Lumbar spondylosis
DR KS Dhillon
Introduction
Terms such as lumbar osteoarthritis, degenerative disc disease, and lumbar spondylosis are used to describe changes that occur in the vertebral bodies and intervertebral disk spaces.
Spinal osteoarthritis (OA) is a degenerative process that is defined radiologically by disc space narrowing, osteophytosis, subchondral sclerosis, and cyst formation [1]. There are two types of osteophytes [2]. The first is spondylosis deformans. These are bony outgrowths arising primarily along the anterior and lateral perimeters of the vertebral end-plate apophyses. These osteophytes are believed to develop at sites of stress to the annular ligament. They most often occur at thoracic T9–10 and lumbar L3 levels [3]. These osteophytes are usually asymptomatic. Rarely they can cause complications that arise due to their close anatomic relationship to organs that are anterior to the spine [3].
The second type of osteophytes are known as intervertebral osteochondrosis. These are more pathological end-plate osteophytes that are associated with disc space narrowing, vacuum phenomenon, and vertebral body reactive changes [4]. If these osteophytes protrude within the spinal canal or intervertebral foramina they can compress nerves with resulting radiculopathy or cause spinal stenosis. They can also limit joint mobility.
Degenerative disk disease (DDD) refers to symptoms of back pain that are attributable to intervertebral disc degeneration. Pathologic changes in disc degeneration include disk desiccation, fibrosis, and disc space narrowing. The annulus may bulge, undergo fissuring, or mucinous degeneration. In addition there are defects and sclerosis of the end-plates, and osteophytes at the vertebral apophyses [4]. With these changes included in the radiographic description of both OA and DDD, there exists diagnostic overlap between the conditions and hence these terms are often used interchangeably in the medical literature.
Spondylosis of the lumbar spine is a term with many definitions. It is employed synonymously with arthrosis, hypertrophic arthritis, spondylitis, and osteoarthritis. Spondylosis is often applied nonspecifically to any and all degenerative conditions affecting the discs, vertebral bodies, and/or facet joints of the lumbar spine [5,6].
Epidemiology
Degenerative changes in the lumbar spine are very common. Symmons’ et al. [7] in a study of individuals aged 45–64 years found that 85.5% of the participants had osteophytes in the lumbar spine.
O’Neill et al. [8] in a study of UK adult population over age 50 years, found that 84% of men and 74% of women demonstrated at least one vertebral osteophyte. The incidence was higher among individuals with more physical activity, self reported back pain, or higher BMI scores. Men have more significant degenerative changes than women, both with regard to severity and number of osteophyte formation [8].
Radiographic evidence of degenerative disease of the lumbar spine among asymptomatic individuals is high. Jensen et al [9] carried out MRI imaging of the lumbar spine in asymptomatic patients over the age of 60 years and found disc protrusions in 80% of the individuals and degenerative spinal stenosis in 20% of the individuals.
A study by Frymoyer et al [10] compared radiographic evidence of spine degeneration among categories of men who were without pain, with moderate pain, or with severe lower back pain and they found that frequency of disc space narrowing and bone spurs among all three groups was the same.
Degenerative changes can even appear in young individuals without decades of spine axis loading. Lawrence [11] found disc degeneration in 10% of women aged 20–29.
Lumbar spondylosis affects 80% of patients older then 40 years, and in 3% of individuals aged 20–29 years [3].
The prevalence of radiographic spondylosis increases as we age. In the first few decades of life it is present in a small percentage of the population but is common by the age of 65 years . In individuals with low back pain, the prevalence ranges from 7% to 75%, depending on the diagnostic criteria used. Despite this high prevalence in patients with low back pain, there is no validated correlation between radiographic presence of lumbar spondylosis and the presence of low back pain. Age is the greatest risk factor for spondylosis. Other possibilities include previous injury, disc desiccation, joint overload from malalignment and/or abnormal facet joint orientation, and genetic predisposition. There is no clear correlation between lumbar spondylosis and body mass index (BMI), level of activity, and gender [3].
Pathogenesis
Kirkaldy Willis and Bernard [12] first coined the term ‘‘degenerative cascade’’. It consists of three overlapping phases that may occur over the course of decades. Phase I, called the dysfunction phase, describes the initial effects of repetitive microtrauma to the disc with the development of circumferential painful tears of the outer innervated annulus, and associated endplate separation. Endplate separation may compromise disc nutritional supply and waste removal. Such tears coalesce to become radial tears that make the disc more prone to protrusion. These tears affect the disc’s capacity to maintain water leading to desiccation and reduced disc height. Ingrowing of vascular tissue and nerve endings into the fissures can increase the disc’s capacity for pain signal transmission [13].
Phase II known as the instability phase is characterized by the loss of mechanical integrity of the disc. There are progressive disc changes of internal disruption, resorption, and additional annular tears. These changes are combined with further facet degeneration. This can induce subluxation of the vertebrae and instability.
During Phase III, also known as stabilization phase, the disc space continues to narrow and fibrosis occurs along with the formation of osteophytes and transdiscal bridging occurs [14].
With disc space narrowing the adjacent pedicles approximate leading to a narrowing of the superior–inferior dimension of the intervertebral canal. This produces redundancy of the longitudinal ligaments and cause bulging of the ligamentum flavum, leading to laxity and instability of the spine.
This laxity leads to Increased spine movements that permits subluxation of the superior articular process. This subluxation can cause narrowing of the anteroposterior dimension of the intervertebral and upper nerve root canals.
Laxity of the spinal column can also alter weight distribution on the vertebrae and joint spaces leading to osteophyte formation and facet hypertrophy. The hypertrophied facets can project into the intervertebral canal and the central canal. Oblique orientation of the articular processes can cause retrospondylolisthesis, leading to anterior encroachment of the spinal canal, nerve root canal, and intervertebral canal [5].
Osteophytes are formed at periosteum through the proliferation of peripheral articular cartilage which subsequently undergoes endochondral calcification and ossification [15]. Mesenchymal stem cells of the synovium or periosteum are likely precursors. Synovial macrophages and growth factors and extracellular matrix molecules act as mediators in this process [16].
Clinical presentation of lumbar spondylosis
Nociceptive pain generators have been identified within facet joints, intervertebral discs, sacroiliac joints, nerve root dura, and myofascial structures around the spine [17]. Hence there can be pain within the axial spine at the site of degeneration of the spine.
Besides back pain, patients with lumbar spondylosis can present with radiculopathy or spinal stenosis. Clinical presentations of radiculopathy can result from many sources in patients with spondylosis. Bulging discs can affect the descending rootlets of the cauda equina, nerve roots, and the spinal nerve within its ventral ramus, if protruding centrally, posterolaterally, or laterally respectively [18].
Osteophytes on the posterior aspect of vertebral bodies, along upper or lower margins, can also affect the rootlets, nerve roots and the spinal nerve.
Hypertrophic changes to the superior articular process can compress the nerve roots within the upper nerve root canal, dural sac, or prior to exiting from the next lower intervertebral canal. A 70% reduction or 30% residual diameter of the neuroforaminal space is regarded as the critical amount of occlusion needed to induce neural compromise [3]. Compression of the posterior disc to less than 4 mm height, or the foraminal height to less than 15 mm has also been found to be the critical dimensions for foraminal stenosis and nerve impingement [19].
