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Neurology and Neurosurgery/Incomplete Spinal Cord Injuries/Failed Back Syndrome

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

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, hypermobility (increased mobility) with instability, scar tissue (fibrosis), psychological depression (mood disorder), 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 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 nerve stimulator TENS, behavioral medicine, non-steroidal anti-inflammatory drug medication(NSAID), 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

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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 journal articles which reported 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 and 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 most 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. (See discussion on disc replacement infra.)

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.[21][22][23][24] 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.

Patient selection

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Patients who have sciatic pain (pain in the back, radiating down the buttock to the leg) and clear clinical findings of an identifiable radicular nerve loss caused by a herniated disc will have a better post operative course that those who simply have low back pain. If a specific disc herniation causing pressure on a nerve root cannot be identified, the results of surgery are likely to be disappointing. Patients involved in worker’s compensation, tort litigation or other compensation systems tend to fare more poorly after surgery. Surgery for spinal stenosis usually has a good outcome, if the surgery is done in an extensive manner, and done within the first year or so of the appearance of symptoms. [31][32][33][34][35]

Oaklander and North define the Failed Back Syndrome as a chronic pain patient after one or more surgical procedure to the spine. They delineated these characteristics of the relation between the patient and the surgeon: (1) The patient makes increasing demands on the surgeon for pain relief. The surgeon may feel a strong responsibility to provide a remedy when the surgery has not achieved the desired goals. (2) The patient grows increasingly angry at the failure and may become litigious. (3) There is an escalation of narcotic pain medication which is habituating or addictive. (4) In the face of expensive conservative treatments which are likely to fail, the surgeon is persuaded to attempt further surgery, even though this is likely to fail as well. (5) The probability of returning to gainful employment decreases with increasing length of disability. (6) The financial incentives to remain disabled far outweigh the incentive to recover. [36]

In the absence of a generous or comfortable economic package for disability or worker’s compensation, other psychological features may limit the ability of the patient to recover from surgery. Some patients are simply unfortunate, and fall into the category of “chronic pain” despite their desire to recover and the best efforts of the physicians involved in their care. [37][38][39][40][41][42][43][44][45][46][47] Even less invasive forms of surgery are not uniformly successful; approximately 30,000-40,000 laminectomy patients obtain either no relief of symptomatology or a recurrence of symptoms.[48] Another less invasive form of spinal surgery, percutaneous disc surgery, has reported revision rates as high as 65%.[49] It is no surprise, therefore, that FBSS is a significant medical concern which merits further research and attention by the medical and surgical communities.[18][19]

Pathology

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Before the advent of CT scanning, the pathology in failed back syndrome was difficult to understand. Computerized tomography in conjunction with metrizamide myelography in the late 1960s and 1970s allowed direct observation of the mechanisms involved in post operative failures. Six distinct pathologic conditions were identified:

  • Recurrent or persistent disc herniation
  • Spinal stenosis
  • Epidural post-operative fibrosis
  • Adhesive arachnoiditis
  • Nerve Injury
  • Pathologic location

Recurrent or persistent disc herniation

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CT scan image of large herniated disc in the lumbar spine.

Removal of a disc at one level can lead to disc herniation at the same level or a different level at a later time. Even the most complete surgical excision of the disc still leaves 30-40% of the disc, which cannot be safely removed. This retained disc can re-herniate sometime after surgery. Virtually every major structure in the abdomen and posterior retroperitoneal space has been injured removing discs from posterior laminetomy/discectomy surgical procedures. The most prominent of these is a laceration of the left internal iliac vein which lies in close proximity to the anterior portion of the disc. [50][51] In some studies, recurrent pain in the same radicular pattern or a different pattern can be as high as 50% after disc surgery. [52][53] Many observers have noted that the most common cause of a failed back syndrome is caused from recurrent disc herniation at the same level originally operated. A rapid removal in a second surgery can be curative. The clinical picture of a recurrent disc herniation usually involves a significant pain free interval. However, physical findings may be lacking, and a good history is necessary. [54][55][56][57] The time period for the emergence of new symptoms can be short or long. Diagnostic signs such as the straight leg raising test may be negative even if real pathology is present. [58][59] The presence of a positive myelogram may represent a new disc herniation, but can also be indicative of a post operative scarring situation simply mimicking a new disc. Newer MRI imaging techniques have clarified this dilemma somewhat. [60][61][62][63][64][65] Conversely, a recurrent disc can be difficult to detect in the presence of post op scarring. Myelography is inadequate to completely evaluate the patient for recurrent disc disease, and CT or MRI scanning is necessary. Measurement of tissue density can be helpful. [66][67][68][69][70]

Even though the complications of laminectomy for disc herniation can be significant, a recent series of studies involving thousands of patients published under auspices of Dartmouth Medical School concluded at four year follow-up that those who underwent surgery for a lumbar disc herniation achieved greater improvement than nonoperatively treated patients in all primary and secondary outcomes except work status. [71]

Spinal stenosis

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CT scan of laminectomy showing scar formation (highlighted in red)causing new stenosis.

Spinal Stenosis can be a late complication after laminectomy for disc herniation or when surgery was performed for the primary pathologic condition of spinal stenosis. [72][73][74] In the Maine Study, among patients with lumbar spinal stenosis completing 8- to 10-year follow-up, low back pain relief, predominant symptom improvement, and satisfaction with the current state were similar in patients initially treated surgically or nonsurgically. However, leg pain relief and greater back-related functional status continued to favor those initially receiving surgical treatment. [75]

A large study of spinal stenosis from Finland found the prognostic factors for ability to work after surgery were ability to work before surgery, age under 50 years, and no prior back surgery. The very long-term outcome (mean followup time of 12.4 years) was excellent-to-good in 68% of patients (59% women and 73% men). Furthermore, in the longitudinal follow-up, the result improved between 1985 and 1991. No special complications were manifested during this very long-term follow-up time. The patients with total or subtotal block in preoperative myelography achieved the best result. Furthermore, patients with block stenosis improved their result significantly in the longitudinal follow-up. The postoperative stenosis seen in computed tomography (CT) scans was observed in 65% of 90 patients, and it was severe in 23 patients (25%). However, this successful or unsuccessful surgical decompression did not correlate with patients' subjective disability, walking capacity or severity of pain. Previous back surgery had a strong worsening effect on surgical results. This effect was very clear in patients with total block in the preoperative myelography. The surgical result of a patient with previous back surgery was similar to that of a patient without previous back surgery when the time interval between the last two operations was more than 18 months. [76]

Post-operative MRI findings of stenosis are probably of limited value compared to symptoms experienced by patients. Patients' perception of improvement had a much stronger correlation with long-term surgical outcome than structural findings seen on postoperation magnetic resonance imaging. Degenerative findings had a greater effect on patients' walking capacity than stenotic findings [77][78]

