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Causes and Sources of Chronic Low Back Pain

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Written by: Dr Jeremy Steinberg – created: 17 June 2020; last modified: 3 November 2022

This page is probably complete!
It is awaiting peer review


Figure 1. Sources of pain in chronic low back pain as a function of age.[1] Copyright © 2020 American Academy of Pain Medicine

Chronic low back pain does not defy diagnosis. While the causes of acute low back pain are largely unknown, this is not the case for chronic low back pain, where a biomedical diagnosis is possible in the majority of cases.[2] The causes of radicular pain and radiculopathy are discussed elsewhere (See Lumbar Radicular Pain).

The exact figures depend on the age (figure 1), but around 40% have disc pain, around 10-30% have facet joint pain, and around 10-20% have sacroiliac joint pain.[3][4] An example published worst case estimate for the percentage of diagnosable chronic low back pain using the lower end of the 95% confidence intervals from multiple studies is 46%[2]

Overview and Postulates

The source of the pain refers to the anatomical structure which has nociceptive activity leading to pain perception. The cause of the pain is the disease process or disorder that is responsible for the nociceptive activity. The most well established causes of chronic low back pain are the lumbar intervertebral discs, and the lumbar zygapophysial joints.

Bogduk's postulates are analogous to Koch's postulates for bacterial diseases, and are the philosophical considerations concerning whether any structure can be deemed to be a credible cause of back pain:[4]

  1. Innervated: The structure should have a nerve supply.
  2. Experimental pain in normal volunteers: The structure should be capable of causing pain, similar to that seen clinically, ideally in normal volunteers, e.g. with noxious injection
  3. Pathology known: The structure should be susceptible to diseases or injuries that are known to be painful. Certain conditions however are not detectable using currently available imaging techniques, and in these cases the next line of evidence is used which is evidence from post-mortem studies or biomechanical studies, e.g. with facet joint pain.
  4. Identified in patients: The structure should be a source of pain in patients, using validated diagnostic techniques such as positive controlled nerve blocks to the sensory supply of a joint. Due to false-positive responses, diagnostic blocks must be controlled. Prevalence data can be determined here.

Following these postulates, it has been determined that the most common sources of chronic low back pain are the lumbar discs, facet joints, and sacroiliac joints (table 1). Internal disc disruption fulfils postulates 1, 3, and 4. Sacroiliac joint and zygapophysial joint pain fulfils postulates 1, 2 and 4. These three diagnoses have survived copious scientific scrutiny. Interspinous ligament pain fulfils postulates 2-4, and probably fulfils the first postulate, but it is thought to be an uncommon cause.

Table 1. Examples of Reported Prevalence Studies for Different Sources of Chronic Low Back Pain, and 95% Confidence Intervals (Not complete list)
Study Intervertebral Disc Facet Joint Sacroiliac Joint
Manchikanti 2020[5] 34.1% (28.8 - 39.8)
DePalma 2011[1] 41.8% (34.6 - 49.3) 30.6% (24.2 - 37.9) 18.2% (13.2 - 24.7)
Sembrano 2009[6] 14.5%
Manchikanti 2008[7] 18 - 44%
Irwin 2007[8] 26.6%
Manchikanti 2004[9] 31% (27 - 36)
Manchikanti 2001[10] 30% adults, 52% elderly
Manchikanti 2000[11] 42%
Manchikanti 1999[12] 45% (36 - 54)
Maigne 1996[13] 18.5%
Schwarzer 1995[14] 30% (16-44)
Schwarzer 1995[15] 39% (29 - 49)
Schwarzer 1995[16] 32% (20 - 44)
Schwarzer 1994[17] 15%
Schwarzer 1994[18] 37%

Non-Specific Low Back Pain

Main article: Non-Specific Chronic Low Back Pain

It is often incorrectly stated that the cause of low back pain cannot be diagnosed in 85% of cases with exact figure differing with different publications (some say 80%, some say 90%)[19] This "convenient truth" has been proven to be false time and time again. Unlike acute low back pain where the causes are largely unknown, The causes of chronic low back pain are largely known. History, examination, and radiography are insufficient for diagnosis, but the cause can be established with at least moderate certainty in around 90% of cases as long as there is access to appropriate investigations and the investigations are done in a logical manner.[20][21][22][23][24]

Red Flag Conditions

The red flag section in the acute low back pain article is still relevant for chronic low back pain. The four most common red flag conditions are fracture, infection, malignancy, and cauda equina syndrome.[25]

Red flag conditions, such as tumours and infections are uncommon, if not rare causes of chronic low back pain. They are however accepted causes. Some also include fractures here, however vertebral fractures may or may not be painful. Bogduk provides the following for mathematical illustration:[2]