The degenerative anatomical changes can cause narrowing of the spinal canal leading to a clinical presentation of spinal stenosis. Progressive ingrowth of osteophytes, hypertrophy of the inferior articular process, disc herniation, bulging of the ligamentum flavum or degenerative spondylolisthesis can produce canal narrowing. The spinal stenosis can produce neurogenic claudication. Neurogenic claudication can produce low back pain, leg pain, as well as numbness and weakness of the lower limbs that worsen with standing and walking, and improve with sitting and supine positioning.
Risk factors
What are the factors that mediate degenerative progression in the spine? What leads to a large portion of the population developing spondylosis, even early in their lives? Answers to these questions can help to broaden treatment options.
1. The influence of age
There are large studies of osteoarthritis which have recognized that the aging process is the strongest risk factor for bony degeneration, particularly in the spine [20]. An extensive autopsy study by Heine in 1926 reported that spondylitis deformans increases in a linear fashion from 0% to 72% between the ages of 39 and 70 years [21]. A subsequent autopsy study by Miller et al. [23] also showed an increase in disc degeneration from 16% at age 20 to about 98% at age 70 years. There are other studies which corroborate this finding [8,23].
Several studies have demonstrated the presence of significant lumbar degeneration to be evident even within the first two decades of life [22,23].
There is variability, within members of the same age, in the presence and extent of degenerative changes in the spine. This variability suggests the influence of other contributing factors.
2.The impact of activity and occupation
Disc degeneration is associated with certain activities. The likelihood and severity of spondylosis is associated with several factors such as Body Mass Index, back trauma, daily spine loading by twisting, lifting, bending, and sustained nonneutral postures, and whole body vibration from vehicular driving [8,24].
Though these correlations exist, a study by Hassett et al [25] did not find significant associations of lumbar spondylosis with the extent of physical activity. They found that only age, back pain, and associated hip OA to be predictive of degenerative spine disease and osteophyte changes [25].
3. The role of heredity
Genetic factors are known to influence disc degeneration and the formation of osteophytes. According to Spector and MacGregor [26] classic twin studies have shown that the influence of genetic factors is between 39% and 65% in radiographic OA of the hand and knee in women, about 60% in OA of the hip, and about 70% in OA of the spine. Taken together, these estimates suggest a heritability of OA of 50% or more. This indicates that half the variation in susceptibility to disease in the population is explained by genetic factors.
Similarly, studies of degenerative changes in lumbar spine on MRI imaging in twins showed that approximately 47% to 66% of the variance could be explained by genetic and environmental factors, and only 2% to 10% of variance can be attributed to physical loading and resistance training [27].
Another twin study by Battié et al [28] revealed a high degree of similarity in disc space narrowing, signal intensity, disk bulging, and end-plate changes.
A study by Videman et al [29] found that specific vitamin D receptor alleles were associated with intervertebral disc degeneration as measured by T2-weighted signal intensity on MRI. They demonstrated for the first time, the existence of genetic susceptibility to this progressive, age-related degenerative process.
4. A functional adaptation?
There have been questions as to whether osteophyte formation is inherently pathological? An osteophyte is a fibrocartilage-capped bony outgrowth. There are three types of osteophytes namely the traction spur at the insertion of tendons and ligaments, the inflammatory spur as seen in ankylosing spondylitis, and the genuine osteophyte or osteochondrophyte (chondro-osteophyte) that arises in the periosteum overlying the bone at the junction between cartilage and bone [30].
van der Kraan and van den Berg [31] were of the opinion that osteophyte formation may represent a remodeling process and the osteophytes functionally adapt to the instability of the spine and the changes in the demands of the spine.
Osteophytes can form in the absence of other degenerative processes, and cartilaginous damage can exist without corresponding osteophytes [31]. Although there exists a strong association between the presence of osteophytes and other degenerative changes in the spine, isolated instances of one without the other can occur.
Diagnostic approach
Patients who present with low back pain (LBP) are initially evaluated by taking a good history and through physical examination. Plain x rays of the spine will show the level of the degenerative changes. Pain x rays can be supplemented with CT, CT myelogram, or MRI of the spine to localize a degenerative lesion and the area of nerve compression.
In the absence of clear disc herniation or neurological deficit, imaging can only identify the underlying cause of LBP in 15% of patients [13]. Frequently, there is no correlation between the symptom severity and the degree of anatomical or radiographic changes [6].
There is, however, some correlation between the number and severity of osteophytes and back pain [8,10]. The prevalence of degenerative changes among asymptomatic patients makes it difficult to assign clinical relevance to observed radiographic changes in patients with LBP.
In patients with nerve compression symptoms, the presence of nerve compression can be confirmed by electromyographic studies. Diagnostic injections can help to localize the nerve compression by isolating and anesthetizing irritated nerve roots (via epidural), or by blocking suspected pain generators within facet joints, sacroiliac joints, or the disc space itself by discography [32].
Treatment options
We have limited ability to isolate the cause of chronic lower back pain, hence the difficulty in reaching a consensus with regard to a definitive treatment approach. There is substantial variation in management of back pain by conservative and invasive approaches between practitioners [33]. There are four main treatment options for the treatment of chronic low back pain. These include physical therapy (exercise and behavioral intervention), pharmacotherapy, injection therapy, and surgical intervention.
1.Exercise and behavioral interventions
Exercise therapy (ET)
One of the conservative mainstays of treatment for chronic lumbar spine pain is exercise therapy. It includes aerobic exercise, muscle strengthening, and stretching exercises [33]. There are significant variations in regimen, intensity, and frequency of prescribed exercise programs [34]. One meta-analysis of the current literature that explored the role of ET in patients with varying duration of symptoms found that a graded exercise program implemented within the occupational setting demonstrated effectiveness in subacute low back pain (LBP). In patients suffering from chronic pain symptoms, there was a small, but statistically significant improvement of pain and functional improvement [32].
The best exercise therapy for chronic low back appears to be regimens involving an individually designed exercise program emphasizing stretching and muscle strengthening, with high frequency and close supervision and adherence. Exercise therapy is complemented by other conservative approaches, such as manual therapies, NSAIDS and daily physical activity [34].
Transcutaneous electrical nerve stimulation (TENS)
A ‘‘TENS’’ unit consists of skin surface electrodes that deliver electrical stimulation to peripheral nerves to relieve pain noninvasively. Such devices are usually available in outpatient exercise therapy settings. Upto a third of patients experience mild skin irritation following treatment [35].
A systematic review by Milne et al [36] to determine the efficacy of TENS in the treatment of chronic LBP found no evidence to support the use of TENS in the treatment of chronic low back pain.
In 2008 Khadilkar et al [37] carried out a Cochrane systematic review to determine whether TENS is more effective than placebo for the management of chronic LBP. They found that the evidence from a small number of placebo-controlled trials does not support the use of TENS in the routine management of chronic LBP.
Back school
The back school was first introduced in Sweden with the purpose of treating low back pain and recurrence of back pain through review with patients about the concepts of posture, ergonomics, and appropriate back exercises [38].
There are two meta-analyses which concluded that there is moderate evidence for improvement of both pain and functional status in patients with chronic low back pain within short and intermediate time courses, when measured against other modalities such as joint manipulation, exercise, myofascial therapy, and or other educational therapy [38,39].
