Discogenic Pain, Internal Disc Disruption, and Radicular Pain

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39 Discogenic Pain, Internal Disc Disruption, and Radicular Pain

Discogenic pain (DP) and internal disc disruption (IDD) imply that the disc is the source of a patient’s spinal pain. As will be discussed further in this chapter, DP is a conceptual label that can be ascribed to a presentation of spinal pain but which cannot be verified by any known test. IDD is a specific entity that by definition pertains only to the lumbar discs and is diagnosed according to a tight protocol by provocation discography (PD). Both are diagnosed from a cohort of patients who present with nonspecific spinal pain (NSSP). Radicular pain is pain from a spinal nerve root. It is most commonly caused by disc prolapse and canal stenosis. It is far less common than NSSP and has a better natural history. Interventional management of NSSP is predicated on the ability to make a tissue-specific diagnosis, a process that requires the judicious use of interventional diagnostic techniques.

This chapter concerns the diagnosis of spinal pain; diagnosis being the cornerstone of a doctor/patient relationship. Various spinal interventions will be discussed in following chapters. Each intervention requires particular knowledge and technical ability. Unfortunately, knowledge of the indications for these procedures and more importantly, their technical performance, have often fallen short of the mark—even in scientific publications.^1,² This has lead to a persistent skepticism about their efficacy. This fact is most evident in the development of radiofrequency neurotomy (RFN) treatments, and in subsequent meta-analyses and systematic reviews that gave equal credence to results, whether or not the technique was accurate.³

Social and Economic Dimension of Spinal Pain

Low back pain (LBP) is a major health problem particularly in industrialized countries,⁴ affecting approximately 60% to 80% of the adult population at some stage⁵^–⁷ and about 6% of people each day.⁶ LBP affects up to 80% of the working population during their lifetime and is the second most common reason for physician visits,⁸ and for work disability.⁹ Although LBP is typically self-limiting,¹⁰ it is still associated with substantial health care costs and absenteeism from work.^4,^11,¹² Neck pain is also extremely common with a lifetime prevalence of 70%, a 1-year prevalence of 40%, and a point prevalence of 10% to 20%.¹³ Generalized musculoskeletal pain is also common: in one study of kitchen-hand workers it was present in 87%, and often present in multiple sites. In this study, neck pain was present in 71%, LBP in 50%, and forearm/hand pain in 49%;¹⁴ 73% had pain in at least two sites, 36% in four or more, and 10% in six to seven sites.¹⁴ In another study of 4006 workers from industrial and service companies, only 7.7% were free of regional pain of any description.¹⁵

In Australia, back problems are the most frequently seen musculoskeletal condition in general practice and the seventh most common reason for seeking care.¹⁶ In Australia, a 2001 survey found the point prevalence of LBP to be 26%, the 12-month prevalence 68%, and lifetime prevalence 79%.⁷ Only about 50% of the adult population experience low-intensity pain and low disability from it and another 11% experience high-intensity-pain but still low disability in a 6-month period.⁷ However, about 11% of the population experience high-disability LBP,^7,¹⁷ and it is to this group that most resources are presumably directed.

LBP is a costly problem. In early 2000, the cost of headache, LBP, arthritis and other muscle and joint pain to U.S. employers was more than $60 billion per year (these costs may have been underestimated because lost productivity among workers affected by a coworker’s diminished productivity was not taken into account).¹⁸ The majority of these costs (77%) related to reduced performance rather than work absence (workers who experienced lost productive time from a pain condition lost a mean of 4.6 hours/week). Workers who reported arthritis or LBP had mean lost productive times of 5.2 hours/week. It was established that these pains were directly associated with a 13% loss in productive time. Headache was the most common (5.4%) pain condition resulting in lost productive time. It was followed by LBP (3.2%), arthritis pain (2.0%), and other musculoskeletal pain (2.0%).

Furthermore, the total health care expenditure only for LBP in the United States is even more alarming. When studied in 1998, total health care expenditures incurred by individuals with LBP in the United States reached $90.7 billion and total incremental expenditures attributable to LBP among these persons were approximately $26.3 billion. On average, individuals with LBP incurred health care expenditures at 60% higher than people without LBP.¹⁹ The lead researcher, Xuemei Luo, put these figures into the perspective of the U.S. economy by noting: “The total $90 billion spent in 1998 represented 1% of the U.S. Gross Domestic Product, and the $26 billion in direct back pain costs accounted for 2.5% of all health care expenditures for that year.”

The largest proportion of direct medical costs for LBP is spent on physical therapy (17%) and inpatient services (17%), followed by pharmacy (13%) and primary care (13%).²⁰ However, indirect costs, especially resulting from lost work productivity, outweigh other costs substantially.²⁰

Nonspecific Spinal Pain

Nonspecific spinal pain (NSSP) is somatic referred pain derived from any spinal structure that is not associated with a specified “legitimate” or named condition. The issues for the clinician faced with a patient presenting with pain that appears to derive from the spine include (1) how to reliably determine that the pain indeed comes from the spine at all, (2) how to label the pain, (3) whether or not to try and make a tissue-specific diagnosis, and, if so, (4) how to make this tissue-specific diagnosis.

Careful history and examination may at least be helpful in determining that the pain comes from the spine and whether or not it is caused by a red-flag condition. If clinical examination produces pain, it is likely that the pain derives from the spine. As a corollary, the absence of any painful restriction of movement on clinical examination should alert the clinician to the possibility of distant referred pain and such a negative finding is, in itself, a “red-flag sign”.²¹ Radiologic techniques are not helpful in resolving whether or not regional spinal pain originates from a spinal structure at all; imaging can exclude only red-flag or exotic causes of pain.

Numerous studies on all imaging modalities used in the detection of morphologic changes in symptomatic and asymptomatic populations have failed to find significant differences that can be considered useful in any individual presentation of NSSP.²²^–⁴⁶ Astoundingly, this well developed scientific fact has still not penetrated into standard health care practice; consequently, certainly the public and regrettably, some heath practitioners, remain misinformed about the relevance of technology as it applies to NSSP. The perceived contribution of the disc to spinal pain has been skewed by inappropriate use of labeling in the field of radiology.⁴⁷ The label degenerative disc disease (DDD) pervades imaging reports and the scientific literature, yet there is no reasonable evidence to confirm DDD as being of any particular relevance to any single manifestation of NSSP. DDD is not a legitimate label for a patient with NSSP.

The convenient and honest label to apply to otherwise unidentifiable somatic referred pain from the spine is the generic term NSSP, a label that means that the pain is derived from some unspecified site and related to some unspecified pathologic process. A label of NSSP means that for most patients presenting with somatic referred pain that appears to derive from a spinal structure there is no tissue or pathology-specific diagnosis.

