- Failed back syndrome
Failed back syndrome or post-
laminectomysyndrome is a condition characterized by persistent pain following back surgeries.
Failed back syndrome (FBS), more commonly referred to as "failed back surgery syndrome" (FBSS), refers to chronic back and/or leg pain that occurs after back (spinal) surgery. [Long, D. M. (1991). "Failed back surgery syndrome." Neurosurg Clin N Am 2(4): 899-919. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1840393&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum National Library of Medicine PubMed link] ] [Ekkehard FW, Heisel J, Rupp S. The failed back surgery syndrome: Reasons, intraoperative findings, and long term results: a report of 182 operative treatments. Spine 1996;21: 626–33.] 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, sleeplessnessand spinal muscular deconditioning. An individual may be predisposed to the development of FBS due to systemic disorders such as diabetes, autoimmune diseaseand peripheral blood vessels (vascular) disease. Smoking is a risk for poor recovery from such an operation as is anything that constricts the blood vessels.
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 has been shown to decrease the frequency and intensity of the pain. The targeted anatomic use of a potent anti-inflammatory anti-TNF therapeutic is an emerging treatment option for patients with severe back or neck disc-related pain associated with FBSS (see below).
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. [Deyo, R. A., D. T. Gray, et al. (2005). "United States trends in lumbar fusion surgery for degenerative conditions." Spine 30(12): 1441-5; discussion 1446-7. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15959375&ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] Abelson, R and Petersen, M. “An operation to ease back pain bolsters the bottom line, too.” New York Times, December 31, 2003.] Abelson, R. “Surgeons invest in makers of hardware”. New York Times, December 30, 2006.] In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year. A single screw that goes into the spine may sell for $1,000. In 2004, the average hospital bill, excluding professional fees was $34,000 for fusion surgery; if one adds the fee of the surgeon, the assistant surgeon, and the anesthesiologist, one can easily see how fusion surgery alone generates billions of dollars per year in fees for hospitals and surgeons.Deyo, R. A., A. Nachemson, et al. (2004). "Spinal-fusion surgery - the case for restraint." N Engl J Med 350(7): 722-6. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=14960750&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ]
With these increasing numbers of operations, one would expect the incidence of FBSS to also have increased. In contrast to the representation that “spine surgery is no more than 95% predictive of a successful result”,fact |date=January 2008 other sources document a success rate as low as 49%, depending upon the evaluation criteria used. [Slipman, C. W., C. H. Shin, et al. (2002). "Etiologies of failed back surgery syndrome." Pain Med 3(3): 200-14; discussion 214-7.] Other forms of spinal surgery are less invasive than
spinal fusion; one such operation is laminectomy, performed more than 250,000 times per year in the U.S. [Taylor VM, Deyo RA, Cherkin DC, Kreuter W. Low back pain hospitalization. Recent United States trends and regional variations. Spine 1994;19: 1207–13.] But even this less invasive form of surgery is not uniformly successful; approximately 30,000-40,000 laminectomypatients obtain either no relief of symptomatology or a recurrence of symptoms. [Keane GP. Failed low back surgery syndrome. In: Cole AJ, ed. The low back pain handbook. Philadelphia: Mosby; 1997: 269–81.] Another less invasive form of spinal surgery, percutaneous disc surgery, has reported revision rates as high as 65%. [Chatterjee S, Foy PM, Findlay GF. Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy in the treatment of contained lumbar disc herniation. Spine 1995;20: 734–8.] It is no surprise, therefore, that FBSS is a significant medical concern which merits further research and attention by the medical and surgical communities.