Pa% = prevalence of serious conditions in patients with acute back pain

Z% = the percentage of patients with a serious cause for acute low back pain that develop chronic low back pain

Pc% = Prevalence of serious condition in patients with chronic low back pain

Then if it is assumed that everyone with a serious condition develops chronic low back pain:

Pc% = (Pa/Z)%

E.g. tumours: P=1%, If 30% of acute patients become chronic, prevalence in chronic low back pain = (1/30)% = 3%

The prevalence of red flag conditions in chronic low back pain is thought to be less than 5%.[26]

Zygapophysial Joint Pain

Figure 2: Probability of CLBP sources by age and BMI for males and females.[22] FJP = facet joint pain, SIJP = sacroiliac joint pain, IDD = internal disc disruption.
Main article: Lumbar Zygapophysial Joint Pain

Zygapophysial joints are innervated (postulate 1), they produce pain with noxious stimulation in normal volunteers (postulate 2), and there is validated diagnostic methodology in the form of controlled blocks (postulate 4). The pathology however is not completely known. Experimental laboratory studies with compression and torsion are able to produce small fractures and capsular avulsions. Postmortem studies have also shown various injuries. There are however not validated techniques of identifying pathology during life.[26]

Lumbar zygapophysial joint pain cannot be diagnosed through standard clinical means, nor through plain films, CT, or MRI. It can only be diagnosed by controlled diagnostic medial branch blocks.

Medial branch blocks is when a needle is placed onto each of the two nerves that innervate the target facet joint. A tiny amount of local anaesthetic is injected (0.3-0.5mL) to achieve specificity for the target. This is visualised under fluoroscopy, however there has been more recent research using ultrasound.

Lumbar medial branch blocks have face validity (makes sense based on anatomical data)[27], construct validity (they selectively block the target, they protect from experimentally induced pain in volunteers, and with controls reduce the rate of false-positives)[28][18], and therapeutic utility (they frequently provide several months of significant relief without even doing neurotomy, and predict response to sustained relief from neurotomy)[29][30].

For the prevalence figures in table 1, complete relief of pain was not a diagnostic criterion, but was usually 50% or 80%. As a diagnostic test, there is a balance between sensitivity and specificity depending on the cut off, with a higher relief of pain criterion resulting in a higher specificity but lower sensitivity.

Controlled blocks are required to reduce the rate of false positives, as single blocks have high false positive rates between 25-41 percent[18][12][31], this is why the results from single block studies are effectively meaningless. There are two types of controls. Pharmaceutical controls use different agents (such as bupivacaine and lidocaine) on the same target at two different instances in time (such as separated by one week). Anatomic control involves injecting the agent to a different substance.

The ultimate pharmaceutical control is the placebo block (bupivacaine, lidocaine, and placebo). A local anaesthetic is used first, because if the pain isn't relieved then there is no point proceeding further. The second block is a random choice between placebo (normal saline), and a different local anaesthetic to the first one. In this setting, a positive response is relief of pain when an anaesthetic was used, and no relief when a placebo was used.

This scenario is only an ideal, as various forces make it difficult to undergo three separate diagnostic procedures. What is done as a practical alternative in many high quality studies and in reality in New Zealand is doing comparative local anaesthetic blocks.[32] With the protocol, the same block is done twice on two separate occasions, but with different local anaesthetics that are blinded to the patient. A concordant response is having a duration of relief that is concordant with the expected duration of the local anaesthetic, i.e. short lasting relief with lidocaine and long-lasting relief with bupivacaine. A discordant response is when the opposite situation occurs with longer relief with lidocaine, which is likely to have a higher false positive rate.

The argument of using a cut-off lower than 100% is usually around the possibility of having more than one source of pain. King and Bogduk[26] reference two studies[33][14] to argue that patients with chronic low back pain only rarely have concurrent sources of pain, and so placebo responses can't be excluded. They note that if 100% relief of pain is used then the prevalence drops to about 5% or less.[34][35][36][37]

They continue however that the prevalence appears to be highly dependent on age. In a study of the elderly using a 90% criteron, 34% were positive.[16] A later study with two publications found that the prevalence was 2% in those 20-35, 5-10% in those 35-50, 20% in those 50-65, and 30-40% in those over 65. There was also an association with increasing age and BMI.[22][1] (figure 2) It appears that in certain groups the prevalence is as high as internal disc disruption.

