Back pain

In an effort to standardise the use of terms and to set standards of diagnostic practice, the International Association for the Study of Pain (IASP) published the second edition of its taxonomy.¹ This document provides definitions of clinical terms used to describe pain and sets criteria for the diagnosis of specific entities.

With respect to presenting complaints, the taxonomy defines spinal pain topographically. It recognises ‘lumbar spinal pain’ and ‘sacral spinal pain’.¹ Lumbar spinal pain is defined as pain perceived within a region bounded laterally by the lateral borders of the erector spinae, superiorly by an imaginary transverse line through the T12 spinous process, and inferiorly by a line through the S1 spinous process. Sacral spinal pain is defined as pain perceived within a region overlying the sacrum, bounded laterally by imaginary vertical lines through the posterior superior and posterior inferior iliac spines, superiorly by a transverse line through the S1 spinous process, and inferiorly by a transverse line through the posterior sacrococcygeal joints.

Low back pain can then be defined as pain perceived as arising from either of these two areas or from a combination of both. Whether or not the pain radiates elsewhere is another matter. The cardinal feature is that it appears to arise in these areas.

This definition does not presuppose the cause of pain, nor does it imply that the source of pain actually lies in the lumbar spine or sacrum. It is simply a definition based essentially on where a patient points to when they indicate where they feel their pain is stemming from.

Somatic pain

Somatic pain is pain that results from noxious stimulation of one of the musculoskeletal components of the body.^1,2 Neurophysiologically, the essential feature is that it arises as a result of the stimulation of nerve endings in a bone, ligament, joint or muscle.

’Somatic pain’ is a term that stands in contrast to ‘visceral pain’, in which the noxious stimulus occurs in a body organ, and in contrast to ‘neurogenic pain’ in which the nociceptive information arises as a result of irritation or damage, not to nerve endings but to the axons or cell bodies of a peripheral nerve.

Referred pain

Referred pain is pain perceived in a region innervated by nerves other than those that innervate the actual source of pain.^1,2 As such, referred pain may be perceived in areas relatively remote from the source of pain, but often the distinction is blurred when the regions of local pain and referred pain are contiguous and the two pains appear to be confluent. A knowledge of the innervation of the affected regions, however, serves to make the distinction.

An example is low back pain associated with pain in the buttock. In this case, the low back pain appears to spread (i.e. radiate) into the buttock, but although the lumbosacral region and the buttock share a similar segmental nerve supply (L4, L5, S1), the back is innervated by the dorsal rami of these nerves, whereas the deep tissues of the buttock are innervated by the ventral rami (represented in the superior gluteal and inferior gluteal nerves). The buttock pain is therefore an example of referred pain.

The physiological basis for referred pain is convergence.¹ Within the spinal cord and in the thalamus, sensory neurones that subtend different peripheral sites converge onto common neurones that relay to higher centres. In the absence of any additional sensory information, the brain is unable to determine whether activity in the common neurone was initiated by one or the other of its peripheral inputs.

When the source of pain lies in a viscus, referred pain may be perceived in those parts of the body wall with a similar segmental nerve supply as the viscus. This type of referred pain may be described as visceral referred pain. In contrast, when the source of pain lies in skeletal or muscular structures, the referred pain may be described as somatic referred pain to emphasise its somatic, as opposed to visceral, origin.

Clinically, the characteristic features of somatic referred pain are that it is perceived deeply, it is diffuse and hard to localise and it is aching in quality.² Physiologically, the critical feature is that it is evoked by the stimulation of nerve endings in the structure that is the primary source of pain. The sensory nerves that innervate the region of referred pain are not activated by the primary stimulus, nor do they convey the referred pain. Referred pain occurs because of a misperception of the origin of the signal which reaches the brain by a convergent sensory pathway. These features underlie the distinction between somatic referred pain and radicular pain.

Postulates

From a philosophical perspective, the status of any conjecture concerning the possible causes of back pain can be evaluated by adopting certain criteria analogous to Koch’s postulates for bacterial diseases. For any structure to be deemed a cause of back pain:

In the shadow of these postulates, the possible sources and causes of back pain can be determined by reviewing the anatomy of the lumbar spine and sacrum. The credibility of any source or of any cause can be measured by determining how well it satisfies the postulates.

Posterior elements

The posterior elements of the lumbar vertebrae may be affected by disorders such as secondary tumours in the pedicle and fractures of the transverse processes, and the mechanisms of pain in these disorders are understandable in terms similar to those applied for tumours and fractures of the vertebral body. Otherwise, there are several distinctive lesions of the posterior elements of the lumbar vertebrae.

Sprain

A belief in the concept of muscle sprain stems from everyday experience and sports medicine where it is commonplace for muscles of the limbs to become painful following severe or sustained exertion, or after being suddenly stretched. It is therefore easy to postulate that analogous injuries might befall the back muscles, but what remains contentious is the pathology of such injuries.

Animal studies have shown that when muscles are forcibly stretched against contraction, they characteristically fail at the myotendinous junction.^146–148 The resulting lesion would presumably evoke an inflammatory repair response, which is easily accepted as a source of pain. In the case of the back muscles, such lesions could be incurred during lateral flexion or combined flexion–rotation injuries of the trunk and would be associated with tenderness near the myotendinous junctions of the affected muscles. Some of these sites are superficial and accessible to clinical examination, but others are deep. Deep sites lie near the tips of the transverse and accessory processes of the lumbar vertebrae. Accessible myotendinous junctions lie just short of the ribs near the insertions of the iliocostalis lumborum.

More diffuse muscle pain following exertion is theoretically explicable on the basis of ischaemia. One can imagine that during sustained muscle contraction the endomysial circulation is compressed, on the one hand obstructing washout of metabolites such as lactic acid and ADP which are algogenic, or on the other hand reducing arterial blood flow and causing muscle cell death, the breakdown products of which are also algogenic. Such mechanisms probably underlie some cases of exertional back pain, but this pain should be self-limiting as in the case of muscular pains of the limbs following severe exercise or unaccustomed activity.