Etiology of the failed back surgery syndrome
For patients with continued severe pain following spinal surgery the surgeon's first responsibility is to rule out a serious treatable cause of pain:
infection, tumor, fracture, spinal instability, or abscess. If present, these causes are usually ferreted out early-on. Surgeons will argue that the etiology of FBSS "can be poor patient selection, incorrect diagnosis, suboptimal selection of surgery, poor technique ...and/or recurrent pathology", as well as including "failure to achieve surgical goals". [Guyer RD, Patterson M, Ohnmeiss DD.Failed back surgery syndrome: diagnostic evaluation.J Am Acad Orthop Surg. 2006 Sep;14(9):534-43. Review.PMID: 16959891] Commonly, however, causes of continued pain are difficult to unequivocally identify, and the patient suffers from chronic pain, not readily amenable to surgical intervention.Deyo RA. Diagnostic evaluation of LBP: reaching a specific diagnosis is often impossible.Arch Intern Med. 2002 Jul 8;162(13):1444-7. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12090877&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] Carragee, E. J. (2005). "Clinical practice. Persistent low back pain." N Engl J Med 352(18): 1891-8.] For those contemplating more surgery additional complications must be considered. Complications of spinal fusion surgery may include instrument failure, bone-donor site infection or chronic pain; neural injuries, pulmonary embolus, infections, vascular complications (rare but potentially catastrophic), failure to achieve a solid fusion, and blindness.
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. Obviously, 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. The reason for this is that many patients with
chronic painoften have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain. In addition, spinal fusionitself, particularly if more than one spinal level is operated on, may result in “adjacent segment degeneration”. Levin DA, Hale JJ, Bendo JA. Adjacent segment degeneration following spinal fusion for degenerative disc disease.Bull NYU Hosp Jt Dis. 2007;65(1):29-36. Review. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17539759&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum link to free full-text article] ] This is thought to occur because the fused segments may result in increased torsional and stress forces being transmitted to the intervertebral discslocated above and below the fused vertebrae. This pathology is one reason behind the development of artificial discs as a possible alternative to fusion surgery. But the fusion surgeons would argue that spinal fusionis 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.
Another highly relevant consideration is the increasing recognition of the importance of “chemical radiculitis” in the generation of
back pain.Peng, B., W. Wu, et al. (2007). "Chemical radiculitis." Pain 127(1-2): 11-6. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16963186&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] 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. [Marshall, L. L. and E. R. Trethewie (1973). "Chemical irritation of nerve-root in disc prolapse." Lancet 2(7824): 320.] [McCarron, R. F., M. W. Wimpee, et al. (1987). "The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain." Spine 12(8): 760-4.] [Takahashi, H., T. Suguro, et al. (1996). "Inflammatory cytokines in the herniated disc of the lumbar spine." Spine 21(2): 218-24. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8720407&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain. [Igarashi, T., S. Kikuchi, et al. (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. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11145807&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] [Sommer, C. and M. Schafers (2004). "Mechanisms of neuropathic pain: the role of cytokines." Drug Discovery Today: Disease Mechanisms 1(4): 441-448.] 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. [Igarashi, A., S. Kikuchi, et al. (2004). "Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders." Spine 29(19): 2091-5.] [Sakuma, Y., S. Ohtori, 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.] [Sekiguchi, M., S. Kikuchi, et al. (2004). "Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain." Spine 29(10): 1105-11.] In addition to causing pain and inflammation, TNFmay also contribute to disc degeneration. [Seguin, C. A., R. M. Pilliar, et al. (2005). "Tumor necrosis factor-alpha modulates matrix production and catabolism in nucleus pulposus tissue." Spine 30(17): 1940-8.] 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.
