Neurology and Neurosurgery/Incomplete Spinal Cord Injuries/Spinal Stenosis

Spinal stenosis is a medical condition in which the spinal canal narrows and compresses the spinal cord and nerves. This is usually due to the common occurrence of spinal degeneration that occurs with aging. It can also sometimes be caused by spinal disc herniation, osteoporosis or a tumor. In the cervical (neck) and lumbar (low back) region it can be a congenital condition to varying degrees.

Spinal stenosis may affect the cervical, thoracic or lumbar spine. In some cases, it may be present in all three places in the same patient. Lumbar spinal stenosis results in low back pain as well as pain or abnormal sensations in the legs, thighs, feet or buttocks, or loss of bladder and bowel control.

Diagnosis of stenosisEdit

Normal lumbar vertebra showing large, round spinal canal.

Spinal stenosis began to be recognized as an impairing condition in the 1960s and 1970s. Porter et al. discovered that individuals who experience back pain and other symptoms are likely to have smaller spinal canals than those who are asymptomatic.[1] Rothman reported that a normal sized lumbar canal is rarely encountered in persons with either disc disease or those requiring a de-roofing (laminectomy) procedure.[2] The natural evolution of disc disease and degeneration lead to stiffening of the intervertebral joint. This leads to osteophyte formation -a bony overgrowth about the joint. This process is called spondylosis, and is part of the normal aging of the spine. This has been seen in studies of normal and diseased spines. Degenerative changes begin to occur without symptoms as early as 25–30 years. It is not uncommon for people to experience at least one severe case of low back pain by the age of 35 years. This can be expected to improve and become less prevalent as the individual develops osteophyte formation around the discs.[3]

Lumbar vertebra showing central stenosis and lateral recess stenosis.

A certain minority of patients will go on to develop spinal stenosis by the age of 60 years.[4] Plain x-rays of the lumbar or cervical spine may or may not show spinal stenosis. The definitive diagnosis is established by either CT (computerized tomography) or MRI scanning. Identifying the presence of a narrowed canal makes the diagnosis of spinal stenosis.[5][6][7][8] However, the diagnosis is based on clinical findings. Some patients can have a narrowed canal without symptoms, and do not require therapy. Stenosis can occur as either central stenosis - the narrowing of the entire canal, or foraminal stenosis - the narrowing of the foramen through which the nerve root exits the spinal canal. Severe narrowing of the lateral portion of the canal is called “lateral recess stenosis". The ligamentum flavum (yellow ligament), an important structural component intimately adjacent to the posterior portion of the dural sac (nerve sac) can become thickened and cause stenosis. The articular facets, also in the posterior portion of the bony spine can become thickened and enlarged causing stenosis. These changes are often called “trophic changes” or “facet trophism” in radiology reports. As the canal becomes smaller and resembles a triangular shape, it is called a "trefoil" canal.

The normal lumbar central canal has a midsagittal diameter (front to back) greater than 13 mm., with an area of 1.45 square cm. Relative stenosis is said to exist when the anterior-posterior canal diameter between 10 and 13 mm. Absolute stenosis of the lumbar canal exists anatomically when the anterior-posterior measurement is 10 mm. or less.[9][10][11]

The first symptoms of stenosis are bouts of low back or neck pain. After a few months or years, this may progress to pain that is described as claudicant pain or claudication. This is a sensation of not getting enough blood to the arms or legs. It occurs more frequently in the legs. The pain may also be radicular in nature, following the classic neurologic pathways. This occurs as the spinal nerves or spinal cord becomes increasing trapped in a smaller space within the canal. It can be difficult to determine whether pain in the elderly is caused by lack of blood supply or stenosis. Modern testing can usually differentiate between them.Sometimes, patients will have both vascular disease in the legs and spinal stenosis.[12][13][14][15]

Bicycle test of van GelderenEdit

In 1977, Dyck and Boyd[16] reported on the bicycle test of van Gelderen. The test has been intermittently reported in various places since then. It is a simple procedure in which the patient is placed upon a stationary bicycle, and asked to pedal. If the symptoms are caused by peripheral vascular disease, the patient will experience claudication (def: limping; experienced as a sensation of not getting enough blood to the legs), by pedaling the bicycle in any position. If the symptoms are caused by lumbar stenosis, symptoms will be relieved when the patient is leaning forward while bicycling. Despite the fact that diagnostic progress has been made with newer technical advances, the bicycle test remains a cheap and easy way to distinguish between claudication caused by vascular disease and spinal stenosis. Dyck and Boyd wrote in their 1977 article: The authors describe a simple clinical adjunct to the routine neurological examination of patients with intermittent cauda equina compression syndrome. The "bicycle test" helps exclude intermittent claudication due to vascular insufficiency and frequently confirms the relationship of posture to radicular pain.

MRI (magnetic resonance imaging)Edit

MRI image showing stenosis of the lumbar spine.

MRI findings of spinal stenosis failed to correlate with ability of patients to walk distances.[17] Despite this, MRI remains the best method of diagnosing and evaluating spinal stenosis of all areas of the spine, including cervical, thoracic and lumbar. Newer enhanced MRI techniques have been recently introduced which lead to improved visualization of cervical spondylotic myelopathy (degenerative arthritis of the cervical spine with associated damage to the spinal cord).[18][19][20][21][22][23][24][25][26] The finding of degeneration of the cervical spinal cord on MRI can be ominous. The condition is called myelomalacia or cord degeneration. It is seen as an increased signal on the MRI. In myelopathy (pathology of the spinal cord) from degenerative changes, the findings are usually permanent and decompressive laminectomy will not reverse the pathology. Surgery can stop the progression of the condition. In cases where the MRI changes are due to Vitamin B-12 deficiency, a brighter prospect for recovery can be expected.[27][28][29] The detection of spinal stenosis in the cervical, thoracic or lumbar spine confirms only the anatomic presence of a stenotic condition. This may or may not correlate with the diagnosis of spinal stenosis which is based on clinical findings of radiculopathy, neurogenic claudication, weakness, bowel and bladder dysfunction, spasticity, motor weakness, hyperreflexia and muscular atrophy. These findings, taken from the history and physical examination of the patient, along with the anatomic demonstration of stenosis with an MRI or CT scan establish the diagnosis.

Stenosis of the cervical spineEdit

Anterior and posterior fusion of C4 to C6 of the cervical spine with metal implants (right). Although this was done for a C5 fracture (left), fusion for stenosis would be similar in appearance.

The developmental anatomy and biomechanics of the upper cervical spine are unique in children. Congenital osseous anomalies in this region may be associated with an increased risk for subsequent neurological compromise from instability and/or spinal cord encroachment. In a review of the medical records and imaging studies of all children with anomalies of the upper cervical spine seen at his institution between 1988 and 2003, Holsalker found multiple bony and neurologic abnormalities in 79% of the patients. Many of these had been identified as having a named syndrome. The most common findings were spinal stenosis of the bony cervical canal, segmental instability and central nervous system abnormalities. Thorough examination and MRI exam of the cervical spine are recommended in such patients.[30]

The sagittal (front to back) diameter of the cervical spinal canal is of clinical importance in traumatic, degenerative and inflammatory conditions. A small canal diameter has been associated with an increased risk of injury. More than 400 specimens from the Hamann-Todd Collection in the Cleveland Museum of Natural History were examined. From C3 to C7, the average diameter of the canal was 14.1 ± 1.6 mm. Stenosis was defined as <12 mm. Men had significantly larger cervical canals than women at all levels. Specimens from donors older than 60 years of age had significantly narrower canals than younger patients. There was no difference observed between black and white groups. The authors concluded that spinal stenosis of the cervical spine is common and usually is not diagnosed during life.[31]

In a review of 108 patients with cervical spondylotic myelopathy who had been managed with anterior decompression and arthrodesis (fusion), it was noted that anterior cervical fusion was fairly reliable in providing relief of symptoms in the cervical spine. Operative treatment consisted of anterior discectomy, partial corpectomy (removal of part of the cervical vertebral body), or subtotal corpectomy at one or more levels, followed by placement of autogenous bone graft from the iliac crest or the fibula. Of 87 patients who had a pre-operative motor deficit, 54 had a complete recovery. A pseudoarthrosis (failure of fusion) developed in 16 patients. Recurrent myelopathy was rare, but when it occurred, it was related to a failure of the fusion and recurrence of stenosis at another level.[32]

