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SECTION I: SYMPOSIUM II: Surgical versus Nonsurgical Management of Spinal Disorders

Lumbar Disc Herniations

Surgical versus Nonsurgical Treatment

Awad, John N MD; Moskovich, Ronald MD, FRCS

Editor(s): Moskovich, Ronald MD, Guest Editor; Nordin, Margareta DrSci, Guest Editor

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Clinical Orthopaedics and Related Research: February 2006 - Volume 443 - Issue - p 183-197
doi: 10.1097/01.blo.0000198724.54891.3a
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Lower-back pain (LBP) is the second most common reason for physician visits in the United States.43 Throughout his or her lifetime, the average working individual has a 60% to 80% chance of developing LBP.31 One common reason for LBP is herniation of the intervertebral disc into the spinal canal. Although our understanding of lumbar disc herniations (LDH) has well advanced since the first anatomic description in 1911,98 there is still more to uncover to comprehend the etiology of pain and the mechanisms of degeneration, to develop techniques to prevent disc herniations, and to treat their occurrences.

Lumbar disc herniations do occur in children and adolescents; however, the incidence peaks in the 4th to 5th decades of life.43 Fortunately, only 4% to 6% of LDHs become symptomatic, with men being up to three times more likely than women to sustain a LDH.44 The lifetime prevalence for surgical intervention varies from 1% to 3%.39,72,80

During the past several decades, the pendulum regarding the best treatment with which to treat LDH has shifted between surgery and physical therapy. Before Weber's landmark paper, in 1983, many considered LDH to be a surgical issue.141 Since then, the pendulum has swung toward nonoperative treatment, with the subsequent development of new treatment options. This growth of alternative medical specialties has been mirrored by an increased use of nonsurgical options by patients. The maturation of spinal surgery as a specialty has also led to the development of new surgical techniques ranging from minimally invasive operations to disc repair and disc replacement.13,17,37,64,74,75 Advances in research of the biological processes involved in LDH may allow targeted nonoperative methods to develop as well, such as the use of tumor necrosis factor antagonists.103

The questions that must be asked in observing the treatment of LDH within the current multifaceted setting of care are: (1) What are the current operative and nonoperative methods applied to the treatment of LDH? (2) What are the current recommendations of each based on best studies available? (3) Do the complexities of the condition effect choices in care, and if so, how? (4) Are the existing investigations adequate to answer the questions regarding treatment choice? (5) What are some of the new operative and nonoperative treatment options available to patients currently and in the future? and (6) What are the best currently available recommendations for a patient presenting with LBP caused by an LDH event, which is the primary question of this review.

A literature search was conducted manually, seeded from classic references and using Medline to review recent studies of various types of treatments for LHD and was directed toward current uses of traditional and new and/or alternative nonoperative and operative treatment methods. A brief review of the anatomy and pathophysiology is presented to support the rationale of different treatment options and their review. The effectiveness of select alternative treatments and newer surgical options is discussed and compared with traditional lines of treatment to explore the advantages of one treatment versus the other.

Anatomy and Pathophysiology

The intervertebral disc is one component of the spinal motion segment. The disc consists of three zones: (1) the outer annulus fibrosus, which is a lamellated ring of alternately obliquely oriented, densely packed Type I collagen fibers that insert onto the vertebral bodies; (2) the fibrocartilaginous inner annulus fibrosus, which consists of a Type II collagen fibrous matrix; and (3) the viscoelastic central nucleus pulposus, which has a high concentration of proteoglycans. The normal disc's blood supply is restricted to the peripheral outer annulus of the normal disc. The vertebral body's blood vessels lie directly against the end plates but do not enter the disc itself. The nutrition of the more centrally located disc cells is derived from diffusional and convective transport of nutrients and wastes through the porous solid matrix. The surface of the outer annulus is innervated, but no nerves have been identified in the substance of the disc itself.23

The cause of annular fissures largely is unknown but is presumed to be the result of degeneration of the annulus fibrosus, intradiscal dehydration and fragmentation, and/or excessive loading, which results in altered biomechanics.100,124 Interestingly, disc herniation occurs more commonly in the morning soon after waking. The inter-vertebral disc is unloaded during the prior evening's recumbence, which permits rehydration of the nucleus pulposus.94,101 This results in increased disc turgor during sleep. In the morning, posture alterations on rising increase the vertical load. Vigorous early morning activities may then result in vertical loads and hoop stresses that could exceed the collagen strength of the annulus, resulting in injury. The disc turgor normalizes after a period of upright posture and light to moderate activity. Other proposed risk factors for LDH include lifting heavy loads, torsional stress, strenuous physical activity, and occupational driving of motor vehicles.57

As one ages, the nucleus pulposus slowly degrades from a resilient well-hydrated proteoglycan gel to a desiccated fibrocartilaginous substance that more closely resembles the inner annulus. Once a radial tear exposes the nucleus pulposus to the outside environment, the disc will begin to degenerate.22 Disc herniations may be purely annular, purely nuclear, or consist of a combination of annular and nuclear tissues. Nuclear disc herniations track posteriorly between the anterior surface of the posterior longitudinal ligament and the posterior surfaces of the annulus and vertebral body and then into the spinal canal.24

The mechanistic cause for pain still is under investigation. The fragmentation and fissuring of the nucleus pulposus and inner annulus is largely asymptomatic secondary to the lack of innervation. This is clinically evident by the observation of degenerated, dehydrated intervertebral discs on magnetic resonance imaging (MRI) in 20% to 30% of asymptomatic individuals.16 When the outer annulus is breached, pain ensues. The mechanism is most likely multifactorial but involves mechanical stimulation of the nerve endings in the outer annulus, direct compression on the nerve root, and/or the chemical inflammatory cascade induced by the exposed nucleus pulposus.51,79

Clinical Presentation and History and Physical Examination

The usual presenting complaint is acute or chronic intermittent LBP associated with sciatica, which is radiating pain in a dermatomal distribution and classically described as a burning, stabbing, or electric sensation, sometimes accompanied with paresthesias. This type of pain should be differentiated from the less well-defined deep aching pain that is confined to the sclerotomes of the spine, commonly known as referred pain. The presence of sciatica is a sensitive and specific symptom of LDH. Most symptomatic LDHs do not present with the so-called classic presentation of acute, unilateral well-defined radicular pain after a strenuous episode of activity. Notably, stepwise multivariate analysis of patients with LDH showed that most of the diagnostic information discovered by physical examination findings had already been revealed by the history.135

Central disc herniations or herniations that have migrated can each result in a mixed clinical picture or, alternatively, signs of stenosis may predominate. There also can be considerable overlap of innervation between the dermatomes.36,134

Further delineating the pain is critical to the diagnosis of LDH and to rule out other serious pathologic conditions. These so-called red flags consist of a history of significant trauma, cancer, constitutional symptoms, night pain, immunosuppression, recent infection, bladder and/or bowel dysfunction, bilateral neurologic deficits, saddle anesthesia, progressive neurologic deficit, and unremitting pain.15 If a patient reports any of these symptoms or signs, then further work up is urgently warranted.65 This especially is true for large central herniations that cause cauda equina syndrome.3,117

Patients with a herniated disc may have a loss of lumbar lordosis, a functional scoliosis secondary to leaning away from the painful side, and the affected hip and knee may be slightly flexed and externally rotated to relieve tension on the nerve root.6,97

Macnab's and Hoppenfeld's classic texts describe the provocative maneuvers.63,97 The classic straight leg raising (SLR) test or Lasegue test is thought to be a useful clinical test to demonstrate an inflammatory compressive process across a spinal nerve root.87,118,121 Intraoperative straight-leg-raising reduces the blood flow in the nerve.81 Absence of SLR limitation does not, however, preclude the presence of a herniated lumbar disc.41,87 A positive crossed straight-leg raise test may offer a higher specificity than a positive ipsilateral test but the sensitivity is variable and some feel not reliable.73 These maneuvers are based on the premise that, normally, nerve roots have an excursion of 1.5 to 3 mm for L4, L5, and S1, respectively.49 When a nerve root is compressed, the lack of mobility creates pain. The bowstring test increases nerve root tension and may exacerbate the pain.58 The tripod test is one of the Waddell maneuvers to confirm a positive straight leg raising test when the patient is seated.139 The SLR and other neurologic signs, such as paresis, sensory loss, and change of reflexes, are neither reliable nor specific markers for LDH. If there is a correlation between motor weakness and dermatomal sensory changes that correspond to the same nerve root, the accuracy of these tests are improved.6

The femoral stretch test places L2-3 and L3-4 nerve roots under tension by bending the knee and extending the hip with the patient prone. Ensuing pain is diagnostic of compression of these roots which is accounted for by a diminution in radicular blood flow.82

Imaging and Classification

A clinical correlation is paramount when interpreting imaging studies. This is especially true for LDHs where there is a high rate of LDH found on MRIs in asymptomatic individuals.16,71 Kortelainen et al86 reported that the most common symptom was an S1 radiculopathy; however, imaging and/or intraoperative findings showed that the most common herniation is the L4-5 disk. Kortelainen et al86 also reported that a significant number of patients had symptoms corresponding to two or more levels. They found that for LDHs at or above L4 relying solely on the clinical diagnosis was fairly inaccurate. Another study showed that only 70% of patients who were diagnosed with a LDH based on clinical examination had a LDH confirmed by MRI.99 In a classic study by Weber,141 nearly 70% of patient symptoms resolved within 4 to 6 weeks. Other studies have reported similar results.25,113 Therefore, no imaging is needed for patients who are clinically diagnosed with a LDH unless one of the red flags is discovered. If this is the case, then further work up is warranted before the 4 to 6 week observational period.

