Epidemiology

Low back pain (LBP) is the leading cause of years lived with disability worldwide. In the United States, LBP is the most common reason for lost productivity, workers’ compensation claims, and early social security disability benefits. Annually, nearly 50% of adults will have an episode of significant and disabling LBP, which will be protracted in a majority of cases. As a result, poorly controlled LBP is one of the most common motivations for visits to emergency departments and primary care physicians. The economic impact of LBP is exorbitant and consists of direct costs of treatment and indirect costs from lost wages, disability benefits, and litigation fees. The overall annual cost of LBP amounts to over 100 billion dollars in the United States alone. Moreover, costs related to LBP have increased immensely in recent decades, mainly due to the availability of new and expensive treatments and an exponential rise in litigation costs and disability benefits paid. Despite the wide availability of treatment options and the enormous cost incurred by this prevalent and disabling health issue, LBP is often poorly controlled and thus remains a significant source of frustration for both sufferers and treating providers. A main contributor to this dissatisfaction is the often concurrent presentation of the various syndromes causing LBP, making diagnosis of a particular or group of etiologies very challenging for the treating physician. Physical exam and imaging studies employed to diagnose LBP syndromes have low sensitivity and specificity and are often incapable of determining the precise source of pain. Additionally, although a wide array of treatments for LBP are available, they are not consistently effective and rarely alter progression of the disease process.

Anatomy

The majority of LBP originates from the spine and contiguous paraspinal musculature; a basic understanding of spinal anatomy, mechanics, and physiology is therefore crucial to the pain physician. The vertebral column is composed of 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 3–5 coccygeal vertebrae. With the exception of the sacral and coccygeal vertebrae, which are ordinarily fused, the two adjacent vertebral bodies (VBs) and the intervening intervertebral disc (IVD) comprise a vertebral motion segment. Anteriorly, the linear arrangement of the adjacent vertebral motion segments forms the continuum of the spinal column. The remainder of the spinal column consists of the neural arch, which includes the spinous processes, laminae and the ligamenta flava posteriorly and pedicles, facet joints, and intervertebral foraminae laterally. The neural arch forms the spinal canal, which houses the thecal sac, the layer of fused dura, and arachnoid mater that envelops the spinal cord and nerve roots of the cauda equina. At the most inferior portion of the spinal cord, the conus medullaris, lies the origin of the fibrous filum terminale, which extends to insert on the caudal dura and anchor the cord in the aqueous thecal sac. The spinal cord characteristically ends at the L1–L2 vertebral level, but the thecal sac extends more inferiorly, normally terminating at the S2–S4 level. In addition to the linkage of the VBs by IVDs, each adjacent VB articulates dorsally by way of a pair of synovial joints known as the zygapophysial (facet) joints. The various components of the spinal column also enable attachment of the powerful trunk muscles and spinal ligaments: the ligamentum flavum and the anterior and posterior longitudinal ligaments. A pair of large synovial-fibrous joints, the sacroiliac joints, absorb the tremendous forces transmitted from the spinal column and distribute the pressure equally to the bilateral lower extremities.

The VBs are composed largely of cancellous bone, but this is sheathed in a thin layer of cortical bone. An IVD consists of the outer annulus fibrosus (AF), the inner nucleus pulposus (NP), and vertebral endplates. The distinction between the AF and NP is more pronounced in lower levels of the spinal column but diminishes in cephalad regions and also loses definition with advancing age. Both the NP and the AF consist mainly of an abundant intercellular matrix that is only sparsely populated by cells. The cells contained in the NP are found in clusters and are reminiscent of chondrocytes, whereas cells found in the AF have fibrocytic characteristics. The intercellular matrix composition of the two disc compartments also differs significantly. The NP matrix is gelatinous and has a high concentration of water and proteoglycans, whereas the AF is collagenous and is arranged in interlacing lamellae. These lamellae have increased density in the anterior portion of the disc and are firmly attached to the entire border of each adjacent VB. Although the cancellous VBs and all spinal canal contents are highly vascular, the NP and inner two-thirds of the AF are nearly avascular. The VB endplate cartilage is also avascular and acts as a barrier to separate VB vasculature from the IVDs.

