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. 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. 
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.  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. 
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.  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. 
In 1992, Turner et al.  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.  found that a concomitant spinal arthrodesis (fusion) had a greater success rate. Herron and Trippi  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  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. In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year. 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. 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. In addition, spinal fusion itself, particularly if more than one spinal level is operated on, may result in “adjacent segment degeneration”. 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. 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. 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. In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain. 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. In addition to causing pain and inflammation, TNF may also contribute to disc degeneration. 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.
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. 
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. 
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.  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. Another less invasive form of spinal surgery, percutaneous disc surgery, has reported revision rates as high as 65%. It is no surprise, therefore, that FBSS is a significant medical concern which merits further research and attention by the medical and surgical communities.
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 herniationEdit
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.  In some studies, recurrent pain in the same radicular pattern or a different pattern can be as high as 50% after disc surgery.  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.  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.  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.  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. 
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. 
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.  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. 
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. 
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 
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. 
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. 
Post operative infectionEdit
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%.  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.  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.  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. 
Epidural post-operative fibrosisEdit
Epidural scarring following a laminectomy for disc excision is a common feature when re-operating for recurrent sciatica or radiculopathy.  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.  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. 
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.  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. 
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. 
Return to workEdit
In a groundbreaking Canadian study, Waddell et al.  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. 
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.  Individual psychological and social work factors, as well as worker-employer relations are also likely to be associated with time and rates of recovery. 
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. 
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. 
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.
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 prioriy 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. 
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.  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. 
Chronic pain and narcotic usageEdit
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. 
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. 
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.  The beneficial experience of methadone usage in some chronic pain patients was also found in Canada. 
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. 
Total disc replacementEdit
Lumbar total disc replacement was originally designed to be an alternative to lumbar arthodesis (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.  Various failure rates, and strategies for revision of total disc replacement have been reported.  The role of artificial or total disc replacement in the treatment of spinal disorders remains ill-defined and unclear.  Evaluation of any new technique is difficult or impossible because physician experience may be minimal or lacking. Patient expectations may be distorted.  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.  The role of disc replacement must come from new indications not defined in today’s literature or a relaxation of current contraindications. 
A younger age was predictive of a better outcome in several studies.  In others it has been found to be a negative predictor or of no predictive value.  Older patients may have more complications. 
Prior spinal surgery has mixed effects on disc replacement. It has been reported to be negative in several studies.  It has been reported to have no effect in other studies.  Many studies are simply inconclusive.  Existing evidence does not allow drawing definite conclusions about the status of disc replacement at present. 
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.  Success rates for implanted neurostimulation has been reported to be 25% to 55%. Success is defined as a relative decrease in pain. 
Smoking and failed backEdit
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. 
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. 
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. 
Regular smoking in adolescence was associated with low back pain in young adults. Pack-years of smoking showed an exposure-response relationship among girls. 
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. 
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.  In a massive study of 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. 
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. 
A report from Spain noted that the investigation and development of new techniques for intrumented 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. 
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.  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.,  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. 
Investigative treatment optionsEdit
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. Targeted anatomic administration of one of these anti-TNF agents, etanercept, a patented treatment method, has been suggested in published pilot studies to be effective for treating selected patients with chronic disc-related pain and FBSS. The scientific basis for pain relief in these patients is supported by the many current review articles. 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. 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”. 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. In addition, epidural steroid injections, in certain settings, may result in serious complications. Fortunately there are now emerging new methods that directly target TNF. 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.
Social Security DisabilityEdit
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). 
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.
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.
- Long DM (Oct 1991). "Failed back surgery syndrome". Neurosurg Clin N Am. 2 (4): 899–919. PMID 1840393.
- Fritsch EW, Heisel J, Rupp S (Mar 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=21&issue=5&spage=626.
- Slipman CW, Shin CH, Patel RK, et al. (Sep 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.
- Taylor VM, Deyo RA, Cherkin DC, Kreuter W (Jun 1994). "Low back pain hospitalization. Recent United States trends and regional variations". Spine 19 (11): 1207–12; discussion 13. PMID 8073311.