Magnetic resonance imaging has become the examination of choice for diagnosing LDHs.68 It has the advantage of having no known side effects or morbidity, no radiation exposure, and is noninvasive. With MRI it is possible to identify the separate constituents of the disc based upon the differing concentrations of water, proteoglycan, and collagen.60 Caution must be exercised in interpreting MRI studies and inferring prognoses based on the radiologic findings, although several newer studies have helped clarify the role of MRI. In a classic study by Borenstein et al,20 67 asymptomatic individuals with no history of back pain underwent MRI of their lumbar spines and were followed for 7 years. Thirty-one had repeat MRI. Low-back pain developed in 21 subjects during the 7-year study period. The original scans of these subjects demonstrated normal findings in twelve, a herniated disc in five, stenosis in three, and moderate disc degeneration in one. Repeat MRIs revealed a greater frequency of disc herniation, bulging, degeneration, and spinal stenosis than did the original scans, but the findings on MRIs were not predictive of the development or duration of LBP.

The sensitivity and specificity of MRI in detecting annular tears, disc herniations, and nerve root swelling has been confirmed in several studies.68,136 Magnetic resonance imaging findings have been correlated to clinical findings and are strong predictors of surgical outcomes. A robust correlation appears to exist between larger antero-posterior disc length, small disc widths, and large medio-lateral canal widths and good surgical outcomes.27 The authors of this report also noted that demographic and clinical features appeared to predict outcomes of nonoperative treatment. Another study also suggested that physical job characteristics and psychological aspects of work were more powerful than MRI-identified disc abnormalities in predicting the need for medical consultation related to lower-back pain and the resultant work incapacity.19 In 71 patients who had preoperative gadolinium DPTA enhanced MRI studies Annular rupture and disc enhancement were found to be closely related, and correlated with sensory loss and paresis. Nerve root enhancement was found to be related to neurologic deficits in general and sensory impairment in particular.136 The degree of nerve root enhancement with gadolinium also correlates with the severity of sciatic pain in patients with LDH.125

Though MRI has a higher sensitivity and specificity than CT and or myelography, there are certain circumstances where CT-myelography is superior. Fifty-nine patients, all of whom had surgical exploration, were imaged using MRI, CT myelogram, CT, and plain myelography.68 Magnetic resonance imaging was the most accurate test with the lowest rate of false positives. However, the false-negative rate was lowest for CT myelogram. In a postoperative subset, myelography was the most accurate means of diagnosing LDH, followed by MRI, CT myelography, and CT, respectively.

Knowing the type of disc herniation and exact position of the compression is paramount for treatment planning. There are documented cases where the disc material has actually eroded through the dura and lies against the spinal cord itself.29,30 These are known as intradural herniations and can be seen by MRI. Disc material may also herniate into the intervertebral foramen or far laterally, compressing the nerve as it exits from the foramen. These types of herniation require a different surgical approach from the standard posterior or paramedian disc and may also respond differently to nonoperative treatment.48,62,123

Differential Diagnosis

When establishing a clinical diagnosis of LDH, it is imperative to rule out other serious causes of back or leg pain. These include other space occupying lesions such as an abscess, tumor, epidural hematoma, stenosis, and intradural pathology. Direct compression of the sciatic nerve in the pelvis and upper thigh may also present as sciatica. These can usually be detected if one of the red flags exist alerting the physician that further work up is warranted.15

Natural History

Henrik Weber's 1983 prospective study remains the classic reference when evaluating a patient with LDH.141 This study included 280 patients who were diagnosed with an L4-L5 or L5-S1 LDH clinically and by myelography. None of the patients had a previous spinal operation or spondylolisthesis. After 14 days in the hospital, the patients were re-examined and divided into three groups. The first group of 126 patients had “uncertain operative indications” in that they still had moderate symptoms and signs of LDH. These patients were randomized to operative versus nonoperative treatment. Followup was done at 1, 4, and 10 years after treatment. The group became the main focus of the paper. The second group, totaling 67 patients, had severe sciatica and/or neurologic compromise that did not improve with physical therapy and received operative treatment. The third group consisted of 87 patients who had mild to moderate symptoms and improved with nonoperative care.

Of the 66 patients treated nonoperatively during the first year, 26% (17 of 66) eventually received operative treatment. Assuming that all these patients had poor results, the overall satisfaction rate for patients having good to fair results was 61% whereas the surgical group had 92% good to fair results. The superior results of surgery became statistically insignificant by the fourth year after surgery; however, a trend for better outcomes in the surgical group remained. The initial recovery period was longer in the surgical group (11 weeks) than the successfully treated nonoperative group (7 weeks). The number of relapses was less than in the surgical group during the first 4 years (15% versus 24%). However, at 10 years there was no difference between the two groups. There was no difference in recovery of muscle strength between the two groups and it was found that improvement could continue over a 3-year period. Combining the two groups, nearly 16% had residual motor deficits while nearly 35% had sensory dysfunction at the last follow-up. Ultimately, there was no difference between the two groups with regard to pain and spinal mobility.141

Weber also attempted to identify risk and prognostic factors. Men outnumbered women by a ratio 1.4:1. Most symptomatic individuals had an episode of acute LBP in their late 20s, the majority of which were associated with a traumatic event. However, no prognostic factors could be found that identified which patients would go on to develop a LDH. An average of 10 years passed between the first episode and disc herniation. The herniation was usually preceded by at least a few days of LBP. Overall, patients without psychosocial stresses had better outcomes, but this result was not statistically different. Twenty-nine percent of the individuals had an element of psychosocial dysfunction consistent with the general population, but when combined with lack of physical activity, it was found to be a significant risk factor. Men tended to have better outcomes than women. A poorer prognosis was found in patients who had at least 3 months of sick leave before hospital admission; patients who were more physically active had an improved prognosis. Younger patients (average age 40 years) fared better than older patients (average age, 47 years). Factors that did not correlate with prognosis were occupation, build, stressful work environment, previous attacks of sciatica, type of herniation at onset, interval between the onset of LBP and the sciatica, and finally, the level of herniation. At 10 years, the only factor associated with a poor outcome was older age (47 years).141

Weber141 concluded that in the short term the surgical group fared better than the nonoperative group, but the difference diminished over time with no significant difference after 4 years. In the nonoperative group, 25% had good results and 36% had fair results; therefore, 60% of patients receiving operative treatment could have been spared the risks of surgery and treated nonoperatively. He found that a period of 3 months was necessary to decide whether nonoperative therapy would provide satisfactory results. If no or little improvement occurred during this period, then the patient would be a good candidate for surgical intervention. He did acknowledge that this may cause the patient undue pain and psychosocial stress, so the treatment algorithm should be discussed to permit the patient to make an educated decision concerning treatment.141

Other studies25,113,142 have supported Weber's141 conclusions. The study by Bush et al25 concluded that it was unnecessary to obtain imaging studies for the first 4 to 6 weeks of symptoms (in the absence of neurologic compromise) given that nearly 70% of patients will improve over this time period. Bassette et al14 questioned the validity of Weber's study, stating that it was not a carefully randomized, blinded study, and there were a large number of crossovers, a small sample size, and insensitive outcome measurements. It is also known that the degree of neurologic deficit does not correlate with outcome, and patients with weakness can improve with nonoperative treatment. In Weber's141 study, these patients would have been automatically placed in the operative group.84,113

When reviewing the literature, it is difficult to assess the success of different types of nonoperative treatment. The majority of studies also focus on LBP and not LDH specifically. Several factors affect outcome, such as selecting a homogeneous cohort, objective assessment of pain, psychosocial environment, cooperation with the study, and motivation of the patient to improve and resume their occupation.143

Nonoperative Treatment

To date, nonoperative care of LDH includes a wide range of qualitatively different methods: lumbar supports, bed rest, oral analgesics and muscle relaxants, spinal manipulation, physical therapy, epidural steroid injections, and behavioral therapy. Not unsurprisingly, there are also either a wide range of different levels of success or little information available.