NSSP concentrates along the spine; early studies on pain referral patterns have shown that all of the innervated back structures can produce local pain with or without more distant referred pain.⁴⁸^–⁵⁴ When the pain is concentrated in the lumbar spine, it can be called nonspecific low back pain (NSLBP); in the cervical region, it is called nonspecific neck pain (NSNP). These terms are synonymous and equally as useful as terms such as idiopathic back (or neck) pain and low back (or neck) pain of unknown origin.

The pain experienced in NSSP is not necessarily confined to the region immediately adjacent to the spine, and it is this characteristic that provides the potential for errors in clinical judgment. The fact that NSSP can be associated with more distant referred pain (to the head particularly from the cervical spine, to the shoulder girdle and upper limb from the cervical and thoracic spines, to the chest and abdomen particularly from the thoracic spine, and to the lower limb from the lumbar spine and pelvis), has lead to mistaken management of many patients because it has often been assumed that NSSP in association with limb pain must be radicular pain. Radicular pain is not the same as referred pain—and this single differentiation is perhaps the most important fact to elicit on clinical examination after red-flag conditions have been eliminated as a possibility.

NSSP can be interpreted as being any pain that is thought to arise from an innervated somatic spinal structure where there is no substantive proof implicating any one structure. The label NSLBP means that the pain seems to come from some structure in the lumbar spine, and implies that there is no other information that can be simply gleaned to determine the source of this pain. On anatomic grounds, NSLBP could mean pain from one or more of any innervated structure, such as the discs, the zygapophyseal joints (ZJs), the sacroiliac joints, multifidus muscle, etc. However, as discussed earlier, NSLBP does not mean pain from disc or ZJ degeneration.

When a patient presents with NSNP or NSLBP this is the diagnosis, even though it is semantically unsatisfactory, especially to the patient. However, such a label provides a good model for explanation of the possible pathology that might be causing or contributing to their pain. When a named condition is determined, it is removed from the general category, such as NSLBP, to a specific category, such as ZJ pain. For example, if a patient presents after a motor vehicle accident with somatic referred type neck pain spreading to the shoulder girdle and there are no red-flag conditions, the initial diagnosis is NSNP or one of its cogeners. If double-blind diagnostic blocks are used to diagnose or exclude say C2-3 ZJ pain in a patient presenting with suboccipital pain and headache after a motor vehicle accident, and the result is positive, then there is a high certainty that the diagnosis is C2-3 ZJ pain. Thus, the patient presenting initially with the general diagnosis of NSNP is then placed into a more structured subgroup, in this case ZJ pain, or more specifically, C2-3 ZJ pain, but only after the appropriate tests have been undertaken. The same could apply to DP if there was a valid test. A patient presenting with NSSP can be slotted into the subgroup of DP if it is considered that there is a diagnostic test used for DP that is accurate. It should be noted that medial branch blocks for the diagnosis of ZJ pain, and discography for the diagnosis of IDD, are currently the best tests for each condition, because diagnosis based on history, physical examination, and investigations, including MRI, have proved to be invalid and generally unreliable. As has been discussed, there is at this stage no test for DP. There is a test for IDD.

A diagnosis of NSLBP is reasonable when a patient presents with, say, focal LBP with typical referred pain into the buttock and leg. One huge dilemma that has never been satisfactorily addressed is how to label the LBP component of a person who presents with widespread pain or pain in multiple sites, or how to label LBP if it is largely neuropathic in nature. Multiple pain sites might be present in a person with multiple injuries, but it also suggests a central pain processing process, and if so, it might suggest that tissue-specific diagnosis is likely to prove not helpful.

Referred Pain

Referred pain can theoretically derive from any locally innervated spinal structure. The mechanism for referred pain is convergence.⁵⁵ Somatic referred pain is pain evoked by the stimulation of the peripheral endings of nociceptive afferent fibers and is perceived in an ambiguous site due to the phenomenon of convergence when these afferents converge on second-order or third-order neurons in the central nervous system that happen also to receive afferents from the region to which the pain is referred.⁵⁶ Under those conditions, and in the absence of additional sensory input to clarify the situation, the brain is unable to identify the source of the pain accurately, and attributes it erroneously to the entire area subtended by the common neurons.^57,⁵⁸ Ambiguity as to the source of information arises, either or both, because the painful structure is not densely innervated, and the central pathways along which the information is relayed are not highly organized somatotopically.⁵⁹ NSSP is, therefore, different to radicular pain. Hence, lumbar ZJ pain,⁶⁰ lumbar disc pain,⁶¹^–⁶³ and sacroiliac joint pain⁶⁴ are described very differently to lumbar radicular pain.

Information about referred pain from deep somatic structures has arisen from numerous important studies that identified the nature and spread of referred pain.⁴⁸^–⁵⁴ Experiments on deep somatic referred pain by Kellgren⁵² in 1939 and Feinstein⁴⁴ in 1954 showed that pain from deep somatic structures can be felt not only locally but also in distant areas; pain from deep lumbar structures refers into the legs as far as the feet; similarly pain from deep cervical structures refers into the arms and hands (Fig. 39-1). Later Hirsch and colleagues placed needles into various lumbar structures in people with LBP and reported that the disc was the most sensitive area for LBP.⁵⁴ In this experiment, needles were placed into one or both of the lower two discs and into the ZJs, followed by the ligamentum flavum and the posterior ligamentous structures. When the disc was injected with 0.3 mL of saline a deep aching occurred across the low back. When the ZJ was injected, also with 0.3 mL saline, the ache spread also into the buttocks and lateral hips. Additionally, deep somatic pain felt three dimensional; it was described typically as deep and aching, but other terms used included gripping, boring, crampy, and lumpy.⁴⁸ Subsequently the pain from lumbar PD, in which intradiscal pressures probably rise above that used by Hirsch and colleagues, has been shown to be experienced as central low back pain that can also spread diffusely into the legs,⁶⁵ and certainly below the knees.⁶⁶ From these studies, various referral pain maps have been created, demonstrating that segmental referral patterns overlap substantially, and structures at one segmental level have similar pain referrals to other structures at the same level.⁶⁷ Thus, although the site of pain may be a clue to a particular spinal segment, it is not a pointer to the specific anatomic origin of pain.

Figure 39-1 Illustrations of referred pain patterns from injections of the interspinous ligaments with 6% saline using a 24 gauge needle.

(From Feinstein B, Langton JB, Jameson RM, et al: Experiments on pain referred from deep somatic tissues. J Bone Joint Surg Am 1954;36-A:981-997.)

From these studies, it is possible to construe that lumbar DP, or perhaps more specifically, lumbar IDD, is predominantly deep three-dimensional LBP that can spread diffusely into the legs. It is therefore possible to construct a clinical presentation that might be considered to be archetypal of, but not specific to, DP.