Lumbar supports
Lumbar back supports can provide benefit to patients suffering chronic LBP due to lumbar spondylosis through several potential, debated mechanisms. Supports limit spine motion, stabilize, correct deformity, and reduce mechanical forces on the spine. The supports can also help by providing beneficial heat to the back. The supports, however, may also function as a placebo.
There is moderate evidence available that lumbar supports are not more effective then other forms of treatment of patients with acute, subacute, and chronic LBP. The data is conflicting with regard to patient improvement and functional ability to return to work [39].
Traction
Lumbar or pelvic traction applies a longitudinal force to the axial spine through use of a harness attached to the iliac crest, with weights attached at the edge of the bed, to relieve chronic low back pain. The forces open intervertebral space and decrease spine lordosis. The traction temporarily realigns the spine to improve symptoms related to degenerative disease of the spine by relieving nerve compression, mechanical stress, and adhesions of the facet and annulus. The traction also disrupts nociceptive pain signals [39].
However, studies show that patients with chronic symptoms and radicular pain have not found traction to provide significant improvement in daily functioning nor pain [40,41,42].
Spine manipulation
Spine manipulation involves low-velocity, long lever manipulation of the spine beyond the accustomed range of motion. The precise mechanism by which it helps improve the back pain remains unclear. There are several ways in which manipulative therapy may function. These include release of entrapped synovial folds, unbuckling of motion segments that have undergone disproportionate displacement, reduction of disc bulge, relaxation of hypertonic muscle, change in neurophysiological function, disruption of articular or periarticular adhesion, repositioning of miniscule structures within the articular surface, mechanical stimulation of nociceptive joint fibers, and reduction of muscle spasm [43].
Available research shows that spinal manipulation is more effective compared to sham manipulation of the spine with regard to both short- and long-term relief of pain, as well as short term functional improvement [39]. Spinal manipulation appears to be comparable in its effectiveness both in short- and long-term to other conventional, conservative treatment approaches such as exercise therapy, back school, and NSAID [39,44].
Spinal manipulation among trained therapists is relatively safe with a very low risk of complications. Worsened disk herniation or cauda equina syndrome occurring in fewer than 1 in 3.7 million has been reported [45].
Massage therapy
Massage therapy appears to provide some beneficial relief in patients with chronic low back pain. When compared with other interventions, it has proved to be less efficacious than TENS and manipulation. Its efficacy is comparable with corsets and exercise regimens. It is superior to acupuncture and other relaxation therapies, when followed over a period of one year. Such preliminary results, however, need confirmation, and evaluation for cost-effectiveness. Massage therapy nevertheless has a potential role in patients who are interested in it [46].
Multidisciplinary back therapy: the biopsychosocial approach
Psychopathology has been recognized for its association with chronic spinal pain, and, when untreated, it can compromise management efforts of spinal pain. Patients with spinal pain can find relief through learned cognitive strategies known as behavioral, or bio-psychosocial therapy.
These strategies include reinforcement, modifying expectations, relaxation techniques, and control of physiological responses aimed at reducing the patient’s perception of disability and pain. To date, evidence is limited with regard to the efficacy of these strategies [47].
Pharmacotherapy
Patients with low back pain often require medications to complement nonpharmacologic interventions. Extensive research effort has gone into exploration to assess the efficacy of different oral medications in the management of low back pain secondary to lumbar spondylosis. There, however, remains no clear consensus regarding the gold-standard approach to pharmacologic management of chronic back pain [48].
1.NSAIDS
NSAIDs are essentially the first step in the pharmacological treatment of chronic low back pain. NSAIDs are used for their analgesic and anti-inflammatory effects.
There have been several studies that have compared the effectiveness of NSAIDs for low back pain versus placebo. Nine studies have been identified [53]. Two studies reported on low back pain without radiation [54, 55], two on sciatica [56,57], and the other five on a mixed population.
There was conflicting evidence that NSAIDs provide better pain relief than placebo in LBP. Six of the nine studies which compared NSAIDs with placebo for LBP reported dichotomous data on global improvement [53]. The pooled RR for global improvement after 1 week using the fixed effects model was 1.24, indicating a statistically significant effect in favour of NSAIDs compared to placebo.
Two studies reported no difference between NSAIDs and paracetamol [58,59]. There is conflicting evidence that NSAIDs are more effective than paracetamol for acute LBP.
There are six studies that report effectiveness of NSAIDs versus other drugs. Five of them did not find any differences between NSAIDs and narcotic analgesics or muscle relaxants [53]. These studies had small numbers of patients and lacked power to detect a statistically significant difference. There is only moderate evidence that NSAIDs are not more effective than other drugs for treatment of acute LBP.
One small cross-over study (n=37) found that naproxen sodium 275 mg bd decreased pain more than placebo at 14 days [60]. There are other studies that show that NSAIDS are effective in treatment of chronic low back pain [49-52]. The use of NSAIDS is most commonly limited by gastrointestinal (GI) side effects.
There are four trials that compared COX2 inhibitors versus placebo for the treatment of low back pain. The studies showed that there is strong evidence that COX2 inhibitors (etoricoxib, rofecoxib and valdecoxib) decreased pain and improved function compared with placebo at 4 and 12 weeks [53]. COX2 inhibitors elicit fewer GI complications, but their use has been restricted due to evidence of increased cardiovascular risk (myocardial infarction and stroke) with prolonged use [61].
2.Opioid medications
Patients who have poor control of pain with NSAIDs and in patients who cannot take NSAIDs due to gastrointestinal side effects opioid medications may be considered as an alternative. Between 3% to 66% of patients with chronic low back take some form of opioids [62].
There are two meta-analyses that showed a modest short-term benefit of opioid use for treatment of chronic LBP. The studies were of limited quality. There was a high rate of tolerance and abuse associated with long-term narcotic use [48,62].
3.Antidepressants
There were 2 systematic reviews that studied the effectiveness of antidepressants for chronic LBP versus placebo [63,64]. There were a total of nine trials in the reviews. One of the reviews found that antidepressants significantly increased pain relief compared with placebo but found no significant difference in function [63]. The other review did not statistically pool data but found similar results [64].
Adverse effects of antidepressants include drowsiness, dry mouth, urinary retention, constipation, orthostatic hypotension, and mania [65]. One randomised control trial found that the prevalence of insomnia, dry mouth, sedation, and orthostatic symptoms was 60–80% with tricyclic antidepressants [66]. The rates, however, were only slightly lower in the placebo group and none of the differences were significant.
4.Muscle relaxants
The term muscle relaxants is very broad and includes a wide range of drugs with different mechanisms of action and indications. Muscle relaxants can be divided into two categories: antispasticity and antispasmodic medications.
Antispasmodics can be further subclassified into benzodiazepines and non-benzodiazepines.
Three studies that have evaluated the efficacy of benzodiazepines versus placebo for the treatment of chronic low back pain [67,68,69]. Two high quality trials showed that there is strong evidence that tetrazepam 50 mg t.i.d. is more effective than placebo for short-term pain relief and overall improvement [67,69]. One of the studies showed that there is moderate evidence that tetrazepam is more effective than placebo on short-term decrease of muscle spasm [67].