Importantly, there is no correlation between radiological signs on plain films or CT of osteoarthritis and the joint being painful. Future research is likely to look at the correlation between inflammatory changes on MRI and positive blocks.[26]

Another important point is that with intraarticular blocks, pharmacologic controls can't be used. This is because the normal duration of action of local anaesthetics within joints is unknown. Anatomic controls can be used with intraarticular blocks, i.e. the doctor targets a structure that they don't believe is causing the pain. The target and control must both be small and very close to each other.[38]

Discogenic Pain

Internal Disc Disruption

Figure 3. Compression of an intervertebral disc may result in vertebral endplate fracture. This may heal or it may trigger nuclear degradation. Degradation may lead to isolated disc resorption or extend to the anulus and cause internal disc disruption (grade III shown). Internal disc disruption may lead to disc herniation
See also: Internal Disc Disruption

The innervation of the disc is well documented (postulate 1), the pathology of internal disc disruption is also well documented (postulate 3), and validated diagnostic techniques exist in the form of provocation discography (postulate 4).

Internal disc disruption is a condition that affects lumbar intervertebral discs and is the cause of pain in around 40% of individuals with chronic low back pain, but is dependent on age with a prevalence as high as 90% in those under 50, around 60% in those 50-65, and 20% in those over 65 (figure 2). As a diagnostic concept it has the most research evidence amongst all causes of chronic low back pain.

The inciting event is fatigue failure of the vertebral endplate (figure 3), which leads to degradation of the nuclear matrix. Subsequently radial and circumferential fissures develop that penetrate from the nucleus pulposus through to the anulus fibrosus, however the outer anulus is not breached. Pain is thought to arise through chemical nociception around the fissures ,as well as through mechanical nociception from the degraded nuclear matrix leading to greater loads being placed on the posterior anulus fibrosus.

Internal disc disruption can be diagnosed through provocation discography, post-discography CT, and imperfectly through MRI.

Discitis and Vertebral Osteomyelitis

Chemical nociception can occur with irritation of the nociceptive fibres of an infected disc, and this is a red flag condition. The most common organism is Staphylococcus aureus which accounts for more than 50% of cases. Bacteria can enter a disc or vertebra through:

  • Haematogenous spread form a distant site such as the genitourinary tract, skin, soft tissue, respiratory tract, intravascular devices, infective endocarditis, and dental infection. This is the most common cause.
  • Direct inoculation from trauma, provocation discography, spinal surgery, or other procedures.
  • Contiguous spread from adjacent soft tissue infection.

Torsion Injuries

With forcible rotation of a vertebra, the initial axis of rotation is about the posterior anulus which prestresses it. With further rotation there is impaction of a zygapophysial joint leading to an impaction microfracture which is one of the features. This impaction leads to a new axis of rotation which additionally laterally shears the anulus, and the combination of torsion and lateral shears causes an annular tear. Meanwhile, the opposite zygapophysial joint is distracted and there is an avulsion fracture or capsular tear. The risk is greater when rotation occurs in flexion due to flexion prestressing the anulus.

This is still an experimental entity with an unknown prevalence, and incompletely developed techniques for diagnosis. It can be diagnosed by a negative provocation discography, and then injecting contrast and local anaesthetic into the anulus which will relieve the pain and also show the tear on post-contrast CT imaging.[4]

Sacroiliac Pain

Main article: Sacroiliac Joint Pain

Sacroiliac Joint Pain

The innervation of the sacroiliac joint is well documented (postulate 1), studies in normal volunteers have shown noxious stimulation produces low back pain (postulate 2), and there is a validated diagnostic methodology in the form of controlled intraarticular blocks (postulate 4). The pathology may be degenerative changes that are often precipitated by trauma,[39] peripartum changes to the ligaments, increased stress post lumbar fusion. However the pathology is overall incompletely known.[4]

Studies based on diagnostic blocks yields a prevalence range of 20-30% among patients that have suspected SIJ pain based on history and examination.[40] The prevalence again varies with age, with it being more common in older, lighter individuals, and females.[22]

Sacroiliac joint pain is generally perceived as low back, or buttock pain, felt below the L5 level. Some patients will have referred pain down the leg and into the foot. Fortin et al found a 3x10cm area, just inferior to PSIS, thought to be specific for SI joint pain.[41]

Sacroiliac Ligament Pain

Sacroiliac ligament pain on the other hand may be a separate entity. It refers to pain arising from the interosseous or dorsal ligamentous complex of the sacroiliac joint.