Conspicuously, what is lacking in the case of back muscle injuries is any direct evidence of the responsible lesion. The only data that might be invoked come from experiments in animals in which the muscles of the limbs, not the back muscles, were studied. Biopsy data in humans or imaging data have not been published. For this reason a workshop sponsored by the American Academy of Orthopedic Surgeons and the National Institutes of Health was circumspect and inconclusive in its approach to the notion that sprained back muscles were a common cause of pain.¹⁴⁹ However, the advent of MRI may now provide a suitable non-invasive tool with which traumatic lesions of the back muscles might be identified.¹⁵⁰

Spasm

Although myotendinous tears might underlie cases of acute back pain stemming from muscle, it is more difficult to explain chronic back pain in terms of muscle pain. A popular belief is that of muscle ‘spasm’.¹⁵¹ The implication is that as a result of some postural abnormality, or secondary to some articular source of pain, muscles become chronically active and therefore painful. If it occurs, such pain can only be explained on the basis of ischaemia, but the greatest liability of this model of muscular pain is that the purported evidence for its existence is inconclusive.¹⁵¹ Electromyographic data are inconsistent, and it is unclear what so-called muscle spasm constitutes in objective physiological terms: whether it is tonic contraction or simply hyperreflexia. Further research data are required before this notion can become more acceptable, together with an explanation of whether the pain arises as a result of ischaemia, strain on the muscle attachments or some other mechanism.

Imbalance

Another concept is that of ‘muscle imbalance’.¹⁵² It is believed that aberrations in the balance of tone between postural and phasic muscles, or between flexors and extensors, can give rise to pain. In the case of the lumbar spine, the imbalance is said to occur between the trunk extensors and psoas major on the one hand, and the trunk flexors and hip extensors on the other. While attractive to some, this theory is without proper foundation. In the first instance, it is unclear how the imbalance comes to be painful: whether the pain arises from one or other of the muscles involved or whether the imbalance somehow stresses an underlying joint. Belief in the theory is founded on the clinical detection of muscle imbalance, but the reliability and validity of the techniques used have never been determined, and so-called muscle imbalances have been pronounced as abnormal without proper comparison to normal biological variation. Objective corroborating evidence is required before this theory attracts more widespread credibility.

Trigger points

Trigger points are tender areas occurring in muscle capable of producing local and referred pain. They are characterised by points of exquisite tenderness located within palpable bands of taut muscle fibres. Clinically, they are distinguished from tender areas by the presence of the palpable band of fibres, which, when snapped, elicits a localised twitch response in the muscle, and which when pressed reproduces the patient’s referred pain.¹⁵³ The pain is relieved if the trigger point is injected with local anaesthetic.

Trigger points are believed to arise as a result of acute or chronic repetitive strain of the affected muscle,¹⁵³ or ‘reflexly’ as a result of underlying joint disease.¹⁵⁴ Histological and biochemical evidence as to the nature of trigger points are incomplete or inconclusive,¹⁵³ but they are believed to represent areas of hypercontracted muscle cells that deplete local energy stores and impair the function of calcium pumps, thereby perpetuating the contraction.^153–155 Pain is said to occur as a result of obstruction of local blood flow and the accumulation of algogenic metabolites such as bradykinin.¹⁵³

Trigger points have been reported to affect the multifidus, longissimus and iliocostalis muscles,¹⁵⁶ and the quadratus lumborum.¹⁵⁷ However, it is not known how often they are a cause of back pain as the diagnostic criteria are so hard to satisfy.

For the diagnosis of trigger points in the iliocostalis and longissimus muscles, the kappa scores for two observers agreeing ranged from 0.35 to 0.46, which is less than satisfying.¹⁵⁸ Similar scores obtain for trigger points in the quadratus lumborum and gluteus medius.¹⁵⁹ It is only if the diagnostic criteria for trigger points are relaxed, to exclude palpable band and twitch response, that acceptable kappa scores are achieved,¹⁵⁹ but this changes the diagnosis from one of ‘trigger point’ to one of ‘tender point’ in the muscle.

Without reliable criteria for diagnosis, it is not possible to estimate the prevalence of trigger points as a cause of back pain. If classic criteria are used strictly, trigger points seem to be uncommon.¹⁵⁹ Tenderness, on the other hand, seems to be quite common but does not constitute a diagnosis.

Compartment syndrome

At its attachment to the supraspinous ligaments, the thoracolumbar fascia is well innervated.^126,127,160 However, little is known about the innervation of its central portions. There is only a mention in one study that it contains nociceptive nerve endings.¹⁶¹ Nevertheless, it would appear that the fascia is appropriately innervated to be a source of pain if excessively stretched.

Since the thoracolumbar fascia encloses the back muscles, it forms a compartment surrounding them, and this has attracted the proposal that the back may be affected by a compartment syndrome.^162,163 The concept is that, in susceptible patients, the back muscles swell during and following activity but their expansion is restricted by the thoracolumbar fascia. Pain presumably arises as a result of excessive strain in the fascia.

The clinical marker of such a compartment syndrome would be raised intracompartmental pressure, but clinical studies have yielded mixed results. In one study, a series of 12 patients was investigated for suspected compartment syndromes. Only one patient exhibited sustained, elevated pressures in the compartment on the side of pain.¹⁶⁴ In another study, however, seven patients were identified whose compartment pressure rose above normal upon flexion and was associated with the onset of back pain; fasciotomy reportedly relieved their pain.¹⁶⁵ However, while offering intriguing results, this study did not rigorously report the variance of pressures in the control group and other diagnostic groups who also exhibited raised pressures. Therefore, it is not evident how unique the feature of raised pressure is to compartment syndrome.

Fat herniation

The posterior layer of thoracolumbar fascia is fenestrated to allow the transmission of the cutaneous branches of the dorsal rami. These sites may be associated with painful herniations of fat.^166–173 It is unclear exactly how these herniations actually cause pain, but reportedly the pain can be relieved by infiltrating the site with local anaesthetic. In this regard, painful fat herniations resemble trigger points, but are distinguished clinically from trigger points by their extramuscular, subcutaneous location. Their prevalence is unknown.