There are three studies that evaluated the efficacy of non-benzodiazepines versus placebo [70,71,72]. One high quality trial showed that there is moderate evidence that flupirtine is more effective than placebo for patients with chronic low back pain for short-term pain relief and overall improvement after 7 days, but not on reduction of muscle spasm [72]. One high quality trial showed that there is moderate evidence that tolperisone is more effective than placebo for patients with chronic low back pain for short-term overall improvement after 21 days, but not for pain relief and reduction of muscle spasm [71].
Strong evidence from eight trials on acute LBP (724 people) showed that muscle relaxants are associated with more adverse effects and central nervous system adverse effects than placebo, but not with more gastrointestinal adverse effects [53]. The most common adverse events involving the central nervous system were drowsiness and dizziness. For the gastrointestinal tract it was nausea.
Antispasticity medications such as baclofen and dantrolene are used for spastic, upper motor neuron syndromes. They are used to reduce spasticity that interferes with therapy or function, such as in cerebral palsy, multiple sclerosis, and spinal cord injuries. The mechanism of action of the antispasticity drugs within the peripheral nervous system is the blockade of the sarcoplasmic reticulum calcium channel. This blockade reduces the calcium concentration and diminishes actin–myosin interaction.
Two high quality trials showed that there is strong evidence that antispasticity muscle relaxants are more effective than placebo for patients with acute low back pain on short-term pain relief and reduction of muscle spasm after 4 days [73,74]. One high quality trial showed moderate evidence on short-term pain relief, reduction of muscle spasm, and overall improvement after 10 days [74].
Injection therapy
1.Epidural steroid injections
Epidural steroid injections (ESI) have become a common interventional strategy in the treatment of chronic axial and radicular pain due to lumbar spondylosis. These injections can be performed through transforaminal, interlaminar, or caudal approaches. The needles for injection are guided under fluoroscopy, and then contrast is injected to localise the tip of the needle. Once the appropriate location is reached, then local anesthetic and steroid are infused into the epidural space at the target vertebral level and the infusion will bathe the exiting nerve roots.
Symptomatic relief occurs through complementary mechanisms whereby the local anesthetics provide quick diagnostic confirmation, and therapeutically it short circuits the pain spasm cycle and blocks pain signal transmission [75]. Corticosteroids on the other hand reduce inflammation through blockade of pro-inflammatory mediators.
In less then a decade (1998–2005), the number of ESI procedures performed have increased by 121% [75]. Despite this widespread use, controversy remains regarding the efficacy of these injections. The procedure is also expensive and can be associated with infrequent but potential risks related to needle placement as well as adverse medication reactions.
There are wide ranges in reported success rates in literature due to variation in study designs, small cohorts, distinct procedural techniques, and imperfect control groups [76].
Prior to the year 2000, few efficacy studies of lumbar epidural steroid injection utilized fluoroscopy to establish needle position. Without fluoroscopic guidance confirmation, needle position is often wrong in 25% of cases [77].
Abdi et al [78] carried out a systematic review to study the efficacy of epidural steroids in the management of chronic spinal pain. They concluded that there is strong evidence for short-term pain relief and limited benefit for long-term following interlaminar steroid injection. They also found that for transforaminal injection of steroids for unilateral sciatica there was strong evidence for short-term, and moderate evidence for long-term pain relief and functional improvement.
Vad et al. [79] studied 48 patients with herniated disc with radicular pain, who were treated with transforaminal steroid injection versus trigger point injections. They found 84% improvement in functional scoring compared with 48% in the control group at follow-up period of 1 year.
Lutz et al. [80] treated a cohort of 69 patients, who had a herniated disc with radicular pain, with transforaminal steroid injection. The patients were followed up for 80 weeks. Seventy five percent of the patients had a successful long-term outcome, which was defined as a 50% reduction in pain scores as well as an ability to return to or near their previous levels of functioning.
In patients with spinal stenosis, transforaminal steroid injections can produce a 50% pain reduction, improve walking, and improve standing tolerance in symptomatic patients at upto 1 year follow-up [81].
Two prospective trials by Riew et al [82,83] and 1 trial by Yang et al [84]
found that patients with severe lumbar radiculopathies and spinal stenosis treated with transforaminal steroid injections experienced sustained functional and symptomatic benefits and they could avoid intended surgical intervention.
2.Facet injection
Facet joints are diarthrodial articulations between adjacent vertebrae.
They are innervated by the medial branches of the dorsal rami. Inflammation to these joints create pain signals in 15–45% of patients with low back pain [13]. For diagnosis local anesthesia is injected directly into the joint space or associated medial branch.
Retrospective and prospective systematic reviews of trials reveal that single diagnostic facet blocks carry a false positive rate of 22% to 47% [85] and medial branch blocks carry false positive rate of 17–47% [86].
Systematic reviews show that there is moderate evidence available for short-term and long-term pain relief with facet blocks [87].
A randomised controlled by Fuch et al [88] showed significant pain relief, functional improvement, and quality of life enhancement at 3 and 6 month intervals. On the other hand, a trial by Carette et al. [89] found no meaningful difference in benefit between patients treated with steroid versus saline injection at 3 and 6 month intervals.
A randomised controlled trial by Manchikanti et al [90] showed significant improvement in overall health status with improvement not only in pain relief, but also with physical, functional, and psychological status, as well as return-to-work status following medial nerve block, with 1–3 injections in 100% patients at 3 months, 75–88% at 6 months, and 17–25% at 1 year.
3.SI joint injections
The sacroiliac joint space is innervated by both myelinated and unmyelinated axons. Injury to or inflammation of the joint produces pain signals which are implicated in 10% to 27% of patients with low back pain [13]. The pain can radiate to the buttocks, groin, and thigh.
There is moderate evidence that support the use of diagnostic and therapeutic blocks of the SI joint [13].
Pereira et al [91] treated 10 patients with MRI-guided bilateral SI joint injections of steroid. Eight of them reported good to excellent pain relief persisting through 13 months followup.
Maugers et al [92] compared corticosteroid injection versus placebo injections under fluoroscopic guidance in SI joints of 10 patients with pain.
They found that only patients in the steroid group reported benefit from the injection. That benefit, however, waned slowly over time, from 70% of patients at 1 month, to 62% at 3 months, and 58% at 6 months.
A systematic review of sacroiliac interventions by Hansen et al [93] showed that the evidence for the specificity and validity of diagnostic sacroiliac joint injections is moderate. The evidence for accuracy of provocative maneuvers in diagnosis of sacroiliac joint pain is limited and the evidence for therapeutic intraarticular sacroiliac joint injections is also limited. They also found that the evidence for radiofrequency neurotomy in managing chronic sacroiliac joint pain is also limited.
In cases of epidural steroid injections, facet, and sacroiliac injections, the diagnostic injections should be considered at intervals of no sooner than 1–2 weeks apart. Therapeutic injections can be performed at most every 2 to 3 months, provided the patient experiences greater than 50% relief within 6 weeks [13].
4.Discal nonoperative therapies for discogenic pain
In 39% of patients with chronic low back pain the source of the pain is discogenic pain. When noninvasive imaging has failed to identify the source of pain, the damaged disc is identified by discography. To perform discography fluid is injected into the disc in an attempt to reproduce patient symptoms. The use of this technique remains controversial since there is significant potential for false positives.