Postoperative radiologic stenosis was very common in patients operated on for lumbar spinal stenosis, but this did not correlate with clinical outcome. The clinician must be cautious when reconciling clinical symptoms and signs with postoperative computed tomography findings in patients operated on for lumbar spinal stenosis. [79]

A study from Georgetown University reported on one-hundred patients who had undergone decompressive surgery for lumbar stenosis between 1980 and 1985. Four patients with postfusion stenosis were included. A 5-year follow-up period was achieved in 88 patients. The mean age was 67 years, and 80% were over 60 years of age. There was a high incidence of coexisting medical diseases, but the principal disability was lumbar stenosis with neurological involvement. Initially there was a high incidence of success, but recurrence of neurological involvement and persistence of low-back pain led to an increasing number of failures. By 5 years this number had reached 27% of the available population pool, suggesting that the failure rate could reach 50% within the projected life expectancies of most patients. Of the 26 failures, 16 were secondary to renewed neurological involvement, which occurred at new levels of stenosis in eight and recurrence of stenosis at operative levels in eight. Reoperation was successful in 12 of these 16 patients, but two required a third operation. The incidence of spondylolisthesis at 5 years was higher in the surgical failures (12 of 26 patients) than in the surgical successes (16 of 64). Spondylolisthetic stenosis tended to recur within a few years following decompression. Because of age and associated illnesses, fusion may be difficult to achieve in this group. [80]

Post operative infection

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A small minority of lumbar surgical patients will develop a post operative infection. In most cases, this is a bad complication and does not bode well for eventual improvement or future employability. Reports from the surgical literature indicate an infection rate anywhere from 0% to almost 12%. [81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96] The incidence of infection tends to increase as the complexity of the procedure and operating time increase. Usage of metal implants (instrumentation) tends to increase the risk of infection. Factors associated with an increased infection include diabetes mellitus, obesity, malnutrition, smoking, previous infection, rheumatoid arthritis, and immunodeficiency. [97][98][99][100][101][102] Previous wound infection should be considered as a contraindication to any further spinal surgery, since the likelihood of improving such patients with more surgery is small. [103][104][105][106][107][108] Antimicrobial prophylaxis (giving antibiotics during or after surgery before an infection begins) reduces the rate of surgical site infection in lumbar spine surgery, but a great deal of variation exists regarding its use. In a Japanese study, utilizing the Center for Disease Control recomendations for antibiotic prophylaxis, an overall rate of 0.7% infection was noted, with a single dose antibiotic group having 0.4% infection rate and multiple dosage antibiotic infection rate of 0.8%. The authors had previously used prophylactic antibiotics for 5 to 7 postoperative days. Based on the Centers for Disease Control and Prevention guideline, their antibiotic prophylaxis was changed to the day of surgery only. It was concluded there was no statistical difference in the rate of infection between the two different antibiotic protocols. Based on the CDC guideline, a single dose of prophylactic antibiotic was proven to be efficacious for the prevention of infection in lumbar spine surgeries. [109]

Epidural post-operative fibrosis

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Epidural scarring following a laminectomy for disc excision is a common feature when re-operating for recurrent sciatica or radiculopathy. [110] When the scarring is associated with a disc herniation and/or recurrent spinal stenosis, it is relatively common, occurring in more than 60% of cases. For a time, it was theorized that placing a fat graft over the dural could prevent post operative scarring. However, initial enthusiasm has waned in recent years. [111][112][113][114][115] In an extensive laminectomy involving 2 or more vertebra, post operative scarring is the norm. It is most often seen around the L5 and S1 nerve roots. [116][117][118]

Adhesive arachnoiditis

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Myelogram showing typical findings of arachnoiditis in the lumbar spine.

Fibrous scarring can also be a complication within the subarachnoid space. It is notoriously difficult to detect and evaluate. Prior to the development of magnetic resonance imaging, the only way to ascertain the presence of arachnoiditis was by opening the dura. In the days of CT scanning and Pantopaque and later, Metrizamide myelography, the presence of arachnoiditis could be speculated based on radiographic findings. Often, myelography prior to the introduction of Metrizamide was the cause of arachnoiditis. It can also be caused by the long term pressure brought about with either a disc herniation or spinal stenosis. [119][120][121][122][123] The presence of both epidural scarring and arachnoiditis in the same patient are probably quite common. Arachnoiditis is a broad term denoting inflammation of the meninges and subarachnoid space. A variety of etiologies exist, including infectious, inflammatory, and neoplastic processes. Infectious etiologies include bacterial, viral, fungal, and parasitic agents. Noninfectious inflammatory processes include surgery, intrathecal hemorrhage, and the administration of intrathecal (inside the dural canal) agents such as myelographic contrast media, anesthetics, and steroids. Neoplasia includes the hematogenous spread of systemic tumors, such as breast and lung carcinoma, melanoma, and non-Hodgkin lymphoma. Neoplasia also includes direct seeding of the cerebrospinal fluid (CSF) from primary central nervous system (CNS) tumors such as glioblastoma multiforme, medulloblastoma, ependymoma, and [w:choroid plexus carcinoma|[choroid plexus carcinoma]]. Strictly speaking, the most common cause of arachnoiditis in failed back syndrome is not infectious or from cancer. It is due to non-specific scarring secondary to the surgery or the underlying pathology. [124][125][126][127][128][129][130][131]

Nerve injury

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Laceration of a nerve root, or damage from cautery or traction can lead to chronic pain, however this can be difficult to determine. Chronic compression of the nerve root by a persistent agent such as disc, bone (osteophyte) or scarring can also permanently damage the nerve root. Epidural scarring caused by the initial pathology or occurring after the surgery can also contribute to nerve damage. In one study of failed back patients, the presence of pathology was noted to be at the same site as the level of surgery performed in 57% of cases. The remaining cases developed pathology at a different level, or on the opposite side, but at the same level as the surgery was performed. In theory, all failed back patients have some sort of nerve injury or damage which leads to a persistence of symptoms after a reasonable healing time. [132][133][134]

Return to work

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CT scan showing post operative scarring and arachnoiditis.

In a groundbreaking Canadian study, Waddell et al. [135] reported on the value of repeat surgery and the return to work in worker’s compensation cases. They concluded that workers who undergo spinal surgery take longer to return to their jobs. Once two spinal surgeries are performed, few if any ever return to gainful employment of any kind. After two spinal surgeries, most people in the worker’s comp system will not be made better by more surgery. Most will be worse after a third surgery.