Interspinous ligaments

The interspinous ligaments receive an innervation from the medial branches of the lumbar dorsal rami,^{44,105,124–127} and experimental stimulation of the interspinous ligament produces low back pain and referred pain in the lower limbs.^190–192 This renders the interspinous ligament as an attractive source of low back pain.

Post-mortem studies have shown that the interspinous ligaments are frequently ‘degenerated’ in their central portions,¹⁸⁶ but it is not known whether or not such lesions are painful. Otherwise, it is conceivable that interspinous ligaments might be subject to strain following excessive flexion of lumbar motion segments, but evidence of this is currently still lacking, even by way of comparing clinical history with the presence of midline interspinous tenderness and relief of pain following infiltration with local anaesthetic.

Clinical studies of the prevalence of interspinous ligament sprain are sobering. Steindler and Luck¹⁹³ reported that in a heterogeneous population of 145 patients, 13 obtained complete relief of their pain following anaesthetisation of interspinous ligaments, suggesting a prevalence of less than 10%. A more recent audit of the experience of a musculoskeletal general practice found only 10 patients in a series of 230 whose pain could be relieved by anaesthetising an interspinous ligament.¹⁹⁴ Since these injections were not controlled, the observed prevalence of 4% must be construed as a best-case estimate.

Iliolumbar ligament

The iliolumbar ligament has not explicitly been shown to have an innervation but presumably it is innervated by the dorsal rami or ventral rami of the L4 and L5 spinal nerves. Biomechanically, the iliolumbar ligament serves to resist flexion, rotation and lateral bending of the L5 vertebra,^195–197 and could therefore be liable to strain during such movements. However, the evidence implicating the iliolumbar ligament as a source of back pain is inconclusive.

Some investigators have regarded tenderness over the posterior superior iliac spine as a sign of iliolumbar ligament sprain¹⁹⁸ but this is hard to credit, for the ligament lies anterior to the ilium and is buried by the mass of the erector spinae and multifidus. Consequently, tenderness in this region cannot be explicitly ascribed to the iliolumbar ligament. Some have claimed to have relieved back pain by infiltrating the iliolumbar ligament,¹⁹⁹ but because of the deep location of this structure, there can be no guarantee that, without radiological confirmation, the ligament was accurately or selectively infiltrated.

Other investigators have been more circumspect in interpreting tenderness near the posterior superior iliac spine, and question whether the pain stems from the iliolumbar ligament, the lumbosacral joint or the back muscles.^200–202 Indeed, radiographic studies of injections made into the tender area reveal spread, not into the iliolumbar ligament but extensively along the iliac crest.¹⁹⁸ Accordingly, the rubric – iliac crest syndrome – has been adopted to describe this entity.^200,201 Others have referred to it simply as lumbosacral strain.²⁰²

What all investigators have overlooked is that the site of tenderness in iliac crest syndrome happens to overlie the site of attachment of the lumbar intermuscular aponeurosis (LIA), which constitutes a common tendon for the lumbar fibres of longissimus thoracis.^203,204 The LIA attaches to the iliac crest rostromedial to the posterior superior iliac spine and exhibits a morphology not unlike that of the common extensor origin of the elbow. Thus, a basis for pain and tenderness in this region could be a tendonopathy of the LIA. On the other hand, it could be no more specific than tenderness in the posterior back muscles, which has been recognised for many years under different rubrics.^202,205,206

Regardless of its underlying pathology, the putative advantage of recognising an iliac crest syndrome is that perhaps specific therapy might be applied. In this regard, if iliac crest syndrome is defined simply as tenderness over the medial part of the iliac crest, the kappa score for its diagnosis is 0.57.²⁰⁷ If the criteria are extended to include reproduction of typical pain, the kappa score rises to 0.66.²⁰⁷ These scores indicate that the syndrome can be identified. Its prevalence seems to be about 30–50%.²⁰⁰ However, as long as the syndrome amounts to no more than tenderness, it is not evident whether it is a unique disorder or a feature that could occur in association with other sources and causes of back pain.

Recognising the syndrome, however, has little impact on treatment. Injecting the area with local anaesthetic is significantly more effective than injecting it with normal saline, but only some 50% of patients benefit and only 30% obtain more than 80% improvement.²⁰⁰

Prevalence

In the past, the criterion standard for diagnosing lumbar zygapophysial joint pain was complete relief of pain following anaesthetisation of one or more of these joints.^236–238 However, it has now been shown that such blocks are not valid because they are associated with an unacceptable false-positive rate.^237,239 Only one in three patients who respond to a first diagnostic block respond to subsequent repeat blocks.²³³ Moreover, the placebo response rate to diagnostic blocks is 32%.²³⁴ This means that previous data, based on uncontrolled diagnostic blocks, overestimate the prevalence of this condition.

To be valid, diagnostic blocks must be controlled in some way, in each and every patient. Unless such precautions are taken, for every three apparently positive cases, two will be false-positive.²³⁴

Using controlled diagnostic blocks, several studies have tried to estimate the prevalence of lumbar zygapophysial joint pain. Variously they have reported the prevalence to be 15% in a sample of injured workers in the USA,²³² 40% in an Australian population of elderly patients in a rheumatology practice²³⁴ and 45% among patients of various ages attending a pain clinic in the USA.²⁴⁰

Collectively, these studies suggest that lumbar zygapophysial joint pain is quite common. However, in all of these studies the criterion for a positive response to blocks was not complete relief of pain but only at least 50% relief of pain. This is a somewhat contentious criterion, for it does not explain the remnant pain. Although the investigators presumed that incomplete relief of pain indicates another, concurrent source of pain, this has never been verified. The only studies that have addressed this question found that multiple sources of pain, in the one patient, were uncommon. Patients tend to have discogenic pain, sacroiliac joint pain, or lumbar zygapophysial joint pain, in isolation. Fewer than 5% have zygapophysial joint pain as well as discogenic pain,²⁴¹ or lumbar zygapophysial joint pain as well as sacroiliac joint pain.²²⁶ The alternative interpretation – that back pain was imperfectly relieved by the blocks – has not been excluded. If the latter applies, the cited prevalence rates may be an overestimate.