As above, in sacroiliac joint pain the diagnosis is made through controlled intra-articular blocks. However, this does not block pain arising from the sacroiliac ligaments. for sacroiliac ligament pain the diagnosis is made through controlled diagnostic lateral branch blocks of the sacral dorsal rami (S1-4). Conversely, as the sacroiliac joint also has a ventral nerve supply, sacroiliac joint pain can't be diagnosed through lateral branch blocks. Lateral branch blocks have been validated but not applied to population studies and so the prevalence is unknown.[42]

Vertebral Pain

Vertebral Bodies

The vertebral bodies are innervated (postulate 1), the pathology is known (postulate 2), and the source has been identified in patients (postulate 4). The production of intra-osseous pain has not been experimented on in normal volunteers except for needling of the periosteum which has been reported to cause pain in certain procedures.

The nerve fibres arise from the plexuses of the anterior and posterior longitudinal ligaments, and innervate the periosteum of the bones and penetrate deep into the vertebral bodies. This deep innervation suggests deep bone pain is possible, but it isn't known if these intraosseous nerves are exclusively vasomotor/vasosensitive as they mostly exist around blood vessels[43], or if they are nociceptive.

In terms of pathologies, the vertebral body can succumb to Paget's disease, oseitis fibrosa, primary or secondary tumours, and infections. The mechanism of pain in these sometimes painful conditions is unknown. Osteoporosis is not painful in the absence of fracture.

For vertebral body compression fractures, there are even less clear conclusions to be made. When fractures are stable elsewhere in the body they aren't painful. One possibility is tissue deformation and periosteal irritation from haematomas and oedema. However this doesn't explain why some patients have chronic pain with vertebral fractures, when presumably the swelling has resolved. One candidate theory is that the pain arises due to the resultant deformity, such as from the posterior elements.[44] Others argue that the pain arises from intraosseous nerves, which is the premise for vertebroplasty,[45] but innervation is scarce.[43] Yet another theory is intraosseuous hypertension, where the intraosseuous veins are distended and stimulate surrounding nociceptors, but this is untested.[4]

Posterior Elements

The pedicles, laminae, and transverse fractures can be affected by fractures and tumours, which are known causes of pain.

Baastrup's disease, also known as "kissing spines" was found to be a rare cause of chronic low back pain, identified in 3/170 (1.8%) patients who were systematically investigated using precision diagnosis techniques in one study.[46] Some distinguish Baastrup's from interspinous oedema which may related to more general disorders of the interspinous space. As this area is innervated by the medial branches[4], some patients diagnosed with "facet joint pain" may actually have interspinous space pain (See Interspinous Oedema).

Lamina impaction is analogous to Baastraps. This is where extension is limited by impaction of an inferior articular process onto the lamina below. Post-mortem studies have found lesions in the periosteum of the lamina. This is a condition that is as yet unproven in living patients. It could be considered in individuals who have repetitive forceful extension such as gymnasts.[4]

Spondylolysis is a disputed cause of chronic low back pain, discussed further below.

Disputed Causes of Pain

One avenue of assessing a given pathology as a potential cause of pain is to compare the prevalence in people with and without pain. If the prevalence is higher in people with pain, an association is established. Another method is to anaesthetise the degenerative structure and if the pain is relieved then it might be the source of pain.[47]

Degenerative Disc Disease

Main article: Lumbar Degenerative Disc Disease

Degenerative disc disease is not a proven cause of pain. Association studies have not found correlations between pain and degenerative findings on plain films or MRI.[47] Internal disc disruption is a separate concept to disc degeneration. While there are many similar processes and features, internal disc disruption is a response to injury that occurs either through single or repetitive compressive loads.[48] For degenerative disc disease genetics and aging play the main roles in its development.

Degenerative Zygapophysial Joint Disease

Degenerative changes of the lumbar zygapophysial joints are not accepted causes of pain, as is the case for the cervical spine.[47] It is a source of great misery for many patients that ACC proclaims ex cathedra that there is indeed a correlation, with the aim of ceasing cover, in spite of the evidence to the contrary.

Osteoarthrosis is in fact equally prevalent amongst symptomatic and asymptomatic individuals. Osteoarthrosis becomes more common with increasing age and this is irrespective of pain.[49][50] One interesting study found no correlation between whether or not a joint was painful as determined by placebo-controlled intra-articular blocks and the severity of the arthropathy.[51]

Low Grade Disc Infection

A disputed cause is chronic low grade infection by Propionibacterium acnes. The hypothesis is that vertebral marrow/endplate oedema caused by low grade bacterial discitis

Some studies have isolated Cutibacterium (Propionibacterium) acnes from discs in people undergoing spinal surgery. A systematic review attempted to clarify this and found that this may be related to abnormal discs being more susceptible to infection, but it is difficult to establish true infection versus contamination (some studies also isolated CONS).[52]