Similar patterns exist in the cervical spine. Cervical ZJ pain, as ascertained by anesthetic blocks rather than provocation, extends beyond the local region to the ipsilateral occiput, shoulder and/or periscapular region (Fig. 39-2).⁶⁷ Cervical disc pain, as ascertained by PD, can spread into the thoracic spine and the arms including the forearms, hands, and fingers.⁶⁸^–⁷⁰ Cervical PD at any level produces local neck pain that is unilateral as often as it is bilateral, with referral patterns as follows: C2-3 suboccipital and facial; C3-4 suboccipital, trapezius, anterior neck, face, shoulder, interscapular, and upper limb; C4-5 shoulder, interscapular, trapezius, extremity, face, chest and suboccipital; C5-6 trapezius, interscapular, suboccipital, anterior neck, chest and face; C6-7 interscapular, trapezius, shoulder, extremity and suboccipital; and C7-T1 interscapular (Fig. 39-3).⁷¹ Thus, cervical referred pain includes headache as well as arm, chest, shoulder, and thoracic pain.

Figure 39-2 Zygapophyseal joint (ZJ) referral patterns: note that the C5-6 and C6-7 segments refer pain into the scapular region.

(From Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns. I: A study in normal volunteers. Spine 1990;15:453-457.)

Figure 39-3 Illustrations of pain maps from cervical discography. A, C2-3 discogram pain referral map. B, C3-4 discogram pain referral map. C, C4-5 discogram pain referral map. D, C5-6 discogram pain referral map. E, C6-7 discogram pain referral map. F, C7-T1 discogram pain referral map.

(From Slipman CW, Plastaras C, Patel R, et al: Provocative cervical discography symptom mapping. Spine J 2005;5:381-388.)

Radicular Pain

NSSP and radicular pain can extend to the limbs; it is therefore important to ascertain which type of pain is more likely because each must be considered differently from clinical and pathophysiologic perspectives (Fig. 39-4).⁷² Radicular pain is not the same as referred pain.⁷⁴ Radicular pain is a particular type of neurogenic pain caused by direct injury to a sensory nerve root or dorsal root ganglion of a spinal nerve.^74,⁷⁵ Radicular pain is sometimes accompanied by objective signs of deficit or loss of neurologic function in a segmental distribution as a result of conduction block and it can coexist with spinal or somatic referred pain.^74,⁷⁵

Figure 39-4 A, Example of radicular pain (L5). B, Example of referred pain.

Cervical radicular pain tends to be deep, severe, aching pain, and as such is different from lumbar radicular pain.⁷⁴ Cervical radicular pain is experienced predominantly in the upper limb and shoulder girdle but when it occurs in the limb its distribution does not correspond to dermatomal maps of sensory deficit due to cervical radiculopathy.⁷³ Cervical radicular pain from the C6, C7, and C8 nerve roots is felt in the arm with pain extending into the forearm and hand (Fig. 39-5).⁷⁵ However, limb pain can also occur in referred pain, and because cervical radicular pain is uncommon, with an annual prevalence rate of 0.083% in one large population study,⁷⁶ deep aching arm pain is much more likely to be somatic referred pain than is cervical radicular pain.

Figure 39-5 Percent occurrence of symptom provocation per bit for C4 to C7 nerve roots. A, C4; B, C5; C, C6; D, C7.⁷³ Note that the figures depict anterior and posterior views.

In contrast, lumbar radicular pain is classically an intense narrow band of lancinating, sometimes burning pain that refers down the limb, and often to the foot.⁷⁷ The leg pain is typically more prominent than any LBP (indeed, LBP frequently is absent), and the leg pain tends to concentrate distally. Coughing, sneezing, straining at the toilet, and lifting will all classically exacerbate radicular pain, but such aggravating features are not specific to radicular pain. Pain is not limited to the dermatome and it may also be experienced in deep tissues innervated by the nerve.⁷⁸

Concepts: Discogenic Pain, Internal Disc

As at least the outer one third of the annulus fibrosus (AF) is innervated,⁷⁹^–⁸¹ the intervertebral disc is considered to be a possible source of pain that is otherwise labeled NSSP. There are five types of nerve terminations found in the lumbar disc: these have various morphologies and include simple and complex free nerve endings that concentrate particularly in the lateral disc, with a smaller amount posteriorly and the least amount anteriorly.⁷⁹ Discogenic pain (DP) is pain that is considered to arise intrinsically from the disc. DP is frequently bandied about and assumed as a diagnosis, but the plain fact is that it is a diagnosis that cannot be substantiated. With the use of PD, the entity IDD has been defined according to specific diagnostic criteria.⁸² IDD is considered to be a subtype of DP.

Is There a Relationship Between Disc Degeneration and Discogenic Pain?

Many published papers make the unsubstantiated statement that DD is a cause of NSSP. In fact, it has been clearly demonstrated that degeneration is not a term that can be used as a diagnosis of NSSP. Furthermore, the difference between aging and degeneration is not always clear; aging itself is not the major factor in the development of degeneration or spinal pain.

Cellular function within the disc is mediated by at least five major factors: genetics, nutrition (diffusion of nutrients and oxygen across the disc matrix), cell function regulation (via IL-1, TNF-α, and TNF-β), age and senescence, and mechanical loading.⁸³ The contribution to DD by genetic factors is highly significant; it may be as high as 80% in the cervical spine,⁸⁴ and general heritability for DD ranges from 29% to 80% in different regions of the spine.⁸⁴^–⁸⁶ In the lumbar spine, the genetic contribution is between 29% and 54%, with environmental influences of about equal importance.⁸⁷ For example, smoking has a moderate influence on the prevalence of DD,⁸⁷ presumably due to its effects on disc nutrition. This emphasizes that DD is not primarily or significantly caused by aging⁸⁸ or by mechanically induced “wear and tear” processes.^85,⁸⁹

Studies with various imaging modalities on symptomatic and asymptomatic populations further emphasize that DD does not imply NSSP. In the cervical spine, radiologic DD is present in 13% of men and 5% of women during the third decade, in 85% to 90% of the population by the sixth decade, and nearly 100% by the age of 70 years.⁹⁰ It occurs most commonly at C5-6, C6-7, and C4-5, respectively.^42,⁹¹ In people aged 60 to 65 years without neck pain, about 95% of men and 70% of women have at least one degenerative change on their cervical spine plain radiographs.⁴² Lumbar degeneration, defined as a grade of ≥2 by the Kellgren-Lawrence scale; is present in Japanese females in 9.7% of the ≤ 39 age group, in 28.6% of those 40 to 49 years, in 41.7% of those 50 to 59 years, in 55.4% of those 60 to 69 years, in 75.1% of those 70 to 79 years, and 78.2% of those ≥ 80 years; and in Japanese males in 14.3% of the ≤ 39 age group, in 45.5% of those 40 to 49 years, in 72.9% of those 50 to 59 years, in 74.6% of those 60 to 69 years, in 85.3% of those 70 to 79 years, and 90.1% of those ≥ 80 years.⁹² Although plain radiographic changes, including vertebral end-plate changes, disc space narrowing, spondylolisthesis, spondylolysis, sacral lumbarization, wedge vertebra, a sagittal diameter of less than 12 mm and abnormal lumbar lordotic angle,^44,^93,⁹⁴ have some predictive value for LBP, the relationship is mild at best,⁹⁵ and their detection is largely not helpful in the management of NSLBP because such changes occur frequently in the asymptomatic population.⁹⁶ Although disc space narrowing at 2 or more levels from L1-2 to L4-5 shows the strongest radiologic relationship with LBP,⁹⁷ similar comments apply. As a consequence, plain radiographs should not be ordered unless there is suspicion of a red-flag condition.⁹⁸^–¹⁰¹