When complete relief of pain, following lumbar zygapophysial joint blocks, has been used as the criterion for zygapophysial joint pain, studies have reported a much lower prevalence: substantially less than 10%.^242,243 In a general population, therefore, lumbar zygapophysial joint pain may not be as common as previously believed. Nevertheless, one study, which used 90% relief of pain as the criterion, did find the prevalence of lumbar zygapophysial joint pain to be 32% in an elderly population.²³⁴

Overall, it would seem that amongst younger workers with a history of injury to their lumbar spine, lumbar zygapophysial joint pain is uncommon, accounting for 10% or less of these patients. Amongst older patients, with no history of injury, the prevalence is greater, and may exceed 30%.

Clinical features

Despite beliefs to the contrary,^244,245 controlled studies have shown that lumbar zygapophysial joint pain cannot be diagnosed clinically.^232,234,246 Controlled diagnostic blocks are the only means available to date of establishing a diagnosis of lumbar zygapophysial joint pain.

Pathology

Although the prevalence of zygapophysial joint pain is known, what remains elusive is its pathology. The lumbar zygapophysial joints can be affected by rheumatoid arthritis,^247–249 ankylosing spondylitis²⁵⁰ or un-united epiphyses of the inferior articular processes,^251–253 and there have been case reports of rare conditions such as pigmented villonodular synovitis^254,255 and suppurative arthritis.^256–259 However, these conditions have not been identified as the cardinal causes of pain in patients responding to diagnostic zygapophysial joint blocks.

Post-mortem studies^131,260,261 and radiological surveys^262,263 have shown that the lumbar zygapophysial joints are frequently affected by osteoarthrosis, and studies of joints excised at operation revealed changes akin to chondromalacia patellae.²⁶⁴ Although it is asserted that zygapophysial arthritis is usually secondary to disc degeneration or spondylosis,¹³¹ in about 20% of cases it can be a totally independent disease.²⁶⁰

The prevalence of zygapophysial osteoarthrosis attracts the belief that this condition is the underlying cause in patients with zygapophysial joint pain.^{244,264–266} However, on plain radiographs zygapophysial osteoarthrosis appears as commonly in asymptomatic individuals as in patients with back pain.^262,263 Features indicative of osteoarthritis on CT scans were once held to be indicative of zygapophysial joint pain^264,265,267 but controlled studies have shown that CT is of no diagnostic value for lumbar zygapophysial joint pain.²⁶⁸ These data preclude making the diagnosis of painful zygapophysial arthropathy on the basis of plain radiography. They also indicate either that osteoarthrosis is not a cause of zygapophysial joint pain or that, when it is, the pain is due to some factor other than the simple radiological presence of this condition.

Injuries

Biomechanics studies have shown that the lumbar zygapophysial joints can be injured in a variety of ways and to various extents.

Extension of the lumbar spine may be limited by impaction of an inferior articular process on the lamina below (see Ch. 8). Under these conditions, continued application of an extension force results in rotation of the affected segment around the impacted articular process, which draws the inferior articular process of the contralateral zygapophysial joint backwards (Fig. 15.1). As a result, the capsule of that joint is disrupted.²⁶⁹

Figure 15.1 Extension injury to a lumbar zygapophysial joint. When extension is arrested by impaction of an inferior articular process on the lamina, the contralateral inferior articular process is forced backwards into rotation, resulting in capsular disruption.

Rotation of a lumbar intervertebral joint normally occurs around an axis located in the posterior third of the vertebral bodies and intervertebral disc (see Ch. 8). Rotation is limited by impaction of the zygapophysial joint opposite the direction of movement but if torque continues to be applied rotation can continue around a new axis located in the impacted joint. As a result, the contralateral inferior articular process is drawn backwards and medially and the joint capsule on that side is disrupted (Fig. 15.2). The lesions that occur in biomechanics experiments include tears of the capsule, avulsion of the capsule or fracture-avulsion of the capsule.²⁷⁰ The impacted joint may sustain fractures of its subchondral bone or articular processes, or the pars interarticularis may fail.^271–276

Figure 15.2 Torsion injuries to a lumbar intervertebral joint. (A) Rotation initially occurs about an axis through the posterior third of the intervertebral disc but is limited by impaction of a zygapophysial joint. (B) Further rotation occurs about a new axis through the impacted joint; the opposite joint rotates backwards while the disc undergoes lateral shear. (C) The impacted joint may suffer fractures of its articular processes, its subchondral bone or the pars interarticularis; the opposite joint may suffer capsular injuries. (D) Subjected to torsion and lateral shear, the anulus fibrosus suffers circumferential tears.

Capsular tears, capsular avulsion, subchondral fractures, intra-articular haemorrhage and fractures of the articular processes, such as those produced in biomechanics studies, have all been found in post-mortem studies.^277,278 However, in no case were any of these lesions evident on plain radiographs.

Fractures of the zygapophysial joints have occasionally been recorded in the past in the radiology literature^{251,279–281} but by and large, these fractures cannot be detected on plain radiographs.^277,278 Fractures should be visible on CT scans although fractures have not been reported in the CT scans of patients with proven painful lumbar zygapophysial joints.²⁶⁸ Thus, fractures are either not the basis for most cases of zygapophysial joint pain, or they are too small or subtle to be detected by conventional use of lumbar CT.

Lesions such as capsular tears cannot be detected by radiography, CT or MRI. It may be that these lesions underlie zygapophysial joint pain, or it may be that the mechanism of pain is due to some process that is both radiologically invisible and still to be determined.

Meniscus extrapment

A relatively common clinical syndrome is ‘acute locked back’. In this condition, the patient, having bent forward, is unable to straighten because of severe focal pain on attempted extension. Because this condition does not lend itself to high resolution investigations like CT scanning and MRI, its cause remains speculative. However, theories have been advanced involving the concept of meniscus extrapment.

Normal lumbar zygapophysial joints are endowed with fibroadipose meniscoids (see Ch. 3),^282,283 and following trauma, segments of articular cartilage still attached to joint capsules may be avulsed from the articular surface to form an acquired cartilaginous meniscoid.²⁸⁴ These meniscoid structures could feasibly act as loose bodies within the joint or be trapped in the subcapsular pockets of the joints.