Episodes of back pain associated with on the job injuries in the worker’s compensation setting are usually of short duration. About 10% of such episodes will not be simple, and will degenerate into chronic and disabling back pain conditions, even if surgery is not performed. [136][137]

It has been hypothesized that job dissatisfaction and individual perception of physical demands are associated with an increased time of recovery or an increased risk of no recovery at all. [138] Individual psychological and social work factors, as well as worker-employer relations are also likely to be associated with time and rates of recovery. [139][140][141]

A Finnish study of return to work in patients with Spinal Stenosis treated by surgery found that: (1) none of the patients who had retired before the operation returned to work afterward. (2) The variables that predicted postoperative ability to work for women were: being fit to work at the time of operation, age < 50 years at the time of operation, and duration of lumbar spinal stenosis symptoms < 2 years. (3) For men, these variables were: being fit to work at the time of operation, age < 50 years at the time of operation, no prior surgery, and the extent of the surgical procedure equal to or less than one laminectomy. Women's and men's working capacity do not differ after lumbar spinal stenosis operation. If the aim is to maximize working capacity, then, when a lumbar spinal stenosis operation is indicated, it should be performed without delay. In lumbar spinal stenosis patients who are > 50 years old and on sick leave, it is unrealistic to expect that they will return to work. Therefore, after such an extensive surgical procedure, re-education of patients for lighter jobs could improve the chances of these patients returning to work. [142]

In a related Finnish study, a total of 439 patients operated on for lumbar spinal stenosis during the period 1974-1987 was re-examined and evaluated for working and functional capacity approximately 4 years after the decompressive surgery. The ability to work before or after the operation and a history of no prior back surgery were variables predictive of a good outcome. Before the operation 86 patients were working, 223 patients were on sick leave, and 130 patients were retired. After the operation 52 of the employed patients and 70 of the unemployed patients returned to work. None of the retired patients returned to work. Ability to work preoperatively, age under 50 years at the time of operation and the absence of prior back surgery predicted a postoperative ability to work. [143]

A report from Belgium noted that patients reportedly return to work an average of 12 to 16 weeks after surgery for lumbar disc herniation. However, there are studies that lend credence to the value of an earlier stimulation for return to work and performance of normal activities after a limited discectomy. At follow-up assessment, it was found that no patient had changed employment because of back or leg pain.

Studies from the University of Washington School of Medicine found 68% of workers undergoing spinal fusion were not working two years post op.

The sooner the recommendation is made to return to work and perform normal activities, the more likely the patient is to comply. Patients with ongoing disabling back conditions have a low priority for return to work. The probability of return to work decreases as time off work increases. This is especially true in Belgium, where 20% of individuals did not resume work activities after surgery for a disc herniation of the lumbar spine. In Belgium, the medical advisers of sickness funds have an important role legally in the assessment of working capacity and medical rehabilitation measures for employees whose fitness for work is jeopardized or diminished for health reasons. The measures are laid down in the sickness and invalidity legislation. They are in accordance with the principle of preventing long-term disability. It is apparent from the authors' experience that these measures are not adapted consistently in medical practice. Most of the medical advisers are focusing purely on evaluation of corporal damage, leaving little or no time for rehabilitation efforts. In many other countries, the evaluation of work capacity is done by social security doctors with a comparable task. [144]

In a comprehensive set of studies carried out by the University of Washington School of Medicine, it was determined that the outcome of lumbar fusion performed on injured workers was worse than reported in most published case series. They found 68% of lumbar fusion patients still unable to return to work two years after surgery. This was in stark contrast to reports of 68% post-op satisfaction in many series. [145][146] In a follow up study it was found that the use of intervertebral fusion devices rose rapidly after their introduction in 1996. This increase in metal usage was associated with a greater risk of complication without improving disability or re-operation rates. [147][148][149][150]

Chronic pain and narcotic usage

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Failed back syndrome (FBS) is a well-recognized complication of surgery of the lumbar spine. It can result in chronic pain and disability, often with disastrous emotional and financial consequences to the patient. Many patients have traditionally been classified as "spinal cripples" and are consigned to a life of long-term narcotic treatment with little chance of recovery. Despite extensive work in recent years, FBS remains a challenging and costly disorder. [151]

A Swedish study of chronic pain and iatrogenic opioid addiction was reported from the methadone program at the Uppsala University Hospital. The aims were to improve pain relief and quality of life in pain patients with problematic opioid use and to investigate background factors explaining problems with opioid use. Titration of oral methadone mixture in daily doses ranging from 10 to 350 mg was done on all patients. Background factors were low back and musculoskeletal pain in 40%, psychiatric disease in 68%, and substance use disorder in 32% of the patients. Before methadone treatment all patients were on sick leave. After treatment five patients returned to work. Ten patients failed treatment, 4 due to intractable nausea, 4 to drug diversion, 1 because of methadone related arrhythmia and 1 because of insufficient analgesia. Pain relief was rated good by 75% and moderate by 25% of the patients. Global quality of life was deemed to have improved, somewhat. It was concluded a structured methadone program can be used for treating chronic pain patients with opioid dependence improving pain relief and quality of life. However, side effects and serious adverse events may limit the beneficial effects of the method. [152]

A study of chronic pain patients from the University of Wisconsin found that methadone is most widely known for its use in the treatment of opioid dependence, but methadone also provides effective analgesia. Patients who experience inadequate pain relief or intolerable side effects with other opioids or who suffer from neuropathic pain may benefit from a transition to methadone as their analgesic agent. Adverse effects, particularly respiratory depression and death, make a fundamental knowledge of methadone's pharmacological properties essential to the provider considering methadone as analgesic therapy for a patient with chronic pain. [153] The beneficial experience of methadone usage in some chronic pain patients was also found in Canada. [154]

A recent Italian study examined the use of fentanyl patches, sustained release morphine and methadone in chronic pain patients with cancer. All the three opioids used as first-line therapy were effective, well tolerated, and required similar amounts of symptomatic drugs or co-analgesics. Methadone was significantly less expensive, but required more changes, up and down, of the doses, suggesting that dose titration of this drug requires major clinical expertise. [155]

Total disc replacement

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Lumbar total disc replacement was originally designed to be an alternative to lumbar arthrodesis (fusion). The procedure was met with great excitement and heightened expectations both in the United States and Europe. In late 2004, the first lumbar total disc replacement received FDA approval in the United States. More experience existed in Europe. Since then, the initial excitement has given way to skepticism and concern. [156][157][158][159][160][161][162] Various failure rates, and strategies for revision of total disc replacement have been reported. [163] The role of artificial or total disc replacement in the treatment of spinal disorders remains ill-defined and unclear. [164] Evaluation of any new technique is difficult or impossible because physician experience may be minimal or lacking. Patient expectations may be distorted. [165][166] It has been difficult to establish clear cut indications for artificial disc replacement. It may not be a replacement procedure or alternative to fusion, since recent studies have shown that 100% of fusion patients had one or more contraindications to disc replacement. [167][168][169] The role of disc replacement must come from new indications not defined in today’s literature or a relaxation of current contraindications. [170]

A study by Regan [171] found the result of replacement was the same at L4-5 and L5-S1 with the CHARITE disc. However, the ProDisc II had more favorable results at L4-5 compared with L5-S1. [172]