The relevance of CT scanning is similar to plain radiographs; it is an excellent test for some red-flag conditions, demonstrates DD well, but it is not helpful in the detection of DP or ZJ pain. CT is better than MRI in detecting ZJ spondylitis,¹⁰² but this is of no particular clinical relevance. A newer technology, F-PET/CT (fluoride positron emission tomography with addition of CT) is more likely to be positive in symptomatic patients,¹⁰³ but only time will tell if it has satisfactory validity in detecting a truly painful structure.

Thus, there is no relationship between degeneration and NSSP and there is no demonstrable relationship between DD and DP.

Internal Disc Disruption and Discogenic Pain

The development of IDD as a concept emphasizes that abnormal morphology is not necessarily related to pain. IDD, a diagnosis that is defined by its diagnostic test, provocation PD, is pain perceived to arise from a disc that has undergone a specific type of degenerative process that is illustrated morphologically by radial tears in the AF. In addition, the diagnostic process recognizes that these changes may occur in the asymptomatic population, and as a consequence, clinicopathologic relationships only become evident when pain provocation or abolition is used to determine the painful from the painless disc. The degree of disc destruction itself is not a factor that can be relied on to delineate a structure causing a patient’s symptoms.

Diagnosis: Discogenic Pain and Internal Disc Disruption

There are two possible methods that can be used to ascertain that a disc is a source of pain—namely PD and specific nerve block. If the nerve supply of the disc could be done efficiently it would establish a prima facie case for DP. However, the complexities of disc innervation may preclude such an eventuality. Nevertheless, some clinicians have made attempts.

The Diagnosis of Discogenic Pain Using Specific Nerve Blocks

Lumbar discs are innervated by the lumbar sinuvertebral nerves, and branches of the lumbar ventral rami and gray rami communicantes (Fig. 39-6).¹⁰⁴^–¹⁰⁶ The posterior and posterolateral portion of each lumbar disc is innervated by a branch of the ventral ramus arising just lateral to the intervertebral foramen and by a branch of the gray ramus communicans just before it connects with the ventral ramus.¹⁰⁶ The sinuvertebral nerves also innervate the posterior longitudinal ligament; the gray rami communicantes also innervate the lateral disc and the anterior longitudinal ligament,^104,¹⁰⁶ and in rats the DRG innervates other lumbar structures, such as, lamina, spinous process, back muscle fascia, and skin.¹⁰⁷ The innervation by the gray rami communicantes is not a direct sympathetic innervation;¹⁰⁶ it has been postulated that somatic and afferent fibers from lumbar structures use the gray rami as transmission pathways only.^104,^108,¹⁰⁹ The rami communicantes branch from the spinal nerves just after they enter the intervertebral foramina, and then run anteriorly along the inferior third aspect of the vertebral body where they connect to the sympathetic trunk before branching to the lateral and anterolateral aspects of the discs above and below.^104,^110,¹¹¹

Figure 39-6 Innervation of the lumbar disc. Diagnostic and therapeutic injections, and thermal lesions, can target the sinuvertebral nerves and gray rami communicantes.

The innervation of the disc might be blocked entirely by dual sinuvertebral nerve root blocks and sympathetic blocks. Sinuvertebral or nerve root blocks target the posterolateral innervation directly, but they are nonspecific because the spinal nerve and DRG are also blocked, and because epidural spread might produce further problems of interpretation.

Various studies have been used to support or refute the utility of blocking the innervation of the disc.¹¹²^–¹¹⁵ Although the nerve supply of the disc is nonspecific, if a local anesthetic block aimed at these nerves totally eradicated pain under controlled conditions, it might be possible to devise a treatment directed at the nerve similar to that performed for medial branch RF neurotomy. If this was the case, the interpretation would be that the pain was mediated by this particular nerve, not that the pain was necessarily discogenic.

The Diagnosis of Discogenic Pain or IDD Using Anesthetic Discography

The disc itself can be blocked by intradiscal injection. Analgesic discography (AD) and functional analgesic discography are refinements of the technique of PD aimed at increasing the utility of discography and, in particular, its specificity.¹¹⁶ However, the current definition of IDD does not include any statement about AD. There is no role for AD in discs with breaches through the outer lamellae (Dallas grade V) because pain reduction with leakage of any anesthetic agent into the epidural space could be a false-positive finding. This is the primary reason why there is at present no method for the diagnosis of DP in general; it is probable that discs with breaches in the outer lamellae can be a source of pain, but there is no valid method to make this connection. The problem with AD is that the anesthetic may not reach the painful radial tear owing to the dilution effect of contrast. If AD is to be used, it probably should be done directly via injection into the radial fissure.

The Diagnosis of IDD with Discography

Although lumbar DP cannot be diagnosed using imaging, there is a significant relationship between disc morphology as determined by discography, and clinical pain as determined by the subjective provocation phase of PD. As a consequence, a particular cohort of otherwise labeled NSLBP patients can be defined as having IDD,¹¹⁷ a specific subtype of DP.

Studies and reports on intradiscal therapies for putative DP have largely been drawn from patients diagnosed with IDD on the basis of PD. Discussion about the role and interpretation of PD can be found in Chapter 38. PD is used to confirm or deny the diagnosis of IDD, allowing for (1) enhanced ability to make a decision on interventional treatment—be it intradiscal therapy or spinal surgery; and (2) cessation of the search for other pain sources. The specificity of PD and, hence, the robustness of the diagnosis IDD has been questioned because of its propensity for false-positive findings.¹¹⁸^–¹²³ This can be minimized by careful patient selection; the risk of false positive findings is substantially diminished by selecting subjects with normal psychometric profiles who do not have pain in other regions.^119,¹²⁰ It would be folly to perform PD on a patient with fibromyalgia! The criteria for IDD are specifically applied to the lower lumbar spine (Table 39-1). There is insufficient research on other areas of the spine to consider that intradiscal therapies have any traction in the cervical and thoracic spine for such regional NSSP presentations. In the cervical spine the disc cannot be pressurized because fissures are present in normal adult discs.¹²⁴ Nevertheless, intradiscal therapies have been trialed in other regions.