Case 1: Undiagnosed cervical stenosisEdit

The patient was a 46-year-old man referred to physical therapy for the treatment of low back pain that was present for the previous 10 months. Neurologic findings were significant, with upper and lower extremity hyperreflexia bilaterally and positive Romberg's test, Lhermitte's sign, and Hoffmann's sign. Due to the strong suspicion of spinal cord involvement, the physical therapist contacted the referring physician and recommended expedited cervical spine magnetic resonance imaging, which revealed severe central canal stenosis at C3-4 and C5-6, secondary to spondylotic changes, and altered spinal cord intensity consistent with myelomalacia (permanent damage to the cervical spinal cord). Despite a neurosurgeon's recommendations, the patient denied surgical intervention. It is recommended that physical therapists utilize screening questions regarding changes in sensation, strength, gait, and bowel and bladder function during the patient interview. A positive response to any of these questions should prompt the completion of a thorough neurological examination, including assessment and interpretation of pathological reflexes.[33]

Klippel-Feil syndromeEdit

Klippel-Feil syndrome is associated with stenosis of the cervical spine. Mutations of the homeobox genes may be responsible for congenital osseous anomalies of the cervical spine. The findings of Klippel-Feil syndrome is associated with central cord syndrome in the participants of winter sports.[34] Congenital osseous anomalies of the cervical spine may herald congenital malformations of other organ systems, such as those of the kidney and heart. Most congenital anomalies of the cervical spine are innocuous and may go undetected throughout life. Translational instability of adjacent vertebral bodies in a congenitally stenotic cervical spinal canal has serious implications. No existing prognostic classification system can predict which patients with a congenital osseous anomaly of the cervical spine are at risk for future neurologic injury.[35]

Stingers and cervical stenosisEdit

A “stinger” is a traumatic condition seen in American football players. It usually follows a severe blow to the head or neck in the course of play. The player experiences immediate pain, numbness and weakness in the upper extremities. Most are not permanent and will resolve in a matter of a few days or weeks. A study looked prospectively at American college football players to determine the risk of an initial stinger while considering the presence of cervical canal stenosis and each player’s position, playing time and body type. The data revealed a 7.7% incidence of initial stinger in the group. In these players, the seventh cervical vertebral level was the narrowest. The presence of spinal stenosis on an anatomic basis was not predictive of who would experience a stinger. Initial stingers were dependent on body habitus and position. Players who experienced multiple stingers did have a higher incidence of cervical stenosis.[36]

Case 2: Athlete with stingersEdit

An 18-year-old male high school student showed great promise to obtain a college scholarship because of his sporting ability. During his senior year, while playing linebacker for the school football team, he experienced a vicious hit to the head. He immediately noticed marked pain in his right arm, followed by numbness. He continued to play, but the pain became so great that he was pulled in the second half. After two weeks, his pain had subsided to the point he could again play. It did not recur. When he attended college the next year, the stingers returned and were worse. He was referred to a spinal surgeon who ordered an MRI of the cervical spine. He was noted to have a small canal between C4 and C7. It was recommended that he not pursue a career in football, and that he should not continue to play college ball.[37]

Thoracic spineEdit

Thoracic stenosisEdit

A report of the surgical treatment results for 7 patients (4 men, 3 women; mean age, 49 years) who presented with myelopathy caused exclusively by primary thoracic spinal stenosis, predominantly in the lower thoracic spine was submitted by Dimar, et al.,[38] (patients with concurrent ascending lumbosacral degenerative disease were excluded). All patients received extensive nonoperative treatment before referral to their center. Surgical treatment consisted of wide posterior decompression and instrumented fusion (5 cases), anterior vertebrectomy and fusion (1), and anterior vertebrectomy with autograft strut followed by wide posterior decompression and instrumented fusion (1). Five patients had significant improvement in myelopathy and were ambulating normally, 1 had modest improvement in ambulation, and 1 remained wheelchair-bound. All patients achieved solid radiographic fusions. Primary thoracic spinal stenosis should be considered in patients who present with isolated lower extremity myelopathy, particularly when no significant pathologic findings are identified in the cervical or lumbosacral spine. Expedient wide decompression with concurrent instrumented fusion is recommended to prevent late development of spinal instability and recurrent spinal stenosis.

Thoracic disc herniationEdit

Drawing of a lumbar disc herniation which can cause a localized stenosis. Thoracic discs though rare are similar.

Thoracic disc herniation is rare, while cervical and lumbar herniations are common. While most cervical and lumbar discs can be safely observed, a true thoracic disc herniation which produces symptoms is a neurosurgical emergency. Laminectomy with removal of the offending disc material is essential, and must be carried out as quickly as possible. Fusion of the segment involved remains controversial. Thoracic disc disease may be accompanied by arthritic symptoms in the lumbar and thoracic spine. A herniated disc can produce radicular pain in the intercostal region, or can present as a Horner syndrome. A true disc herniation can also present as an immediate onset of paralysis of the legs or loss of bowel and bladder function. The diagnosis is confirmed by CT or MRI of the involved spinal area. Often, disc herniations are found incidentally while looking for other pathology. If the disc is not producing any neurologic symptoms, it can be observed and does not need treatment.[39][40][41][42][43]

Case 3: Thoracic disc, college studentEdit

An 18-year-old male college student experienced the onset of paralysis while shooting pool in a local bar. He was 6 foot 3 inches tall and weighed 320 pounds. He was attending college on a football scholarship. The nurse-practitioner at the university was not sure what was wrong with him. He could not walk and was moved about in a wheelchair. He went back to his apartment where he stayed for three days. After that, he was referred to a neurosurgeon. An MRI showed a blockage of the mid-thoracic canal. The diagnosis was not obvious, but it appeared to possibly be a spinal tumor. He was taken to surgery where the spinal canal was opened and a large amount of swelling was found. Biopsy was sent for frozen section, which the pathologist reported was most likely a glioblastoma or astrocytoma. The wound was closed. Paralysis was complete below T6 by this time. The patient was referred to a cancer center. There, two weeks after the onset of paralysis, a second MRI was performed. Now the diagnosis of herniated thoracic disc was made. He was taken to surgery a second time where a disc was removed one level above the first surgery. The patient remained paralyzed below the level of T6 permanently.[44][45][46][47][48]

Case 4: Thoracic disc, lawyerEdit

A 38 year old lawyer had been experiencing mid-thoracic pain and some numbness in the legs for several months. At first she thought it was due to stress and long hours. It became worse. Her family physician thought it might be due to diabetes mellitus, however work-up for this showed no such disease. She tried to ignore the problem. She was not obese, although she was about 20 pounds overweight. She decided her symptoms were due to this condition, so she joined a gym in an effort to lose weight. Her symptoms worsened. She awoke one morning completely numb in the legs. Her physician referred her to a spinal surgeon who diagnosed a herniated thoracic disc at T6 after an MRI of the thoracic spine. He recommended a discectomy with associated fusion. She decided to wait to see if her symptoms would get better, which they did. Two months later, during a jury trial, she experienced complete numbness in the legs, perineum and completely lost bladder function. At this time, she was rushed into surgery where the offending disc was removed and a fusion with metal rods was completed. She completely regained neurologic function within two weeks.[49][50][51][52][53]

Degenerative spondylolisthesis with spinal stenosisEdit

L5 S1 Spondylolisthesis Grade II with forward slipping of L5 on S1 <50%.