- Fager, C. A., Freiberg, S. R., Spine, 5:87-94; 1980
- Spengler, D. M., et al. Spine 5:356-60; 1980
- Wiltse, l. L., Rocchio, P. D., J. Bone Joint Surg.; 57 A:478-83, 1957
- Burton, C. V., et al., Clin. Orthop. 157:191-99; 1981
- Hakelius, A., Acta. Orthop. Scand., Suppl:129-76; 1970
- Turner, J., et al., Spine 1992; 17:1-8
- Mardjetko, S. M., et al., Spine 1994; 20S:2256S-2265S
- Herron, L. D., and Trippi, A. C., Spine 1989; 14:534-538
- Epstein, N. E., J. Spinal Disorder. 1998; 11(2): 116-122
- Deyo RA, Gray DT, Kreuter W, Mirza S, Martin BI (Jun 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=12&spage=1441.
- 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.
- Guyer RD, Patterson M, Ohnmeiss DD (Sep 2006). "Failed back surgery syndrome: diagnostic evaluation". J Am Acad Orthop Surg 14 (9): 534–43. PMID 16959891. http://www.jaaos.org/cgi/pmidlookup?view=long&pmid=16959891.
- Deyo RA (Jul 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. http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=12090877.
- Carragee EJ (May 2005). "Clinical practice. Persistent low back pain". N Engl J Med. 352 (18): 1891–8. doi:10.1056/NEJMcp042054. PMID 15872204.
- 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. http://www.nyuhjdbulletin.org/Permalink.aspx?permalinkId=e6fb30e7-8841-4258-be97-610c1d8e7b9c.
- Peng B, Wu W, Li Z, Guo J, Wang X (Jan 2007). "Chemical radiculitis". Pain 127 (1-2): 11–6. doi:10.1016/j.pain.2006.06.034. PMID 16963186.
- Marshall LL, Trethewie ER (Aug 1973). "Chemical irritation of nerve-root in disc prolapse". Lancet 2 (7824): 320. doi:10.1016/S0140-6736(73)90818-0. PMID 4124797.
- McCarron RF, Wimpee MW, Hudkins PG, Laros GS (Oct 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.
- Takahashi H, Suguro T, Okazima Y, Motegi M, Okada Y, Kakiuchi T (Jan 1996). "Inflammatory cytokines in the herniated disc of the lumbar spine". Spine 21 (2): 218–24. doi:10.1097/00007632-199601150-00011. PMID 8720407. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=21&issue=2&spage=218.
- Igarashi T, Kikuchi S, Shubayev V, Myers RR (Dec 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=25&issue=23&spage=2975.
- Sommer C, Schafers M (Dec 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.
- Igarashi A, Kikuchi S, Konno S, Olmarker K (Oct 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=19&spage=2091.
- Sakuma Y, Ohtori S, Miyagi M, et al. (Aug 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. PMID 17468886.
- Sekiguchi M, Kikuchi S, Myers RR (May 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=10&spage=1105.
- Séguin CA, Pilliar RM, Roughley PJ, Kandel RA (Sep 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=17&spage=1940.
- Spengler, D. M., et al. Spine 5:356-60, 1980
- Wiltse, L. L., Rocchio, P. D., J. Bone Joint Surg., 57A:478-83, 1980
- Weir, B. K. A., J. Neuro. Surg. 50:283-89, 1979
- Weir, B. K. A., Jacobs, G. A., Spine 5:366-70, 1980
- Burton, C. V., et al. Clin Orthop. 157:191-99, 1981
- Oaklnader, A. L., and North, R. B. “Failed back surgery syndrome” In Loeser, J. D., et al., eds. “Bonica’s Management of Pain”, Philadephia, Lippincott Williams & Williams, 2001
- Haider, T T., et al., J. Occup. Rehabil. 8:247-253, 1998
- Tandon. V., Spine 24:1833-1838, 1999
- Turner, J., et al., JAMA 268:907-911, 1992
- Malter, A. D., et al., Spine 21:1048-1055, 1996
- Dvorak, J., et al., Spine 13:1418-1422, 1988
- Deyo, R., et al., J. Bone Joint Surg., 74 A:536-543, 1992
- Gervitz, R. N., et al., Prof. Psychol. Res. Pract. 27:561-566, 1996
- Graver, V., et al., Br. J. Neurosurg. 2:178-184, 1999
- de Groot, K. I., et al., Pain 69:19-25, 1997
- Schade, V., et al., Pain 80:239-249, 1999
- Rosenstiel, A., Keefe, F., Pain 17:33-40, 1983
- Keane GP (1997). "Failed low back surgery syndrome". in Herring SA, Cole AJ. The low back pain handbook: a practical guide for the primary care clinician. Philadelphia: Hanley & Belfus. pp. 269–81. ISBN 1-56053-152-5.