After the diseased disc is identified, there are several treatment options available. Besides surgery, there are minimally invasive options available. Intradiscal electrothermal therapy or radiofrequency posterior annuloplasty can be carried out by placement of an electrode into the disc. Heat that is produced and the electrical current coagulates the posterior annulus, thereby strengthening the collagen fibers, denature inflammatory exudates, and coagulate nociceptors [13]. Current evidence, however, provides moderate support for intradiscal electrothermal therapy in patients with discogenic pain. Preliminary studies of radiofrequency posterior annuloplasty provide limited support for short term relief, with indeterminate long-term value. Both these procedures can be associated with complications that include catheter malfunction, nerve root injuries, postprocedure disk herniation, and infection [13].
5.Operative treatment
Surgical interventions are considered for patients when conservative treatment fails. Surgical options include spinal fusion, spinal decompression or both.
Spinal fusion is usually done in patients with malalignment or excessive motion of the spine, as seen in patients with degenerative disease of the spine and spondylolisthesis.
Decompression surgery is indicated in patients with evidence of neural impingement. Despite dramatic increases in the number of procedures performed on the spine over the last several decades, there remains controversy as to the efficacy of these procedures in resolving chronic low back.
Controversy arises due to the inherent challenges of comparing the available research. Systematic reviews show that there is heterogeneity of current trials that evaluate different surgical techniques with differing comparison groups and limited follow-up. The trials are frequently not patient-centered and do not have pain outcomes included [6].
There are some case series that show promising results [94]. A recent meta-analysis of 31 randomized controlled trials, concluded that there is no clear evidence about the most effective technique of decompression for spinal stenosis or the extent of decompression needed.
There is limited evidence that adjunct fusion to supplement decompression for degenerative spondylolisthesis produces less progressive slip and better clinical outcomes. Another review noted that there is no statistically significant improvement in patients undergoing fusion compared with nonsurgical interventions.
Spinal fusion is the most commonly performed surgical procedure for treatment of lumbar spondylosis [95]. The basis for spinal fusion is that painful diarthrodial joints or joint deformities can be successfully treated by
arthrodesis [95]. It was first introduced in 1911 by Albee [96] and Hibbs [97]. Spinal fusion was initially only used to treat spinal infections and high-grade spondylolisthesis. Later it was used to treat fractures and spinal deformities. Now about 75% of the spinal fusions are carried out for painful degenerative disorders [95].
Although spinal fusion for lumbar spondylosis is carried out frequently, there still is no good scientific evidence of its clinical effectiveness [95,98,99,100]. It was believed for a long time that the outcome of spinal fusions could be significantly improved when the fusion rates come close to 100%. However, it is now quite clear that the outcome is not closely linked to the fusion status [98,99,100,101,102,103].
Spinal fusion is usually recommended when an adequate trial of non-operative treatment has failed to improve the patient’s pain or functional limitations [104,105]. There is, however, no general consensus in the literature on what actually comprises an adequate trial of non-operative care.
A meta-analysis by van Tulder et al. [105] came to the conclusion that fusion surgery can be considered only in carefully selected patients after active rehabilitation programs for a period of 2 years have failed to relieve symptoms. The philosophy that surgery is only indicated if long-term non-operative care has failed has been challenged by the finding that the longer pain persists the less likely it is for the pain to disappear. This is supported by recent advances in our understanding of the pathways of chronic pain and molecular biology of chronic pain. It is well known that returning to work becomes very unlikely after 2 years [106].
Some of the favourable indications for surgery include [107]:
- severe structural alterations
- short duration of persistent symptoms (< 6 months)
- one or two-level disease
- absence of risk factor flags
- clinical symptoms concordant with the structural correlate
- highly motivated patient)
- positive pain provocation and/or pain relief tests
- initial response to a rehab program but frequent
- recurrent episodes
The challenge in spinal fusion is to bridge an anatomic region of the spine with bone that is not normally supported by a viable bone [108].
There are several ways by which the fusion can be achieved. Spinal arthrodesis can be generated by a fusion of [107]:
- adjacent laminae and spinous processes
- facet joints
- transverse processes
- intervertebral disc space
Fusion of the transverse processes is the most common type of fusion performed [109]. The success of intertransverse fusion over posterior fusion (fusion of the laminae and spinous processes) is due the blood supply at the fusion bed which allows for revascularization and reossification of the graft [110].
In a single blinded randomized clinical trial by Brox et al [111] the effectiveness of lumbar instrumented fusion was compared with cognitive intervention and exercises in patients with chronic low-back pain and disc degeneration. They found no significant differences between the two groups in terms of subjective outcome or disability. The authors concluded that the main outcome measure showed equal improvement in patients with chronic low-back pain and disc degeneration who were randomized to cognitive intervention and exercises or lumbar fusion. Spinal fusion and intensive rehabilitation achieve similar outcomes.
Patients with chronic low-back pain who followed cognitive intervention and exercise programmes improved significantly in muscle strength compared with patients who underwent lumbar fusion [112].
The MRC Spine Stabilization Trial [113] assessed the clinical effectiveness of surgical stabilization (fusion) compared with an intensive rehabilitation program which included cognitive behavioral treatment for patients with chronic low-back pain. The authors found no clear evidence that primary spinal fusion surgery was any more beneficial than intensive rehabilitation. A cost-effectiveness analysis by Rivero-Arias [114] showed that surgical stabilization of the spine may not be a cost-effective use of scarce health care resources.
The Swedish Lumbar Spine Study [115] investigated whether lumbar fusion could reduce pain and diminish disability more effectively as compared to non-surgical treatment in patients with severe chronic low-back pain. They found that the surgical patients had a significantly higher rate of subjective favorable outcome and return to work rate compared to the non-surgical group.
There are no significant differences between fusion techniques among the groups in terms of subjective or objective clinical outcome [116].
Complications of spinal fusion
The complication rate of surgical interventions for lumbar spondylosis depends on the extent of the intervention [117]. The reoperation rate varies from 6% in patients undergoing non-instrumented fusion to 17% in patients undergoing combined anterior/posterior fusion [118].
However, the complication rate is also dependent on the surgical skill of the individual surgeon. The most frequent complications after spinal fusion for degenerative disc disease include [107]:
- infection: 0 –1.4%
- non-union: 7 –55%
- de novo neurological deficits: 0 –2.3%
- bone graft donor site pain: 15 –39%
Conclusion
Lumbar spondylosis is a degenerative condition of the spine but definitions vary widely within the literature. It is easily diagnosed radiologically. Its pervasiveness throughout all patient populations makes the exact diagnosis of symptomatic cases very difficult.
There is no concrete, gold-standard treatment approach to the wide range of patient presentations. Most patients can be treated conservatively with medication and physiotherapy. In some cases where patients do not improve with conservative treatment, an invasive therapeutic approach may be needed in the form of injections into the spine. In some patients who are resistant to all such treatment, surgery (spinal fusion) may be needed.
There is no conclusive proof that surgery has better outcome then nonsurgical treatment. Nonsurgical treatment is the first line of treatment for patients with lumbar spondylosis.
Reference
- Pye SR, Reid DM, Lunt M, et al. Lumbar disc degeneration: association between osteophytes, end-plate sclerosis and disc space narrowing. Ann Rheum Dis. 2007;66(3):330–3.