Upon flexion, one of the fibroadipose meniscoids is drawn out of the joint but upon attempted extension it fails to re-enter the joint cavity (Fig. 15.3). Instead, it impacts against the edge of the articular cartilage, and in this location it buckles and acts like a space-occupying lesion under the capsule, causing pain by distending the capsule.²⁸⁵ Maintaining flexion is comfortable for the patient because that movement disengages the meniscoid. Treatment by manipulation becomes logical. Passive flexion of the segment reduces the impaction, and rotation gaps the joint, encouraging the meniscoid to re-enter the joint cavity (see Fig. 15.3).²⁸⁵

Figure 15.3 Meniscus extrapment. (A) Upon flexion, the inferior articular process of a zygapophysial joint moves upwards, taking a meniscoid with it. (B) Upon attempted extension, the inferior articular process returns towards its neutral position but the meniscoid, instead of re-entering the joint cavity, impacts against the edge of the articular cartilage, and buckles, forming a space-occupying ‘lesion’ under the capsule. Pain occurs as a result of capsular tension, and extension is inhibited. (C) Manipulation of the joint, involving flexion and gapping, reduces the impaction and opens the joint to encourage re-entry of the meniscoid into the joint space (D).

This condition of meniscoid entrapment is only theoretical, for it is difficult, if not impossible, to visualise meniscoids radiologically. However, it reigns as one of the plausible explanations for some cases of acute locked back, particularly those amenable to manipulative therapy.²⁸⁵

Disc stimulation

Despite its chequered and controversial history, disc stimulation (formerly known as discography) remains the only means of determining whether or not a disc is painful.^293–295 The procedure involves introducing a needle into the nucleus pulposus of the target disc and using it to distend the disc with an injection of normal saline or contrast medium.²⁹⁵ The test is positive if upon stimulating a disc the patient’s pain is reproduced provided that stimulation of adjacent discs does not reproduce their pain.^1,295,296 Moreover, modern guidelines insist that the pressure of injection is critical.²⁹⁵ Discs are considered symptomatic only if pain is reproduced at pressures of injection less than 50 psi and preferably less than 15 psi.

At low pressures of injection, disc stimulation does not cause pain in normal volunteers. In a normal disc the innervated outer third of the anulus fibrosus is buffered by the dense inner two-thirds of the anulus fibrosus from mechanical and chemical stimuli directed to the central nucleus pulposus. The anulus fibrosus is designed to withstand immense pressures within the nucleus pulposus, and therefore one should not expect disc stimulation to be able to cause pain in a normal disc. Only at high pressures of injection, over the order of 80 psi or more, are some discs painful in normal individuals.

Previous studies that reported painful stimulation of discs in normal volunteers²⁹⁷ have been refuted on methodological grounds,²⁹⁸ and a stringent study found no painful discs in asymptomatic individuals.²⁹⁹ A more recent study found painful discs in only 10% of normal volunteers.³⁰⁰ Another study showed that discs are not painful in normal volunteers if they are stimulated at pressures less than 40 psi.³⁰¹ A systematic review found that disc stimulation has a false-positive rate of less than 10%.³⁰² Disc stimulation, therefore, is specific for painful discs, and a positive response implies an abnormality that has rendered the disc painful.

This experience with stimulation of lumbar discs by injection has been complemented by another approach. Discs can be stimulated thermally, by heating a wire electrode inserted into the anulus of the disc.³⁰³ Heating the disc evokes pain, which is initially perceived in the back, but which can be referred in different patterns into the lower limb. The referred pain may be perceived in the buttock, or posterior thigh, and even in the leg (i.e. below the knee). Since the noxious stimulus is restricted to the disc, and does not affect the nerve roots, thermal heating provides evidence not only that lumbar discs can be painful, but also that they can be responsible for somatic referred pain in the thigh and leg.

Pathology

At present, data on the pathology of disc pain are incomplete and are largely circumstantial but there are sufficient data to enable three entities to be described: discitis; torsion injuries; and internal disc disruption.³⁰⁴

Torsion injury

When an intervertebral joint is forcibly rotated, injuries can occur to the disc as well as the posterior elements (see Fig. 15.2). Rotation about the normal axis of rotation pre-stresses the anulus, but once further rotation ensues around the secondary axis through the impacted zygapophysial joint (see Fig. 15.2B), the disc is subjected to an additional lateral shear. The combination of torsion and lateral shear results in circumferential tears in the outer anulus (see Fig. 15.2D).^270,307,308 The risk of injury is greater if rotation is undertaken in flexion, for then the flexion pre-stresses the anulus to a near maximal extent, and the added rotation takes the collagen fibres of the anulus beyond their normal strain limit.³⁰⁹

In discs with concave posterior surfaces, circumferential tears occur in the posterolateral corner of the anulus fibrosus; in discs with convex posterior surfaces the tears occur posteriorly. The reason for these locations lies in the stress distribution across a disc subjected to torque.^273,308 These are locations where the lamellae of the anulus fibrosus exhibit the greatest relative curvature and where torsional strains are maximal. Consequently, they are sites where collagen fibres are most likely initially to fail under torsion.

Torsion injuries, however, are only a theoretical diagnosis. The condition can be suspected on clinical grounds given the appropriate mechanical history of a flexion–rotation strain. Neurological examination is normal because the lesion is restricted to the anulus fibrosus and does not involve nerve root compression. For the same reason, CT scanning, myelography and MRI are normal, and discography will be normal since the nucleus pulposus is not involved in the lesion. The condition is essentially a ligament sprain and behaves as such. Theoretically, the pain should be aggravated by any movements that stress the anulus fibrosus, but in particular flexion and rotation in the same direction that produced the lesion.³¹⁰ However, these clinical features are not enough to prove the diagnosis.

Circumferential tears of the anulus are not visible on any contemporary imaging technique, including MRI,³¹¹ but it is possible to identify the lesion by other means.^312,313 Contrast medium and local anaesthetic can be injected into the putatively painful tear in the anulus fibrosus. If the tear is painful, the local anaesthetic relieves the pain, and the contrast medium outlines the tear, which can then be seen on a post-procedural CT scan as a crescent in the outer anulus fibrosus (Fig. 15.4).