- Chatterjee S, Foy PM, Findlay GF (Mar 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.
- Linton, R. R., White, P. D., Arch. Surg., 50:6, 1945
- Epps, C. H., “Complications in Orthopedic Surgery”, p. 1009-1037, Lippincott and Co., Philadelphia, 1978
- Cauchoix, J., et al. Spine 3:256-59, 1978
- Weir, BKA., Jacobs, G. A., Spine ibid
- Benoist, M., et al., Spine 5:432-35, 1980
- Benner, B., Ehni, G., Spine 3: 40-44, 1978
- Rothman, R., Orhop. Clin. North Amer. 6:310, 1975
- Quiles, M., et al., Spine 3:45-5-, 1978
- Spangfort, E., Acta Orthop. Scand. Suppl 142:5-93, 1972
- Weir, B. K. A., Spine 5:366-70, 1980
- Benoist, M., et al., Spine 5:432-35, 1980
- Bener, B., Ehni, G., Spine 3:40-44, 1978
- Byrd, S. E., et al., Spine 10:652-61, 1985
- Deburge, A., Badelon, O., Rev. Chir. Orthop. 68:249-54, 1982 (French)
- Irstam, L., Spine 9:759-63, 1984
- Thibierge, M., Metzger, J., Rev. Chir. Orthop. 68:230-33, 1982 (French)
- Burton, C. V., et al., Clin. Orthop. 157:191-99, 1981
- Byrd, S. E., et al., Spine 10:652-61, 1985
- Massare, C., Rev. Chir. Orthop., 68:233-46, 1982
- Teplik, J. G., Haskin, M. E., Am. J. Neuroradiol., 43:845-55, 1984
- Deyo RA, Nachemson A, Mirza SK (Feb 2004). "Spinal-fusion surgery – the case for restraint". N Engl J Med. 350 (7): 722–6. doi:10.1056/NEJMsb031771. PMID 14960750.
- Weinstein, J. N., et al. Spine 33:2789-2800, 2008
- Burton, C. V., et al., Clin Orthop. 157:191-99, 1981
- Crock, H. V., J. Bone Joint Surg. 58B:193-199, 1976
- Crock, H. V., “Practice of Spinal Surgery”, Vienna/New York; Springer Verlag, 1983
- Atlas, S. J., et al. Spine30:857-9, 2005
- Herno, A., Ann. Chir. Gynaecol. Suppl. 210:1-969, 1995
- Herno, A., et al. Spine 24:33-7, 1999
- Herno, A., et al., Spine 24:1010-4, 1999
- Herno, A., et al. Spine 24:2234-9, 1999
- Caputy, A. J., Luessenhop, A. J., J. Neurosurg. 77:669-76, 1992
- Sponseller, P. D., et al., Spine 25:2461-2466:2000
- Weinstein, M. A., et al., J. Spinal Disord. 13:422-426, 2000
- Massie, J. B., et al., Clin. Orthop. Rel. Res. 284:99-108, 1992
- Rechtine, G. R., et al., J. Ortho. Trauma 15:566-569, 2001
- Eck, K. R., et al., Spine 26::E182-E191, 201
- Capen, D. A., et al., Orthop. Clin. North. Am. 27:83-86, 1996
- Hee, H. T., et al., J. Spinal Disord. 14:533-540, 2001
- Aydinli, U., et al., Acta Orthop. Belg. 65:182-187, 1999
- Wimmer, C., et al. J. Spinal Disord. 11:498-500, 1998
- Wimmer, C., et al., J. Spinal Disoder. 11:124-128, 1998
- Hodges, S. D., et al., South. Med. J. 91:1132-1135, 1998
- Perry, J. W., et al., Clin. Infect. Dis. 24:558-561, 1997
- Abbey, D. M., et al., J. Spinal. Disord. 8:278-283, 1995
- West, J. L., et al., Spine 16:576-579, 1991
- Esses, S. I., et al., Spine 18:2238-2239, 1993
- Dave, S. H., and Meyers, D. L., Spine 17:(6 Suppl): S184-189, 1992
- Andreshak, T. G., et al., J. Spinal Disord. 10:376-379, 1997
- Viola, R. W., et al., Spine 22:2450-2451, 1997