In an RCT of 144 patients, there was significant improvement with 100 days of augmentin in chronic low back pain, prior disc herniation, and type 1 Modic changes. Limitations included high proportions of participants having had previous back surgery, no improvement in the control group, and unclear efficacy of blinding.[53] A multi-centre double blinded RCT was done in an attempt to reproduce the results with amoxicillin but it was not successful. See graphic[54]

A recent open access review of this topic has been published which concluded that patients with Modic type 1 changes appear to respond better to antibiotics than those with Modic type 2 changes.[55]

Structural Abnormalities

Structural abnormalities include congenital abnormalities (congenital fusion, spina bifida occulta, and transitional vertebra), spondylolysis, spondylolisthesis, and spondylosis. As is the case for acute low back pain, these abnormalities are equally common in symptomatic and asymptomatic patients and so cannot be causes of chronic low back pain.[56]

For spondylolysis, only amongst sportspeople are pars defects more common. However simply seeing spondylolysis on plain films does not constitute having found the source of pain. For that a pars block is required, with relief of pain supporting the diagnosis, and predicts success with surgery.[57]

Instability

Lumbar instability is a historical term that was debated through the 1980s-90s. It encompasses two types: mechanical (radiographic), and functional (clinical). Topic is subject to much debate and controversy on the exact nature of the problem, correlation with history and relevance to patient management[58] The musculoskeletal medicine view is that instability does not constitute a diagnosis of chronic low back pain.[59]

There are various biomechanical definitions and diagnostic criteria.

The various definitions, which all have limitations include:

  1. Loss of stiffness in spinal motion segments
  2. An increase in the neutral zone of intervertebral movements
  3. Increase in the ratio between the magnitude of translation and the magnitude of rotation that a motion segment exhibits during flexion-extension of the lumbar spine

Instability can also be classified based on the lesions that are postulated to cause the instability:

  1. fractures and fracture-dislocations
  2. infections of anterior elements
  3. neoplasms
  4. spondylolisthesis
  5. degenerative.

In this classification scheme for fractures, infections, and neoplasms one only needs to see the finding, and not demonstrate the instability biomechanically, which is sensible.

For spondylolisthesis, while it can look threatening on radiographs, it rarely progresses, and grade 1 and grade 2 spondylolisthesis is associated with reduced range of motion rather than instability. Further precision studies have shown that motion patterns of patients are indistinguishable from degenerative disc disease. Furthermore spondylolisthesis is not associated with pain, and finding it on x-ray does not constitute a diagnosis.

There are several types of instability that have been attributed to degeneration of the lumbar spine. However there have been no studies proving them as a cause of pain or showing that correcting them resolves pain. These types of instability include:

  • Rotational – hypothetical entity, certain radiographic signs may suggest it, but the reliability and validity has not been studied.
  • Retrolisthetic – occurs during extension, but this movement can occur in asymptomatic individuals.
  • Translational – abnormal forward translation during flexion. There is difficulty in defining the upper limit of normal, with dynamic translations of 4mm occurring in 20% of asymptomatic individuals.

Failed back surgery syndrome

Main article: Failed Back Surgery Syndrome

The pathology of the condition is unknown. Some hypotheses include neuroma formation, deafferentation, epidural scarring, etc. There are no reliable diagnostic techniques where these conjectures can be confirmed. This fact leads to the reason why the term "syndrome" is used, because patho-anatomical diagnosis is usually impossible.

Patients with FBSS can be further categorised into:

  • Correct operation, wrong diagnosis e.g Solid L4-L5 discectomy and fusion but pain arising from L3-4 disc
  • Correct diagnosis, wrong operation e.g L3-4 discogenic pain treated with a posterolateral fusion but no discectomy
  • Wrong diagnosis, wrong operation e.g Laminectomy and discectomy for asymptomatic disc bulge but the source of pain was actually the zygoapophyseal joint
  • A further subset of patients will have a new cause of pain following their procedure e.g Post-operative neuroma, arachnoiditis, nerve injury, epidural scarring, local irritation by a fusion mass/instrumentation

Lumbar Fat Herniation

Main article: Lumbar Fat Herniation

There are two hypotheses regarding the pathophysiology. Some authors state that the condition is where deep fat herniates through the thoracolumbar fascia in a more superficial extramuscular, subcutaneous location. Other authors report that they are discrete lipomata or fibro-fatty nodules. It may be that these are two separate conditions with similar clinical presentations. Fat herniations are commonly asymptomatic, with prevalence rates of 10-58%.[60] Some report relief of pain with diagnostic infiltration.[4]

Muscles

Quadratus lumborum and psoas are supplied by branches of the lumbar ventral rami. The back muscles are supplied by the branches of the dorsal rami. The intertransverse muscles can be supplied by either rami (postulate 1). Muscles have been shown to be painful when injected with hypertonic saline in normal volunteers (postulate 2). Postulates 3 and 4 fall short for identified pathology and identified in patients. The concepts of strain, spasm, imbalance, segmental dysfunction, and trigger points all have various problems including shortfalls in concept validity, reliability, and diagnostic validity.[26]

The general current thinking in Musculoskeletal Medicine is that any muscle pain is an epiphenomenon secondary to the standard proven causes of chronic low back pain (internal disc disruption, facet joint pain, and sacroiliac joint pain). The muscles are innervated.