Forward displacement of a proximal vertebra in relation to its adjacent vertebra in association with an intact neural arch, and in the presence of degenerative changes is known as degenerative spondylolisthesis.[54][55] The term is derived from the Greek word spondylous for vertebra, and olisthesis meaning to slip or slide down a slippery incline. Degenerative spondylolisthesis narrows the spinal canal and symptoms of spinal stenosis is common. Of these, neural claudication is most common. Any forward slipping of one vertebra on another can cause spinal stenosis by narrowing the canal. If this forward slipping narrows the canal sufficiently, and impinges on the contents of the spinal column, it is spinal stenosis by definition. If there are associated symptoms of narrowing, the diagnosis of spinal stenosis is confirmed. With increasing age, the occurrence of degenerative spondylolisthesis becomes more common. The most common spondylolisthesis occurs with slipping of L4 on L5. Frymoyer showed that spondylolisthesis with canal stenosis is more common in diabetic women who have undergone oophorectomy (removal of ovaries). The cause of symptoms in the legs can be difficult to determine. A peripheral neuropathy secondary to diabetes can have the same symptoms as spinal stenosis.[56]

Case 5: Stenosis in spondylolisthesisEdit

A 47-year-old salesman drove a car for more than 200 miles a day in the course of making his sales calls. He began to notice a sensation that he thought was related to lack of blood in his legs around 10 AM several days a week. After six months of increasing symptoms, he was referred to a spinal surgeon who diagnosed a Grade II spondylolisthesis at L5 S1. His symptoms had reached the point that he could no longer work. He underwent a decompressive laminectomy, reduction of the spondylolisthesis with a fusion and metal fixation. After six months, he was able to resume his activities as a salesman. After two years, he was no longer able to take long car trips, and found a job in an office. He filed a worker’s compensation claim, and after a long litigation, his spondylolisthesis was adjudged to have been caused or aggravated by his employment. The insurance carrier argued that the condition of spinal stenosis and spondylolisthesis were preexisting conditions, hence not compensable. The judge determined the company must “take the claimant worker as he is found.”[57][58][59]

Spinal stenosis in ankylosing spondylitisEdit

Lumbar spine showing advanced ankylosing spondylitis which can lead to spinal stenosis.

In a retrospective analysis of vertebral fractures in patients with ankylosing spondylitis, it was shown that 74% experienced some form of trauma. Of these, greater than 60% revealed vertebral fractures with some neurologic symptoms. Of these, a significant number went on to develop spinal stenosis. Paravertebral hematomas (blood clots) were accompanied by a higher incidence of other complications. Females were at greater risk of death from the complications.[60]

Case 6: Stenosis in ankylosing spondylitisEdit

A 32-year-old teacher with ankylosing spondylitis developed intermittent pain and numbness in the legs after she delivered a child. At first, she ignored the problem, thinking it was a side effect of an epidural anesthetic administered during childbirth. The problem continued to worsen over the next year. A spinal surgeon examined her and found from the old medical records that she was positive for HLA-B27 antigen. During the previous year, she had a flare up of her condition with a sed rate of 80 mm/hour and an elevated C-reactive protein titer. Rheumatoid factor (RF) and anti-nuclear antibody (ANA) were negative. Blood sugar was normal, and there was no evidence of diabetes mellitus. She had been placed on anti tumor necrosis factor-alpha (anti-TNF-alpha) therapy of infliximab and etanercept about six months earlier, with a general decrease in symptoms. Recently, the problems with her legs had recurred. An x-ray of the pelvis demonstrated fused sacro-iliac joint (SI joints). Exam showed a diffuse patchy loss of sensation in the legs and perineum. There was not a radicular pattern in the loss. She kept rubbing her legs during the exam, stating there was not enough blood getting to them. Good peripheral pulses were noted with Doppler exam. MRI of the lumbar spine demonstrated marked stenosis of L2-3 and L5-S1. She underwent a successful decompressive laminectomy with resolution of her symptoms.[61][62][63][64][65][66][67]

Surgical proceduresEdit

Surgical versus non-surgical treatment of all spinal disorders remains controversial in most areas. Certain distinct schools of thought with their own studies, literature and justifications have developed concerning most areas of spinal disease. The treatment of spinal stenosis is less controversial than other conditions of the spine. Severe, impairing stenosis of the cervical or lumbar spine should be treated with surgery, although there is often considerable room for expectant and observant therapy for those who do not wish to undergo a surgical procedure. Surgical treatment revolves around a laminectomy of the involved area. This operation is sometimes called a “de-roofing” procedure because the overlying lamina (the “roof”) of the spinal canal is removed, thus relieving the stenosis. The idea is to give the contents of the spinal canal and the dural sac more room, thus relieving the stenosis.[68][69][70][71] Surgical failures most notably occur when scar tissue grows into the laminectomy area causing a “dural scar” or a “stenotic scar” which then can cause the same problem as the original stenosis. The other complication of the surgery is “destabilization” of the spine. In other words, the spine becomes unstable because some of its supporting ligaments have been removed by surgery in treating the underlying stenosis. To counter this problem, many different fusion procedures have been tried. These include:

  • anterior fusion
  • posterior fusion
  • posterior lateral fusion
  • combination of anterior and posterior fusion
  • metal implants consisting of plates, screws, titanium cages and the like

All these are variations on a theme which are intended to restore a stable spine.

Results of treatmentEdit

Non-operative use of salmon calcitoninEdit

Several investigators have examined the use of salmon calcitonin in non-operative treatment of spinal stenosis.[72][73][74][75][76][77][78][79][80][81][82] Many problems have been encountered in this modality. Bioavailability of calcitonin delivered by nasal spray has been difficult to test, and of high variability. If nasal calcitonin cannot be sufficiently delivered into the body, it tends to reinforce the general conclusion that calcitonin does not appear to have a role in conservative treatment of lumbar spinal stenosis.

It has been observed that studies of calcitonin for treatment of stenosis have methodologic flaws.[83] Podichetty has recommended that it will be necessary to investigate the variation of the effect via different administration routes (subcutaneous or intra-nasally) and with a longer follow-up. Randomized trials are lacking and necessary to properly evaluate calcitonin in spinal stenosis.[84]

Depression and surgeryEdit

A study in Finland found that patients with spinal stenosis and depression had significantly less post-operative success and perception of improvement than patients without depression.[85]

Case 7: DepressionEdit

A 37-year-old male with a history of several major depressive episodes, requiring hospitalization for suicide attempts, had long standing complaints of back and leg pain. He had seen several spinal surgeons, who had diagnosed spinal stenosis, but none had recommended surgical intervention. He became obsessed that if he had surgery, he would become cured of his problems. Finally, a surgeon performed a decompressive laminectomy with fusion consisting of bone graft and metal implants. Instead of relieving his symptoms, the surgery did not help him and he only became worse. He experienced another major depressive disorder in the post operative course. His depression became all-consuming and he died from an overdose of narcotics six months after the surgery.[86]

Results of surgeryEdit

Lumbar spine stenosis is a common cause of radicular leg pain and neurogenic claudication in older adults. In a multicenter US Study, investigators compared surgical and nonsurgical care in patients who had experienced at least twelve weeks of symptomatic lumbar spinal stenosis without degenerative spondylolisthesis. The cohort of the study was randomized and included 289 patients who were assigned to either the surgical or non-surgical group. Of those who were assigned to the surgery group, only 67% eventually underwent surgery. The others declined. 43% of the non-surgical group opted to cross over into the surgery category. Over a period of two years, both groups reported a decrease in pain. The surgery group reported less pain, overall. Physical function and disability scores did not differ significantly in the two groups. Other studies have had similar results. The findings of these studies are not clear cut, but suggest that surgery offers more relief in some patients.[87]


Surgery may not be optimal for all patients with spinal stenosis.[88] Dr. Sohail K. Mirza, M.D., Assoc. Professor at the University of Washington School of Medicine, remarked, 12–14 minutes into a downloadable video on a 17% complication rate and a 14% failure rate in lumbar fusions from one Swedish study.[89]

In a study of spinal surgery for herniated nucleus pulposus (slipped disc), chronic low back pain, and spinal stenosis, it was found that the best results were found in stenosis patients. Disc surgery for a herniated nucleus pulposus gave marginal results. Surgery for chronic low back pain with no specific identifiable pathology is marginal at best. Spinal surgery in spinal stenosis, spondylolisthesis and instability had in comparison to other types of elective orthopedic surgery an outstanding better ability to improve the operated subject’s health-related quality of life than other types of elective orthopedic surgery.[90]

Decompression without fusionEdit

L4-5 Spondylolisthesis Grade I with forward slipping of L4 on L5 <25%. Newer laminectomy techniques preserving the posterior elements do not lead to further progression.