- van der Kraan PM, van den Berg WB. Osteophytes: relevance and biology. Osteoarthritis cartilage. 2007;15(3):237–44.
- Rothschild B. Lumbar spondylosis. In: Emedicine publication. 2008. Available via WebMD. http://emedicine.medscape.com/ article/249036-overview.
- Fardon DF, Milette PC. Nomenclature and classification of lumbar disc pathology. Spine. 2001;26(5):E93–113.
- Schneck CD. The anatomy of lumbar spondylosis. Clin Orthop Relat Res. 1985;193:20–36.
- Gibson JNA, Waddell G. Surgery for degenerative lumbar spondylosis. Spine. 2005;20:2312–20.
- Symmons DPM, van Hemert AM, Vandenbrouke JP, et al. A longitudinal study of back pain and radiological changes in the lumbar spines of middle aged women: radiographic findings. Ann Rheum Dis. 1991;50:162–6.
- O’Neill TW, McCloskey EV, Kanis JA, et al. The distribution, determinants, and clinical correlates of vertebral osteophytosis: a population based survey. J Rheumatol. 1999;26:842–8.
- 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(2):69–73.
- Frymoyer JW, Newberg A, Pope MH, et al. Spine radiographs in patients with low-back pain. An epidemiological study in men. J Bone Joint Surg Am. 1984;66(7):1048–55.
- Lawrence JS. Disc degeneration. Its frequency and relationship to symptoms. Ann Rheum Dis. 1969;28:121–38.
- Kirkaldy-Willis W, Bernard T. Managing low back pain. New York: Churchill livingstone; 1983.
- Boswell MV, Trescot AM, Datta S, et al. Interventional techniques: evidence-based practice guidelines in the management of chronic spinal pain. Pain Physician. 2007;10(1):7–111.
- Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine. 1978; 3:319–28.
- Peng B, Hou S, Shi Q, et al. Experimental study on mechanism of vertebral osteophyte formation. Chin J Traumatol. 2000;3(4):202–5.
- Blom AB, van Lent PL, Holfhuysen AE, et al. Synovial lining macrophages mediate osteophyte formation during experimental osteoarthritis. Osteoarthritis Cartilage. 2004;12(8):627–35.
- Bogduk N. The innervation of the lumbar spine. Spine. 1983; 8:286–93.
- Williams AL, Haughton VM, Daniels DL, Thornton RS. CT recognition of lateral lumbar disc herniation. Am J Roentgenol. 1982;139(1):345–7.
- Hasegawa T, An HS, Haughton VM, et al. Lumbar foraminal stenosis: critical heights of the intervertebral discs and foramina. A cryomicrotome study in cadavera. J Bone Joint Surg Am. 1995; 77(1):32–8.
- Buckwalter JA, Saltzman C, Brown T. The impact of osteoarthritis: implications for research. Clin Orthop Relat Res. 2004;427:S6–15.
- Heine J, Uber die Arthritis deformans. Virchows Arch Pathol Anat. 1926;260:521–663.
- Miller JA, Schmatz C, Schultz AB. Lumbar disc degeneration: correlation with age, sex, and spine level in 600 autopsy specimens. Spine. 1988;13:173–8.
- Boos N, Weissbach S, Rohrbach H, et al. Classification of age related changes in lumbar intervertebral discs: 2002 Volvo Award in basic science. Spine. 2002;27:2631–44.
- Videman T, Battie´ MC. Spine update: the influence of occupation on lumbar degeneration. Spine. 1999;24:1164–8.
- Hassett G, Hart DJ, Manek NJ, et al. Risk factors for progression of lumbar spine disc degeneration: the Chingford Study. Arthritis Rheum. 2003;48(11):3112–7.
- Spector TD, MacGregor AJ. Risk factors for osteoarthritis: genetics. Osteoarthritis Cartilage. 2004;12(Suppl A):S39–44.
- Videman T, Battie´ MC, Ripatti S, et al. Determinants of the progression in lumbar degeneration: a 5-year follow-up study of adult male monozygotic twins. Spine. 2006;31(6):671–8.
- Battié MC, Videman T, Gibbons LE, Fisher LD, Manninen H, Gill K. 1995 Volvo Award in clinical sciences. Determinants of lumbar disc degeneration. A study relating lifetime exposures and magnetic resonance imaging findings in identical twins. Spine (Phila Pa 1976). 1995 Dec 15;20(24):2601-12. PMID: 8747238.
- Videman T, Leppävuori J, Kaprio J, Battié MC, Gibbons LE, Peltonen L, Koskenvuo M. Intragenic polymorphisms of the vitamin D receptor gene associated with intervertebral disc degeneration. Spine (Phila Pa 1976). 1998 Dec 1;23(23):2477-85. doi: 10.1097/00007632-199812010-00002. PMID: 9854746.
- Menkes CJ, Lane NE. Are osteophytes good or bad? Osteoarthritis Cartilage 2004;12(Suppl A):S53e4.
- van der Kraan PM, van den Berg WB. Osteophytes: relevance and biology. Osteoarthritis cartilage. 2007;15(3):237–44.
- Hayden JA, van Tulder MW, Malmivaara AV, et al. Meta-analysis: exercise therapy for nonspecific low back pain. Ann Intern Med. 2005;142:765–75.
- Deyo R, Cherkin D, Conrad D. Cost, controversy, crisis: low back pain and the health of the public. Annu Rev Publ Health. 1991; 12:141–56.
- Hayden JA, van Tulder MW, Tomlinson G. Systematic review: strategies for using exercise therapy to improve outcomes in chronic low back pain. Ann Intern Med. 2005;142:776–85.
- Deyo RA, Walsh NE, Martin DC, et al. A controlled trial of transcutaneous electrical nerve stimulation (TENS) and exercise for chronic low back pain. N Engl J Med. 1990;322:1627–34.
- Milne S, Welch V, Brosseau L, Saginur M, Shea B, Tugwell P, Wells G. Transcutaneous electrical nerve stimulation (TENS) for chronic low back pain. Cochrane Database Syst Rev. 2001;(2):CD003008. doi: 10.1002/14651858.CD003008. PMID: 11406059.
- Khadilkar A, Odebiyi DO, Brosseau L, Wells GA. Transcutaneous electrical nerve stimulation (TENS) versus placebo for chronic low-back pain. Cochrane Database Syst Rev. 2008 Oct 8;2008(4):CD003008. doi: 10.1002/14651858.CD003008.pub3. PMID: 18843638; PMCID: PMC7138213.
- Heymans MW, van Tulder MW, Esmail R, et al. Back schools for nonspecific low back pain: a systematic review within the framework of the cochrane collaboration back review group. Spine. 2005; 30(19):2153–63.
- Van Tulder MW, Koes B, Malmivaara. Outcome of non-invasive treatment modalities on back pain: an evidence-based review. Eur Spine J. 2006;15(1):S64–81.
- Van der Heijden GJMG, Beurskens AJHM, Dirx MJM, et al. Efficacy of lumbar traction: a randomized clinical trial. Physiotherapy. 1995;81:29–35.
- Borman P, Keskin D, Bodur H. The efficacy of lumbar traction in the management of patients with low back pain. Rheumatol Int. 2003;23:82–6.