A younger age was predictive of a better outcome in several studies. [173][174][175] In others it has been found to be a negative predictor or of no predictive value. [176][177][178][179][180] Older patients may have more complications. [181]

Prior spinal surgery has mixed effects on disc replacement. It has been reported to be negative in several studies. [182][183][184][185][186][187] It has been reported to have no effect in other studies. [188][189][190][191][192][193] Many studies are simply inconclusive. [194] Existing evidence does not allow drawing definite conclusions about the status of disc replacement at present. [195]

Electrical stimulation

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Many failed back patients are significantly impaired by chronic pain in the back and legs. Many of these will be treated with some form of electrical stimulation. This can be either a transcutaneous electrical nerve stimulation device placed on the skin over the back or a nerve stimulator implanted into the back with electrical probes which directly touch the spinal cord. Also, some chronic pain patients utilize fentanyl or narcotic patches. These patients are generally severely impaired and it is unrealistic to conclude that application of neurostimulation will reduce that impairment. For example, it is doubtful that neurostimulation will improve the patient enough to return to competitive employment. Neurostimulation is palliative. TENS units work by blocking neurotransmission as described by the pain theory of Melzack and Wall. [196] Success rates for implanted neurostimulation has been reported to be 25% to 55%. Success is defined as a relative decrease in pain. [197]

Smoking and failed back

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CT scan showing markedly thickened ligamentum flavum (yellow ligament) causing Spinal Stenosis in the lumbar spine.

Recent studies have shown that cigarette smokers will routinely fail all spinal surgery, if the goal of that surgery is the decrease of pain and impairment. Many surgeons consider smoking to be an absolute contraindication to spinal surgery. Nicotine appears to interfere with bone metabolism through induced calcitonin resistance and decreased osteoblastic function. It may also restrict small blood vessel diameter leading to increased scar formation. [198][199][200][201][202][203][204]

There is an association between cigarette smoking, back pain and chronic pain syndromes of all types. [205][206][207][208][209]

In a report of 426 spinal surgery patients in Denmark, smoking was shown to have a negative effect on fusion and overall patient satisfaction, but no measurable influence on the functional outcome. [210]

There is a validation of the hypothetical assumption that postoperative smoking cessation helps to reverse the impact of cigarette smoking on outcome after spinal fusion. If patients cease cigarette smoking in the immediate post operative period, there is a positive impact on success. [211]

Regular smoking in adolescence was associated with low back pain in young adults. Pack-years of smoking showed an exposure-response relationship among girls. [212]

A recent study suggested that cigarette smoking adversely affects serum hydrocodone levels. Prescribing physicians should be aware that in some cigarette smokers, serum hydrocodone levels might not be detectible. [213]

In a study from Denmark reviewing many reports in the literature, it was concluded tha smoking should be considered a weak risk indicator and not a cause of low back pain. In a multitude of epidemiologic studies, an association between smoking and low back pain has been reported, but variations in approach and study results make this literature difficult to reconcile. [214] In a massive study of 3482 patients undergoing lumbar spine surgery from the National Spine Network, comorbidities of (1) smoking, (2) compensation, (3) self reported poor overall health and (4) pre-existing psychological factors were predictive in a high risk of failure. Followup was carried out at 3 months and one year after surgery. Pre-operative depressive disorders tended not to do well. [215]

Smoking has been shown to increase the incidence of post operative infection as well as decrease fusion rates. One study showed 90% of post infections occurred in smokers, as well as myonecrosis (muscle destruction) around the wound. [216][217]

Worldwide perspective

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CT scan showing two views of L4-5 disc herniation

A report from Spain noted that the investigation and development of new techniques for instrumented surgery of the spine is not free from conflicts of interest. The influence of financial forces in the development of new technologies and its immediate application to spine surgery, shows the relationship between the published results and the industry support. Authors who have developed and defended fusion techniques have also published new articles praising new spinal technologies. The author calls spinal surgery the "American Stock and Exchange" and "the bubble of spine surgery". The scientific literature doesn't show clear evidence in the cost-benefit studies of most instrumented surgical interventions of the spine compared with the conservative treatments. It has not been yet demonstrated that fusion surgery and disc replacement are better options than the conservative treatment. It's necessary to point out that at present "there are relationships between the industry and back pain, and there is also an industry of the back pain". Nonetheless, the "market of the spine surgery" is growing because patients are demanding solutions for their back problems. The tide of scientific evidence seems to go against the spinal fusions in the degenerative disc disease, discogenic pain and in specific back pain. After decades of advances in this field, the results of spinal fusions are mediocre. New epidemiological studies show that "spinal fusion must be accepted as a non proved or experimental method for the treatment of back pain". The surgical literature on spinal fusion published in the last 20 years establishes that instrumentation seems to slightly increase the fusion rate and that instrumentation doesn't improve the clinical results in general. We still are in need of randomized studies to compare the surgical results with the natural history of the disease, the placebo effect, or conservative treatment. The European Guidelines for lumbar chronic pain management show "strong evidence" indicating that complex and demanding spine surgery where different instrumentation is used, is not more effective than a simple, safer and cheaper posterolateral fusion without instrumentation. Recently, the literature published in this field is sending a message to use "minimally invasive techniques"; - the abandonment of transpedicular fusions. Surgery in general, and usage of metal fixation should be discarded in most cases. [218]

In Sweden, the national registry of lumbar spine surgery reported in the year 2000 that 15% of patients with spinal stenosis surgery underwent a concomitant fusion. [219] Despite the traditionally conservative approach to spinal surgery in Sweden, there have been calls from that county for a more aggressive approach to lumbar procedures in recent years.

Cherkin et al., [220] evaluated worldwide surgical attitudes. There were twice the number of surgeons per capita in the United States compared to the United Kingdom. Numbers were similar to Sweden. Despite having very few spinal surgeons, the Netherlands proved to be quite aggressive in surgery. Sweden, despite having a large number of surgeons was conservative and produced relatively few surgeries. The most surgeries were done in the United States. In the UK, more than a third of non-urgent patients waited over a year to see a spinal surgeon. In Wales, more than half waited over three months for consult. Lower rates of referrals in the United Kingdom was found to discourage surgery in general. Fee for service and easy access to care was thought to encourage spinal surgery in the United States, whereas salaried position and a conservative philosophy led to less surgery in the United Kingdom. There were more spinal surgeons in Sweden than in the United States. However, it was speculated that the Swedish surgeons being limited to compensation of 40–48 hours a week might lead to a conservative philosophy. It should be noted that there have been calls for a more aggressive approach to lumbar surgery in both the United Kingdom and Sweden in recent years. [70][221][222]

Investigative treatment options

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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 TNF became available in the U.S. in 1998, and were demonstrated to be potentially effective for treating sciatica in experimental models beginning in 2001.[223][224][225] Targeted anatomic administration of one of these anti-TNF agents, etanercept, a patented treatment method,[226] has been suggested in published pilot studies to be effective for treating selected patients with chronic disc-related pain and FBSS.[227][228] The scientific basis for pain relief in these patients is supported by the many current review articles.[229][230] 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. These treatments are still experimental.