Table 39-1 Eligibility Criteria for IDD Treatment

Chronic, disabling NSLBP

Failure to respond to noninvasive treatments

No red-flag conditions

No evidence of radicular or neuropathic pain

No psychological barriers

No greater than 25% loss of disc height

Criteria for IDD by provocation discography satisfied

IDD, internal disc disruption; NSLBP, nonspecific low back pain.

Discography arose because of its ability to detect morphologic changes in the disc that were not seen on other imaging techniques. However, the defining component of discography has been the pain response, not the morphologic changes alone. Clinicopathologic correlations have been found implicitly in IDD. The concept of IDD is supported by various biomedical features.

• Degenerative changes do not correlate with either positive pain response from discography or pain prevalence in general.

• Grade 3 fissures correlate strongly with pain, and are not related to age changes.

• IDD discs have abnormal stress profilometry:¹²⁵

• NP stresses are irregular and reduced, even to zero, whereas in normal discs there is uniform distribution of stress throughout all components.

• Posterior AF stresses are increased.

• Altered NP pressure can arise experimentally from end-plate fatigue failure,¹²⁶ which has been demonstrated to occur with loads that are consistent with moderately heavy work activities.¹²⁷

• The biologic features of IDD have been reproduced in live animal experiments.¹²⁸

• The process of fibrosis is distinctly different in discs with IDD compared to control discs.¹²⁹

This last point is likely to be highly significant. The histology of discs that have been diagnosed with IDD using PD is different for discs in patients without LBP that have been assessed by PD as negative but degenerate on MRI and for cadaver discs that are macroscopically normal; the major difference is that in IDD there is a chronic inflammatory reaction with variable blood vessel infiltration.¹²⁹ More specifically, the AF loses its normal lamellar structure, is disorganized and disrupted, and the fibers are cross-fused; the NP is markedly fibrosed, inflamed, and infiltrated with blood vessels.¹²⁹ Additionally, immunohistochemical staining shows strong connective tissue growth factor (CTGF) expression in IDD discs, weak expression in asymptomatic DDs, and no expression in adjacent control discs in patients with IDD.¹²⁹

CTGF is the downstream effector mediated by transforming growth factor-β1 (TGF-β1).¹³⁰ CTGF is “closely associated with the regulation of cell proliferation and differentiation and the fibrosis of tissues and organs, and can induce the in vivo expression of the gene involved with fibroblast extracellular matrix composition.”¹³⁰ CTGF has a number of functions, one of which is the creation of some of the components of fibrosis by the production and accumulation of extracellular matrix.¹³¹ Healing of disc tissue is different to most other tissues because it is relatively avascular and takes place either from peripheral structures such as the outer AF and posterior longitudinal ligament,¹³¹ or via the end plate.^132,¹³³ Healing after injury to the AF or end plate is promoted and accompanied by vascular ingrowth, which stimulates vascular inflammatory reactions and the production of growth factors including TGF-β1 and CTGF.¹³³ Aberrations of growth factor contribution to healing after injury to the AF or end plate are postulated to be a significant cause of DP.

The validity of the diagnosis IDD is predicated first on the methodology of the PD, and second on patient selection for the procedure. The International Spine Interventional Society mandates the protocol as follows:⁸² (1) reproduction of the patient’s pain by stimulation of the affected disc; (2) such that the evoked pain has an intensity of at least 7 on a 10-point scale; and (3) pain is reproduced at a pressure of stimulation of < 15 psi; (4) provided that stimulation of adjacent discs does not reproduce pain; and (5) post-discography CT demonstrates a grade III or IV fissure. That is, the disc is morphologically abnormal internally, but it is intact peripherally. A diagnosis of IDD can be made, therefore, on a disc that is normal on CT scan, and, dependent on the sensitivity of MRI, on a normal MRI.¹³⁴ Patients with concordant pain at 15 to 50 psi might be labeled as having indeterminate pain, and those without pain until above 50 psi as definitely negative. Presumably, alterations in the pressure parameters used to diagnose IDD alter the robustness of PD to truly detect DP; however, this is a somewhat ethereal statement because there is no standardized criterion against which the concept of IDD can be tested.

The features of IDD are characterized morphologically by: (1) degradation of the matrix of the NP, and (2) radial fissures, with or without a circumferential extension, that penetrate the AF without breaching the outer lamella. Fissures are graded on their extent, depending on whether they reach the inner, middle, or outer third of the AF,¹³⁵ or if they extend circumferentially.¹³⁶ The more extensive fissures that do not breach the outer lamellae of the AF correlate strongly with clinical pain and are associated with abnormal stress profilometry throughout the disc, including reduction and irregularity of NP stress, and increase in AF stress.¹²⁵ Additionally, altered NP pressure can arise experimentally from end-plate fatigue failure,¹²⁶ which has, in turn, been demonstrated to occur with loads that are consistent with moderately heavy work activities.

Although it is likely that intrinsic DP can occur in discs that are disrupted to the point where the outer lamellae of the AF are breached (a grade 5 annular tear), it is not possible to determine that such a disc is the source of pain with PD (Fig. 39-7). On morphologic grounds alone, a discogram finding of a grade 5 disc disruption negates the diagnosis of IDD. On pain provocation grounds it is not possible to state that a disc with grade 5 change is the source of pain because of the high chance of invalid responses. If the outer lamellae are breached during discography, the provocation phase might not only produce a false-positive result because contrast and pressure is exerted into the epidural space, but also a false-negative response because the disc may not be able to be pressurized to the degree required by protocol or to a sufficient degree to reproduce the index pain.

Figure 39-7 The Dallas discogram description.

(From Sachs BL, Vanharanta H, Spivey MA, et al: Dallas discogram description. A new classification of CT/discography in low-back disorders. Spine 1987;12:287-294.)

How Useful Is MRI as a Predictor of IDD?

As discussed earlier, MRI changes occur in the asymptomatic population,^38,^137,¹³⁸ and apart from the finding of a high intensity zone (HIZ) or Modic type 1 and 2 changes in the lumbar spine, the extent of changes are not predictive of the development or duration of future back pain.¹³⁸ Attempts have been made to determine whether or not MRI can be used to predict PD outcome because PD is not without morbidity.¹³⁹^–¹⁴¹ Although MRI is somewhat predictive of a positive PD test when an HIZ or Modic type I or II changes are found, it is somewhat insensitive.