Figure 15.4 A CT scan diagram of a torsion injury. Contrast medium and local anaesthetic were injected into a putatively painful circumferential tear in the anulus fibrosus. The contrast medium shows that the injectate was deposited in a crescent fashion in the anulus. The local anaesthetic abolished the patient’s pain. The nucleus is outlined because of an earlier discogram, which was painless.

(Courtesy of Hunter Valley X-Ray, Newcastle, Australia.)

This procedure, however, is still experimental, and no studies have reported the prevalence of torsion injuries diagnosed in vivo. Consequently, torsion injury remains a theoretical diagnosis but one that may assume greater prominence in the future.

Internal disc disruption

Internal disc disruption (IDD) has emerged as the most extensively studied, and best understood, causes of chronic low back pain. For no other condition are there such strong correlations between the morphology of the condition, its biophysics and pain.

Morphologically, IDD is characterised by degradation of the nuclear matrix and the presence of radial fissures, extending from the nucleus into the anulus fibrosus. For descriptive purposes, the fissures can be graded according to the extent to which they penetrate the anulus (Fig. 15.5):³¹⁴

• Grade 1 fissures reach only the inner third of the anulus.

• Grade 2 fissures reach the second, or middle, third.

• Grade 3 fissures extend into the outer third of the anulus.

• Some investigators recognise a fourth grade, which is a grade 3 fissure that expands circumferentially around the outer anulus.³¹⁵

Figure 15.5 Grades of radial fissures in internal disc disruption. Grade 1: disruption extends into the inner third of the anulus fibrosus. Grade 2: disruption extends as far as the inner two-thirds of the anulus. Grade 3: disruption extends into the outer third of the anulus fibrosus. Grade 4: a grade 3 fissure spreads circumferentially between the lamellae of the outer anulus.

IDD is not disc degeneration, as commonly understood. It is not a diffuse process affecting the entire disc. Rather, it is a focal disorder, affecting a single sector of the anulus fibrosus. The remainder of the anulus remains intact and normal.

Also, IDD is not equivalent to disc herniation. Although the radial fissures contain nuclear material, that material has not herniated. It remains contained within the disc. The external perimeter of the anulus remains intact. The disc may exhibit a diffuse bulge, but there is no focal protrusion of nuclear material beyond the normal perimeter of the anulus.

The extent to which the anulus is penetrated by radial fissures correlates strongly with the affected disc being painful on disc stimulation.^316,317 Grade 1 fissures are typically not painful. Grade 2 fissures may or may not be painful but some 70% of grade 3 fissures are associated with pain, and some 70% of painful discs exhibit a grade 3 fissure.³¹⁶.

This pattern correlates with the density of innervation of the disc. The inner third of the anulus lacks an innervation and so grade 1 fissures do not have access to a nerve supply. The middle third of the anulus may or may not have an innervation. So, grade 2 fissures may or may not have access to a nerve supply. The outer third of the anulus is consistently innervated. So, grade 3 fissures consistently have access to the nerve supply of the disc.

Studies using multivariate analysis have shown that IDD is independent of degenerative changes.³¹⁷ Degenerative changes increase with age but do not correlate with the disc being painful. Radial fissures occur at an early age and their prevalence does not increase with age. Yet fissures are strongly correlated with pain, independently of age changes (Table 15.2).³¹⁷

Table 15.2 The correlation between anular disruption and reproduction of pain by disc stimulation. The numbers refer to the number of patients exhibiting the features tabulated. χ² = 148; P < 0.001. (Based on Moneta et al. 1994.³¹⁷)

Discs affected by IDD exhibit abnormal stress profiles (see Ch. 8). Nuclear stresses are reduced, irregular or absent (Fig. 15.6).³¹⁸ Meanwhile, stresses in the posterior anulus are increased greatly above normal. These features indicate that the degraded nuclear matrix is no longer able to retain water and does not contribute to sustaining compression loads on the disc. Instead, the compression load is transferred to the posterior anulus.

Figure 15.6 The stress profile of a disc with internal disc disruption. The graph shows the irregular and reduced stress profile across the nucleus pulposus and a raised stress in the posterior anulus. The dotted line indicates the normal stress profile.

(Based on McNally et al. 1996.³¹⁸)

Each of these changes in the biophysical properties of the disc correlate with the disc becoming painful. Decreased nuclear stresses and increased stresses in the posterior anulus each correlate with reproduction of pain by disc stimulation (Table 15.3).³¹⁸

Table 15.3 The correlation between disc stimulation and changes in stress profile of the disc (Based on McNally et al. 1996.³¹⁸)

Collectively, these data constitute evidence of convergent validity. Different, and independent, techniques point to the same conclusion. IDD has a distinctive morphology that correlates strongly with pain and IDD has biophysical properties that correlate strongly with pain. For no other cause of low back pain have such multiple and strong correlations been demonstrated.

For many years, the aetiology of IDD remained elusive. It was addressed only by theoretical arguments. The reasons for this were that it was ethically impossible to induce IDD in normal volunteers, and it was not possible to study the evolution of the disorder in individuals affected by it because there is no marker of its onset.

Early proponents argued that IDD was the result of compression injuries to the disc. This proposition was based on intuition and studies of the mechanism of failure of discs subjected to compression.^{273,308,319,320} This is consonant with the available biomechanical evidence.

Despite traditional wisdom in this regard, when compressed, intervertebral discs do not fail by prolapsing. In biomechanical experiments, it is exceedingly difficult to induce disc failure by prolapse. Even if a channel is cut into the anulus fibrosus, the nucleus fails to herniate.^321–323 A normal nucleus is intrinsically cohesive and resists herniation. Even in specimens with partially herniated discs, completion of the prolapse rarely occurs even after repeated flexion and compression.³²⁴

When compressed, intervertebral discs typically fail by fracture of a vertebral endplate.^{323,325–330} The forces required are usually quite large,^327,331 of the order of 10 000 N, but can be as low as 3000 N.³³² Although seemingly large, these forces are of a magnitude such as might be encountered in a sudden fall, landing on the buttocks or as a result of forceful muscle activity.³³³ In a heavy lift, the back muscles can exert a longitudinal force of some 4000 N.³³⁴ It transpires, therefore, that certain individuals could be susceptible to compression injury of their vertebral endplates if their vertebral bodies were weaker than the maximum strength of their muscles.