The reported success rates for decompressive surgery for stenosis vary greatly in the literature. Good to excellent results are noted in the immediate post op period up to about six months after the surgery. These results tend to deteriorate after about one year post op.[91][92][93][94][95][96]

In a report of the outcome of 50 patients with degenerative lumbar spinal stenosis who were treated surgically by spinal decompression without fusion between 1984 and 1995, it was found that the length of pre-operative symptoms could predict the satisfaction of patients postoperatively. The longer the symptoms had existed pre-op, the worse the general result of the surgery. The mean age at the time of surgery was 59.9 years (45–77 years) and the mean follow-up was 11.6 years (6.1-17.2 years). Five patients had a concomitant spinal fusion. The outcome was rated as excellent in 23 patients, good in 13 patients, fair in 9 patients and poor in 5 patients. Patients with concomitant fusion had good to excellent results and were more satisfied, whereas patients with long-standing preoperative symptoms had poor to fair result and were less satisfied.[97]

In 1992, Turner et al.[98] published a survey of 74 articles on the results after decompression for spinal stenosis. Good to excellent results were on average reported by 64% of the patients. There was, however, a wide variation in outcomes reported. There was a better result in patients who had a degenerative spondylolishesis. A similarly desigined study by Mardjekto et al.[99] found that a concomitant spinal arthrodesis (fusion) had a greater success rate. Herron and Trippi[100] 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[101] reported on 290 patients treated over a 25 year period. Excellent results were obtained in 69% and good results in 13%.

Johnsson et al.[102] studied postoperative slipping after lumbar decompression without fusion. In the group with degenerative spondylolisthesis, progression of the slip occurred in 65% of the patients. However, this progression did not appear to influence the result of the surgery. At that time, a wide decompression with removal of the facets (facetectomy) was common. More recent studies have shown that preservation of the posterior elements in the spine does not lead to further progression of the spondylolisthesis in the majority of cases.[103][104][105][106] There is still no consensus regarding treatment of patients with stenosis.[107][108]

Case 8: Multiple surgeriesEdit

A 34-year-old female was involved in a motor vehicle accident with resultant low back and leg pain. She was diagnosed with lumbar stenosis by MRI. After nine months of expectant therapy, she did not improve. She underwent a decompressive laminectomy with excellent results for about two years. After that, her symptoms of leg and back pain returned. At three years after her first surgery, she underwent a second surgery to remove the scar tissue that had formed over the previous laminectomy area, and fusion. The second surgery was complicated by an undetected tear of the dural. This required a third surgery to repair the leak. By the time she was dismissed from the hospital from the second and third surgeries, she was taking morphine sulfate 80 mg. per day. She had recurrence of her symptoms at one month post op and remained significantly impaired and unable to resume employment.[109][110][111]

Decompression with lateral fusionEdit

Patients with spinal stenosis and degenerative spondylosis (degenerative disc disease) or degenerative spondylolisthesis (degenerative disc disease with forward or backward slipping of one vertebra on another) may be candidates for a decompression and lateral fusion. This technique represents its own school of thought and has an extensive surgical literature. It involves placement of bone graft over the lateral vertebral processes (transverse processes), and may comprise some kind of internal fixation with metal implants.[112][113][114][115][116][117] In general, any patient who has a spinal stenosis can also be fused. Most patients with lumbar stenosis do not show signs of spinal instability. The lateral fusion may be combined with instrumentation such as pedicle screws or metal rods. Internal fixation with metal devices has been found to increase fusion rates[118][119][120][121]

Decompression and lateral fusion is thought to be a safe procedure with a low complication rate. Decompression alone, or with fusion can be complicated by a dural tear, motor or sensory loss and infection.[122][123][124]

Case 9: Stenosis and vascular diseaseEdit

A 72-year-old man had noticed he was unable to play nine holes of golf without developing severe pain in the legs. After about a year, he was unable to play, even if he rode in a golf cart. On exam, he was noted to have markedly advanced atherosclerotic vascular disease in his legs as well as a severe L4-5 stenosis of the lumbar spine. It was decided to perform a decompressive laminectomy. He had some improvement in his symptoms for about six months. Then his pain in the legs returned. At this time it was determined that his vascular situation had worsened. He underwent a vascular bypass on the left leg. This was successful in relieving his symptoms for about three years, although he continued to experience some element of pain in the right leg. This case demonstrates a situation in which both stenosis and peripheral vascular disease occurred concurrently in the same patient.

Anterior interbody fusionEdit

The most extensive experience with anterior interbody fusion has been accumulated in the Japanese surgical literature. The anterior interbody fusion involves placement of bone graft into the anterior portion of the disc from a retroperitoneal approach. This requires surgery from the front of the abdomen or the flank. Adhesion of the peritoneum is a relative contraindication. It has been reported that patients can expect a satisfactory result up to about 65 years of age.[125][126][127] Anterior interbody fusion should be reserved for younger patients (those under 50).[128][129][130] Patients with osteoporosis have a poorer result. Degeneration of an adjacent segment can lead to greater degeneration after surgery. (This is a phenomenon noted in all fusions.) [131] Anterior fusion is not indicated for patients with multilevel involvement. Patients with single level involvement are the best candidates.[132][133] Satisfactory results have been reported in the range of 76% to 60% depending on the length of followup. A strict postoperative course is recommended, including up to three weeks in bed.[134]

Case 10: Anterior interbody fusionEdit

40 year old Japanese business man had severe pain and numbness in the legs. He was diagnosed with spinal stenosis of the lumbar spine. After he failed conservative therapy, an anterior spinal fusion was carried out at L4-5 and L5-S1 combined with a decompression. He was kept at strict bed rest for three weeks, then allowed slow progression of ambulation. At two years post op, he reported his symptoms were 95% improved. He continued to pursue his business career.[135][136][137]

Decompression with instrumentationEdit

Spinal instrumentation can increase the fusion rate.

Arguably, inclusion of a fusion procedure along with decompression has become accepted. Usage of metal instrumentation has remained controversial. Also correction of the slippage with reduction of the spondylolisthesis remains controversial. Such a reduction can be done only with some kind of metal fixation. Some authors recommend metal placement in recurrent surgery for failed stenosis procedures.[138] Instrumentation certainly improves the successful fusion rate, but there is no conclusive evidence that it improves the clinical outcome. Several studies have compared the role of instrumentation in improving fusion rates. Several of these have found an increased fusion rate with internal fixation.[139][140] In general, those with a higher fusion rate also report a greater functional capacity after the surgery. The potential complications of decompression and pedicle screw fixation include wound infection, dural tear and misplacement of the screws. Adjacent stenosis has been reported to occur in 42% of lumbar fusion patients treated with decompression and fusion.[141] Whitecloud found a similarly high rate of adjacent stenosis which was also associated with a pseudarthrosis (failure of fusion). Use of metal fixation reduced the rate of fusion failrue.[142] Patel found that adjacent stenosis occurred with greater frequency and earlier in patients with instrumental fixation.[143] Bony regrowth around the laminectomy may occur in up to 88% of cases with or without associated fusion. This can lead to failure of the surgery and recurrence of the stenotic condition.[144]

Dartmouth studyEdit

A large study under the auspices of Dartmouth Medical School found that surgery for stenosis was effective, but may not be justified based on cost.