- Klein, J. D., et al., Spine 22:2676-2682, 1996
- Swank, S. M., et al., J. Bone Joint Surg., 63 A: S268, 1981
- Klein, J. D., Garfin, S. R., Orthop. Clin. North. Am. 27:33-36, 1996
- Heary, R. F., et al., Surg. Neurol. 42:417-423, 1994
- Bertrand, G., Orthop. Clin. North America, 6:305-310, 1975
- Depalma and Rothman, “The Intervertebral Disc”, Philadelphia, W. B. Saunders, 1970
- Finnegan, W., Rothman, R., et al., J. Bone Joint Surg., 57A:1034, 1975
- Ghormley, R. K., Instructional Course Lecture, The American Academy of Orthopedic Surgeons, Vol. 14, pp 56-63, Ann Arbor, J. W. Edwards, 1957
- Greenwood, J., et al., J. Neurosurg. :15-20, 1952
- Hirsch, C., J. Bone Joint Surg. 47 A: 991-1004, 1965
- Kanayama, M., et al. J. Neurosurg. Spine 6:327-9, 2007
- Benoist, M., et al., Spine 5:432-35, 1980
- Langenskold, A., Valle, M., Clin. Orthop. 115:92-95, 1976
- La Rocca, H., Macnab, I., J. Bone Joint Surgery 56B:545-50, 1974
- Law, J. D., et al. J. Neurosurgery 48:259-63, 1978
- Lee, C. K., Alexander, H., Spine 9:305-12, 1984
- Lehmann, T. R., La Rocca, H., Spine 6:615-19,1981
- Lahde, S., Puranen, J., Eur. J. Radiol. 5:190-192, 1985
- Hinton, J. L. Jar, Wreck, D. J., Spine 20:564-570, 1995
- Fischgrund, J. S., J. Am. Acad. Orthop. Surg. 8:339-343, 2000
- Benoit, M., et al., Spine 5:432-35, 1980
- Benner, B., Ehni, G., Spine 3:40-44, 1978
- Brodsky, A. E., Spine 3:88-91, 1978
- Burton, C. V., Spine 3:24-30, 1978
- Quiles, M., et al., Spine 3:45-50, 1978
- Brammah, T. B., Jayson, M. I.,Spine 19(22):2603-5, 1994
- Georgy, B. A., et al., AJR Am. J. Roentgenol., 166(1):173-9, 1996
- Gero, B., et al., AJNR Am. J. Neuroradiol., 12(5):1009-19, 1991
- Gupta, R. K., et al., Neuroradiology 36:(1):39-43, 1994
- Johnson, C. E., Sze, G., AJNR Am. J. Neuroradiol. 11(4):763070, 1990
- Munoz, A., et al., AJNR 28:889-894, 2007
- Sharma, A., et al., AJR Am. J. Roentgenol. 168:807-12, 1997
- Tali. E. T., et al., Invest. Radiol. 37:152-9, 2002
- Chacoix, J., et al., Spine 3:256-59, 1978
- Weir, B.K.A., Jacobs, G. A., Spine 5:366-70, 1980
- Yong, H. K., et al., Spine 5:59-64, 1980
- Waddell, G., et al. J. Bone Joint Surgery, 61 A, 201-206, 1979
- Waddell, G., “The Back Pain Revolution”, London: Churchill Livingstone; 1998
- Litton, S., van Tulder, M., Spine 26:339-44, 2001
- Mielenz, T. J., et al., Spine 33:1270-1275, 2008
- Hoogendoorn, W. E., et al., Spine 25:2114-25, 2000
- Davis, K., Heaney, C., Clin. Biomech. 15:389-406, 2000
- Linton, S., et al., J. Occup. Rehab., 4:1-10, 1994
- Herno, A., et al., Am. J. Ind. Med. 30:473-8, 1996
- Airaksinen, O., et al., Eur Spine J. 3:261-4, 1994
- Donceel, P, et al., Spine 24:872, 1999
- Franklin, G. M., et al., Spine 19:1897-1904, 1994
- Turner, J. A., et al., JAMA 268:907-11,1992
- Maghout-Juratli, S., et al., Spine 31, 2715-2723, 2006
- Romano, P. S., et al., Am. J. Med. Qual. 17:145-54, 2002
- Murphy, P. L., Volinn, E., Spine 24:691-7, 1999