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.[19] 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”.[231] 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.[232] In addition, epidural steroid injections, in certain settings, may result in serious complications.[233] Fortunately there are now emerging new methods that directly target TNF.[227] These TNF-targeted methods represent a highly promising new approach for patients with chronic severe spinal pain, such as those with FBSS.[227] Ancillary approaches, such as rehabilitation, physical therapy, anti-depressants, and, in particular, graduated exercise programs, may all be useful adjuncts to anti-inflammatory approaches.[19] 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.[234][235]

Social Security Disability

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Under rules promulgated by Titles II and XVI of the United States Social Security Act, chronic radiculopathy, arachnoiditis and spinal stenosis are recognized as disabling conditions under Listing 1.04 A (radiculopathy), 1.04 B (arachnoiditis) and 1.04 C (spinal stenosis). [236][237]

Representative cases

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Case 1

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A 42 year old male working as a truck driver and delivery man for a local dairy experienced pain while lifting a milk case at a stop. The pain was immediate and went from his low back to the left leg. He tried to continue working, but was unable to finish his route. The pain persisted unabated for a week, when he was referred to a spinal surgeon by the company doctor. On exam he was found to have an absent left ankle jerk reflex (S 1) and some nerve loss and motor weakness in S1. An MRI was ordered which showed a large extruded disc at L5-S1 on the left. He was taken to surgery where the disc was removed. He returned to work in 6 weeks with no modification of the schedule. He was able to perform his duties for about 2 years when increasing pain in the back and leg caused him to quit his job. He again consulted a spinal surgeon who diagnosed a new disc herniation at the L4-5 level and post operative scarring at the previous laminectomy site. He was taken to surgery where the scar was removed and the new disc herniation was removed. After 8 weeks he tried to return to his old job, but was unable to do it. He tried to get retrained in sedentary type work. Finally, after 2 years, he found new employment in computer related services. He was able to do this work for about 3 years. He had a slow increase in back and leg symptoms. He underwent a third surgery which consisted of a wide decompressive laminectomy from L3 to S1 with a posterior lateral fusion. This did not relieve his pain and he was never able to return to work. After the last surgery, he was maintained on prescription narcotics Norco and percocet and sought disability.

Case 2

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A 27 year old male sheet rock worker and day laborer, smoker of one pack per day, experienced pain in the back while lifting building materials weighing about 100 pounds in the course of his employment. He tried to continue working but was unable to finish the day. He reported the problem and was sent to the company doctor who sent him to a spinal surgeon. There, a herniated L5-S1 disc with right sided S1 radiculopathy was diagnosed. He underwent a course of conservative therapy for three weeks, and did not improve. He continued to lose motor strength in the right S1 muscles. It was decided to perform a limited laminotomy with disc removal. The patient did well the first three days post-operatively and had relief of his symptoms. He was sent home in good spirits and seemingly better. He became ill on the fourth post op day. He was seen in the emergency room where he had a fever of 101.4, white cell count of 12,200 with slight left shift. He was complaining of severe pain in the surgical incision. On exam, the incision was red and pus could be expressed. Cultures were taken and he was returned to the operating room where an abscess was drained which went down to the dura. Tube suction drainage was placed and he was started on methicillin and gentamicin. The cultures grew methicillin sensitive staph aureus (MSSA). He was continued on IV antibiotics for two weeks. His pain continued unabated in both the low back and his right leg. He was maintained on percodan while in the hospital. At two years after his injury, he was still unemployed and maintained on methadone with vicodin and percodan for breakthrough pain. He sought disability as his spinal surgeon advised him it would be unlikely he would ever return to work.