There are no studies that show lumbar supports are more effective than other interventions for treatment of LBP.70

Bed rest places the least amount of pressure on the intervertebral disc and has, therefore, led many practitioners to recommend patients initially remain in a supine position for a specified period of time. However, there are no prospective randomized studies describing the efficacy of bed rest or the appropriate duration. A maximum of 1 week of bed rest followed by gradual resumption of normal activity has been recommended.143 Deyo et al34 conducted a randomized trial, comparing the consequences of recommending 2 days versus 7 days of bed rest. The group that was assigned to 2 days of bed rest missed 45% fewer days of work than those assigned to the 7 day period (3.1 versus 5.6 days). No differences were observed in other functional, physiologic, or perceived outcomes. Gilbert et al compared bed rest with a formal physiotherapy and education program for patients with an acute episode of LBP.47 They found no beneficial effect of either treatment with regards to several clinical outcome measures, including straight leg raising, lumbar flexion, activities of daily living, and pain. In fact, the results favored early mobilization over bed rest and suggested that the physiotherapy and education program was doing more harm than good. They found that the bed rest group took 42% longer to achieve normal level of activity, suggesting that general mobilization alone was good enough to treat LBP.

Pharmacologic treatment is widely used, but with wide-ranging results. Nonsteroidal anti-inflammatory drugs (NSAIDs) have shown mixed results on long-term reduction of back pain and sciatica.56,142 A meta-analysis of over 51 clinical trials concluded it was beneficial to use NSAIDs in acute LBP when compared with placebo, but there was little to support the use of NSAIDS for chronic LBP. There is conflicting evidence that NSAIDs are more effective than muscle relaxants, and there is moderate evidence that NSAIDs are not more effective than other medications for acute LBP. No specific NSAID was shown to be more efficacious than another.132 There is little literature on the use of oral steroids and its effect on LDHs. A recent meta-analysis reported muscle relaxants are more effective than placebo in patients with LBP but care should be taken because the incidence of adverse affects was not negligible. No difference in efficacy between benzodiazepines, nonbenzodiazepines, and antispasticity muscle relaxants was found.133

Most published studies of spinal manipulation reported mixed efficacy for the technique and were found to be low-quality studies without long-term results beyond 3 months for most.83 Just more than 1½ of the studies showed limited positive results. One study showed a beneficial effect for patients with acute onset (< 4 weeks) of LBP but the effects were not long lasting.52 A meta-analysis of all prospective randomized trials found no statistically or clinically significant advantage over general practitioner care, analgesics, physical therapy, exercises, or back school.8 Massage was shown to be effective for persistent back pain and may have a role in treatment cost-reduction.28 Acupuncture has become a popular alternative for the treatment of LBP and LDH. However, no definitive studies have been done that indicate a clear benefit of its use as a sole treatment or as an adjunct.28,129 Traction had no benefit except for those patients who experienced pain relief during the actual traction; they were slightly more likely to avoid surgery.35 The overall ineffectiveness of traction has been confirmed in another study looking at patients with LBP and sciatica.105 Interestingly, authors of one study showed a lasting benefit in increasing lumbar lordosis (mean, 5-10°) and decreasing pain with the use of an extension type of traction.55 A prospective randomized trial has yet to support this.

Physical therapy as been shown to be extremely beneficial for patients with LBP and LDHs.112,113,141 Physical therapy not only reduces pain but it also limits days off from work.85 It is suggested that bed rest deconditions the paraspinal and abdominal musculature but there are no studies documenting which types of exercises are beneficial. In another review, there was no evidence that specific exercises are affective for acute LBP.130 A trend showing that multidisciplinary rehabilitation (eg, workplace visits, comprehensive occupational physical therapy) helps patients to return to work faster, take less sick leave, and alleviate subjective disability is seen in the literature. This conclusion should be prefaced with the acknowledgment that few studies have been done and that before undertaking such a cost prohibitive approach further studies need to be completed.78 The same is true for the common approach of back schools.130 One prospective, randomized placebo controlled study, evaluated the efficacy of exercise therapy for acute LBP.40 The subjects received exercise instruction with advice for daily life activities by a physiotherapist, placebo ultrasound therapy by a physiotherapist, or usual care by the general practitioner. All patients received analgesics and information on LBP before randomization. They found no difference in functional status, number of recurrences, or medical care usage. Recurrence duration was shorter and less fatigue was observed during the first 3 months in the exercise group when compared with the usual care group. There was no difference between the exercise and placebo groups. The overall conclusion was that nonspecific therapy for a non-specific diagnosis had no advantage over usual care from the general practitioner.

There is, however, a new concept of directional preference that specifically may be elicited when patients achieve an immediate, lasting improvement in pain from performing repeated lumbar flexion, extension, or side glide/rotation movements.92 Some patients may not exhibit a preference. Directional preference therapy where flexion or extension is limited depending on the cause for pain has been shown to be superior to non-directional therapy and placebo. These results, however, diminish in the long term with no difference found at 5 years when comparing a directional protocol (McKenzie method) with education in back school.120

Epidural steroid injections to decrease inflammation have been increasingly utilized with the growing evidence that inflammatory agents released by the herniation are a significant contributor to the pain and nerve root irritation. Epidural steroid injection was successful in about 1½ the patients prospectively randomized to receive them who had not responded to an initial 6-week period of nonoperative care for LDH.26 The treatment was effective for up to 3 years. There was no difference between the patients who responded and those who did not with regard to regression of the size of the herniation. The 50 patients randomized to surgery had the most rapid reduction of symptoms with 92% to 98% reporting successful treatment. Other studies have confirmed the benefits of epidural steroid injection when compared with control groups.9,25,140 Authors of one study found epidural steroid injections had a 77% success rate for decreasing symptoms up to 27 months in patients who had poor results after nonoperative treatment and who were considered surgical candidates.140 Controversies regarding injections remain in the literature. Epidural steroids have proven to be beneficial, but more prospective studies are needed to further elucidate the efficacy of the modality.

Behavioral therapies have had a major impact on the treatment and understanding of long-term effects of LDH on patients. Gordon Waddell and his colleagues are credited with identifying and describing various psychosocial factors associated with spinal pathology and the subjective complaints of patients. In 1980, “Waddell signs” were published that distinguished whether pain was organic or non-organic in nature.139 These investigators also found that the most important psychological disturbance in low-back pain was emotional distress, measured as increased bodily awareness and depression. Emotionally distressed patients tended to present inappropriate descriptions of symptoms as well as inappropriate responses to physical examination.138 Furthermore they found that the amount of treatment patients received was influenced more by their distress and illness behavior than by the actual physical disease.137 These findings have been misinterpreted by many practitioners in that behavioral signs are not, on their own, a valid test of credibility or faking.95 Behavioral responses to examination, while they provide useful clinical information, need to be carefully interpreted. Patients require both physical treatment of their pathology as well as treatment of the psychosocial and behavioral aspects of their condition.

The multiple-factor etiology and long-term chronicity of LDH can leave the examiner with the proverbial “chicken and the egg” dilemma. We know now that psychosocial factors play an important role in patient symptoms and signs and in patient response to both non-operative and operative measures. No one has yet been able to definitively demonstrate whether depression precedes and predisposes patients to pain or occurs afterwards and is the result of having pain. It has been suggested that depression appears to the result of being in pain rather than the cause of pain.54 In the current authors' experience, it is not uncommon to see an exacerbation of behavioral symptoms during both acute crises and as pain develops into a chronic problem. Positive responses indicating depression were found in 38.4% of 2878 patients with disc herniation who took a validated three-question depression screening test which is included in the Health Status Questionnaire 2.0 (which is comprised of the Short-Form 36-Item Health Survey and the three-question depression screener.)90 In multivariate analyses of this group, positive depression screener responses were significantly associated with an attorney's services and a longer duration of symptoms. Another study of 106 lumbar discectomy patients found the hypochondriasis, depression, hysteria, psychopathic deviate, psychasthenia, and schizophrenia scales on the Minnesota Multiphasic Personality Inventory were useful predictors of surgical outcomes.59 Psychological factors clearly play a role in patient wellness. Authors of another study showed that carefully selected and presented educational information on back pain can have a positive effect on patients' beliefs and clinical outcomes, especially those patients with an initially high fear-avoidance beliefs score.24 A systematic review of randomized controlled trials of the effect of behavioral therapy on patients with chronic LBP showed it to be effective compared with waiting-list controls or no treatment, but it is still unknown what type of behavioral therapy is appropriate for the several different subgroups of patients who suffer from LBP.131

Operative Treatment

Walter Dandy is credited with the first documented surgical decompression for disc herniation.33 Since that time, countless debates and clinical investigations have been done comparing the results of operative versus nonoperative treatment and the results of different surgical techniques with an emphasis on minimizing soft tissue disruption.