- Greenough, C. G., Fraser, R. D., Spine 14: 947-55, 1989
- Onesti, S. T., Neurologist 10(5):259-64, 2004
- Rhodin, A., et al. Eur. J. Pain 10:271-8, 2006
- Brown, R., et al., Postgrad. Med. J. 80:854-9, 2004
- Gardner-Nix, J. S., J. Pain Symptom Manage. 11:321-8, 1996
- Mercandante, S., et al., Eur. J. Pain 12:1040-6, 2008
- Fritzell, P., et al., Spine, 26:2521-32, 2001
- LeHuec, J. C., et al., Orthop. Clin. North Am., 36:315-22, 2005
- Guyer, R. D., et al., Spine J., 4 (6 Suppl):252S-259S, 2004
- Blumenthal, S., et al., Spine 30:1565-75, 2005; Discussion E387-91
- McAfee, P. C., et al., Spine 30:1576-83, 2005; Discussion E 388-90
- Zeegers, W. S., et al., Eur. Spine J., 8:210-17, 1999
- Putzier, M., Eur. Spine J., 15:183-95, 2006
- Patel, A. A., et al., Spine 33:1276-1283, 2008
- Zindrick, M. R., et al. Spine 33:1262-1269, 2008
- Straus, S., et al. “Evidence Based Medicine, 3rd ed.” London; Elsevier Churchill Livingstone, 2005
- Sackett, D. L., et al., “Evidence-Based Medicine. How to Practice and Teach EBM”, New York:: Churchill Livingstone, 2000
- Lemaire, J. P., et al., J. Spinal Disord. Tech. 18:353-9, 2005
- Huang, R. C., et al. Spine 29:2538-41, 2004
- Wong, D. A., et al., Spine J., 7:5-11, 2007
- Zindrick, M. R., et al. Spine ibid.
- Regan, J. J., Orthop. Clin. North Am., 36:323-40, 2005
- Siepe, C. J., et al., Spine 32:782-90, 2007
- Zeegers, W. S., et al., Eur. Spine J. 8:210-17, 1999
- Siepe, C. J., et al., Spine 31:1923-32, 2006
- Le Huec, J. C., et al. J Spinal Disord. Tech., 18:219-32, 2005
- Tropiano, P., et al., J. Bon Joint Surg., 87 A: 490-6, 2005
- Sott, A. H., Harrison, D. J., Int Orthop. 24:50-3, 2000
- Chung, S. S., et al., J. Spinal. Disord. Tech. 19:411-5, 2006
- Bertagnoli, R., et al., J Neurosurg. Spine 4:85-90, 2006
- Tropiano, P., et al., J. Spinal Disord. Tech., 16: 362-8, 2003
- Bertagnoli, R., et al., J. Neurosurg. Spine 4:85-90, 2006
- David, T., Spine 32:661-6, 2007
- Cinotti, G., et al., Spine 21:995-1000, 1996
- Bertagnoli, et al., Spine 30:2192-9, 2005
- Tropiano, P., et al., J. Bone Joint Surg., 87 A: 490-6, 2005
- Tropiano, P., et al., J. Spinal Disord. Tech. 16:362-8, 2003
- Le Huec, J. C., J. Spinal Disord. Tech. 18:219-23, 2005
- Lemaire, J. P., et al., Clin Orthop. Rel. Res. 337:64-76, 1997
- Siepe, C. J., et al., Spine 31:1923-32, 2006
- Chung, S. S., et al., J. Spinal. Disord. Tech. 19:411-5, 2006
- Bertognoli, R.,Spine 30: 2192-9, 2005
- Mayer, H. M., et al., Eur. Spine J., 11 (Suppl 2): S124-30, 2002
- Zeegers, W. S., et al., Eur. Spine J.8:210-7, 1999
- Tropiano, P., et al., J. Bone Joint Surg., 87 A: 490-6, 2005
- Zindrick, M. R., et al., ibid
- Wang, J. K., Mayo Clinic Proc. 51:28-30, 1976
- Laporte, de C, Siegfried, J., Spine 18:593-603, 1983
- Frymoyer, J. W., et al., J. Bone Joint Surg., 65 A; 213-218; 1983
- Deyo, R. A., Bass, J. E., Spine, 14:501-506, 1989
- Svensson, H. O., et al., Spine, 8;277-285, 1983