References

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  1. ↑ Long DM (1991). "Failed back surgery syndrome". Neurosurg Clin N Am. 2 (4): 899–919. PMID 1840393. {{cite journal}}: 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  15. ↑ a b 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  18. ↑ a b c Deyo RA (2002). "Diagnostic evaluation of LBP: reaching a specific diagnosis is often impossible". Arch Intern Med. 162 (13): 1444–7, discussion 1447–8. doi:10.1001/archinte.162.13.1444. PMID 12090877. {{cite journal}}: Unknown parameter |month= ignored (help)
  19. ↑ a b c d Carragee EJ (2005). "Clinical practice. Persistent low back pain". N Engl J Med. 352 (18): 1891–8. doi:10.1056/NEJMcp042054. PMID 15872204. {{cite journal}}: Unknown parameter |month= ignored (help)
  20. ↑ a b 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ↑ a b c 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  31. ↑ Spengler, D. M., et al. Spine 5:356-60, 1980
  32. ↑ Wiltse, L. L., Rocchio, P. D., J. Bone Joint Surg., 57A:478-83, 1980
  33. ↑ Weir, B. K. A., J. Neuro. Surg. 50:283-89, 1979
  34. ↑ Weir, B. K. A., Jacobs, G. A., Spine 5:366-70, 1980
  35. ↑ Burton, C. V., et al. Clin Orthop. 157:191-99, 1981
  36. ↑ Oaklnader, A. L., and North, R. B. “Failed back surgery syndrome” In Loeser, J. D., et al., eds. “Bonica’s Management of Pain”, Philadelphia, Lippincott Williams & Williams, 2001
  37. ↑ Haider, T T., et al., J. Occup. Rehabil. 8:247-253, 1998
  38. ↑ Tandon. V., Spine 24:1833-1838, 1999
  39. ↑ Turner, J., et al., JAMA 268:907-911, 1992
  40. ↑ Malter, A. D., et al., Spine 21:1048-1055, 1996
  41. ↑ Dvorak, J., et al., Spine 13:1418-1422, 1988
  42. ↑ Deyo, R., et al., J. Bone Joint Surg., 74 A:536-543, 1992
  43. ↑ Gervitz, R. N., et al., Prof. Psychol. Res. Pract. 27:561-566, 1996
  44. ↑ Graver, V., et al., Br. J. Neurosurg. 2:178-184, 1999
  45. ↑ de Groot, K. I., et al., Pain 69:19-25, 1997
  46. ↑ Schade, V., et al., Pain 80:239-249, 1999
  47. ↑ Rosenstiel, A., Keefe, F., Pain 17:33-40, 1983
  48. ↑ Keane GP (1997). "Failed low back surgery syndrome". In Herring SA, Cole AJ (ed.). The low back pain handbook: a practical guide for the primary care clinician. Philadelphia: Hanley & Belfus. pp. 269–81. ISBN 1-56053-152-5.
  49. ↑ Chatterjee S, Foy PM, Findlay GF (1995). "Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation". Spine. 20 (6): 734–8. doi:10.1097/00007632-199503150-00016. PMID 7604351. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  50. ↑ Linton, R. R., White, P. D., Arch. Surg., 50:6, 1945
  51. ↑ Epps, C. H., “Complications in Orthopedic Surgery”, p. 1009-1037, Lippincott and Co., Philadelphia, 1978
  52. ↑ Cauchoix, J., et al. Spine 3:256-59, 1978
  53. ↑ Weir, BKA., Jacobs, G. A., Spine ibid
  54. ↑ Benoist, M., et al., Spine 5:432-35, 1980
  55. ↑ Benner, B., Ehni, G., Spine 3: 40-44, 1978
  56. ↑ Rothman, R., Orhop. Clin. North Amer. 6:310, 1975
  57. ↑ Quiles, M., et al., Spine 3:45-5-, 1978
  58. ↑ Spangfort, E., Acta Orthop. Scand. Suppl 142:5-93, 1972
  59. ↑ Weir, B. K. A., Spine 5:366-70, 1980
  60. ↑ Benoist, M., et al., Spine 5:432-35, 1980
  61. ↑ Bener, B., Ehni, G., Spine 3:40-44, 1978
  62. ↑ Byrd, S. E., et al., Spine 10:652-61, 1985
  63. ↑ Deburge, A., Badelon, O., Rev. Chir. Orthop. 68:249-54, 1982 (French)
  64. ↑ Irstam, L., Spine 9:759-63, 1984
  65. ↑ Thibierge, M., Metzger, J., Rev. Chir. Orthop. 68:230-33, 1982 (French)
  66. ↑ Burton, C. V., et al., Clin. Orthop. 157:191-99, 1981
  67. ↑ Byrd, S. E., et al., Spine 10:652-61, 1985
  68. ↑ Massare, C., Rev. Chir. Orthop., 68:233-46, 1982
  69. ↑ Teplik, J. G., Haskin, M. E., Am. J. Neuroradiol., 43:845-55, 1984
  70. ↑ a b Deyo RA, Nachemson A, Mirza SK (2004). "Spinal-fusion surgery – the case for restraint". N Engl J Med. 350 (7): 722–6. doi:10.1056/NEJMsb031771. PMID 14960750. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  71. ↑ Weinstein, J. N., et al. Spine 33:2789-2800, 2008
  72. ↑ Burton, C. V., et al., Clin Orthop. 157:191-99, 1981
  73. ↑ Crock, H. V., J. Bone Joint Surg. 58B:193-199, 1976
  74. ↑ Crock, H. V., “Practice of Spinal Surgery”, Vienna/New York; Springer Verlag, 1983
  75. ↑ Atlas, S. J., et al. Spine30:857-9, 2005
  76. ↑ Herno, A., Ann. Chir. Gynaecol. Suppl. 210:1-969, 1995
  77. ↑ Herno, A., et al. Spine 24:33-7, 1999
  78. ↑ Herno, A., et al., Spine 24:1010-4, 1999
  79. ↑ Herno, A., et al. Spine 24:2234-9, 1999
  80. ↑ Caputy, A. J., Luessenhop, A. J., J. Neurosurg. 77:669-76, 1992
  81. ↑ Sponseller, P. D., et al., Spine 25:2461-2466:2000
  82. ↑ Weinstein, M. A., et al., J. Spinal Disord. 13:422-426, 2000
  83. ↑ Massie, J. B., et al., Clin. Orthop. Rel. Res. 284:99-108, 1992
  84. ↑ Rechtine, G. R., et al., J. Ortho. Trauma 15:566-569, 2001
  85. ↑ Eck, K. R., et al., Spine 26::E182-E191, 201
  86. ↑ Capen, D. A., et al., Orthop. Clin. North. Am. 27:83-86, 1996
  87. ↑ Hee, H. T., et al., J. Spinal Disord. 14:533-540, 2001
  88. ↑ Aydinli, U., et al., Acta Orthop. Belg. 65:182-187, 1999
  89. ↑ Wimmer, C., et al. J. Spinal Disord. 11:498-500, 1998
  90. ↑ Wimmer, C., et al., J. Spinal Disoder. 11:124-128, 1998
  91. ↑ Hodges, S. D., et al., South. Med. J. 91:1132-1135, 1998
  92. ↑ Perry, J. W., et al., Clin. Infect. Dis. 24:558-561, 1997
  93. ↑ Abbey, D. M., et al., J. Spinal. Disord. 8:278-283, 1995
  94. ↑ West, J. L., et al., Spine 16:576-579, 1991
  95. ↑ Esses, S. I., et al., Spine 18:2238-2239, 1993
  96. ↑ Dave, S. H., and Meyers, D. L., Spine 17:(6 Suppl): S184-189, 1992
  97. ↑ Andreshak, T. G., et al., J. Spinal Disord. 10:376-379, 1997
  98. ↑ Viola, R. W., et al., Spine 22:2450-2451, 1997