References

  1. ↑ 1.0 1.1 1.2 DePalma MJ, Ketchum JM, Saullo T. What is the source of chronic low back pain and does age play a role? Pain Med. 2011 Feb;12(2):224-33. doi: 10.1111/j.1526-4637.2010.01045.x. Epub 2011 Jan 25. PMID: 21266006.
  2. ↑ 2.0 2.1 2.2 Bogduk and McGuirk. Causes and sources of chronic low back pain In: Medical Management of Acute and Chronic Low Back Pain. Elsevier 2002
  3. ↑ DePalma MJ. Diagnostic Nihilism Toward Low Back Pain: What Once Was Accepted, Should No Longer Be. Pain Med. 2015 Aug;16(8):1453-4. doi: 10.1111/pme.12850. Epub 2015 Jul 27. PMID: 26218010.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Bogduk. Low back pain In: Clinical and Radiological Anatomy of the Lumbar Spine. 5th Edition. Elsevier 2012
  5. ↑ Manchikanti L, Kosanovic R, Pampati V, Cash KA, Soin A, Kaye AD, Hirsch JA. Low Back Pain and Diagnostic Lumbar Facet Joint Nerve Blocks: Assessment of Prevalence, False-Positive Rates, and a Philosophical Paradigm Shift from an Acute to a Chronic Pain Model. Pain Physician. 2020 Sep;23(5):519-530. PMID: 32967394.
  6. ↑ Sembrano JN, Polly DW Jr. How often is low back pain not coming from the back? Spine (Phila Pa 1976). 2009 Jan 1;34(1):E27-32. doi: 10.1097/BRS.0b013e31818b8882. PMID: 19127145.
  7. ↑ Manchikanti L, Manchikanti KN, Cash KA, Singh V, Giordano J. Age-related prevalence of facet-joint involvement in chronic neck and low back pain. Pain Physician. 2008 Jan;11(1):67-75. PMID: 18196171.
  8. ↑ Irwin RW, Watson T, Minick RP, Ambrosius WT. Age, body mass index, and gender differences in sacroiliac joint pathology. Am J Phys Med Rehabil. 2007 Jan;86(1):37-44. doi: 10.1097/phm.0b013e31802b8554. PMID: 17304687.
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  13. ↑ Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine (Phila Pa 1976). 1996 Aug 15;21(16):1889-92. doi: 10.1097/00007632-199608150-00012. PMID: 8875721.
  14. ↑ 14.0 14.1 Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine (Phila Pa 1976). 1995 Jan 1;20(1):31-7. doi: 10.1097/00007632-199501000-00007. PMID: 7709277.
  15. ↑ Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine (Phila Pa 1976). 1995 Sep 1;20(17):1878-83. doi: 10.1097/00007632-199509000-00007. PMID: 8560335.
  16. ↑ 16.0 16.1 Schwarzer AC, Wang SC, Bogduk N, McNaught PJ, Laurent R. Prevalence and clinical features of lumbar zygapophysial joint pain: a study in an Australian population with chronic low back pain. Ann Rheum Dis. 1995 Feb;54(2):100-6. doi: 10.1136/ard.54.2.100. PMID: 7702395; PMCID: PMC1005530.
  17. ↑ Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. Clinical features of patients with pain stemming from the lumbar zygapophysial joints. Is the lumbar facet syndrome a clinical entity? Spine (Phila Pa 1976). 1994 May 15;19(10):1132-7. doi: 10.1097/00007632-199405001-00006. PMID: 8059268.
  18. ↑ 18.0 18.1 18.2 Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial joints. Pain. 1994 Aug;58(2):195-200. doi: 10.1016/0304-3959(94)90199-6. PMID: 7816487.
  19. ↑ Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Häuser W. Nociplastic pain: towards an understanding of prevalent pain conditions. Lancet. 2021 May 29;397(10289):2098-2110. doi: 10.1016/S0140-6736(21)00392-5. PMID: 34062144.
  20. ↑ DePalma et al.. What is the source of chronic low back pain and does age play a role?. Pain medicine (Malden, Mass.) 2011. 12:224-33. PMID: 21266006. DOI.
  21. ↑ DePalma et al.. Etiology of chronic low back pain in patients having undergone lumbar fusion. Pain medicine (Malden, Mass.) 2011. 12:732-9. PMID: 21481166. DOI.