As mentioned in the previous section, most patients can be treated successfully by nonoperative means if the patient can comply with physical therapy, medications, and epidural steroids and most importantly, allow adequate time.10,67,147 Time also should be spent educating the patient when discussing treatment options. Our society has placed an importance on short-term outcomes. Patients who undergo decompression will have more rapid resolution of symptoms, especially those who have mild or no LBP and an acute onset of severe sciatica.108 Patients treated operatively have a shorter recovery period, return to work in less time, and overall, place less of a financial and social burden on the health care system when compared with patients treated nonoperativly.109 The results are not as promising for patients who have longstanding LBP or chronic sciatica. In one study, patients who were candidates for lumbar disc surgery were examined with a standardized dynamic mechanical form of spinal assessment using repeated end-range test movements while monitoring patterns of pain response. Three subgroups based on patients' patterns of pain response were identified: reversible condition, irreversible condition, or unaffected condition. Reversible conditions include acute or chronic LBP and/or leg pain and are often rapidly recoverable using nonoperative care. Pain centralization, defined as an improvement in pain location in response to repetitive end-range testing and typically occurring with only one direction of test movement(s), predicted a successful response to nonoperative treatment, even in the presence of neurologic deficits. Irreversible conditions are characterized by pain in all directions of testing and absence of the centralization response, predicting a poor response to nonoperative care. When pain was unaffected with repeated end-range of motion testing, the authors concluded that the pain was likely to be non-discogenic.144

The long-term results of surgical intervention are of great interest to us; can we improve on the natural history of LDH? Ten years after lumbar discectomy the average recovery rate calculated by using Japanese Orthopedic Association scores was 73.5 +/− 22% in one group. These results equal Weber's findings for nonoperative treatment.141,146 Seventy-four percent of patients still complained of LBP but only 12% of these were classified as severe. There was also a 12% reoperation rate. One can conclude that this indicates failure of surgery; however, the purpose of surgical intervention is to address the leg symptoms not the back pain. Also as mentioned previously, because there is a genetic and familial predisposition this may represent the individual's natural tendency for disc degeneration and herniation rather than a result of surgery.88,107,111

McCulloch96 stated that there are eight basic principles that the surgeon and the patient should understand when operative treatment is recommended: (1) LDHs are common (1% of the total population); (2) more than 90% have some improvement with nonoperative treatment; (3) 2% to 4% of patients with LDHs are surgical candidates; (4) MRI will reveal a LDH in approximately 20% to 30% of asymptomatic patients younger than 60 years of age; (5) surgical intervention will improve short-term outcomes, but long-term studies show little difference with those treated nonoperatively; (6) surgical intervention rarely is indicated before 6 weeks from the onset of symptoms but should not be delayed to beyond 3 to 4 months; (7) the disc will continue to degenerate with either form of treatment; and (8) scar tissue will form, possibly creating a poorer prognosis in the future if repeated discectomy is required.

With the knowledge that the majority of patients will have satisfactory outcomes with nonoperative or operative treatment, surgical indications need to be established clearly. The one absolute indication is cauda equina syndrome. Most practitioners would also consider a progressive motor deficit as a strong indication for surgery. These two situations, however, are rare. The majority of cases are not as straightforward. Most texts would agree that the relative indications for surgery are: (1) failure of an adequate trial of nonoperative treatment, (2) recurrent sciatica after a successful trial of nonoperative treatment, (3) significant motor deficit with positive nerve root tension signs, (4) a herniation into an already stenotic spinal canal, (5) large extruded fragments, and/or (6) intractable pain.96 The standard of care remains an open partial discectomy in which the herniation is removed through a small annulotomy. The remainder of the stable disc is preserved. Throughout the years, many attempts have been made to refine the procedure to minimize the soft tissue dissection and ultimately, scar tissue formation. Minimally invasive techniques have been developed with a focus on minimizing the soft tissue dissection, creating a laminotomy without creating instability, safely retracting the cauda equina and the individual nerve root, and finally, excising the disc herniation. The use of magnification (microscope or magnification glasses) has assisted in achieving these goals. Microdiscectomy gradually has risen to become the standard operative technique for discectomy and has been shown to be superior to traditional open discectomy with regards to in-patient cost effectiveness, postoperative pain, and work days missed.7,11,18 The rate of recurrent LDH may differ depending on the surgical technique but more likely reflect surgical experience and individual technique. Authors of independent studies performed more than a decade apart showed no difference in results or recurrence rates of disc herniation treated by open discectomy or microdiscectomy.126,127 Patient factors that are predictors of favorable outcomes are an absence of LBP, radicular pain distribution with positive tension signs, non-work related injury, higher socioeconomic status, and minimal psychosocial stressors.1

Surgery provides nearly 85% to 95% of patients with good to excellent short-term results.53,141 These results can, however, deteriorate with time.93 Lower-back pain is usually the cause for the drop in satisfaction and, in the long term, no differences have been found between those treated operatively and nonoperatively. Lewis et al91 reported that the long-term good to excellent results diminished to approximately 55% to 70%, with 18% requiring additional back surgery.114 It is unclear whether this is a direct result of surgery or just the natural history of lumbar degeneration.42

Questions arise whether nonoperative treatment sets patients up for less than satisfactory results if operative intervention is subsequently instituted? Approximately 15% of patients who have surgery after an adequate trial of nonoperative treatment show no improvement, while the majority of patients experience significant relief of LBP.126 Patient's age, type of disc herniation, recurrence, and need for reoperation are significantly related to the patient's satisfaction with the outcome of surgery. 45Satisfaction was not found to depend on the interval between clinical onset and diagnosis or on the timing of surgery. The degree of return to activities of daily living (ADL) was found to be significantly related to age, need for re-operation, type of disc herniation, and timing of surgery. The authors concluded that that age and type of disc herniation are important to consider when deciding whether to operate on a patient and that return to ADL postoperatively correlated with disc disease recurrence.45 Patients with an extruded herniated disc had a shorter duration of symptoms and a better functional outcome than those with a contained herniation.102 Their study also suggests that patients with sciatica for more than 12 months have a less favorable outcome, and there was no difference in outcomes for surgical patients in whom the duration was less than 12 months. In another study, investigators looked at the risk of “getting worse.”119 Using the Oswestry disability index as their measure, they found that 4% of patients deteriorated. Independent risk factors of deterioration were a long duration of sick leave and a better functional status and quality of life prior to operation. These findings should be discussed with patients when advising them on the course of treatment.

Arthroscopic techniques have recently emerged as an alternative to microdiscectomy. Clinical results are similar to microdiscectomy, however, there is a slightly higher rate of retained disc material and residual symptoms. The advantages are less operative time, avoidance of general anesthesia, minimal blood loss, and less scarring in the spinal canal.76 Patient selection and surgical expertise are paramount for the success of arthroscopic techniques. At this time, these techniques are still being investigated.

Another method of discectomy is chemonucleolysis with chymopapain, which basically is an enzymatic dissolution of the herniated portion of the nucleus pulposus. Under conscious sedation, chymopapain is injected percutaneously guided by fluoroscopic visualization of the needle. Short-term satisfaction is approximately 80%, which is slightly below those of standard laminectomy.21 After reports of paraplegia and transverse myelitis the use of chymopapain diminished significantly. With the current improved imaging methods and strict adherence to technique and indications this alternative may once again become a viable option. There is strong evidence on the relative effectiveness of surgical discectomy versus chemonucleolysis versus placebo46

Postoperative care is variable. In a recent meta-analysis, it was concluded there was no evidence that postoperative activity restriction was required after a primary discectomy. Physical therapy initiated 4 to 6 weeks postoperatively reduced the number of work days missed and increased general functional status. There was no evidence that therapy increased the rate of recurrence or the need for reoperation.104

Since Weber's141 landmark findings there has been a trend towards nonoperative treatment. Postachinni107 summarized it well when he stated:

“In the last two decades, we have shifted from an aggressive surgical approach for the treatment of patients with a herniated disc to an excess of nonoperative management, passing through chemonucleolysis and the various methods of percutaneous discectomy, which have clearly shown their limits. In the next decade, we must reach a new equilibrium between nonoperative and operative treatment. We should better understand which patients are likely to obtain full and satisfactory results in a reasonably short period after nonoperative care; which are the few candidates for the various percutaneous modalities of discectomy; which are the patients in whom surgery, done with minimally invasive techniques, is the treatment of choice in terms of clinical efficacy and rapidity of return to activities of daily living; and which can be better treated with a fusion or a disc prosthesis because of chronic back pain related to the herniated disc.”