If chronic pain in FBSS has a chemical component producing inflammatory pain, then prior to additional surgery it may make sense to use an anti-inflammatory approach. Often this is first attempted with non-steroidal anti-inflammatory medications, but the long-term use of NSAIDS for patients with persistent back pain is complicated by their possible cardiovascular and gastrointestinal toxicity; and NSAIDs have limited value to intervene in TNF-mediated processes. An alternative often employed is the injection of cortisone into the spine adjacent to the suspected pain generator, a technique known as “epidural steroid injection”. [Fredman, B., M. B. Nun, et al. (1999). "Epidural steroids for treating "failed back surgery syndrome": is fluoroscopy really necessary?" Anesth Analg 88(2): 367-72.] Although this technique began more than a decade ago for FBSS, the efficacy of epidural steroid injections is now generally thought to be limited to short term pain relief in selected patients only. [ Landau, W. M., D. A. Nelson, et al. (2007). "Assessment: use of epidural steroid injections to treat radicular lumbosacral pain: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology." Neurology 69(6): 614; author reply 614-5.] In addition, epidural steroid injections, in certain settings, may result in serious complications. [ Abbasi, A., G. Malhotra, et al. (2007). "Complications of interlaminar cervical epidural steroid injections: a review of the literature." Spine 32(19): 2144-51. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17762818&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] Fortunately there are now emerging new methods that directly target TNF. Tobinick, E. L. and S. Britschgi-Davoodifar (2003). "Perispinal TNF-alpha inhibition for discogenic pain." Swiss Med Wkly 133(11-12): 170-7.] These TNF-targeted methods represent a highly promising new approach for patients with chronic severe spinal pain, such as those with FBSS. Ancillary approaches, such as rehabilitation,
physical therapy, anti-depressants, and, in particular, graduated exercise programs, may all be useful adjuncts to anti-inflammatory approaches. In addition, more invasive modalities, such as spinal cord stimulation, may offer relief for certain patients with FBSS, but these modalities, although often referred to as “minimally invasive", require additional surgery, and have complications of their own. [Bell, G. K., D. Kidd, et al. (1997). "Cost-effectiveness analysis of spinal cord stimulation in treatment of failed back surgery syndrome." J Pain Symptom Manage 13(5): 286-95.] [ Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, Molet J, Thomson S, O'Callaghan J, Eisenberg E, Milbouw G, Buchser E, Fortini G, Richardson J, North RB. Spinal cord stimulation versus conventional medical management for neuropathic pain: A multicentre randomised controlled trial in patients with failed back surgery syndrome. Pain. 2007 Sep 12; [Epub ahead of print] PMID: 17845835.]
Emerging treatment options
The identification of
tumor necrosis factor-alpha( TNF) as a central cause of inflammatory spinal pain now suggests the possibility of an entirely new approach to selected patients with FBSS. Specific and potent inhibitors of TNFbecame available in the U.S. in 1998, and were demonstrated to be potentially effective for treating sciaticain experimental models beginning in 2001. [ Sommer, C., M. Schafers, et al. (2001). "Etanercept reduces hyperalgesia in experimental painful neuropathy." J Peripher Nerv Syst 6(2): 67-72. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11446385&ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] [Olmarker, K. and B. Rydevik (2001). "Selective inhibition of tumor necrosis factor-alpha prevents nucleus pulposus-induced thrombus formation, intraneural edema, and reduction of nerve conduction velocity: possible implications for future pharmacologic treatment strategies of sciatica." Spine 26(8): 863-9. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11317106&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] [Murata, Y., A. Onda, et al. (2004). "Selective inhibition of tumor necrosis factor-alpha prevents nucleus pulposus-induced histologic changes in the dorsal root ganglion." Spine 29(22): 2477-84.] Targeted anatomic administration of one of these anti-TNF agents, etanercept, a patented treatment method, [U.S. patent 6,537,549 and others] has been suggested in published pilot studies to be effective for treating selected patients with chronic disc-related pain and FBSS. [Tobinick, E. and S. Davoodifar (2004). "Efficacy of etanercept delivered by perispinal administration for chronic back and/or neck disc-related pain: a study of clinical observations in 143 patients." Curr Med Res Opin 20(7): 1075-85. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15265252&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] The scientific basis for pain relief in these patients is supported by the most current review articles. [Myers, R. R., W. M. Campana, et al. (2006). "The role of neuroinflammation in neuropathic pain: mechanisms and therapeutic targets." Drug Discov Today 11(1-2): 8-20. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16478686&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum PubMed link] ] [Uceyler, N. and C. Sommer (2007). "Cytokine-induced Pain: Basic Science and Clinical Implications." Reviews in Analgesia 9(2): 87-103.] In the future new imaging methods may allow non-invasive identification of sites of neuronal inflammation, thereby enabling more accurate localization of the "pain generators" responsible for symptom production.
* [http://health.nytimes.com/health/guides/symptoms/back-pain-low/overview.html New York Times Back Pain]
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