- de Vernejoul, M.C., et al., Clin. Orthop., 179:107-115, 1989
- An, H. S., et al., J. Spinal Disord., 7:369-373, 1994
- Hollo, I., et al., JAMA ,237; 2470, 1977
- Iwahashi, M., et al., Spine, 27:1396-1401, 2002
- Biering-Sorensen, F., Thomsen, C., Spine 11:720-5, 1986
- Boshuizen, H., et al., Spine 18:35-40, 1993
- Deyo, R. A., et al., Spine 14:501-506, 1989
- Heliovaara, M., et al., Spine 16:608-14, 1991
- Heliovaara, M., et al., Ann. Med., 21:257-64, 1989
- Andersen, T., et al., Spine 26:2623, 2001
- Glassman, S. D.., et al., Spine 25:2608-08, 2000
- Mikkonen, P., et al., Spine 33:527-32, 2008
- Ackerman, W. E., and Ahmad, M., J. Ark. Med. Soc. 104:19-21, 2007
- Leboeuf-Yde, C., Spine 24:1463, 1999
- Slover, J., et al., Spine 31:1974-1988, 2006
- Porter, S. E., and Hanley, E. N., J. AAOS 9:9-17, 2001
- Thalgott, J. S., et al., Spine 16:981-984, 1991
- Rabaina-Paderon, F. J., Neurocirugia (Astur) 18:406-13, 2005
- Stromquist, B., et al., Acta Orhop. Scand. 72:99-106, 2001
- Cherkin, D. C., et al., Spine 19:1201-1206, 1994
- Bunker, J. P., N. Engl. J. Med. 282:135-144, 1970
- Lewis, C. E., N. Engl. J. Med., 281, 880-994, 1969
- Sommer C, Schäfers M, Marziniak M, Toyka KV (Jun 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. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1085-9489&date=2001&volume=6&issue=2&spage=67.
- Olmarker K, Rydevik B (Apr 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=26&issue=8&spage=863.
- Murata Y, Onda A, Rydevik B, Takahashi K, Olmarker K (Nov 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=22&spage=2477.
- U.S. Patent 6,537,549 and others
- Tobinick EL, Britschgi-Davoodifar S (Mar 2003). "Perispinal TNF-alpha inhibition for discogenic pain". Swiss Med Wkly 133 (11-12): 170–7. doi:2003/11/smw-10163. PMID 12715286.
- Tobinick E, Davoodifar S (Jul 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.
- Myers RR, Campana WM, Shubayev VI (Jan 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.
- Uceyler N, Sommer C (2007). "Cytokine-induced Pain: Basic Science and Clinical Implications". Reviews in Analgesia 9 (2): 87–103. doi:10.3727/000000007783992807.
- Fredman B, Nun MB, Zohar E, et al. (Feb 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. http://www.anesthesia-analgesia.org/cgi/pmidlookup?view=long&pmid=9972758.
- Landau WM, Nelson DA, Armon C, Argoff CE, Samuels J, Backonja MM (Aug 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.
- Abbasi A, Malhotra G, Malanga G, Elovic EP, Kahn S (Sep 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.
- Bell GK, Kidd D, North RB (May 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. http://linkinghub.elsevier.com/retrieve/pii/S0885392496003235.
- Kumar K, Taylor RS, Jacques L, et al. (Nov 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.
- Social Security; "Disability Evaluation Under Social Security", June 2006