Any surgical procedure, no matter how carefully it is done, has risks. Most can be avoided with proper patient selection, education, thorough preoperative planning, and meticulous attention to anatomy and surgical technique. Fortunately, these risks are the exception rather than the rule. More common complications include wrong level surgery, missed pathology and/or retained disc, durotomy, epidural venous bleeding, lesions from positioning, residual back and/or leg symptoms, recurrent disc herniation, cauda equina, epidural hematoma, infection, discitis, iatrogenic instability, thromboembolism, and postoperative epidural fibrosis and/or arachnoiditis.

Operating on the wrong disc level for herniated disc disease is a rarely reported complication.50 One group of experienced surgeons operated on the wrong spinal level in 1.2% of their cases compared to a rate of 3.3% with less experienced surgeons in the group.145 The American Academy of Orthopaedic Surgeons has spearheaded an initiative to eliminate wrong-site and wrong-level surgery.

Wrong-site surgery is preventable by having the surgeon, in consultation with the patient when possible, place his or her initials on the operative site using a permanent marking pen and then operating through or adjacent to his or her initials. Spinal surgery done at the wrong level can be prevented with an intraoperative xray that marks the exact vertebral level (site) of surgery.2

Inadvertent durotomies occurred in 0.8% to 7.2% in different series. Nerve root lesions occurred on average 0.2% of the time. Infections occur in 2% to 3% of all cases across the board. A review of the literature indicates that recurrent herniations occur with a frequency of 5% to 15%, with the risk decreasing over time.69,122 Lack of physical activity is a significant risk factor for recurrence.77 Traditionally, an open discectomy was used to treat recurrent herniations; however, as the endoscopic and percutaneous techniques have improved, many authors have demonstrated comparable results in terms of patient satisfaction and safety.4,66,89

Distinguishing between recurrent disc herniation and epidural fibrosis can be difficult. Contrast enhanced MRI has become the study of choice to differentiate between nonenhancing disc material and vascularized fibrosis. Unfortunately, there is no direct correlation between the amount of fibrosis and the patient's symptoms and therefore, clinical judgment must intervene when interpreting these studies. However, one series reports that patients with extensive fibrosis were 3.2 times more likely to experience radicular symptoms.12 To this date, no intervention or material has been shown to alter the formation of scar tissue enough to influence clinical results. Interestingly, one prospective study showed that the use of closed suction drainage decreased the quantity of epidural fibrosis.116

Special Cases

Approximately 5% of all LDHs occur in the upper lumbar spine (L1-L2, L2-L3, L3-L4).115 These herniations present the practitioner with multiple difficulties. First, the symptoms of upper LDH are not as consistent as those of L4-L5 and L5-S1 herniations. Imaging methods are not as reliable in detecting herniations of the upper lumbar spine.5 The surgical outcomes are less promising for lower lumbar levels, especially for L1-L2, L2-L3.115 This has been attributed to the fact that the interlaminar space is not as large and more of the lamina has to be removed to gain access to the disc, which potentially creates more instability. Another factor is that the spinal canal is smaller and the nerve roots have a more horizontal course, making these herniations more technically challenging.

Herniations occurring in the very young or the elderly present a unique dilemma. It has been shown that patients aged over 40 years tend to fare worse than younger patients, but no significant difference could be found in patients over 65 compared to those over 40 years.114 Interestingly, the level of herniation tends to be more proximal as patients age.32 Nearly 60% of children and adolescents have recurring symptoms in adulthood, and 28% require a reoperation during their lifetime.106

Far lateral disc herniations account for 1% to 12% of all disc herniations, with L4-L5 level being the most common.61 The unique characteristic of these herniations is that instead of compressing the traversing nerve root of the level below, the herniation extends into or through the foramen and compresses the corresponding exiting nerve root. Myelography may miss identifying these herniations because there may be no contour defect in the dye column, but with good quality CT scanning or the use of MRI the diagnostic dilemma may be elucidated. The parasagittal views may indicate occlusion of the affected neural foramen. Several surgical techniques have been developed to address these types of herniations. Total unilateral facet-ectomy has fallen out of favor because of the likely development of iatrogenic instability consequent on resection of the facet and concomitant discectomy. The Wiltse paraspinal approach is a paramedian muscle-splitting technique which provides direct visualization and access to extraforaminal and foraminal disc herniations.38 There is less intraspinal scar formation and less muscle disruption than the standard midline approach, and the facet joint remains largely competent.


Operative treatment clearly is indicated in cauda equina and possibly for patients with progressive motor deficit, where such treatment is conservative treatment. Otherwise, no one method of nonoperative or operative treatment seems definitively to be superior on reviewing the literature. Severe neurologic deficits without pain also may be a good reason to consider operative treatment. A dissociation between pain and sensorimotor dysfunction should not be a contraindication to providing the patient an opportunity to receive surgical relief for nerve compression if nonoperative measures fail. Limitations of a surgical solution include that the more immediate pain relief possible by decompression and the benefit of shorter recovery times do not reliably apply to patients with chronic LBP or chronic sciatica, and acute LBP (known as reversible conditions that have pain of a directed nature); non-operative care appears to afford more rapid recovery in these latter situations. The average long-term recovery following surgery, 73% (with 74% of these postoperative patients complaining of continued mild to moderate LBP pain)146 is similar to Weber's141 finding for longer-term recovery of nonoperative therapy; one would hope that the risks and discomfort of operative solutions would offer a longer benefit overall, but this cannot be said at this time. However, because the indication for surgery in the former study146 mainly was for leg pain, to focus on less than superior results for LBP may be an unfair assessment. Another limitation of surgery is that there appears to be a window of 4 to 6 months or possibly 1 year from onset, beyond which benefits from surgery may be less reliable.102 Although the short-term surgical benefits are attractive and extend beyond pain relief to early work benefits for the vast majority of properly selected patients (85-95%), authors of an older study suggested the results may deteriorate with time, reducing that percentage to 55% to 70%, with some patients possibly headed for re-operation.114

The goal of minimizing soft tissue trauma is laudable and microdiscectomy is used more commonly. Arthros-copy, which has become the standard of care for soft tissue knee derangements, offers benefits over open surgery but a less than optimal rate of good outcome in spine surgery has prevented it from acquiring a similar standard of care position.

There also are limitations of nonoperative therapies, one of them being the wide qualitative differences among them, which make combinatorial efforts limited and difficult to investigate formally. Behavioral therapy and steroid injections benefit some patients but many other techniques seem to have more limited value; and lack of research prevents knowing the conditions under which they may be applied usefully. Some level of general mobility has replaced the previously longstanding “wisdom” of bed rest, although no prospective randomized studies have defined its proper role.34 Physical therapy or exercise has been shown to reduce pain consistently and to limit the amount of work days missed to know it is a reliable form of therapy.112,113 Oral analgesics and muscle relaxants suffer similarly from too little investigation, and although NSAIDS have received the greater attention, both show mixed results and use of either is associated with adverse side effects. Spinal manipulation, massage, and acupuncture cannot be supported by high-level research as to their benefit.128

Multidisciplinary programs may be a cost-prohibitive choice in chronic situations but can be cost-effective for early intervention.129 Investigations into behavioral therapies related to stress factors, depression, and the effects of chronicity may hold the best promise to add new information to the existing nonoperative therapies.131 A major contribution has been to increase awareness that LDH has a greater number of multifactorial components than considered prior to research in this area.

Despite the high prevalence of LDH and numerous studies on the subject, many of the treatment decisions still depend on the art of medicine and clinical expertise. It is difficult to design a decision flow chart that encompasses well all of the different presenting situations. General treatment guidelines included in Figure 1 are an umbrella to the difficult decisions lying within the “stations” of the included flowchart (Fig 1). Specifics of imaging studies and choice of actual treatment is not detailed here. Most practitioners would agree that as long as the patient does not have a progressive or significant neurologic deficit, cauda equina, or severe intractable pain, a minimum of 6 to 8 weeks should be reserved for non-operative treatment. There is no need for immediate radiologic work-up absent “red flags,” and the history and physical examination are consistent with LDH. Nonoperative treatment methods should not extend beyond 4 to 6 months if the patient shows only minimal improvement; the results of surgery are diminished if the patient has surgery past this time and the success rate of nonoperative treatment also declines. The majority of patients treated by nonoperative methods will experience substantial improvement of their symptoms. For the patient who has not improved in the initial 6-week to 8-week period, a radiologic workup should be done and surgical options should be discussed and realistically compared with options and outcomes for continued non-operative care or no further treatment.