- Werners R, Pynsent PB, Bulstrode CJK. Randomized trial comparing interferential therapy with motorized lumbar traction and massage in the management of low back pain in a primary care setting. Spine. 1999;24:1579–84.
- Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low back pain. A meta-analysis of effectiveness relative to other therapies. Ann Intern Med. 2003;138:871–81.
- Bromfort G, Haas M, Evans RL, et al. Efficacy of spinal manipulation and mobilization for low back pain and neck pain: a systematic review and best evidence synthesis. Spine. 2004; 4(3):335–56.
- Oliphant D. Safety of spinal manipulation in the treatment of lumbar disk herniations: a systematic review and risk assessment. J Manipulative Physiol Ther. 2004;27:197–210.
- Furlan AD, Brosseau L, Imamura M, et al. Massage for low-back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 2002;27(17):1896–910.
- Middleton and Fish. Lumbar spondylosis: clinical presentation and treatment approaches. Curr Rev Musculoskelet Med (2009) 2:94–104.
- Schnitzer TJ, Ferraro A, Hunsche E, et al. A comprehensive review of clinical trials on the efficacy and safety of drugs for the treatment of low back pain. J Pain Symptom Manage. 2004;28: 72–95.
- Hickey RF. Chronic low back pain: a comparison of diflunisal with paracetamol. N Z Med J. 1982;95(707):312–4.
- Videman T, Osterman K. Double-blind parallel study of piroxicam versus indomethacin in the treatment of low back pain. Ann Clin Res. 1984;16:156–60.
- Berry H, Bloom B, Hamilton EB, et al. Naproxen sodium, diflunisal, and placebo in the treatment of chronic back pain. Ann Rheum Dis. 1982;41(2):129–32.
- DeMoor M, Ooghe R. Clinical trial of oxametacin in low back pain and cervicobrachialgia. Ars Medici Revue Internationale De Therapie Pratique. 1982;37:1509–15.
- van Tulder MW, Koes B, Malmivaara A. Outcome of non-invasive treatment modalities on back pain: an evidence-based review. Eur Spine J. 2006;15 Suppl 1(Suppl 1):S64-S81.
- Amlie E, Weber H, Holme I. Treatment of acute low back pain with piroxicam: results of a double-blind placebo-controlled trial. Spine. 1987;12:473–476. doi: 10.1097/00007632-198706000-00010.
- Szpalski M, Hayez JP. Objective functional assessment of the efficacy of tenoxicam in the treatment of acute low back pain: a double blind placebo-controlled study. Br J Rheumatol. 1994;33:74–78. doi: 10.1093/rheumatology/33.1.74.
- Goodkin K, Gullion CM, Agras WS. A randomised double blind, placebo-controlled trial of trazodone hydrochloride in chronic low back pain syndrome. J Clin Psychopharmacol. 1990;10:269–278.
- 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.
- Milgrom C, Finestone A, Lev B, Wiener M, Floman Y. Overexertional lumbar and thoracic back pain among recruits: a prospective study of risk factors and treatment regimens. J Spinal Disord. 1993;6:187–193. doi: 10.1097/00002517-199306030-00001.
- Wiesel SW, Cuckler JM, Deluca F, Jones F, Zeide MS, Rothman RH. Acute low back pain: an objective analysis of conservative therapy. Spine. 1980;5:324–330.
- Berry H, Bloom B, Hamilton EBD, Swinson DR. Naproxen sodium, diflunisal, and placebo in the treatment of chronic back pain. Ann Rheum Dis. 1982;41:129–132. doi: 10.1136/ard.41.2.129.
- Topol EJ. Failing the public health—rofecoxib, Merck, and the FDA. N Engl J Med. 2004;351:1707–1709.
- Martell BA, O’Connor PG, Kerns RD, et al. Systematic review: opioid treatment for chronic back pain: prevalence, efficacy, and association with addition. Ann Intern Med. 2007;146(2):116–27.
- Salerno SM, Browning R, Jackson JL. The effect of antidepressant treatment in chronic back pain: a meta-analysis. Arch Intern Med. 2002;162:19–24. doi: 10.1001/archinte.162.1.19.
- Staiger O, Barak G, Sullivan MD, Deyo RA. Systematic review of antidepressants in the treatment of chronic low back pain. Spine. 2003;28:2540–2545.
- Bigos S, Bowyer O, Braen G (1994) Acute low back problems in adults. Clinical Practice Guideline No. 14. AHCPR Publication No. 95-0642. Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services, Rockville.
- Atkinson JH, Slater MA, Williams RA. A placebo-controlled randomized clinical trial of nortriptyline for chronic low back pain. Pain. 1998;76:287–296. doi: 10.1016/S0304-3959(98)00064-5.
- Arbus L, Fajadet B, Aubert D, Morre M, Goldfinger E. Activity of tetrazepam in low back pain. Clin Trials J. 1990;27:258–267.
- Basmajian J. Cyclobenzaprine hydrochloride effect on skeletal muscle spasm in the lumbar region and neck: two double-blind controlled clinical and laboratory studies. Arch Phys Med Rehabil.
- Salzmann E, Pforringer W, Paal G, Gierend M. Treatment of chronic low-back syndrome with tetrazepam in a placebo controlled double-blind trial. J Drug Dev. 1992;4:219–228.
- Basmajian J. Cyclobenzaprine hydrochloride effect on skeletal muscle spasm in the lumbar region and neck: two double-blind controlled clinical and laboratory studies. Arch Phys Med Rehabil. 1978;59:58–63.
- Pratzel HG, Alken R-G, Ramm S. Efficacy and tolerance of repeated oral doses of tolperisone hydrochloride in the treatment of painful reflex muscle spasm: results of a prospective placebo-controlled double-blind trial. Pain. 1996;67:417–425.
- Wörz R, Bolten W, Heller J, Krainick U, Pergande G. Flupirtin im vergleich zu chlormezanon und placebo bei chronische muskuloskelettalen ruckenschmerzen. Fortschritte der Therapie. 1996;114(35–36):500–504.
- Casale R. Acute low back pain: symptomatic treatment with a muscle relaxant drug. Clin J Pain. 1988;4:81–88.
- Dapas F. Baclofen for the treatment of acute low-back syndrome. Spine. 1985;10:345–349.
- Abdi S, Datta S, Trescot AM, et al. Epidural steroids in the management of chronic spinal pain: a systematic review. Pain Physician. 2007;10:185–212.
- Koes BW, Scholten RJ, Mens JM, et al. Efficacy of epidural steroid injections for low-back pain and sciatica: a systematic review of randomized clinical trials. Pain. 1995;63(3):279–88.
- Stitz MY, Sommer HM. Accuracy of blind versus fluoroscopically guided caudal epidural injection. Spine. 1999;24(13):1371–6.
- Abdi S, Datta S, Trescot AM, et al. Epidural steroids in the management of chronic spinal pain: a systematic review. Pain Physician. 2007;10:185–212.
- Vad VB, Bhat AL, Lutz GE, et al. Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine. 2002;27:11–6.
- Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study. Arch Phys Med Rehabil. 1998;79:1362–6.
- Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transforaminal epidural steroid injections in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil. 2002;81:898–905.