  99. ↑ Klein, J. D., et al., Spine 22:2676-2682, 1996
  100. ↑ Swank, S. M., et al., J. Bone Joint Surg., 63 A: S268, 1981
  101. ↑ Klein, J. D., Garfin, S. R., Orthop. Clin. North. Am. 27:33-36, 1996
  102. ↑ Heary, R. F., et al., Surg. Neurol. 42:417-423, 1994
  103. ↑ Bertrand, G., Orthop. Clin. North America, 6:305-310, 1975
  104. ↑ Depalma and Rothman, “The Intervertebral Disc”, Philadelphia, W. B. Saunders, 1970
  105. ↑ Finnegan, W., Rothman, R., et al., J. Bone Joint Surg., 57A:1034, 1975
  106. ↑ Ghormley, R. K., Instructional Course Lecture, The American Academy of Orthopedic Surgeons, Vol. 14, pp 56-63, Ann Arbor, J. W. Edwards, 1957
  107. ↑ Greenwood, J., et al., J. Neurosurg. :15-20, 1952
  108. ↑ Hirsch, C., J. Bone Joint Surg. 47 A: 991-1004, 1965
  109. ↑ Kanayama, M., et al. J. Neurosurg. Spine 6:327-9, 2007
  110. ↑ Benoist, M., et al., Spine 5:432-35, 1980
  111. ↑ Langenskold, A., Valle, M., Clin. Orthop. 115:92-95, 1976
  112. ↑ La Rocca, H., Macnab, I., J. Bone Joint Surgery 56B:545-50, 1974
  113. ↑ Law, J. D., et al. J. Neurosurgery 48:259-63, 1978
  114. ↑ Lee, C. K., Alexander, H., Spine 9:305-12, 1984
  115. ↑ Lehmann, T. R., La Rocca, H., Spine 6:615-19,1981
  116. ↑ Lahde, S., Puranen, J., Eur. J. Radiol. 5:190-192, 1985
  117. ↑ Hinton, J. L. Jar, Wreck, D. J., Spine 20:564-570, 1995
  118. ↑ Fischgrund, J. S., J. Am. Acad. Orthop. Surg. 8:339-343, 2000
  119. ↑ Benoit, M., et al., Spine 5:432-35, 1980
  120. ↑ Benner, B., Ehni, G., Spine 3:40-44, 1978
  121. ↑ Brodsky, A. E., Spine 3:88-91, 1978
  122. ↑ Burton, C. V., Spine 3:24-30, 1978
  123. ↑ Quiles, M., et al., Spine 3:45-50, 1978
  124. ↑ Brammah, T. B., Jayson, M. I.,Spine 19(22):2603-5, 1994
  125. ↑ Georgy, B. A., et al., AJR Am. J. Roentgenol., 166(1):173-9, 1996
  126. ↑ Gero, B., et al., AJNR Am. J. Neuroradiol., 12(5):1009-19, 1991
  127. ↑ Gupta, R. K., et al., Neuroradiology 36:(1):39-43, 1994
  128. ↑ Johnson, C. E., Sze, G., AJNR Am. J. Neuroradiol. 11(4):763070, 1990
  129. ↑ Munoz, A., et al., AJNR 28:889-894, 2007
  130. ↑ Sharma, A., et al., AJR Am. J. Roentgenol. 168:807-12, 1997
  131. ↑ Tali. E. T., et al., Invest. Radiol. 37:152-9, 2002
  132. ↑ Chacoix, J., et al., Spine 3:256-59, 1978
  133. ↑ Weir, B.K.A., Jacobs, G. A., Spine 5:366-70, 1980
  134. ↑ Yong, H. K., et al., Spine 5:59-64, 1980
  135. ↑ Waddell, G., et al. J. Bone Joint Surgery, 61 A, 201-206, 1979
  136. ↑ Waddell, G., “The Back Pain Revolution”, London: Churchill Livingstone; 1998
  137. ↑ Litton, S., van Tulder, M., Spine 26:339-44, 2001
  138. ↑ Mielenz, T. J., et al., Spine 33:1270-1275, 2008
  139. ↑ Hoogendoorn, W. E., et al., Spine 25:2114-25, 2000
  140. ↑ Davis, K., Heaney, C., Clin. Biomech. 15:389-406, 2000
  141. ↑ Linton, S., et al., J. Occup. Rehab., 4:1-10, 1994
  142. ↑ Herno, A., et al., Am. J. Ind. Med. 30:473-8, 1996
  143. ↑ Airaksinen, O., et al., Eur Spine J. 3:261-4, 1994
  144. ↑ Donceel, P, et al., Spine 24:872, 1999
  145. ↑ Franklin, G. M., et al., Spine 19:1897-1904, 1994
  146. ↑ Turner, J. A., et al., JAMA 268:907-11,1992
  147. ↑ Maghout-Juratli, S., et al., Spine 31, 2715-2723, 2006
  148. ↑ Romano, P. S., et al., Am. J. Med. Qual. 17:145-54, 2002
  149. ↑ Murphy, P. L., Volinn, E., Spine 24:691-7, 1999
  150. ↑ Greenough, C. G., Fraser, R. D., Spine 14: 947-55, 1989
  151. ↑ Onesti, S. T., Neurologist 10(5):259-64, 2004
  152. ↑ Rhodin, A., et al. Eur. J. Pain 10:271-8, 2006
  153. ↑ Brown, R., et al., Postgrad. Med. J. 80:854-9, 2004
  154. ↑ Gardner-Nix, J. S., J. Pain Symptom Manage. 11:321-8, 1996
  155. ↑ Mercandante, S., et al., Eur. J. Pain 12:1040-6, 2008
  156. ↑ Fritzell, P., et al., Spine, 26:2521-32, 2001
  157. ↑ LeHuec, J. C., et al., Orthop. Clin. North Am., 36:315-22, 2005
  158. ↑ Guyer, R. D., et al., Spine J., 4 (6 Suppl):252S-259S, 2004
  159. ↑ Blumenthal, S., et al., Spine 30:1565-75, 2005; Discussion E387-91
  160. ↑ McAfee, P. C., et al., Spine 30:1576-83, 2005; Discussion E 388-90
  161. ↑ Zeegers, W. S., et al., Eur. Spine J., 8:210-17, 1999
  162. ↑ Putzier, M., Eur. Spine J., 15:183-95, 2006
  163. ↑ Patel, A. A., et al., Spine 33:1276-1283, 2008
  164. ↑ Zindrick, M. R., et al. Spine 33:1262-1269, 2008
  165. ↑ Straus, S., et al. “Evidence Based Medicine, 3rd ed.” London; Elsevier Churchill Livingstone, 2005
  166. ↑ Sackett, D. L., et al., “Evidence-Based Medicine. How to Practice and Teach EBM”, New York:: Churchill Livingstone, 2000
  167. ↑ Lemaire, J. P., et al., J. Spinal Disord. Tech. 18:353-9, 2005
  168. ↑ Huang, R. C., et al. Spine 29:2538-41, 2004
  169. ↑ Wong, D. A., et al., Spine J., 7:5-11, 2007
  170. ↑ Zindrick, M. R., et al. Spine ibid.
  171. ↑ Regan, J. J., Orthop. Clin. North Am., 36:323-40, 2005
  172. ↑ Siepe, C. J., et al., Spine 32:782-90, 2007
  173. ↑ Zeegers, W. S., et al., Eur. Spine J. 8:210-17, 1999
  174. ↑ Siepe, C. J., et al., Spine 31:1923-32, 2006
  175. ↑ Le Huec, J. C., et al. J Spinal Disord. Tech., 18:219-32, 2005
  176. ↑ Tropiano, P., et al., J. Bon Joint Surg., 87 A: 490-6, 2005
  177. ↑ Sott, A. H., Harrison, D. J., Int Orthop. 24:50-3, 2000
  178. ↑ Chung, S. S., et al., J. Spinal. Disord. Tech. 19:411-5, 2006
  179. ↑ Bertagnoli, R., et al., J Neurosurg. Spine 4:85-90, 2006
  180. ↑ Tropiano, P., et al., J. Spinal Disord. Tech., 16: 362-8, 2003
  181. ↑ Bertagnoli, R., et al., J. Neurosurg. Spine 4:85-90, 2006
  182. ↑ David, T., Spine 32:661-6, 2007
  183. ↑ Cinotti, G., et al., Spine 21:995-1000, 1996
  184. ↑ Bertagnoli, et al., Spine 30:2192-9, 2005
  185. ↑ Tropiano, P., et al., J. Bone Joint Surg., 87 A: 490-6, 2005