The Spine Patient Outcomes Research Trial (known by the acronym "SPORT”) done under the auspices of Dartmouth Medical School, but involving other institutions, reported favorable surgery outcomes over two years among patients with stenosis and without degenerative spondylolisthesis. The economic value of these surgeries is uncertain. Among 634 patients with stenosis, 394 (62%) had surgery. Most often this was a decompressive laminectomy without fusion. Stenosis surgeries improved health to a greater extent than nonoperative care. Among 601 patients with degenerative spondylolisthesis, 368 (61%) had surgery. Of this group, most had decompression with fusion (93%). The majority had instrumentation (78%). Degenerative spondylolistheiss surgeries significantly improved health versus nonoperative care. Costs for both decompressive laminectomy ($77,600 average; range $49,600 to $120,000) and laminectomy with fusion (average $115,600; range $90,800 to $144,900) were considered to be a hindrance in the total care of stenosis patients. The expenditure per patient may be difficult to justify, despite the apparent improvement of stenosis patients with surgery. In other words, the economic value of these surgeries is uncertain.[145][146]

In another closely related study, 289 stenosis patients were enrolled in a randomized cohort, and 365 were enrolled in an observational cohort. At two years, 67% of the patients in the randomized cohort had undergone surgery, whereas 43% of those who were randomly assigned to receive non-surgical care had also undergone surgery. In the combined group, patients who inderwent surgery showed significantly more improvement in all primary outcomes than did patients who were treated non-surgically.[147]

In a preliminary report to the one cited supra, the authors noted that management of degnerative spondylolisthesis with spinal stenosis is controversial. Surgery is widely used, but its effectiveness in comparison with that of non-surgical treatment has not been demonstrated in controlled trials. Surgical candidates from 13 centers in 11 US States who had at least 12 weeks of symptoms and image confirmed degenerative spondylolisthesis were offered enrollment in a randomized cohort or an observational cohort. Treatment was standard decompressive laminectomy with or without fusion, or usual non-surgical care. 304 patients were enrolled in the randomized cohort and 303 in the observational cohort. They concluded that in non-randomized as-treated comparisons with careful control for potentially confounding baseline factors, patients with degenerative spondylolisthesis and spinal stenosis treated surgically showed substantially greater improvement in pain and function during the two years than patients treated non-surgically.[148]

In the four year follow-up of the SPORT/Dartmouth study, patients who underwent surgery for a lumbar disc herniation achieved greater improvement than nonoperatively treated patients in all primary and secondary outcomes except work status.[149]

Steroid epidural injectionsEdit

In a study of steroid epidural injections, the authors noted that spinal stenosis is one of the three most common diagnoses of low back and leg symptoms which also include disc herniation and degenerative spondylolisthesis. Spinal stenosis is a narrowing of the spinal canal with encroachment on the neural structures by surrounding the bone and soft tissue. In the United States, one of the most commonly performed interventions for managing chronic low back pain are epidurual injections, including their use for spinal stenosis. However, there have been no randomized trials and evidence is limited with regards to the effectiveness of epidural injections in managing chronic function limiting low back and lower extremity pain secondary to lumbar spinal stenosis. The study found caudal epidural injections with or without steroids may be effective in patients with chronic function-limiting low back and leg pain with associated spinal stenosis in approximately 60% of patients.[150]

Case 11: Steroid epidural injectionEdit

42 year old with spinal stenosis was injured on the job. He was lifting boxes while sorting inventory at a store. The boxes weighed about 30 pounds each. He experienced low back pain which then became a diffuse numbness in the legs. It persisted for two months. He was referred to a spinal surgeon who diagnosed multilevel stenosis between L2 and S1. He was given a series of steroid epidural injections over a three month period. These provided relief for about six months, but then his symptoms returned, when it was decided he should undergo an extensive decompression from L2 to S1.[151]

Case 12: Steroid injection in failed back syndromeEdit

38 year old male truck driver was injured when his truck inadvertently drove over a large pot hole which was about two feet deep. He experienced a jarring sensation in his back. This progressed to generalized leg pain. He was diagnosed with a stenotic segment at L3-4. After six months he underwent a surgical decompression. This relieved his symptoms for about six months. He returned to truck driving, when his symptoms returned. He underwent another surgical procedure with removal of scar from the previous laminectomy and posterior fusion with metal placement. He was never able to return to work, and developed a chronic pain syndrome with consumption of large amounts of prescribed narcotics on a daily basis. At three years post op, he was diagnosed with arachnoiditis of the lumbar spine. He was given a series of steroid epidural injections, but without any lasting benefit. Finally, he had a third surgery for placement of a spinal cord stimulator. This reduced his perception of pain by about 25%, but he continued with the same consumption of narcotics as before surgery. He was now diagnosed as a Failed Back Syndrome.[152][153][154]

Failed surgeryEdit

(See main article: Failed back syndrome or WikiBooks Neurology and Neurosurgery/Incomplete Spinal Cord Injuries/Failed Back Syndrome)

Failure to return to workEdit

In a landmark Canadian study, Waddell et al. found that in the worker’s compensation system, once the threshold of two major spinal surgeries is reached, the vast majority of workers will never return to any form of gainful employment. Beyond two spinal surgeries, any more are likely to make the patient worse, not better. Very few studies in the worldwide surgical literature actually document return to work after spinal surgery, or lack thereof.[155]

Failure to relieve symptomsEdit

The biggest risk of spinal stenosis surgery is that it might not be effective in relieving the symptoms. Compared to surgery for disc herniation and radiculopathy, spinal stenosis surgery has a greater effectiveness. The beneficial results of the surgical decompression may deteriorate with time. This can lead to a recurrence of symptoms, or the development of new ones. In the most common forms of degenerative stenosis, the pathology is characterized pathologically by degenerative hypertrophy of the facet joints, the vertebral body margins, thickening of the ligamentum flavum and narrowing of the discs with osteophyte formation.[156] The combined effect of these changes is a narrowing of the canal with leg pain, paresthesias, varying degree of back pain and limitation of walking distance with a good peripheral circulation. The lower limb pain is increased by bending forward. The incidence of unsatisfactory results after surgery for lumbar stenosis is not known. Despite studies which describe a “good” or “excellent” result, the parameters are not the same for different studies. Many studies rely upon a third party filling out a questionnaire. Some patients are lost to follow-up. Most studies never look at such important factors as “return to previous work”, “use of narcotics” or “ability to reenter the competitive work force”. Therefore, there is no correlation between reported results and ability to return to work.[157]

Post op infectionEdit

Post operative infection in the site of the dural canal is relatively infrequent, reported in the surgical literature to be 1% to less than 12%.[158][159][160][161][162][163][164][165][166][167][168][169][170][171][172][173] The longer the surgical procedure, and the more complicated, the greater the risk of infection. When it occurs, it is usually a devastating complication, if the space around the dural canal is involved, and will leave the patient with significant permanent impairment. 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.[174][175][176][177][178][179] 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 recommendations 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 five to seven postoperative days. Based on the Center for Disease Control guidelines, 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.[180]

Case 13: Post op infectionEdit

MRI showing localized stenosis at L2-3, L3-4 and L4-5.

A 41-year-old welder fell approximately eight feet onto a concrete surface at a construction site where he was working. He landed on his back and buttocks. He immediately experienced low back pain and leg pain. He ignored it for the rest of the day. He tried to continue working, but over the next two weeks, his pain in the back became worse, and his legs began to go numb for several hours at a time. He filed a comp claim and was sent to the company doctor who referred him to a spinal surgeon. There, he was diagnosed with L2-3, L3-4 and L4-5 spinal stenosis. It was felt this had been a previously undiagnosed and asymptomatic condition which had been aggravated by the fall. Since his symptoms were not improving after a few months, a decompressive laminectomy was advised. He underwent the surgery. On the fourth post-op day, he spiked a fever of 102 degrees F. His white count was 13,500. He appeared in some distress. His sed rate was 110 mm/hour. His wound in the lumbar spine was red and draining pus. It had a foul, fecal odor to it. A diagnosis of wound infection was made, and he was returned to surgery where the wound was opened, drained and irrigated. Cultures grew methicillin sensitive staphylococcus aureus and streptopeptcoccus. Two more surgeries were necessary, along with a two month course of intravenous antibiotics. He was cured of the infection after two months. He continued to have sharp and unrelenting pain in his back and radiating into his legs. Severely impaired from his pain, at two years he was still unemployed and maintained on the oral narcotics morphine sulphate, 80 mg. per day supplemented with OxyContin and Percocet for breakthrough pain. He was now diagnosed as a Failed Back Syndrome.[181][182][183][184][185][186][187][188]

Recurrence of stenosisEdit

Drawing of lumbar vertebra after decompressive laminectomy with scar covering the dural canal which can cause a new stenosis.