  22. ↑ 22.0 22.1 22.2 22.3 DePalma et al.. Multivariable analyses of the relationships between age, gender, and body mass index and the source of chronic low back pain. Pain medicine (Malden, Mass.) 2012. 13:498-506. PMID: 22390231. DOI.
  23. ↑ DePalma et al.. Structural etiology of chronic low back pain due to motor vehicle collision. Pain medicine (Malden, Mass.) 2011. 12:1622-7. PMID: 21958329. DOI.
  24. ↑ DePalma. Diagnostic Nihilism Toward Low Back Pain: What Once Was Accepted, Should No Longer Be. Pain medicine (Malden, Mass.) 2015. 16:1453-4. PMID: 26218010. DOI.
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  26. ↑ 26.0 26.1 26.2 26.3 26.4 King and Bogduk. Chronic Low Back Pain In: Bonica's Management of Pain 2018
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  28. ↑ Kaplan M, Dreyfuss P, Halbrook B, Bogduk N. The ability of lumbar medial branch blocks to anesthetize the zygapophysial joint. A physiologic challenge. Spine (Phila Pa 1976). 1998 Sep 1;23(17):1847-52. doi: 10.1097/00007632-199809010-00008. PMID: 9762741.
  29. ↑ Manchikanti L, Singh V, Falco FJ, Cash KA, Pampati V. Evaluation of lumbar facet joint nerve blocks in managing chronic low back pain: a randomized, double-blind, controlled trial with a 2-year follow-up. Int J Med Sci. 2010 May 28;7(3):124-35. doi: 10.7150/ijms.7.124. PMID: 20567613; PMCID: PMC2880841.
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  34. ↑ Carette S, Marcoux S, Truchon R, Grondin C, Gagnon J, Allard Y, Latulippe M. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. N Engl J Med. 1991 Oct 3;325(14):1002-7. doi: 10.1056/NEJM199110033251405. PMID: 1832209.
  35. ↑ Jackson RP, Jacobs RR, Montesano PX. 1988 Volvo award in clinical sciences. Facet joint injection in low-back pain. A prospective statistical study. Spine (Phila Pa 1976). 1988 Sep;13(9):966-71. doi: 10.1097/00007632-198809000-00002. PMID: 2974632.
  36. ↑ Laslett M, Oberg B, Aprill CN, McDonald B. Zygapophysial joint blocks in chronic low back pain: a test of Revel's model as a screening test. BMC Musculoskelet Disord. 2004 Nov 16;5:43. doi: 10.1186/1471-2474-5-43. PMID: 15546487; PMCID: PMC534802.
  37. ↑ Laslett M, McDonald B, Aprill CN, Tropp H, Oberg B. Clinical predictors of screening lumbar zygapophyseal joint blocks: development of clinical prediction rules. Spine J. 2006 Jul-Aug;6(4):370-9. doi: 10.1016/j.spinee.2006.01.004. PMID: 16825041.
  38. ↑ Bogduk. Diagnostic Procedures in Chronic Pain In: Wilson's Chronic Pain. 2008
  39. ↑ Murakami, E. (2019). Pathophysiology of Sacroiliac Joint Disorder BT - Sacroiliac Joint Disorder: Accurately Diagnosing Low Back Pain. In E. Murakami (Ed.) (pp. 33–53)
  40. ↑ Kennedy DJ, Engel A, Kreiner DS, Nampiaparampil D, Duszynski B, MacVicar J. Fluoroscopically Guided Diagnostic and Therapeutic Intra-Articular Sacroiliac Joint Injections: A Systematic Review. Pain Med. 2015 Aug;16(8):1500-18. doi: 10.1111/pme.12833. Epub 2015 Jul 14. PMID: 26178855.
  41. ↑ Fortin JD, Dwyer AP, West S, Pier J. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: Asymptomatic volunteers.Spine (Phila Pa 1976). 1994;19(13):1475-1482.
  42. ↑ Bogduk N. A Commentary on Appropriate Use Criteria for Sacroiliac Pain. Pain Med. 2017 Nov 1;18(11):2055-2057. doi: 10.1093/pm/pnx234. PMID: 29092066.
  43. ↑ 43.0 43.1 Buonocore M, Aloisi AM, Barbieri M, Gatti AM, Bonezzi C. Vertebral body innervation: Implications for pain. J Cell Physiol. 2010 Mar;222(3):488-91. doi: 10.1002/jcp.21996. PMID: 20020509.