Fig 1:
An algorithm for treating LHD is shown.

The ideal is to provide an evidence-based approach to the treatment of LDH and to tailor the specific treatment to the individual patient's spinal pathology, socioeconomic status, and behavioral environment.


1. Abramovitz JN, Neff SR. Lumbar disc surgery: Results of the Prospective Lumbar Discectomy Study of the Joint Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. Neurosurgery. 1991;29:301-307.
2. Advisory Statement. Wrong-site surgery. Available at: Accessed on November 29, 2005.
3. Ahn UM, Ahn NU, Buchowski JM, et al. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine. 2000;25:1515-1522.
4. Ahn Y, Lee SH, Park WM, et al. Percutaneous endoscopic lumbar discectomy for recurrent disc herniation: surgical technique, outcome, and prognostic factors of 43 consecutive cases. Spine. 2004;29:E326-E332.
5. Albert TJ, Balderston RA, Heller JG, et al. Upper lumbar disc herniations. J Spinal Disord. 1993;6:351-359.
6. Andersson GB, Deyo RA. History and physical examination in patients with herniated lumbar discs. Spine. 1996;21:10S-18S.
7. Andrews DW, Lavyne MH. Retrospective analysis of microsurgical and standard lumbar discectomy. Spine. 1990;15:329-335.
8. Assendelft WJ, Morton SC, Yu EI, Suttorp MJ, Shekelle PG. Spinal manipulative therapy for low back pain. Cochrane Database Syst Rev CD000447, 2004.
9. Autio RA, Karppinen J, Kurunlahti M, et al. Effect of periradicular methylprednisolone on spontaneous resorption of intervertebral disc herniations. Spine. 2004;29:1601-1607.
10. Balague F, Nordin M, Sheikhzadeh A, et al. Recovery of severe sciatica. Spine. 1999;24:2516-2524.
11. Barrios C, Ahmed M, Arrotegui J, Bjornsson A, Gillstrom P. Microsurgery versus standard removal of the herniated lumbar disc. A 3-year comparison in 150 cases. Acta Orthop Scand. 1990;61:399-403.
12. BenDebba M, Augustus van Alphen H, Long DM. Association between peridural scar and activity-related pain after lumbar discectomy. Neurol Res. 1999;21 (Suppl 1): S37-S42.
13. Bertagnoli R, Karg A, Voigt S. Lumbar partial disc replacement. Orthop Clin North Am. 2005;36:341-347.
14. Bessette L, Liang MH, Lew RA, Weinstein JN. Classics in Spine. Surgery literature revisited. Spine. 1996;21:259-263.
15. Bigos SJ. Acute low back pain in adults. Rockville, MD, Department of Health Services, Public Health Service, Agency for Health Care Policy and Research, 1994.
16. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg. 1990;72A:403-408.
17. Boelen EJ, van Hooy-Corstjens CS, Bulstra SK, et al. Intrinsically radiopaque hydrogels for nucleus pulposus replacement. Biomaterials. 2005;26:6674-6683.
18. Bookwalter JW III, Busch MD, Nicely D. Ambulatory surgery is safe and effective in radicular disc disease. Spine. 1994;19:526-530.
19. Boos N, Semmer N, Elfering A, et al. Natural history of individuals with asymptomatic disc abnormalities in magnetic resonance imaging: Predictors of low back pain-related medical consultation and work incapacity. Spine. 2000;25:1484-1492.
20. Borenstein DG, O'Mara JW Jr, Boden SD, et al. The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects: A seven-year follow-up study. J Bone Joint Surg. 2001;83A:1306-1311.
21. Brown MD. Update on chemonucleolysis. Spine. 1996;21: 62S-68S.
22. Buckwalter JA. Aging and degeneration of the human intervertebral disc. Spine. 1995;20:1307-1314.
23. Buckwalter JA, Mow VC, Boden SD, Eyre DR, Weidenbaum M. Intervertebral disc Structure, Composition, and Mechanical Function. In: Buckwalter JA, Einhorn TA, Simon SR, eds. Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2000:547.
24. Burton AK, Waddell G, Tillotson KM, Summerton N. Information and advice to patients with back pain can have a positive effect. A randomized controlled trial of a novel educational booklet in primary care. Spine. 1999;24:2484-2491.
25. Bush K, Cowan N, Katz DE, Gishen P. The natural history of sciatica associated with disc pathology. A prospective study with clinical and independent radiologic follow-up. Spine. 1992;17: 1205-1212.
26. Buttermann GR. Treatment of lumbar disc herniation: Epidural steroid injection compared with discectomy. A prospective, randomized study. J Bone Joint Surg. 2004;86A:670-679.
27. Carragee EJ, Kim DH. A prospective analysis of magnetic resonance imaging findings in patients with sciatica and lumbar disc herniation. Correlation of outcomes with disc fragment and canal morphology. Spine. 1997;22:1650-1660.
28. Cherkin DC, Sherman KJ, Deyo RA, Shekelle PG. A review of the evidence for the effectiveness, safety, and cost of acupuncture, massage therapy, and spinal manipulation for back pain. Ann Intern Med. 2003;138:898-906.
29. Clatterbuck RE, Belzberg AJ, Ducker TB. Intradural cervical disc herniation and Brown-Sequard's syndrome. Report of three cases and review of the literature. J Neurosurg Spine. 2000;92:236-240.
30. D'Andrea G, Trillo G, Roperto R, et al. Intradural lumbar disc herniations: The role of MRI in preoperative diagnosis and review of the literature. Neurosurg Rev. 2004;27:75-80.
31. Damkot DK, Pope MH, Lord J, Frymoyer JW. The relationship between work history, work environment and low-back pain in men. Spine. 1984;9:395-399.
32. Dammers R, Koehler PJ. Lumbar disc herniation: Level increases with age. Surg Neurol. 2002;58:209-212.
33. Dandy WE. Loose cartilage from intervertebral disk simulating tumor of the spinal cord. Clin Orthop Relat Res. 1989;238:4-8.
34. Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med. 1986;315:1064-1070.
35. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med. 1990;112:598-603.
36. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268:760-765.
37. Di MA, Vaccaro AR, Lee JY, Denaro V, Lim MR. Nucleus pulposus replacement: Basic science and indications for clinical use. Spine. 2005;30:S16-S22.
38. Epstein NE. Different surgical approaches to far lateral lumbar disc herniations. J Spinal Disord. 1995;8:383-394.
39. Evans W, Jobe W, Seibert C. A cross-sectional prevalence study of lumbar disc degeneration in a working population. Spine. 1989;14:60-64.
40. Faas A, Chavannes AW, van Eijk JT, Gubbels JW. A randomized, placebo-controlled trial of exercise therapy in patients with acute low back pain. Spine. 1993;18:1388-1395.
41. Fisk JW. The straight leg raising test: Its relevance to possible disc pathology. N Z Med J. 1975;81:557-560.
42. Fraser RD, Sandhu A, Gogan WJ. Magnetic resonance imaging findings 10 years after treatment for lumbar disc herniation. Spine. 1995;20:710-714.
43. Frymoyer JW. Back pain and sciatica. N Engl J Med. 1988;318: 291-300.
44. Frymoyer JW. Lumbar disk disease: Epidemiology. Instr Course Lect. 1992;41:217-223.
45. Gaetani P, Aimar E, Panella L, et al. Surgery for herniated lumbar disc disease: Factors influencing outcome measures. An analysis of 403 cases. Funct Neurol. 2004;19:43-49.
46. Gibson JN, Grant IC, Waddell G. The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine. 1999;24:1820-1832.
47. Gilbert JR, Taylor DW, Hildebrand A, Evans C. Clinical trial of common treatments for low back pain in family practice. Br Med J (Clin Res Ed). 1985;291:791-794.
48. Gioia G, Mandelli D, Capaccioni B, Randelli F, Tessari L. Surgical treatment of far lateral lumbar disc herniation. Identification of compressed root and discectomy by lateral approach. Spine. 1999;24:1952-1957.
49. Goddard MD, Reid JD. Movements induced by straight leg raising in the lumbo-sacral roots, nerves and plexus, and in the intrapelvic section of the sciatic nerve. J Neurol Neurosurg Psychiatry. 1965;28:12-18.
50. Goodkin R, Laska LL. Wrong disc space level surgery: Medico-legal implications. Surg Neurol. 2004;61:323-341.