The HIZ, defined on sagittal MRI as a very bright signal (equal to or brighter than CSF on T2-weighted scans) contained within the posterior AF,¹³⁶ has been shown to have appreciable but variable correlation with positive PD in patients presenting with NSLBP.¹²⁷ The initial study showed that an HIZ increases the odds that PD will be positive in that patient at that level by a factor of 6.5.¹³⁶ Studies on the HIZ since that time have all shown that HIZ is highly specific (range 0.74 to 0.93)¹⁴²^–¹⁴⁶ but that it has variable sensitivity, from as low as 0.09,¹⁴⁶ to as high as 0.78.¹⁴⁴ Thus, it is uncommon for an HIZ to occur in a disc that is not painful to PD, and the calculated likelihood ratios (ranging from 1.3 to 6.5 and averaging 4.1) indicate that an HIZ increases the odds that a PD will be positive by at least 50%.¹²⁷ Additionally, although HIZs are present in both asymptomatic and symptomatic subjects, they are found significantly more in symptomatic (prevalence 60% ± 15%) than asymptomatic subjects (24% ± 11%).¹⁴⁷

Modic changes have also been studied in relationship to NSLBP and PD.^148,¹⁴⁹ The overall rate of vertebral end-plate signal changes (VEPSC) is about 43% in patients with NSLBP and 6% in those without.¹⁵⁰ The most common association of VEPSC and NSLBP is extensive Modic type 1 changes at L5-S1.¹⁵¹ Overall, VEPSCs are relatively insensitive, but quite specific, for the diagnosis of IDD established by discography, with sensitivity of 23.2%, specificity 96.8%, PPV 91.3%, and NPV 46.5% in one study.¹⁴⁸ When Modic changes are studied according to type, the type 1 end plate has the highest PPV for positive PD at 81% (±7%).¹⁴⁹

One of the problems of proton MRI is that the traditional T1 and T2 images measure the end stages of proteoglycan breakdown, by which stage water depletion is more severe. The earlier, more subtle, changes are not able to be detected with these sequences. As proteoglycans are highly negatively charged they attract cations, particularly Na⁺. Sodium MRI measures Na⁺ levels in the disc, thereby giving a direct measurement of proteoglycan levels. Depletion of Na⁺ is, therefore, a direct measure of degree of disc degeneration.¹⁵² Sodium MRI does not have the resolution of proton MRI, but it can now be studied as a potential surrogate for PD.

Can Clinical Tests Predict IDD?

The prevalence of IDD in a population of NSLBP patients considered to be having sufficient pain and disability to undergo PD is about 35% to 40%.^61,¹⁵³ The prevalence of IDD in a group of patients with positive clinical indicators increases to 52% to 69%.¹⁵³ The centralization phenomenon, or pain centralization, which is the retreat of referred pain toward the spinal midline during specified clinical examination, a history of persistent pain between acute episodes, a significant loss of extension, and a subjective report of so-named “vulnerability in the neutral zone” individually and in combination increase the likelihood of an eventual diagnosis of IDD in a group of highly disabled and psychosocially distressed patients with otherwise diagnosed NSLBP.^153,¹⁵⁴ Additionally, if vibration applied over individual spinous processes is considered a positive test, then the odds of a positive PD increases significantly.^155,¹⁵⁶ These clinical tests and protocols will need further validity and reliability studies before they can be considered to be adequate surrogates for PD.

The Diagnosis of Radicular Pain Due to a Contained Disc Prolapse

The nature of radicular pain has been described. Apart from the description of pain, various clinical tests such as the straight leg raise test are used as aids to the diagnostic process, but their clinical utility is questionable,¹⁵⁷ and radicular pain lends itself to imaging investigation. In the cervical spine, the neck compression, the axial manual traction test, and the shoulder abduction test are highly specific but poorly sensitive for the diagnosis of root compression.¹⁵⁸ CT scan, MRI, and CT myelography can all be used in different clinical settings. If the morphologic findings match the clinical picture, then the cause of radicular pain can be assumed. The most common cause is some degree of disc prolapse. However, it should be noted that disc prolapse is also commonly seen in the asymptomatic population.^34,^36,^41,¹⁵⁹

Which Patients Should Be Considered for Intradiscal Therapies?

Internal Disc Disruption and Discogenic Pain

The patient with putative IDD or DP being considered for an intradiscal therapy should have had considerable NSLBP for at least 6 months. Each patient should have exhausted the options provided in less invasive care, and the pattern of pain should be such that it might reasonably be expected that the condition will not recover spontaneously. By the time a patient is being considered for PD, there is a reasonable chance that the pain and disability will be similar at 2 years, and perhaps improved by 5 years. The natural history of IDD over a 5-year period has been studied in a group of patients who elected not to have the subsequently offered posterolateral fusion surgery.¹⁶⁰ In this study, 25 patients underwent PD after experiencing incapacitating NSLBP for a period of at least 6 months. The patients (n = 36) were selected from all patients who underwent PD (n = 432) over a 3-year period. Eligibility included single level PD positive (morphology and pain response), normal plain radiographs, and a minimum of 3-year follow-up. Of these, 25 patients were able to be studied, with average age at time of discography being 43 years, and at a mean follow-up time of 4.9 years, 68% had improved, 8% had stayed the same, and 24% were worse; 80% of those receiving worker’s compensation had improved. No patient had recovered fully. The natural history of IDD in a group of 36 patients undergoing placebo intradiscal injection over a 2-year period has also been documented by Peng and colleagues in their study on methylene blue.¹⁶¹ In this study, patients also had IDD using similar selection criteria but they elected to have the injection treatment. At 2 years the placebo group, with an average age of 42, had not undergone much change in either disability or pain levels: there was a weak statistically insignificant trend to improvement of pain.

The ideal patient has focal pain, with or without a component of referred pain, little or no other pain in other areas of the body, minimal disc space narrowing at the level to be treated, and a fairly normal psychosocial profile (Fig. 39-8). These are the ideal prerequisites in any case for a patient to be assessed with high quality PD that complies with recognized standards. If the PD is positive, the diagnosis of IDD (and thus DP) is then made (Figs. 39-8 through 39-10).

Figure 39-8 Ideal prerequisites if provocation discography (PD) is to be used as a test before an intradiscal procedure.

Figure 39-9 Cellular function within the disc is mediated by at least five major factors.

(From Freemont AJ: The cellular pathobiology of the degenerate intervertebral disc and discogenic back pain. Rheumatology [Oxford] 2009;48:5-10.)

Figure 39-10 Illegitimate labels for a presentation of neck pain.

The diagnosis of IDD does not imply that specific interventional treatment including surgery to the disc will produce good results.^162,¹⁶³ The cohort or cohorts of patients who might respond best to treatments arising from a diagnosis of IDD are still being defined.