  186. ↑ Tropiano, P., et al., J. Spinal Disord. Tech. 16:362-8, 2003
  187. ↑ Le Huec, J. C., J. Spinal Disord. Tech. 18:219-23, 2005
  188. ↑ Lemaire, J. P., et al., Clin Orthop. Rel. Res. 337:64-76, 1997
  189. ↑ Siepe, C. J., et al., Spine 31:1923-32, 2006
  190. ↑ Chung, S. S., et al., J. Spinal. Disord. Tech. 19:411-5, 2006
  191. ↑ Bertognoli, R.,Spine 30: 2192-9, 2005
  192. ↑ Mayer, H. M., et al., Eur. Spine J., 11 (Suppl 2): S124-30, 2002
  193. ↑ Zeegers, W. S., et al., Eur. Spine J.8:210-7, 1999
  194. ↑ Tropiano, P., et al., J. Bone Joint Surg., 87 A: 490-6, 2005
  195. ↑ Zindrick, M. R., et al., ibid
  196. ↑ Wang, J. K., Mayo Clinic Proc. 51:28-30, 1976
  197. ↑ Laporte, de C, Siegfried, J., Spine 18:593-603, 1983
  198. ↑ Frymoyer, J. W., et al., J. Bone Joint Surg., 65 A; 213-218; 1983
  199. ↑ Deyo, R. A., Bass, J. E., Spine, 14:501-506, 1989
  200. ↑ Svensson, H. O., et al., Spine, 8;277-285, 1983
  201. ↑ de Vernejoul, M.C., et al., Clin. Orthop., 179:107-115, 1989
  202. ↑ An, H. S., et al., J. Spinal Disord., 7:369-373, 1994
  203. ↑ Hollo, I., et al., JAMA ,237; 2470, 1977
  204. ↑ Iwahashi, M., et al., Spine, 27:1396-1401, 2002
  205. ↑ Biering-Sorensen, F., Thomsen, C., Spine 11:720-5, 1986
  206. ↑ Boshuizen, H., et al., Spine 18:35-40, 1993
  207. ↑ Deyo, R. A., et al., Spine 14:501-506, 1989
  208. ↑ Heliovaara, M., et al., Spine 16:608-14, 1991
  209. ↑ Heliovaara, M., et al., Ann. Med., 21:257-64, 1989
  210. ↑ Andersen, T., et al., Spine 26:2623, 2001
  211. ↑ Glassman, S. D.., et al., Spine 25:2608-08, 2000
  212. ↑ Mikkonen, P., et al., Spine 33:527-32, 2008
  213. ↑ Ackerman, W. E., and Ahmad, M., J. Ark. Med. Soc. 104:19-21, 2007
  214. ↑ Leboeuf-Yde, C., Spine 24:1463, 1999
  215. ↑ Slover, J., et al., Spine 31:1974-1988, 2006
  216. ↑ Porter, S. E., and Hanley, E. N., J. AAOS 9:9-17, 2001
  217. ↑ Thalgott, J. S., et al., Spine 16:981-984, 1991
  218. ↑ Rabaina-Paderon, F. J., Neurocirugia (Astur) 18:406-13, 2005
  219. ↑ Stromquist, B., et al., Acta Orhop. Scand. 72:99-106, 2001
  220. ↑ Cherkin, D. C., et al., Spine 19:1201-1206, 1994
  221. ↑ Bunker, J. P., N. Engl. J. Med. 282:135-144, 1970
  222. ↑ Lewis, C. E., N. Engl. J. Med., 281, 880-994, 1969
  223. ↑ Sommer C, Schäfers M, Marziniak M, Toyka KV (2001). "Etanercept reduces hyperalgesia in experimental painful neuropathy". J Peripher Nerv Syst. 6 (2): 67–72. doi:10.1046/j.1529-8027.2001.01010.x. PMID 11446385. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  224. ↑ Olmarker K, Rydevik B (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. doi:10.1097/00007632-200104150-00007. PMID 11317106. {{cite journal}}: Unknown parameter |month= ignored (help)
  225. ↑ Murata Y, Onda A, Rydevik B, Takahashi K, Olmarker K (2004). "Selective inhibition of tumor necrosis factor-alpha prevents nucleus pulposus-induced histologic changes in the dorsal root ganglion". Spine. 29 (22): 2477–84. doi:10.1097/01.brs.0000144406.17512.ea. PMID 15543058. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  226. ↑ U.S. Patent 6,537,549 and others
  227. ↑ a b c Tobinick EL, Britschgi-Davoodifar S (2003). "Perispinal TNF-alpha inhibition for discogenic pain". Swiss Med Wkly. 133 (11–12): 170–7. doi:2003/11/smw-10163. PMID 12715286. {{cite journal}}: Check |doi= value (help); Unknown parameter |month= ignored (help)
  228. ↑ Tobinick E, Davoodifar S (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. doi:10.1185/030079903125004286. PMID 15265252. {{cite journal}}: Unknown parameter |month= ignored (help)
  229. ↑ Myers RR, Campana WM, Shubayev VI (2006). "The role of neuroinflammation in neuropathic pain: mechanisms and therapeutic targets". Drug Discov. Today. 11 (1–2): 8–20. doi:10.1016/S1359-6446(05)03637-8. PMID 16478686. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  230. ↑ Uceyler N, Sommer C (2007). "Cytokine-induced Pain: Basic Science and Clinical Implications". Reviews in Analgesia. 9 (2): 87–103. doi:10.3727/000000007783992807.
  231. ↑ Fredman B, Nun MB, Zohar E; et al. (1999). "Epidural steroids for treating "failed back surgery syndrome": is fluoroscopy really necessary?". Anesth Analg. 88 (2): 367–72. doi:10.1097/00000539-199902000-00027. PMID 9972758. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  232. ↑ Landau WM, Nelson DA, Armon C, Argoff CE, Samuels J, Backonja MM (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. doi:10.1212/01.wnl.0000278878.51713.c8. PMID 17679685. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  233. ↑ Abbasi A, Malhotra G, Malanga G, Elovic EP, Kahn S (2007). "Complications of interlaminar cervical epidural steroid injections: a review of the literature". Spine. 32 (19): 2144–51. doi:10.1097/BRS.0b013e318145a360. PMID 17762818. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  234. ↑ Bell GK, Kidd D, North RB (1997). "Cost-effectiveness analysis of spinal cord stimulation in treatment of failed back surgery syndrome". J Pain Symptom Manage. 13 (5): 286–95. doi:10.1016/S0885-3924(96)00323-5. PMID 9185434. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  235. ↑ Kumar K, Taylor RS, Jacques L; et al. (2007). "Spinal cord stimulation versus conventional medical management for neuropathic pain: a multicentre randomised controlled trial in patients with failed back surgery syndrome". Pain. 132 (1–2): 179–88. doi:10.1016/j.pain.2007.07.028. PMID 17845835. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  236. ↑ Social Security; "Disability Evaluation Under Social Security", June 2006
  237. ↑ http://www.ssa.gov/disability/professionals/bluebook/adultlistings.pdf
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