In such individuals, fracture of the vertebral endplate could occur during unaccustomed inordinate heavy lifting, or if they maximally exerted their back muscles in activities such as pulling on a stubborn tree root while gardening. In these situations the individual voluntarily exerts their back muscles to a severe degree, but the muscles act on a vertebral column that is unaccustomed to bearing the large loads involved. Training and physical exercise appear to condition vertebral bodies, rendering them stronger and better able to withstand the longitudinal stresses imposed upon them by severe efforts of the back muscles,^331,335 but the risk of endplate fracture prevails if athletes, workers and other individuals with relatively weak vertebral endplates are not conditioned to their task, and take on lifting activities for which their back muscles might be capable but their vertebrae are not.

These considerations presuppose sudden static loading. However, modern research has shown that endplate failure can occur at loads substantially less than ultimate failure strength of the endplate, if the endplate is fatigued (see Ch. 8).

If a normal disc is repetitively loaded, in compression or in compression with flexion, at loads between 37 and 50% of its ultimate failure strength, it can resist 1000 or 2000 repetitions without failing.^336,337 However, if it is loaded to between 50% and 80% of its ultimate strength, the endplate can fail, by fracturing, after as few as 100 repetitions.³³⁶

These latter figures are within the ranges encountered during normal working activities. Loads of between 50% and 80% of ultimate compression strength of the disc are not atypical of those encountered in heavy lifting or bending, and 100 repetitions are not atypical of a normal course of work. Thus, instead of sudden compression loads, endplate fractures can occur as a result of fatigue failure after repeated, submaximal compression loading.

An endplate fracture is of itself not symptomatic and may pass unnoticed. Furthermore, an endplate fracture may heal and cause no further problems (Fig. 15.7). However, it is possible for an endplate fracture to set in train a series of sequelae that manifest as pain and a variety of endstages.

Figure 15.7 Endplate fracture. Compression of an intervertebral disc results in fracture of a vertebral endplate. The fracture may heal or may trigger degradation of the intervertebral disc.

Early proponents of internal disc disruption argued that an endplate fracture simply elicited an unbridled, inflammatory repair response^{273,274,308,319} that failed to heal the fracture but proceeded to degrade the matrix of the underlying nucleus pulposus.

Others subsequently ventured a bolder interpretation, suggesting that through the fracture, the proteins of the nuclear matrix are exposed to the circulation in the vertebral spongiosa, and elicit an autoimmune inflammatory response.^304,338,339 This proposal was based on evidence that showed that disc material was antigenic^55–59340 and was consistent with observations that acute intraosseous disc herniation was associated with inflammation of the spongiosa.³⁴¹ The model invited an analogy with the condition of sympathetic ophthalmia in which release of lens proteins after an injury to an eye causes an autoimmune reaction that, in due course, threatens the integrity of the healthy eye. What lens proteins and disc proteins have in common is that neither has ever been exposed to the body’s immune system, because the two tissues are avascular. Their proteins, therefore, are not recognised as self.

A more conservative interpretation could be that an endplate fracture interferes with the delicate homeostasis of the nuclear matrix. The matrix contains degradative enzymes whose activity is normally limited by tissue inhibitors of metalloproteinases.^{60,61,342–345} Furthermore, the balance between synthesis and degradation of the matrix is very sensitive to changes in pH.^344,346 This invites the conjecture that an injury, such as an endplate fracture, might disturb the metabolism of the nucleus, perhaps by lowering the pH, and precipitate degradation of the matrix without an explicit inflammatory reaction. Indeed, recent biochemical studies suggest that increased activation of disc proteinases occurs progressively from the endplate into the nucleus, and that these proteinases either may be activated by blood in the vertebral body or may even stem from cells in the bone marrow.³⁴⁷

Regardless of its actual mechanism, the endplate theory supposes that fractures result in progressive degradation of the nuclear matrix. Nuclear ‘degradation’ may appear synonymous with disc ‘degeneration’ and, indeed, other authors have implicated the same biochemical processes described above as the explanation for disc degeneration.³⁴⁸ However, they view this as an idiopathic phenomenon, and do not relate it to endplate fracture. In the present context, nuclear ‘degradation’ is not intended to mean ‘degeneration’. ‘Degeneration’ is an emotive term, conjuring images of inevitable decay and destruction, yet many of the pathological changes said to characterise disc degeneration are little more than normal age changes (see Ch. 13). In contrast, nuclear degradation is a process, initiated by an endplate fracture, that progressively destroys the nucleus pulposus. It is an active consequence of trauma not a passive consequence of age.

When degradation is restricted to the nucleus pulposus, proteolysis and deaggregation of the nuclear matrix result in a progressive loss of water-binding capacity and a deterioration of nuclear function. Less able to bind water, the nucleus is less able to sustain pressures, and greater loads must be borne by the anulus fibrosus. In time, the anulus buckles under this load and the disc loses height, which compromises the functions of all joints in the affected segment (Fig. 15.8). As a result, reactive changes occur in the form of osteophyte formation in the zygapophysial joints and anulus fibrosus. This state, characterised by osteophytes and disc narrowing, has been recognised clinically and described as ‘isolated disc resorption’,^348,349 which becomes symptomatic if nerve roots are compromised by canal stenosis or foraminal stenosis.

Figure 15.8 Disc degradation. If restricted to the nucleus pulposus, disc degradation may lead to isolated disc resorption. Otherwise, it results in internal disc disruption, which is characterised by degradation of the nucleus pulposus and radial fissuring of the anulus fibrosus. If fissures reach the periphery of the anulus fibrosus, the degraded nucleus may herniate if the disc is subjected to compression.

In Chapter 13, it was explained that disc narrowing is not a consequence of age: discs retain their height with age.³⁵⁰ A different explanation is required for disc narrowing, especially if it occurs at only one in five lumbar segments. The explanation lies in disc narrowing being a consequence of nuclear degradation following endplate fracture. However, disc narrowing and isolated disc resorption comprise only one possible endstage of disc degradation. This occurs when the anulus fibrosus remains intact circumferentially but when nuclear degradation and dehydration are severe.