51. Gordon SJ, Yang KH, Mayer PJ, et al. Mechanism of disc rupture. A preliminary report. Spine. 1991;16:450-456.
52. Hadler NM, Curtis P, Gillings DB, Stinnett S. A benefit of spinal manipulation as adjunctive therapy for acute low-back pain: A stratified controlled trial. Spine. 1987;12:702-706.
53. Hanley EN Jr, Shapiro DE. The development of low-back pain after excision of a lumbar disc. J Bone Joint Surg. 1989;71A:719-721.
54. Hansen FR, Biering-Sorensen F, Schroll M. Minnesota Multiphasic Personality Inventory profiles in persons with or without low back pain. A 20-year follow-up study. Spine. 1995;20:2716-2720.
55. Harrison DE, Cailliet R, Harrison DD, Janik TJ, Holland B. Changes in sagittal lumbar configuration with a new method of extension traction: Nonrandomized clinical controlled trial. Arch Phys Med Rehabil. 2002;83:1585-1591.
56. Hatori M, Kokubun S. Clinical use of etodolac for the treatment of lumbar disc herniation. Curr Med Res Opin. 1999;15:193-201.
57. Heliövaara M. Risk factors for low back pain and sciatica. Ann Med. 1989;21:257-264.
58. Herron LD Pheasant HC. Bilateral laminotomy and discectomy for segmental lumbar disc disease. Decompression with stability. Spine. 1983;8:86-97.
59. Herron LD, Turner J, Clancy S, Weiner P. The differential utility of the Minnesota Multiphasic Personality Inventory. A predictor of outcome in lumbar laminectomy for disc herniation versus spinal stenosis. Spine. 1986;11:847-850.
60. Herzog RJ. The radiologic assessment for a lumbar disc herniation. Spine. 1996;21:19S-38S.
61. Hodges SD, Humphreys SC, Eck JC, Covington LA. The surgical treatment of far lateral L3-L4 and L4-L5 disc herniations. A modified technique and outcomes analysis of 25 patients. Spine. 1999;24:1243-1246.
62. Hodges SD, Humphreys SC, Eck JC, Covington LA. The surgical treatment of far lateral L3-L4 and L4-L5 disc herniations. A modified technique and outcomes analysis of 25 patients. Spine. 1999;24:1243-1246.
63. Hoppenfeld S. Physical Examination of the Lumbar Spine. In: Physical Examination of the Spine and Extremities. East Norwalk, CT: Appleton-Century-Crofts; 1976:237.
64. Huang RC, Wright TM, Panjabi MM, Lipman JD. Biomechanics of nonfusion implants. Orthop Clin North Am. 2005;36:271-280.
65. Humphreys SC, Eck JC. Clinical evaluation and treatment options for herniated lumbar disc. Am Fam Physician. 1999;59:575-578.
66. Isaacs RE, Podichetty V, Fessler RG. Microendoscopic discectomy for recurrent disc herniations. Neurosurg Focus. 2003;15: E11.
67. Ito T, Takano Y, Yuasa N. Types of lumbar herniated disc and clinical course. Spine. 2001;26:648-651.
68. Jackson RP, Cain JE Jr, Jacobs RR, Cooper BR, McManus GE. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus: II. A comparison of computed tomography (CT), myelography, CT-myelography, and magnetic resonance imaging. Spine. 1989;14:1362-1367.
69. Jansson KA, Nemeth G, Granath F, Blomqvist P. Surgery for herniation of a lumbar disc in Sweden between 1987 and 1999. An analysis of 27,576 operations. J Bone Joint Surg. 2004;86B:841-847.
70. Jellema P, van Tulder MW, van Poppel MN, Nachemson AL, Bouter LM. Lumbar supports for prevention and treatment of low back pain: A systematic review within the framework of the Cochrane Back Review Group. Spine. 2001;26:377-386.
71. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994;331:69-73.
72. Johnson MG, Errico TJ. Lumbar disc Herniation. In: Fardon DF, Garfin SR, Abitbol JJ, Boden SD, Mayer TG, eds. Orthopedic Knowledge Update: Spine. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2002:323.
73. Jonsson B, Stromqvist B. Clinical appearance of contained and noncontained lumbar disc herniation. J Spinal Disord. 1996;9: 32-38.
74. Joshi A, Fussell G, Thomas J, et al. Functional compressive mechanics of a PVA/PVP nucleus pulposus replacement. Biomaterials. 2006;27:176-184.
75. Joshi A, Mehta S, Vresilovic E, Karduna A, Marcolongo M. Nucleus implant parameters significantly change the compressive stiffness of the human lumbar intervertebral disc. J Biomech Eng. 2005;127:536-540.
76. Kambin P, Savitz MH. Arthroscopic microdiscectomy: An alternative to open disc surgery. Mt Sinai J Med. 2000;67:283-287.
77. Kara B, Tulum Z, Acar U. Functional results and the risk factors of reoperations after lumbar disc surgery. Eur Spine J. 2005;14: 43-48.
78. Karjalainen K, Malmivaara A. van TM, et al. Multidisciplinary biopsychosocial rehabilitation for neck and shoulder pain among working age adults. Cochrane Database Syst Rev. CD002194, 2003.
79. Kawakami M, Tamaki T, Hayashi N, Hashizume H, Nishi H. Possible mechanism of painful radiculopathy in lumbar disc herniation. Clin Orthop Relat Res. 1998;351:241-251.
80. Kelsey JL, White AA III. Epidemiology and impact of low-back pain. Spine. 1980;5:133-142.
81. Kobayashi S, Shizu N, Suzuki Y, Asai T, Yoshizawa H. Changes in nerve root motion and intraradicular blood flow during an intraoperative straight-leg-raising test. Spine. 2003;28:1427-1434.
82. Kobayashi S, Suzuki Y, Asai T, Yoshizawa H. Changes in nerve root motion and intraradicular blood flow during intraoperative femoral nerve stretch test. Report of four cases. J Neurosurg. 2003;99:298-305.
83. Koes BW, Assendelft WJ, van der Heijden GJ, Bouter LM. Spinal manipulation for low back pain. An updated systematic review of randomized clinical trials. Spine. 1996;21:2860-2871.
84. Komori H, Shinomiya K, Nakai O, et al. The natural history of herniated nucleus pulposus with radiculopathy. Spine. 1996;21: 225-229.
85. Kool J, de BR, Oesch P, et al. Exercise reduces sick leave in patients with non-acute non-specific low back pain: A meta-analysis. J Rehabil Med. 2004;36:49-62.
86. Kortelainen P, Puranen J, Koivisto E, Lahde S. Symptoms and signs of sciatica and their relation to the localization of the lumbar disc herniation. Spine. 1985;10:88-92.
87. Kosteljanetz M, Bang F, Schmidt-Olsen S. The clinical significance of straight-leg raising (Lasegue's sign) in the diagnosis of prolapsed lumbar disc. Interobserver variation and correlation with surgical finding. Spine. 1988;13:393-395.
88. la-Kokko L. Genetic risk factors for lumbar disc disease. Ann Med. 2002;34:42-47.
89. Le H, Sandhu FA, Fessler RG. Clinical outcomes after minimal-access surgery for recurrent lumbar disc herniation. Neurosurg Focus. 2003;15:E12.
90. Levy HI, Hanscom B, Boden SD. Three-question depression screener used for lumbar disc herniations and spinal stenosis. Spine. 2002;27:1232-1237.
91. Lewis PJ, Weir BK, Broad RW, Grace MG. Long-term prospective study of lumbosacral discectomy. J Neurosurg. 1987;67:49-53.
92. Long A, Donelson R, Fung T. Does it matter which exercise? A randomized control trial of exercise for low back pain. Spine. 2004;29:2593-2602.
93. Loupasis GA, Stamos K, Katonis PG, et al. Seven-to 20-year outcome of lumbar discectomy. Spine. 1999;24:2313-2317.
94. Lu YM, Hutton WC, Gharpuray VM. Do bending, twisting, and diurnal fluid changes in the disc affect the propensity to prolapse? A viscoelastic finite element model. Spine. 1996;21:2570-2579.
95. Main CJ, Waddell G. Behavioral responses to examination. A reappraisal of the interpretation of ′nonorganic signs. Spine. 1998;23:2367-2371.
96. McCulloch JA. Focus issue on lumbar disc herniation: Macro-and microdiscectomy. Spine. 1996;21:45S-56S.
97. McCulloch JA, Transfeldt EE. Disc Degeneration with Root Irritation: Disc Ruptures. 3rd ed. In: Macnab's Backache. Baltimore, MD: Williams and Wilkins; 1997:500.
98. Middleton GS, Teacher JH. Injury to the spinal cord due to rupture of an intervertebral disc during muscular effort. Glasgow Med J. 2005;76:1-6.
99. Modic MT, Ross JS, Obuchowski NA, et al. Contrast-enhanced MR imaging in acute lumbar radiculopathy: A pilot study of the natural history. Radiology. 1995;195:429-435.