  44. ↑ Bogduk N, MacVicar J, Borowczyk J. The pain of vertebral compression fractures can arise in the posterior elements. Pain Med. 2010 Nov;11(11):1666-73. doi: 10.1111/j.1526-4637.2010.00963.x. PMID: 21044256.
  45. ↑ Niv D, Gofeld M, Devor M. Causes of pain in degenerative bone and joint disease: a lesson from vertebroplasty. Pain. 2003 Oct;105(3):387-392. doi: 10.1016/S0304-3959(03)00277-X. PMID: 14527699.
  46. ↑ DePalma MJ, Ketchum JM, Saullo T. What is the source of chronic low back pain and does age play a role? Pain Med. 2011 Feb;12(2):224-33. doi: 10.1111/j.1526-4637.2010.01045.x. Epub 2011 Jan 25. PMID: 21266006.
  47. ↑ 47.0 47.1 47.2 Bogduk N. Degenerative joint disease of the spine. Radiol Clin North Am. 2012 Jul;50(4):613-28. doi: 10.1016/j.rcl.2012.04.012. PMID: 22643388.
  48. ↑ Bogduk N, Aprill C, Derby R. Lumbar discogenic pain: state-of-the-art review. Pain Med. 2013 Jun;14(6):813-36. doi: 10.1111/pme.12082. Epub 2013 Apr 8. PMID: 23566298.
  49. ↑ Lawrence JS, Bremner JM, Bier F. Osteo-arthrosis. Prevalence in the population and relationship between symptoms and x-ray changes. Ann Rheum Dis. 1966 Jan;25(1):1-24. PMID: 5905334; PMCID: PMC2453365.
  50. ↑ Kalichman L, Li L, Kim DH, Guermazi A, Berkin V, O'Donnell CJ, Hoffmann U, Cole R, Hunter DJ. Facet joint osteoarthritis and low back pain in the community-based population. Spine (Phila Pa 1976). 2008 Nov 1;33(23):2560-5. doi: 10.1097/BRS.0b013e318184ef95. PMID: 18923337; PMCID: PMC3021980.
  51. ↑ Schwarzer AC, Wang SC, O'Driscoll D, Harrington T, Bogduk N, Laurent R. The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine (Phila Pa 1976). 1995 Apr 15;20(8):907-12. doi: 10.1097/00007632-199504150-00005. PMID: 7644955.
  52. ↑ Urquhart DM et al. Could low grade bacterial infection contribute to low back pain? A systematic review.BMC Med 2015;13:13.
  53. ↑ Albert H, Sorensen J, Christensen B, Manniche C. Antibiotic treatment in patients with chronic low back pain and vertebral bone edema (Modic type 1 changes): a double-blind randomized clinical controlled trial of efficacy.Eur Spine J.2013;22:697–707
  54. ↑ Bråten LCH, Rolfsen MP, Espeland A, et al. Efficacy of antibiotic treatment in patients with chronic low back pain and Modic changes (the AIM study): double blind, randomised, placebo controlled, multicentre trial [published correction appears in BMJ. 2020 Feb 11;368:m546]. BMJ. 2019;367:l5654. Published 2019 Oct 16. doi:10.1136/bmj.l5654
  55. ↑ Manniche C, Hall GM. Chronic low back pain, Modic changes and low-grade virulent infection: efficacy of antibiotic treatment. Future Sci OA. 2021 Apr 7;7(6):FSO703. doi: 10.2144/fsoa-2021-0026. PMID: 34046205; PMCID: PMC8147823.
  56. ↑ van Tulder MW, Assendelft WJ, Koes BW, Bouter LM. Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies. Spine (Phila Pa 1976). 1997 Feb 15;22(4):427-34. doi: 10.1097/00007632-199702150-00015. PMID: 9055372.
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  58. ↑ Lumbar instability: an evolving and challenging concept. J. Beazell. Journal of Manual and Manpulative Therapy. Vol 18 1 (2010)
  59. ↑ Bogduk. Instability In: Clinical and Radiological Anatomy of the Lumbar Spine. 5th Edition. 2012
  60. ↑ Tiegs-Heiden CA, Murthy NS, Glazebrook KN, Skinner JA. Subfascial fat herniation: sonographic features of back mice. Skeletal Radiol. 2018 Jan;47(1):137-140. doi: 10.1007/s00256-017-2772-9. Epub 2017 Sep 15. PMID: 28914351.

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