It has been recognized for many years that spinal surgery can be complicated by recurrence of the same symptoms which originally provided the indications for the initial surgery. Decompressive laminectomy remains the mainstay of operative treatment for stenosis of the spine, whether it is combined with fusion or not. Failure of fusion can lead to a condition called pseudoarthosis. Repeat surgery to repair a pseudarthrosis has been documented in the surgical literature to be futile for decades. Despite this, there remains a school of thought which continues to recommend repeat surgery for repair of failed fusion.[189][190] There has never been an established link between pseudarthrosis and recurrent back pain.[191] Scar tissue frequently fills in the area of laminectomy creating a new stenotic condition. The nerve roots can become encased in scar tissue, causing new, painful symptoms. It has been long recognized that neurolysis (a surgery to remove the scar tissue from the dura and nerve roots) is futile, and will only lead to more scar tissue.[192][193][194][195][196][197]

Recurrent or multiple surgeries in the lumbar spine quickly lead to successively worsening results. When surgery is carried out in the worker’s compensation system, it is even worse. [198] The development of arachnoiditis, a chronic and often non-specific inflammation of the epidural space can be particularly vexing to the treating physician.

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.[199][200][201][202][203][204][205]

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.[206][207][208][209][210][211][212][213]

Most Failed Back Syndrome patients who have had two or more surgeries will become chronic pain patients, addicted or habituated to heavy narcotics, unemployed and experiencing a limited social existence.[214][215][216][217][218]

Neuro-modulation techniquesEdit

A Spanish study noted that following lumbar disc surgery, or lumbar spine surgery in general, several chronic pain syndromes can result, either in the lumbar region or the lower limbs. The current indication for spinal surgery is to relieve chronic pain in the degenerative spine (degenerative disc disease and lumbar stenosis) which causes symptoms of pain in the legs. A review of the methodology of evidence based medicine shows that the use of spinal fusion, instrumentation, and decompression laminectomy have not answered the problem of chronic pain, despite more than 20 years experience. Neuro-modulation techniques described as spinal electronic stimulation techniques or injections in the dural sac. These may be of benefit in the chronic pain patient, as an alternative to more surgery, in the face of failed surgery.[219] Once the patient is deemed to need the placement of a neurostimulator, or a transcutaneous nerve stimulator (TENS), the condition is quite poor and highly impaired. The outlook for such patients is usually quite guarded.[220] Success rates for implanted neurostimulation has been reported to be 25% to 55%. Success is defined as a relative decrease in pain.[221]

Social Security DisabilityEdit

Under rules promulgated by Titles II and XVI of the United States Social Security Act, spinal stenosis is recognized as a disabling condition under Listing 1.04 C. The listing states: "Lumbar pseudoclaudication, established by findings on appropriate medically acceptable imaging, manifested by chronic nonradicular pain and weakness, and resulting in inability to ambulate effectively, as defined in 1.00B2b." 1.00B2b states, "b. What we mean by Inability to Ambulate Effectively. (1) Definition. Inability to ambulate effectively means an extreme limitation of the ability to walk; i.e., an impairment(s) that interferes very seriously with the individual's ability to independently initiate, sustain, or complete activities. Ineffective ambulation is defined generally as having insufficient lower extremity functioning (see 1.00J) to permit independent ambulation without the use of a hand-held assistive device(s) that limits the functioning of both upper extremities. (2) To ambulate effectively, individuals must be capable of sustaining a reasonable walking pace over a sufficient distance to be able to carry out activities of daily living. They must have the ability to travel without companion assistance to and from a place of employment or school. Therefore, examples of ineffective ambulation include, but are not limited to, the inability to walk without the use of a walker, two crutches or two canes, the inability to walk a block at a reasonable pace on rough or uneven surfaces, the inability carry out routine ambulatory activities, such as shopping and banking, and the inability to climb a few steps at a reasonable pace with the use of a single hand rail. The ability to walk independently about one's home without the use of assistive devices does not, in and of itself, constitute effective ambulation."

Note that the regulation is written specifically for lumbar stenosis. Inclusion of cervical stenosis requires either a meet or equal depending on the idiosyncrasy of the trier of fact in federal disability hearings.[222][223]