100. Moore RJ, Vernon-Roberts B, Fraser RD, Osti OL, Schembri M. The origin and fate of herniated lumbar intervertebral disc tissue. Spine. 1996;21:2149-2155.
101. Nachemson AL. Disc pressure measurements. Spine. 1981;6: 93-97.
102. Ng LC, Sell P. Predictive value of the duration of sciatica for lumbar discectomy. A prospective cohort study. J Bone Joint Surg. 2004;86B:546-549.
103. Olmarker K, Nutu M, Storkson R. Changes in spontaneous behavior in rats exposed to experimental disc herniation are blocked by selective TNF-alpha inhibition. Spine. 2003;28:1635-1641.
104. Ostelo RW, de Vet HC, Waddell G, et al. Rehabilitation following first-time lumbar disc surgery: A systematic review within the framework of the Cochrane collaboration. Spine. 2003;28:209-218.
105. Pal B, Mangion P, Hossain MA, Diffey BL. A controlled trial of continuous lumbar traction in the treatment of back pain and sciatica. Br J Rheumatol. 1986;25:181-183.
106. Papagelopoulos PJ, Shaughnessy WJ, Ebersold MJ, Bianco AJ Jr, Quast LM. Long-term outcome of lumbar discectomy in children and adolescents sixteen years of age or younger. J Bone Joint Surg. 1998;80A:689-698.
107. Postacchini F, Lami R, Pugliese O. Familial predisposition to discogenic low-back pain. An epidemiologic and immunogenetic study. Spine. 1988;13:1403-1406.
108. Postacchini F. Results of surgery compared with conservative management for lumbar disc herniations. Spine. 1996;21:1383-1387.
109. Postacchini F. Management of herniation of the lumbar disc. J Bone Joint Surg. 1999;81B:567-576.
110. Postacchini F. Lumbar disc herniation: A new equilibrium is needed between nonoperative and operative treatment. Spine. 2001;26:601.
111. Richardson JK, Chung T, Schultz JS, Hurvitz E. A familial predisposition toward lumbar disc injury. Spine. 1997;22:1487-1492.
112. Saal JA. Natural history and nonoperative treatment of lumbar disc herniation. Spine. 1996;21:2S-9S.
113. Saal JA, Saal JS. Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy. An outcome study. Spine. 1989;14:431-437.
114. Salenius P, Laurent LE. Results of operative treatment of lumbar disc herniation. A survey of 886 patients. Acta Orthop Scand. 1977;48:630-634.
115. Sanderson SP, Houten J, Errico T, et al. The unique characteristics of “upper” lumbar disc herniations. Neurosurgery. 2004;55:385-389.
116. Sen O, Kizilkilic O, Aydin MV, et al. The role of closed-suction drainage in preventing epidural fibrosis and its correlation with a new grading system of epidural fibrosis on the basis of MRI. Eur Spine J. 2004;14:409-414.
117. Shapiro S. Medical realities of cauda equina syndrome secondary to lumbar disc herniation. Spine. 2000;25:348-351.
118. Smith SA, Massie JB, Chesnut R, Garfin SR. Straight leg raising. Anatomical effects on the spinal nerve root without and with fusion. Spine. 1993;18:992-999.
119. Solberg TK, Nygaard OP, Sjaavik K, Hofoss D, Ingebrigtsen T. The risk of “getting worse” after lumbar microdiscectomy. Eur Spine J. 2005;14:49-54.
120. Stankovic R, Johnell O. Conservative treatment of acute low back pain. A 5-year follow-up study of two methods of treatment. Spine. 1995;20:469-472.
121. Summers B, Malhan K, Cassar-Pullicino V. Low back pain on passive straight leg raising: the anterior theca as a source of pain. Spine. 2005;30:342-345.
122. Swartz KR, Trost GR. Recurrent lumbar disc herniation. Neurosurg Focus. 2003;15:E10.
123. Tessitore E. Far-lateral lumbar disc herniation: The microsurgical transmuscular approach. Neurosurgery. 2004;54:939-942.
124. Thompson RE, Pearcy MJ, Barker TM. The mechanical effects of intervertebral disc lesions. Clin Biomech (Bristol, Avon). 2004;19: 448-455.
125. Toyone T, Takahashi K, Kitahara H, et al. Visualisation of symptomatic nerve roots. Prospective study of contrast-enhanced MRI in patients with lumbar disc herniation. J Bone Joint Surg. 1993;75B:529-533.
126. Toyone T, Tanaka T, Kato D, Kaneyama R. Low-back pain following surgery for lumbar disc herniation. A prospective study. J Bone Joint Surg. 2004;86A:893-896.
127. Tullberg T, Isacson J, Weidenhielm L. Does microscopic removal of lumbar disc herniation lead to better results than the standard procedure? Results of a one-year randomized study. Spine. 1993;18:24-27.
128. van Tulder MW, Cherkin DC, Berman B, Lao L, Koes BW. The effectiveness of acupuncture in the management of acute and chronic low back pain. A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 1999;24:1113-1123.
129. van Tulder MW, Esmail R, Bombardier C, Koes BW. Back schools for non-specific low back pain. Cochrane Database Syst Rev. CD000261, 2000.
130. van Tulder MW, Malmivaara A, Esmail R, Koes B. Exercise therapy for low back pain: A systematic review within the framework of the Cochrane collaboration back review group. Spine. 2000;25:2784-2796.
131. van Tulder MW, Ostelo R, Vlaeyen JW, et al. Behavioral treatment for chronic low back pain: A systematic review within the framework of the Cochrane Back Review Group. Spine. 2001;26:270-281.
132. van Tulder MW, Scholten RJ, Koes BW, Deyo RA. Nonsteroidal anti-inflammatory drugs for low back pain: A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 2000;25:2501-2513.
133. van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM. Muscle relaxants for nonspecific low back pain: A systematic review within the framework of the Cochrane collaboration. Spine. 2003;28:1978-1992.
134. Vroomen PC, de Krom MC, Knottnerus JA. Diagnostic value of history and physical examination in patients suspected of sciatica due to disc herniation: A systematic review. J Neurol. 1999;246: 899-906.
135. Vroomen PC, de Krom MC, Wilmink JT, Kester AD, Knottnerus JA. Diagnostic value of history and physical examination in patients suspected of lumbosacral nerve root compression. J Neurol Neurosurg Psychiatry. 2002;72:630-634.
136. Vroomen PC, Van Hapert SJ, Van Acker RE, et al. The clinical significance of gadolinium enhancement of lumbar disc herniations and nerve roots on preoperative MRI. Neuroradiology. 1998;40:800-806.
137. Waddell G, Bircher M, Finlayson D, Main CJ. Symptoms and signs: Physical disease or illness behaviour? Br Med J (Clin Res Ed). 1984;289:739-741.
138. Waddell G, Main CJ, Morris EW, Di Paola M, Gray IC. Chronic low-back pain, psychologic distress, and illness behavior. Spine. 1984;9:209-213.
139. Waddell G, McCulloch JA, Kummel E, Venner RM. Nonorganic physical signs in low-back pain. Spine. 1980;5:117-125.
140. Wang JC, Lin E, Brodke DS, Youssef JA. Epidural injections for the treatment of symptomatic lumbar herniated discs. J Spinal Disord Tech. 2002;15:269-272.
142. Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine. 1983;8:131-140.
143. Weber H, Holme I, Amlie E. The natural course of acute sciatica with nerve root symptoms in a double-blind placebo-controlled trial evaluating the effect of piroxicam. Spine. 1993;18:1433-1438.
141. Weber H. The natural history of disc herniation and the influence of intervention. Spine. 1994;19:2234-2238.
144. Wetzel FT, Donelson R. The role of repeated end-range/pain response assessment in the management of symptomatic lumbar discs. Spine J. 2003;3:146-154.
145. Wiese M, Kramer J, Bernsmann K, Ernst WR. The related outcome and complication rate in primary lumbar microscopic disc surgery depending on the surgeon's experience: Comparative studies. Spine J. 2004;4:550-556.
146. Yorimitsu E, Chiba K, Toyama Y, Hirabayashi K. Long-term outcomes of standard discectomy for lumbar disc herniation: A follow-up study of more than 10 years. Spine. 2001;26:652-657.
147. Zentner J, Schneider B, Schramm J. Efficacy of conservative treatment of lumbar disc herniation. J Neurosurg Sci. 1997;41:263-268.
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