Unknown parameter |month= ignored (help)
  23. ↑ McCarron RF, Wimpee MW, Hudkins PG, Laros GS (1987). "The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain". Spine. 12 (8): 760–4. doi:10.1097/00007632-198710000-00009. PMID 2961088. Unknown parameter |month= ignored (help)
  24. ↑ Takahashi H, Suguro T, Okazima Y, Motegi M, Okada Y, Kakiuchi T (1996). "Inflammatory cytokines in the herniated disc of the lumbar spine". Spine. 21 (2): 218–24. doi:10.1097/00007632-199601150-00011. PMID 8720407. Unknown parameter |month= ignored (help)
  25. ↑ Igarashi T, Kikuchi S, Shubayev V, Myers RR (2000). "2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats". Spine. 25 (23): 2975–80. doi:10.1097/00007632-200012010-00003. PMID 11145807. Unknown parameter |month= ignored (help)
  26. ↑ Sommer C, Schafers M (2004). "Mechanisms of neuropathic pain: the role of cytokines". Drug Discovery Today: Disease Mechanisms. 1 (4): 441–8. doi:10.1016/j.ddmec.2004.11.018. Unknown parameter |month= ignored (help)
  27. ↑ Igarashi A, Kikuchi S, Konno S, Olmarker K (2004). "Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders". Spine. 29 (19): 2091–5. doi:10.1097/01.brs.0000141265.55411.30. PMID 15454697. Unknown parameter |month= ignored (help)
  28. ↑ Sakuma Y, Ohtori S, Miyagi M; et al. (2007). "Up-regulation of p55 TNF alpha-receptor in dorsal root ganglia neurons following lumbar facet joint injury in rats". Eur Spine J. 16 (8): 1273–8. doi:10.1007/s00586-007-0365-3. PMC 2200776. PMID 17468886. Unknown parameter |month= ignored (help)
  29. ↑ Sekiguchi M, Kikuchi S, Myers RR (2004). "Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain". Spine. 29 (10): 1105–11. doi:10.1097/00007632-200405150-00011. PMID 15131438. Unknown parameter |month= ignored (help)
  30. ↑ Séguin CA, Pilliar RM, Roughley PJ, Kandel RA (2005). "Tumor necrosis factor-alpha modulates matrix production and catabolism in nucleus pulposus tissue". Spine. 30 (17): 1940–8. doi:10.1097/01.brs.0000176188.40263.f9. PMID 16135983. Unknown parameter |month= ignored (help)
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