ReferencesEdit

  1. Porter, P. W., et al., J. Bone Joint Surg. 60 B:485-87, 1978
  2. Rothman, R., and Simeone, F., p. 518, “The Spine”, W. B. Saunders Co., Philadelphia, 1982
  3. Rothman, p. 518 ibid
  4. Kirkaldy-Willis, W. H., et al., Spine 3:319-28
  5. Kirkaldy-Willis, W. H., et al., Clin Orthop. Rel. Res. 99:30-50, 1974
  6. Lane, J. M., et al., Eur. Spine J. 12: (suppl 2):S147-54, 2003
  7. Benoist, M., Eur Spine J., 12 (suppl 2):S86-89, 2003
  8. Szapalski, M., Gunzburg, R., Eur. Spine. J. 12 (suppl 2):S170-75, 2003
  9. Ullrich, C. G., et al., Radiology 134:137-43, 1980
  10. Verbiest, H., Orthop. Clin. North Am. 6:177-96, 1966
  11. Eisenstein, S., J. Bone Joint Surg. 59 B:173-80, 1977
  12. Macnab, I., J. Bone Joint Surg. 53 A:663-70, 1971
  13. Macnab, I., J. Bone Joint Surg. 53 A: 891-903, 1971
  14. Falconer, M. A., et al., J. Neurol. Neurosurg. Psychiatry 11:13-26, 1948
  15. Ball, J., Ann. Rheum. Dis., 30:213-23, 1971
  16. Dyck, P., and Boyd, J. B., J. Neurosurg. 1977; May, 46 (5) 667-70
  17. Zeifang, F., et al., BCM Musculoskeletal Disord. 2008, 9:89
  18. Demir, A., et al., Radiology, Oct. 1, 2003; 229(1):37-43
  19. Ellingson, B. M., el al, Am J. Neuroradiol. Nov. 1, 2008; 29(10):1976-82
  20. Ellingson, B. M., et al., Am. J. Neuroradiol. Aug 1, 2008; 29(7):1279-84
  21. Lee, J. W., et al., Am. J. Roentgenol. Aug 1, 2008; 191(2):W52-W57
  22. Seidenwurm, D. J., et al., Am. J. Neuroradiol. May 1, 2008; 29(5):1032-34
  23. Shanmuganathan, R. P., et al., Am. J. Neuroradiol., Apr 1, 2008; 29(4): 655-59
  24. Ozanne, A., et al., Am. J. Neuroradiol. Aug 1, 2007: 28(7):1271-79
  25. Renoux, D., et al., Am. J. Neuroradiol. Oct. 1, 2006: 27(9):1947-51
  26. Facon, D., et al., Am. J. Neuroradiol., Jun 1, 2005; 26(6):1587-94
  27. Kiers, L., Desmons, P., J. Clin. Neurosci. 1999, Jan; 6(1) 49-50
  28. Rimbot, A., et al., J. Radiol. 2004; Mar; 85(3) 326-28
  29. Srilanth, S. G., Neurol. India, 2002; Sept; 50(3):310-2
  30. Holsalker, H., J. Bone Joint Surg.90 A; 333-48, 2008
  31. Lee, M. J., et al., J. Bone Joint Surg. 89 A:376-80, 2007
  32. Emery, S. E., et al., J. Bone Joint Surg., 80 A: 941-51, 1998
  33. Lee, L., and Elliott, R. L. J. Orthop Sports Phys Ther. 2008;38(12):798-98
  34. Matsumoto, K., et a., Am. J. Sports Med., Oct 1, 2006:34(10):1685-89
  35. Guille, J., et al., J. Bone Joint Surg. 84A: 277-88, 2002
  36. Castro, F. P., et al., The American Journal of Sports Medicine 25:603-08, 1997
  37. Castro, F. P., et al., The American Journal of Sports Medicine 25:603-08, 1997
  38. Dimar, J. R., et al., Am. J. Orthop. 2008; Nov: 37(11):564-68
  39. Arce, C. A., et al., Neurol. Clin. 1985; 3:383
  40. Alvarez, O., et al.,J. Comput, Assist. Tomogr., 1988; 12:649
  41. Benson, M. K., Byrnes, D. P., J. Bone Joint Surg. 57 B: 471, 1975
  42. Otani, K., et al., Spine 1988; 13: 1262
  43. Wood, K. B., et al., J. Bone Joint Surg., 77 A; 1631, 1995
  44. Arce, C. A., et al., Neurol. Clin. 1985; 3:383
  45. Alvarez, O., et al.,J. Comput, Assist. Tomogr., 1988; 12:649
  46. Benson, M. K., Byrnes, D. P., J. Bone Joint Surg. 57 B: 471, 1975
  47. Otani, K., et al., Spine 1988; 13: 1262
  48. Wood, K. B., et al., J. Bone Joint Surg., 77 A; 1631, 1995
  49. Arce, C. A., et al., Neurol. Clin. 1985; 3:383
  50. Alvarez, O., et al.,J. Comput, Assist. Tomogr., 1988; 12:649
  51. Benson, M. K., Byrnes, D. P., J. Bone Joint Surg. 57 B: 471, 1975
  52. Otani, K., et al., Spine 1988; 13: 1262
  53. Wood, K. B., et al., J. Bone Joint Surg., 77 A; 1631, 1995
  54. Takahashi, K., et al., Spine 1990; 15, 1211-15
  55. Wiltse, L. L., et al. Clin Orthop Rel Res. 1976, 117; 23-29
  56. Frymoyer, J. W., J. Am. Acad. Orthop. Surg. 1994; 2:9-15
  57. Colonial Ins. Co. V, Industrial Accident Comm., (1946), 29 Cal. 2d 79, 172 P.2d 884,887
  58. C. Finbeiner, Inc. v. Flowers (1971) 251 Ark. 241, 471, S. W. 2d 772
  59. Ingalls Shipbuilding Corp. v. Cahela (1948) 251 Ala. 163, 36 So.2d 531
  60. Altenbernd, J., et al., Rofo 2008, Dec 11
  61. Gorman, J. D., et al., N. Engl. J. Med. 346:1439:2002
  62. Braun, J., et al., Lancet 359:1187, 2002
  63. Brandt, J., et al., J. Rheumatol. 29:118, 2002
  64. Bowness, P, Rheumatology (Oxford) 41:857, 2002
  65. Brown, M. A., Curr. Opin. Rheumatol. 14:354, 2002
  66. Dougados, M., et al., Arthritis Rhem. 34:1218, 1991
  67. Gladman, D. D., Curr. Opin. Rheumatol. 14:361, 2002
  68. Postachinni, F., Spine 1999; 10:1043-47
  69. Katz, J. N., Spine 1996; 1:92-96
  70. Sato, k., et al., Spine 1989; 11:1265-1271
  71. downloadable UWTV videos on spinal surgery
  72. Eskola, A., Alaranta H., Pohjohainen, T., et al., (1989) Calcif. Tissue Int. 45:372-72
  73. Eskola, A., Pohjolainen, T., Alaranta, H., et al., (1992) Calcif. Tissue Int. 50:400-03
  74. Garfin, S., Herkowitz, H., Mirkovic, S. (2000) Spinal Stenosis. AAOS Instr. Course Lect 49:361-74
  75. Huth, E. J. (1986) Ann. Intern. Med. 104:257-59
  76. Jerrells, T. R., 2001 J. Subst. Abuse Treat. 20:111-13
  77. Katz J., Dalgas, M., Stucki, G., Lispon, S., (1994) Rheum. Dis. Clin. North Am. 20: 471-83
  78. Onel, D., Sari, H., Donmez, C., Spine 18:291-98
  79. Podichetty, V. K., Segal, A. M., et al. 2004, Spine 29(21): 2343-43
  80. Porter, R. W., Hibbert, C., Spine 5:90-93,1983,
  81. Streifler, J., et al., J. Neuro. Neurosurg. Psychiatry 52:543-44, 1989
  82. Porter, R. W., Miller, C. G., Spine 13:1061-64, 1988
  83. Podichetty, Vinod, K., Eur. Spine J. 2007, June; 16(6): 851-52
  84. Podichetty, Vinod, K., Eur. Spine J. 2007, June; 16 (6):851-52
  85. Sinikallio, S., et al. Eur. Spine J. 2007 July; 16(7): 905-12
  86. Sinikallio, S., et al. Eur. Spine J. 2007 July; 16(7): 905-12
  87. Hansson, T., et al., Spine Dec 1, 2008; 33 (25):2819-30
  88. Journal Watch 2008; 7 (2).
  89. "Spine: Indications for Lumbar Fusions (2003)", referring to the 2001 Volvo Award winner in Clinical Studies, 'Lumbar Fusion Versus Nonsurgical Treatment for Chronic Low Back Pain', a multicenter randomized-control Swedish study involving 310 patients, published in by Fritzell, et al. Spine 26:2521-32, 2001
  90. Hansson, T., et al., Spine Dec 1, 2008; 33 (25):2819-30
  91. Atlas, S. J., et al., Spine, 25:556-62; 2000
  92. Sanderson, P. L., J. Bone Joint Surg., 75 B 75: 393-97, 1993
  93. Ganz, J. C., J. Neurosurg. 72:71-74, 1990
  94. Herron, L. D., Mangelsdorf, C., J. Spinal Disord., 4:26-33, 1991
  95. Atlas, S. J., et al., Spine, 21:92-98, 1996
  96. Katz, J. N., et al., Spine 21:92-98, 1992
  97. Gelalis, Ioannis D., et al., Int. Orthop. 2006 February; 30(1):59-63
  98. Turner, J., et al., Spine 1992; 17:1-8
  99. Mardjetko, S. M., et al. Spine 1994; 20S:2256S-65S
  100. Herron, L. D., and Trippi, A. C., Spine 1989; 14:534-38
  101. Epstein, N. E., J. Spinal Disorder. 1998; 11(2): 116-22
  102. Johnsson, K. E., et al., Spine 1986; 11:107-10
  103. Jonsson, B., et al., Spine 1997; 24:2938-44
  104. Jonsson, B., et al., Eur. Spine J. 1992; 1:90-94
  105. Kinoshita, T., et al., J. Neurosurg. 2001; 95:11-16
  106. Kleeman, T. J., et al., Spine 2000; 25:865-70
  107. Bassewitz, H., Herkowitz, H., Clin Orth. 2001; 384:54-60
  108. Postachinni, F., Spine 1999; 10:1043-47
  109. Mardjetko, S. M., et al., Spine 1994; 19:S2256-65