IDD can theoretically be treated directly by discectomy and fusion, discectomy and artificial disc replacement or by intradiscal therapies. The rationale for the first two procedures is that the painful structures within the disc are rendered pain free either by removal of the offending algogenic material and/or its immediate nerve supply, and the function of the disc is restored (artificial disc replacement) or made redundant (fusion). The rationales for intradiscal therapies include denervation of the offending tissue and improved tissue healing.

Radicular Pain due to Contained Disc Prolapse

The patient with radicular pain due to a contained disc prolapse considered appropriate for an intradiscal therapy should have considerable pain that is not showing signs of recovery despite the passage of time and perhaps one or more epidural injections. This can be a hard situation to call. Also, if such a therapy is suggested, the clinician should be able to justify using an intradiscal treatment over minimally invasive treatments including minimally invasive spinal surgery.

Surgery for radicular pain caused by a disc protrusion has been considered successful for many years since the discovery of the disc prolapse and its effects on the neural system.¹⁶⁴ It is instructive to consider that the natural history for radicular pain due to disc prolapse is reasonably good in any case,¹⁶⁵^–¹⁶⁸ and surgery has proved popular not necessarily because of its better long-term outcome,¹⁶⁹ but because it provides the quickest route to recovery.¹⁶⁵^–¹⁶⁹ Surgery may be superior to conservative care within 12 months but by 4 years there is no difference in outcome.¹⁷⁰ Large disc protrusions or extrusions treated conservatively for the presentation of radicular pain do resolve when followed with imaging techniques: smaller protrusions tend not to resolve.¹⁷¹

Once a decision is made to perform an invasive technique, any outcome that seems to be predicated on bony canal dimension reduction demands spinal surgery. Intradiscal decompression is for contained and, therefore, small disc protrusions that are not recovering quickly enough.

Which Patients Should Not Be Considered for Intradiscal Therapies?

Purely on face validity grounds, the more that the presenting pain is localized into one region, the more likely that it is derived from a local structure. As a corollary, chronic widespread pain, which is present in about 4.5% of the population,¹⁷² could derive from multiple regions or from an underlying pain dysfunction, such as central sensitization. There are schools of thought postulating that most, if not all, chronic NSSP is caused by central nervous system processing dysfunction independent of any initiating musculoskeletal event.

Fibromyalgia (FM), the most common known cause of chronic, widespread pain,¹⁷³ is an example of a presentation that could mimic DP. It is considered to be present in between 0.5% and 7% of the population at any given time.¹⁷⁴^–¹⁷⁶ It is not uncommon for a patient, who presents to a spinal clinic with a pain diagram demonstrating only focal LBP, to reveal under closer questioning a profile consistent with FM. Additionally, there are others who present somewhere short of the FM diagnostic requirements.¹⁷⁷ They might get labeled with an entity such as diffuse myofascial pain. The essence is that they do not have relatively focal regional pain like that described earlier for focal deep somatic pain referral, and they might have some of the accompanying symptoms of FM, such as sleep disturbance, unrefreshed sleep, and general autonomic symptoms.

Local neuropathic pain should also alert the clinician to be wary. Neuropathic pain can be challenging to diagnose because diagnostic criteria are still developing, and neuropathic pain can manifest simultaneously with somatic referred or other pain.¹⁷⁸ The diagnosis of neuropathic pain is based primarily on history and physical examination.¹⁷⁹ Although neuropathic pain can have deep aching and shooting characteristics, more typical of lumbar radicular pain,75 it also attracts other descriptors such as burning, crushing, punishing, and cruel,¹⁷⁹ and it can be associated with abnormal sensations such as formication. Because it is often unrecognized by clinicians,¹⁸⁰ a range of neuropathic questionnaires, such as StEP,¹⁸¹ PainDETECT,¹⁸² DN4,^183,¹⁸⁴ LANSS¹⁸⁵ and NPS¹⁸⁶ have been developed and reviewed.¹⁸⁷ The prevalence of neuropathic pain in the general population is about 7% of which 70% have pain in the moderate to severe range.¹⁸⁸ Additionally, although some of these questionnaires should be considered a screening tool only and population surveys should be treated with some scepticism,¹⁸⁹ one survey report using PainDETECT found that the prevalence of predominantly neuropathic pain in a population of people with LBP was 37%.¹⁸² In an orthopedic setting of patients with predominantly LBP, those with a positive PainDETECT questionnaire had a median VAS of 5.0, and some had features typically representative of radicular pain and/or radiculopathy, including typical radicular pain (40%), positive Laségue sign (18%), or absent reflex (17%).¹⁹⁰ More than two neuropathic pain characteristics were present in 34% of these patients. Although neuropathic pain may represent radicular pain, it is fair to say that when a person presents with LBP that has neuropathic descriptors rather than deep somatic pain descriptors, clinicians should consider that the pain is more complex than being simply derived from a local somatic structure such as a disc. Pain centralization may be a significant factor.

The patient with significant psychological features in association with pain is difficult to assess from a pain origin perspective. Although it has been reported that alleviation of pain from a surgical procedure can return abnormal psychological parameters to normal,¹⁹¹ the false-positive rate of interventional diagnostic tests such as discography is an example of the difficulty in assessing such a presentation.¹²⁰

In summary, the presentation that might lead a clinician to the suspicion of deep somatic referred pain from a disc is that of deep aching pain that is localized predominantly in one region of the spine with or without referred pain from that region into the limbs or trunk, without any substantial abnormality of psychological profile, perhaps other than distress. The presentation that might lead to the opposite conclusion is when the pain is more widespread or has prominent neuropathic qualities suggestive of radicular pain or central sensitization pain, or if the psychological profile is substantially abnormal.

Why Is There Such A Problem with NSSP?

The essence of tissue-specific spinal pain diagnosis is that it requires the use of invasive special tests such as medial branch blocks and discography. These tests should be performed only when they serve some use. They should be performed when a useful tissue-specific treatment is planned. For the majority of patients presenting with spinal pain these tests are unwarranted because the condition can be dealt with in a less invasive manner or because there is no valid treatment.

When a person presents with spinal pain, the initial aims are to ensure that the pain derives from the spine and that it is not caused by any red-flag condition. The next aim for the clinician is to use the available evidence to guide treatment. There is some good evidence about prevention of LBP chronicity, and this should be used where applicable when a diagnosis of NSLBP is made. As will be discussed, the use of fear-avoidance and “move it or lose it” type models have excellent evidence for prevention of this chronicity, at least for NSLBP. Despite this, evidence has not been converted into practice.

Specific traditional treatments have not proved effective in controlling the epidemic of back pain. Because about 70% of the acute back pain population recovers rapidly, therapies that are no better than placebo have been ascribed healing properties they do not deserve. The challenges for those who manage back pain are to provide a management strategy that actually alters the long-term outcome and to identify, if possible, and as early as possible, the patients who are less likely to recover.