- Riew KD, Park JB, Cho YS, et al. Nerve root blocks in the treatment of lumbar radicular pain: a minimum 5-year follow up. J Bone Joint Surg Am. 2006;88:1722–5.
- Riew KD, Yin Y, Gilula L, Bridwell, et al. The effect of nerve root injections on the need for operative treatment of lumbar radicular pain. J Bone Joint Surg Am. 2000;82:1589–93.
- Yang SC, Fu TS, Lai PL, et al. Transforaminal epidural steroid injection for discectomy candidates: an outcome study with a minimum of 2 year follow-up. Chang Gung Med J. 2006;29:93–9.
- Boswell MV, Singh V, Staats PS, et al. Accuracy of precision diagnostic blocks in the diagnosis of chronic spinal pain of facet or zygapophysial joint origin: a systematic review. Pain Physician. 2003;6:449–56.
- Sehgal N, Dunbar EE, Shah RV, et al. Systematic review of diagnostic utility of facet (zygapophysial) joint injections in chronic spinal pain: an update. Pain Physician. 2007;10(1):213–28.
- Boswell MV, Colson JD, Sehgal N, et al. A systematic review of therapeutic facet joint interventions in chronic spinal pain. Pain Physician. 2007;10:229–53.
- Fuchs S, Erbe T, Fischer HL, et al. Intraarticular hyaluronic acid versus glucocorticoid injections for nonradicular pain in the lumbar spine. J Vasc Interv Radiol. 2005;16:1493–8.
- Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. N Engl J Med. 1991;325:1002–7.
- Manchikanti L, Pampati VS, Bakhit C, et al. Effectiveness of lumbar facet joint nerve blocks in chronic low back pain: a randomized clinical trial. Pain Physician. 2001;4:101–17.
- Pereira PL, Gunaydin I, Trubenbach J, et al. Interventional MR imaging for injection of sacroiliac joints in patients with sacroiliitis. Am J Roentgenol. 2000;175:265–6.
- Maugars Y, Mathis C, Berthelot JM, et al. Assessment of the efficacy of sacroiliac corticosteroid injections in spondylarthropathies: a double-blind study. Br J Rheumatol. 1996;35(8):767–70.
- Hansen HC, McKenzie-Brown AM, Cohen SP, et al. Sacroiliac joint interventions: a systematic review. pain physician. 2007; 10(1): 165–84.
- Katz JN, Lipson SJ, Chang LC, et al. Seven to ten year outcome of decompressive surgery for degenerative lumbar spinal stenosis. Spine. 1996;21:92.
- Deyo RA, Weinstein JN (2001) Low back pain. N Engl J Med 344: 363 –70.
- Albee FH (1911) Transplantation of a portion of the tibia into the spine for Pott’s disease. A preliminary report. JAMA 57:885 –886.
- Hibbs R (1911) An operation for progressive spinal deformities. N Y Med J 93:1013 –1016.
- Gibson JN, Grant IC, Waddell G (1999) The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine 24:1820 –32 103.
- Gibson JN, Waddell G (2005) Surgery for degenerative lumbar spondylosis: updated Cochrane Review. Spine 30:2312 –20.
- Turner JA, Ersek M, Herron L, Deyo R (1992) Surgery for lumbar spinal stenosis. Attempted meta-analysis of the literature. Spine 17:1 –8.
- Boos N, Webb JK (1997) Pedicle screw fixation in spinal disorders: a European view. Eur Spine J 6:2 –18.
- Fritzell P, Hagg O, Wessberg P, Nordwall A (2001) 2001 Volvo Award Winner in Clinical Studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine 26:2521 –32; discussion 2532 –4
- Fritzell P, Hagg O, Wessberg P, Nordwall A (2002) Chronic low back pain and fusion: a comparison of three surgical techniques: a prospective multicenter randomized study from the Swedish lumbar spine study group. Spine 27:1131 –41.
- Hanley EN, Jr, David SM (1999) Lumbar arthrodesis for the treatment of back pain. J Bone Joint Surg Am 81:716 –30.
- van Tulder MW, Koes B, Seitsalo S, Malmivaara A (2006) Outcome of invasive treatment modalities on back pain and sciatica: an evidence-based review. Eur Spine J 15 Suppl 1:S82 –92.
- Waddell G (1987) 1987 Volvo award in clinical sciences. A new clinical model for the treatment of low-back pain. Spine 12:632 –44.
- Merkle et al. Degenerative lumbar spondylosis at https://neurobicetre.com/wp-content/uploads/2018/04/Boose-Degenerative-spondylolisthesis.pdf.
- Burkus JK (2005) Surgical treatment of the painful motion segment: matching technology with indications. Spine 30:S7 –15.
- Boden SD, Schimandle JH, Hutton WC, Chen MI (1995) 1995 Volvo Award in basic sciences. The use of an osteoinductive growth factor for lumbar spinal fusion. Part I: Biology of spinal fusion. Spine 20:2626 –32.
- Macnab I, Dall D (1971) The blood supply of the lumbar spine and its application to the technique of intertransverse lumbar fusion. J Bone Joint Surg 53B:628.
- Brox JI, Sørensen R, Friis A, Nygaard Ø, Indahl A, Keller A, Ingebrigtsen T, Eriksen HR, Holm I, Koller AK, Riise R, Reikerås O. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. Spine (Phila Pa 1976). 2003 Sep 1;28(17):1913-21. doi: 10.1097/01.BRS.0000083234.62751.7A. PMID: 12973134.
- Keller A, Brox JI, Gunderson R, Holm I, Friis A, Reikeras O (2004) Trunk muscle strength, cross-sectional area, and density in patients with chronic low back pain randomized to lumbar fusion or cognitive intervention and exercises. Spine 29:3 –8.
- Fairbank J, Frost H, Wilson-MacDonald J, Yu LM, Barker K, Collins R (2005) Randomised controlled trial to compare surgical stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: the MRC spine stabilisation trial. BMJ 330:1233.
- Rivero-Arias O, Campbell H, Gray A, Fairbank J, Frost H, Wilson-MacDonald J (2005) Surgical stabilisation of the spine compared with a programme of intensive rehabilitation for the management of patients with chronic low back pain: cost utility analysis based on a randomised controlled trial. BMJ 330:1239.
- Fritzell P, Hägg O, Wessberg P, Nordwall A; Swedish Lumbar Spine Study Group. 2001 Volvo Award Winner in Clinical Studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine (Phila Pa 1976). 2001 Dec 1;26(23):2521-32.
- Fritzell P, Hagg O, Wessberg P, Nordwall A (2002) Chronic low back pain and fusion: a comparison of three surgical techniques: a prospective multicenter randomized study from the Swedish lumbar spine study group. Spine 27:1131 –41.
- Thomsen K, Christensen FB, Eiskjaer SP, Hansen ES, Fruensgaard S, Bunger CE (1997) 1997 Volvo Award winner in clinical studies. The effect of pedicle screw instrumentation on functional outcome and fusion rates in posterolateral lumbar spinal fusion: a prospective, randomized clinical study. Spine 22:2813 –22.
- Fritzell P, Hagg O, Nordwall A (2003) Complications in lumbar fusion surgery for chronic low back pain: comparison of three surgical techniques used in a prospective randomized study. A report from the Swedish Lumbar Spine Study Group. Eur Spine J 12:178 –89.