In contrast, the water-binding capacity of the nucleus may not be so severely affected by nuclear degradation, whereupon the disc relatively retains its height. However, in time, nuclear degradation extends peripherally to erode the anulus fibrosus, typically along radial fissures, to establish the definitive features of internal disc disruption (see Fig. 15.8).

Ultimately, it is possible for internal disc disruption to progress to disc herniation (see Fig. 15.8). This occurs if the inflammatory degradation extends along a radial fissure for the entire thickness of the anulus. The conditions for disc herniation are thereby set – a defect has been produced in the anulus fibrosus and the nucleus pulposus has been denatured into a form that is expressible. In such a disc, compression loading during normal flexion may be sufficient to herniate the nucleus.

However, disc herniation is only one possible endstage of internal disc disruption, hence its relative rarity. In the meantime, the condition that prevails and renders the disc painful, without rupturing, is internal disc disruption.

Further evidence

Two lines of evidence have recently corroborated the importance of compression injury and endplate fracture in the aetiology of IDD. Both come from laboratory studies.

When cadaveric discs are repeatedly loading in compression, the onset of fatigue failure of the endplate can be detected by the sudden change in mechanical behaviour.³³³ Harvesting the specimen at this time reveals the endplate fracture (Fig. 15.9). When stress profiles in the disc have been monitored during loading, another correlate has appeared. At the time of failure, the disc exhibits the onset of the biophysical changes of IDD. Nuclear stresses reduce and posterior anulus stress rises sharply (Fig. 15.10).

Figure 15.9 The physical behaviour of a lumbar disc when subjected to cyclic compression loading. During early cycles the disc remains intact. Failure is indicated by a sudden loss of resistance. This coincides with the onset of an endplate fracture.

Figure 15.10 The stress profile of a disc at the time of failure when subjected to cyclic compression loading. There is a sudden decrease in nuclear stress and an increase in stress in the posterior anulus.

(Based on Adams et al. 1993.³³³)

In laboratory animals, experimental induction of an endplate fracture precipitates the biochemical, morphological and biophysical changes of IDD.³⁵¹ The water content of the nucleus decreases, and proteoglycans decrease, the inner anulus delaminates and nuclear pressure falls.

Both of these experiments addressed only the immediate effects of endplate fracture. Neither examined what the long-term effects might be. Therefore, the experiments did not produce the full effects of what might be called ‘full-blown’ IDD. Nevertheless, both showed the onset of the features of IDD. Together they provide strong circumstantial evidence that endplate fracture is the critical, initiating factor for the development of IDD.

Symptoms

The mechanism by which IDD becomes painful has not been explicitly demonstrated but two explanations apply. In the first instance, chemicals from the degraded nuclear matrix that enter the radial fissure might irritate nerve endings in the outer third of the anulus. This becomes the basis for chemical nociception from the disc. To this effect, there is evidence that inflammatory cells penetrate the anulus fibrosus of disrupted discs,³⁵² whereupon inflammatory chemical mediators may trigger nociceptive nerve endings.

Secondly, the disruption of the anulus provides a basis for mechanical nociception. In an intact anulus, mechanical loads would be borne uniformly across all the laminae of the anulus in any given sector. However, when a radial fissure penetrates the anulus, two-thirds or more of the laminae are disrupted and cannot contribute to resisting mechanical loads. Consequently, the load is thrust onto the remaining intact laminae, which, therefore, are required to bear three times their normal load.

Chemical and mechanical processes may act simultaneously. Chemicals may sensitise the nerve endings in the outer anulus and amplify their response to mechanical stimulation.

These models predict the clinical features of IDD. The chemical nociception would produce a background of constant, dull, aching pain that is difficult to localise but which is felt deeply in the back. Mechanical nociception would be manifest as aggravation of that pain by any movements that strain the outer anulus. Movements that strain the anulus most would be the cardinal aggravating factors. Meanwhile, movements that strain the anulus less would be less aggravating.

There would be no other specific clinical features. In particular, since there is no herniation of disc material, radicular pain or radiculopathy would be absent. The features are no more specific than constant pain aggravated by movements. These are the features exhibited by patients in whom IDD is detected.

Diagnosis

There are no means by which IDD can be diagnosed clinically. The diagnosis requires reproduction of the patient’s pain by disc stimulation, and the demonstration by postdiscography CT of a radial fissure (Fig. 15.11).

Figure 15.11 A CT discogram showing internal disc disruption. Contrast medium has been injected into the nucleus but outlines a radial fissure that spreads circumferentially around the anulus. The perimeter of the disc is intact; there is no herniation or disc bulge. This disc was symptomatic.

(Courtesy of Dr Charles Aprill, New Orleans, USA.)

In some patients, the condition can be detected by MRI. In these patients, internal disc disruption is manifest by a signal of high intensity in the posterior anulus (Fig. 15.12). This signal is discontinuous with that of the nucleus and is somewhat brighter. Empirically, the presence of this high-intensity zone correlates strongly both with the disc being painful and with the presence of a grade 4 radial fissure.^315,353 Morphologically, the high-intensity zone seems to have the appearance, in sagittal section, of nuclear material running circumferentially in the posterior anulus.³¹⁵ Its relative brightness distinguishes it from asymptomatic transverse fissures and suggests that symptomatic fissures are ones that somehow have become ‘activated’, perhaps by inflammation of the tissue contained in the fissure.

Figure 15.12 A magnetic resonance image of a lumbar spine showing a high-intensity zone lesion in the posterior anulus of the L4–L5 intervertebral disc.

A high-intensity zone is not exhibited by all patients who have IDD but it is evident in about 30% of patients with chronic back pain. When evident, it strongly implicates the affected disc as the source of pain.

Prevalence

IDD is the single most common detectable cause of chronic low back pain. Under the strictest of diagnostic criteria, and using worst-case analysis, its prevalence has been measured as 39%.²⁹⁶ Under more liberal criteria, and allowing for multilevel disease, its prevalence may be considerable higher than this.