To this end, a number of evidence-based guidelines for the clinical management of acute back pain in primary care have been developed.¹⁹²^–¹⁹⁹ In general, the guidelines subscribe to the concept that exercise is beneficial, fear of movement is harmful, that consequent pain should not be understood to be further injury, and that chronicity is contributed to by avoidance of these concepts. More specifically, they (1) identify potentially serious causes of acute low back pain (< 5%); (2) promote effective self-management of symptoms through the provision of timely and appropriate advice; and (3) maximize functional status and minimize disability.

A multidimensional approach is required to translate these concepts into reality for the public and the medical profession.^200,²⁰¹ One way to promulgate the guideline concepts is with mass-media campaigns, which have been shown to be effective in delivering health information to medical and allied health practitioners and the general public,^202,²⁰³ although the effective penetration relates more to public perception changes than alterations in the attitudes or behaviors of health professionals.²⁰⁴ A mass media campaign that outlined some evidence-based facts about back pain was implemented²⁰⁵ and was found to be useful.^206,²⁰⁷ The campaign issued sharply focused, unambiguous advice directed toward staying active and exercising, not resting for prolonged periods, and remaining at work.²⁰⁸^–²¹¹

Such programs do not necessarily translate into huge savings.²¹⁰ Guidelines in general do not lead to improvement of clinical outcomes, primarily because they are not followed by practitioners.^210,²¹²^–²¹⁸ Reasons for this include poor penetration of clinical guidelines into graduate and postgraduate medical education, lack of awareness, inability to understand the ramifications of referred pain, lack of commitment to change, incomplete understanding of the natural history of LBP, disagreement with evidence-based recommendations, concern for litigation, a belief that guidelines cannot be adequately explained to patients and particularly lack of uniformity in management by the various health professionals.^212,²¹⁸^–²²² It is also not easy to remedy lack of compliance to guidelines.^210,^220,²²³

It is apparent that the proper use of clinical guidelines in the management of LBP produces better outcomes.²²⁴^–²²⁶ Guidelines tend to portray LBP as a benign, self-limiting disease, as single attacks tend to recover.²²⁷ Consequently it is not surprising that some primary care practitioners adopt a blasé attitude to an acute presentation of LBP, despite evidence clearly demonstrating that early diagnosis and suitable advice underpins the long-term outcome for many patients.²²⁴

The end result of lack of compliance to guidelines is prolonged unnecessary disability and increased usage of the health-care system. For example, a survey on the usage of the health care system over a 12-month period in a longitudinal prospective cohort study following presentation with LBP revealed alarming data.²²⁷ Of the 1342 patients, 57% were seeking additional specialist care, 46% had some form of imaging, 49% underwent physiotherapy, and 31% received massage. Because specialist care resulted in more imaging and intervention, it was considered that a significant contribution to the problem was the lack of a well-functioning primary care gate-keeping force.²²⁷

So, one problem is the dissemination and utilization of evidence-based clinical guidelines to those practitioners in the front line of LBP management. Promoting adherence to LBP guidelines requires more than enhancing knowledge about its evidence-based management.²¹² Public education and an interdisciplinary consensus are important requirements for successful guideline implementation into daily practice.²¹² Guideline recommendations need to be adapted to the infrastructure of the health care system in general.²¹² Most guidelines refer to the management of LBP in general. However, in respect to work-related acute LBP, specific guidelines do exist.²²⁸^–²³⁰ In the first instance, we need to know if these guidelines are of sufficient quality on which to base the management of LBP.

Preventative Measures

There are two important studies that emphasize the benefits of early assessment and active management of acute LBP.

In Indahl’s study,²²⁵^–²²⁶ in which workers with LBP were put into one of two groups and followed up for 5 years, 19% of the patients in the intervention group, compared with 34% in the control group, were still on sick leave after 5 years. The successfully treated group was managed with an approach that included clinical examination combined with information for patients about the nature of the problem provided in a manner designed to reduce fear and give them reason to resume light activity. It might be reasonably assumed that Indahl was able to successfully rehabilitate the 15% of people who had a reversible primary psychosocial reason for nonrecovery of function, and that the other 19% who remained disabled had significant underlying pathologic processes or some other unknown factor responsible for this disability.

Evidence-based care has been further studied. A seminal study on WorkCover patients which offered these workers a choice between Indahl’s evidence-based care and usual care (e.g., from the family general practitioner) in four district hospitals in Newcastle, Australia, also showed the benefit of early decisive management of LBP.²²⁴ In this study, the 65% who accepted evidence-based care were compared to the other group. The specialist in this clinic practiced according to Australian Evidence-Based Guidelines for Management of Acute LBP.¹⁹⁸ These guidelines are similar to other published guidelines except that they do not use treatment by manual therapy, a treatment that seems to lack significant positive evidence.²³¹ The emphasis is on explanation, reassurance, encouragement to remain at work, simple analgesics, avoidance of passive therapies, and worksite visit/intervention if indicated. Imaging was performed only if there was a clinical red-flag indicator. Instructions on how to implement these guidelines have been discussed in detail.²³²

In this study, the physician saw the injured worker at the hospital clinic, often on the day and virtually always within 48 hours of injury. At consultation, clinical examination consisted of history of the injury, past history, red-flag checklist, and examination. Management was by explanation of the benign nature of LBP and of its good prognosis. Fears or misconceptions that the patient had were identified and addressed. Workers were specifically reassured on the basis of evidence that a good outcome was highly likely and were encouraged to remain at work. They were given simple analgesics particularly paracetamol and simple McKenzie type stretching exercises. If the worker had any occupational safety issues at work, that was further assessed. The patients were reviewed at 1 week.

This study followed 253 patients. Of these, 62 elected usual care (private general practitioner, etc.), 191 (75%) consulted the staff specialist (of these, 27 [14%] elected to change to usual care after the initial consultation), and 164 (65%) remained under the care of the staff specialist. The outcomes are summarized in Table 39-2.A group of 84 patients who saw the staff specialist were identified as having credible back pain but alleged disability dissonant with the history of injury. Psychosocial factors in this subgroup included job dissatisfaction or dislike of the supervisor. Of these 84 patients, 13 transferred to usual care but 71 remained under evidence-based care. Although they required a longer initial consultation and a greater number of consultations, their outcomes were favorable and did not statistically differ from other patients who pursued evidence-based care. Additionally, of the entire group, 32% accepted evidence-based care readily, 24% came to the consultation with preconceived beliefs about back pain management, and 44% expressed job dissatisfaction and psychosocial difficulties in the workplace. When evidence-based care was explained, most of the group with preconceived beliefs accepted evidence-based care. Patients with psychosocial difficulties required more consultations and care, but ultimately had similar outcomes as the rest.

Table 39-2 Outcomes of Workers Presenting with Acute Back Pain