  110. Banwart, J. C., et al., Spine 1995; 20:1055-60
  111. Colterjohn, N. R., and Bednar, D. A., J. Bone Joint Surg. [Am] 1997; 79:756-59
  112. Feffer, H. L., et al., Spine 1985; 10:287-89
  113. Fox., M. W., et al., J. Neurosurg. 1996; 85:793-802
  114. Herkowitz, H. N., and Kurz, L. T., J. Bone Joint Surg [Am] 1991; 73:802-08
  115. DePalma, A., and Rothman, R., Clin Orth., 59:113-18, 1968
  116. DePalma, A., and Rothman, R., Clin Orth., 63:162-70, 1969
  117. Hirsch, C., J. Bone Joint Surg. 47 A:991, 1965
  118. Bridwell, K. H., et al., J. Spinal Disord. 1993: 6:461-72
  119. Fischgrund, J. S., Spine 1997; 22:2807-12
  120. Yuan, H. A., Spine 1994; 20 S 2279S-96S
  121. Zbelick, T. A., Spine 1993, 18:983-91
  122. Mardjetko, S. M., et al., Spine 1994; 19:S2256-65
  123. Banwart, J. C., et al., Spine 1995; 20:1055-60
  124. Colterjohn, N. R., and Bednar, D. A., J. Bone Joint Surg. [Am] 1997; 79:756-59
  125. Takahashi, K., et al. Spine 1990; 15:1211-15
  126. Satomi, K., Rinshoseikeigeka 1990;25:399-406 [Japanese]
  127. Takahashi, K., et al., Rinshoseikeigeka 1990; 25:473-78 [Japanese]
  128. Fujimura, Y., Kansetsugeka 1997; 16:1520-26 [Japanese]
  129. Hirofuji E., et al., Cent. Jpn. J. Orthop Surg. Traum. 1996; 39-87-88 [Japanese]
  130. Nakai, O., et al., Kansetsugeka 1997;16:1527-33 [Japanese]
  131. Tokioka, T., et al., Seikei Saigaigeka 1991; 34:471-79 [Japanese]
  132. Abe, E., East Jpn. J. Clin. Orthop. 1990; 2:18-21 [Japanese]
  133. Tanaka, M., Seikeigeka 1999;50:1384-88 [Japanese]
  134. Nishizawa, T., et al., Sekitsuisekizui 2000; 13:709-14 [Japanese]
  135. Takahashi, K., et al. Spine 1990; 15:1211-15
  136. Satomi, K., Rinshoseikeigeka 1990;25:399-406 [Japanese]
  137. Takahashi, K., et al., Rinshoseikeigeka 1990; 25:473-78 [Japanese]
  138. Yuan, H. A., et al., Spine 1994; 19{20 Suppl]:2279S-96S
  139. Zbedlick, T. A., Spine 1993; 18(8):983-91
  140. Bridwell, K. H., et al., J. Spinal Disord. 1993 6(6):461-72
  141. Lehmann, T. R., et al., Spine 1987; 12(2):97-104
  142. Whitecloud, T. S., Spine 1994; 19(5):31-536
  143. Patel, C., et al., Spine J. 2002;2(5S):54S
  144. Postacchini, F., and Cinotti, G., J. Bone Joint Surg. [Br] 1992; 74(6):862-69
  145. Tosteson, A. N., Ann. Intern. Med. 2008 Dec. 16; 149(12): 845-53
  146. Tosteson, A. N., et al., Spine 2008, Sept. 1:33 (19); 2108-15
  147. Weinstein, J. N., Tosteson, T. D., et al., N. Engl. J. Med., Feb. 21, 2008; 358 (8): 794-810
  148. Weinstein, J. N., Tosteson, T. D., N. Engl, J. Med. May 31: 2007; 356 (22): 2257-70
  149. Weinstein, J. N., et al. Spine 33:2789-2800, 2008
  150. Manchulunati, L., et al., Pain Physician, 2008, Nov-Dec; 11(6):833-48
  151. Manchulunati, L., et al., Pain Physician, 2008, Nov-Dec; 11(6):833-48
  152. Mardjetko, S. M., et al., Spine 1994; 19:S2256-65
  153. Banwart, J. C., et al., Spine 1995; 20:1055-60
  154. Colterjohn, N. R., and Bednar, D. A., J. Bone Joint Surg. [Am] 1997; 79:756-59
  155. Waddell, G., et a., J. Bone Joint Surgery, 61 A, 201-06, 1979
  156. Hilibrand, A. S., Rand, N., J. Am. Acad. Orthop. Surg. 1999; 7:239-49
  157. Waddell, G., et al., J. Bone Joint Surg., 61A, 201-06, 1979
  158. Sponseller, P. D., et al., Spine 25:2461-66, 2000
  159. Weinstein, M. A., et al., J. Spinal Disord. 13:422-26, 2000
  160. Massie, J. B., et al., Clin. Orthop. Rel. Res. 284:99-108, 1992
  161. Rechtine, G. R., et al., J. Ortho. Trauma 15:566-69, 2001
  162. Eck, K. R., et al., Spine 26::E182-E191, 201
  163. Capen, D. A., et al., Orthop. Clin. North. Am. 27:83-86, 1996
  164. Hee, H. T., et al., J. Spinal Disord. 14:533-540, 2001
  165. Aydinli, U., et al., Acta Orthop. Belg. 65:182-87, 1999
  166. Wimmer, C., et al. J. Spinal Disord. 11:498-500, 1998
  167. Wimmer, C., et al., J. Spinal Disoder. 11:124-28, 1998
  168. Hodges, S. D., et al., South. Med. J. 91:1132-35, 1998
  169. Perry, J. W., et al., Clin. Infect. Dis. 24:558-61, 1997
  170. Abbey, D. M., et al., J. Spinal. Disord. 8:278-83, 1995
  171. West, J. L., et al., Spine 16:576-79, 1991
  172. Esses, S. I., et al., Spine 18:2238-39, 1993
  173. Dave, S. H., and Meyers, D. L., Spine 17: (6 Suppl): S184-89, 1992
  174. Bertrand, G., Orthop. Clin. North America, 6:305-10, 1975
  175. Depalma and Rothman, “The Intervertebral Disc”, Philadelphia, W. B. Saunders, 1970
  176. Finnegan, W., Rothman, R., et al., J. Bone Joint Surg., 57A:1034, 1975
  177. Ghormley, R. K., Instructional Course Lecture, The American Academy of Orthopedic Surgeons, Vol. 14, pp. 56-63, Ann Arbor, J. W. Edwards, 1957
  178. Greenwood, J., et al., J. Neurosurg. :15-20, 1952
  179. Hirsch, C., J. Bone Joint Surg. 47 A: 991-1004, 1965
  180. Kanayama, M., et al. J. Neurosurg. Spine 6:327-29, 2007
  181. Sponseller, P. D., et al., Spine 25:2461-66, 2000
  182. Weinstein, M. A., et al., J. Spinal Disord. 13:422-26, 2000
  183. Massie, J. B., et al., Clin. Orthop. Rel. Res. 284:99-108, 1992
  184. Rechtine, G. R., et al., J. Ortho. Trauma 15:566-69, 2001
  185. Eck, K. R., et al., Spine 26::E182-E91, 201
  186. Capen, D. A., et al., Orthop. Clin. North. Am. 27:83-86, 1996
  187. Hee, H. T., et al., J. Spinal Disord. 14:533-40, 2001
  188. Aydinli, U., et al., Acta Orthop. Belg. 65:182-87, 1999
  189. DePalma, and Rothman, ibid.
  190. Macnab, I “Backache”, Baltimore, Williams and Wilkins, 1977
  191. Barr, J. S., et al., J. Bone Joint Surg., 45A:1553, 1963
  192. Bertrand, G., ibid
  193. Depalma and Rothman, ibid
  194. Finnigan, Rothman, ibid
  195. Ghormley, ibid,
  196. Greenwood, J., et al., ibid
  197. Hirsch, C., ibid
  198. Waddell, G., et al., ibid
  199. Frymoyer, J. W., et al., J. Bone Joint Surg., 65 A; 13-218; 1983
  200. Deyo, R. A., Bass, J. E., Spine, 14:501-06, 1989
  201. Svensson, H. O., et al., Spine, 8;77-285, 1983
  202. de Vernejoul, M.C., et al., Clin. Orthop., 179:107-15, 1989
  203. An, H. S., et al., J. Spinal Disord., 7:369-73, 1994
  204. Hollo, I., et al., JAMA, 237; 2470, 1977
  205. Iwahashi, M., et al., Spine, 27:1396-1401, 2002
  206. Frymoyer, J. W., et al., J. Bone Joint Surg., 65 A; 213-18; 1983
  207. Deyo, R. A., Bass, J. E., Spine, 14:501-06, 1989
  208. Svensson, H. O., et al., Spine, 8;277-85, 1983
  209. de Vernejoul, M.C., et al., Clin. Orthop., 179:107-15, 1989
  210. An, H. S., et al., J. Spinal Disord., 7:369-373, 1994
  211. Hollo, I., et al., JAMA, 237; 2470, 1977
  212. Iwahashi, M., et al., Spine, 27:1396-1401, 2002
  213. Glassman, S. D., et al., Spine 25:2608-15, 2000
  214. Biering-Sorensen, F., Thomsen, C., Spine 11:720-25, 1986
  215. Boshuizen, H., et al., Spine 18:35-40, 1993
  216. Deyo, R. A., et al., Spine 14:501-06, 1989
  217. Heliovaara, M., et a., Spine 16:608-14, 1991
  218. Heliovaara, M., et al., Ann. Med., 21:257-64, 1989
  219. Ribaina Padron F. J., Neurocirurgia (Astur) 2008, Feb.19(1):35-44
  220. Wang, J. K., Mayo Clinic Proc. 51:28-30, 1976
  221. Laporte, de C, Siegfried, J., Spine 18:593-603, 1983
  222. Social Security; "Disability Evaluation Under Social Security", June 2006
  223. http://www.ssa.gov/disability/professionals/bluebook/adultlistings.pdf

See alsoEdit

External linksEdit

Last modified on 1 October 2009, at 13:33