IVDs and the neural canal contents are primarily innervated by nerve plexuses that lie along the anterior longitudinal ligament (ALL) and posterior longitudinal ligament (PLL; Fig. 24.1 ). The nerve plexus along the ALL receives contributions mainly from the gray rami communicans, while the plexus along the PLL receives the majority of its input from the sinuvertebral nerve with only minimal contributions from the gray rami communicans. At each level, the sinuvertebral nerve originates from the segmental spinal nerve as it exits the intervertebral foramen, re-enters the vertebral canal, and receives contributions from the gray rami communicans. The posterior longitudinal ligament plexus innervates the anterior dura and the posterior IVDs. The gray rami communicans emerges from the sympathetic chain and joins the spinal segmental nerve soon after it exits the intervertebral foramina and runs anteriorly along the inferior third of the VB. It connects to the sympathetic trunk before separating into lateral and anterior branches to innervate the lateral and anterior disc annulus of the disc levels above and below the trunk. The posterior primary ramus, soon after its division from the anterior primary ramus, branches into medial and lateral branches. The medial branch of the posterior primary ramus supplies most dorsal spinal column components including the facet joints, posterior neural arch components, and spinous processes. The AF of the IVD therefore has complex innervation from several sources and includes contributions from sinuvertebral nerves, segmental spinal nerves, gray ramus communicans nerves, and the sympathetic trunk. The efferent nerves carrying information from spinal components rarely follow a single pathway but instead branch extensively and undergo interneuronal convergence within the spinal cord. This, when coupled with the rich autonomic connections present in the spinal column, results in the poor topographical localization of pain of spinal origin, particularly pain originating from the IVD. Although all components of a spinal motion segment have been implicated in generating pain, the majority of pain receptors are found in spinal ligaments, paraspinal muscles, VB periosteum, facet joints, and the outer third of the AF.

Segmental innervation of the lumbar spine.

From Paris SV: Anatomy as related to function and pain. Symposium on evaluation and care of lumbar spine problems. Orthop Clin North Am. 14:475-489, 1983.

Spinal Mechanics

The flexibility and remarkable range of motion (ROM) exhibited by an active spine depends almost entirely on the cumulative plasticity exhibited by the IVDs. An individual IVD, however, is only moderately plastic in isolation and the NP is almost incompressible. Forces applied to the spine are substantial and are borne directly by the VBs and IVDs. Extreme compressive forces applied to a healthy IVD can be endured without traumatic injury due to the incompressibility of the NP and equal distribution of tensile force to the AF. Pathophysiologic changes within the degenerated IVD alter the biomechanical properties, causing it to shrink and lose plasticity. These changes in the disc dynamics increase stress on the adjacent vertebral motion segments and propagate dysfunction, hypertrophy, and degenerative changes in several contiguous structures: facet joints, sacroiliac joints, and paraspinal muscles or ligaments. Hypertrophy of the facet joints and ligamenta flava along with bulging of the IVDs leads to narrowing of the spinal canal and the intervertebral foraminae, which can cause pain due to compression of the neural elements. Degenerative changes in one disc can also cause accelerated degenerative changes in the adjacent IVDs. Although the spinal degenerative changes mentioned above are common, their presence or absence correlates poorly to patients’ reported symptoms.

Pathophysiology

The incompressibility exhibited by the NP is a product of its water content, which is the result of osmotic pressure generated by matrix proteoglycans that are synthesized by sparsely present NP cells. Due to its avascularity, the IVD meets its metabolic requirements exclusively through diffusion from capillary beds in adjacent VBs and the outer AF. Matrix metalloproteinases (MMPs) facilitate discal catabolic activities, which exist in delicate balance with anabolic activities. As the IVD lacks scavenger cells, the end products of macromolecular metabolism accumulate within the disc over time. These factors result in a precarious anaerobic environment for the IVD, leaving it vulnerable to a host of hereditary and environmental insults. Lack of nutrition, enhanced MMP activity, and an increase in disc cytokines and proinflammatory mediator concentration all contribute to dysfunction and the decline in the viable NP cell population. Reduced NP cellular anabolic activities can lead to reduced NP proteoglycans, osmotic pressure, and water content, which can lead to reduced NP hydrostatic pressure. Factors analogous to those affecting the NP can affect the AF wherein cellular dysfunction and loss can result in the loss of AF collagen. Loss of hydrostatic pressure results in NP laxity and exposes the AF to direct compressive forces. This, along with loss of collagen, may eventually lead to AF failure and the development of tears and fissures extending from the periphery to the NP. These AF tears are gradually infiltrated by granulation tissue, which is highly vascularized, richly innervated, and is abundant in mononuclear cell infiltrates. These cells then release nerve growth factors, which contribute to nerve in-growth and accelerated IVD degeneration. These nerve fibers include vasoregulatory nerves, which accompany the neovascularization, and free nerve endings, which are high in substance P and are likely nociceptive in nature. The high concentrations of proinflammatory mediators within the disrupted discs can also sensitize the neonociceptive nerve endings, maintaining a state of pain and hyperalgesia within the disrupted disc. Overt disc herniation or occult leakage of disc material through the AF tears can cause inflammation of contiguous structures, especially the spinal nerve roots. This may increase local or, more frequently, remote pain in the distribution of the affected nerve root, causing pain in a dermatomal distribution that is known as radicular pain. Leakage of the inflammatory mediators across the vertebral endplates into the VB may cause inflammation followed by hypertrophic new bone formation and sclerosis in the adjacent VB. These inflammatory changes are visible on imaging and as a whole are termed Modic changes. It is unclear if Modic changes are a true etiology of pain or if they are simply a visible manifestation of a degenerating spinal column’s maladaptive modulation.

Etiology

The majority of LBP originates from the various spinal components such as the spinal nerve roots, facet joints, the contiguous paraspinal muscles and ligaments, sacroiliac joints, and the IVDs and VBs. LBP of spinal origin typically is not life-threatening and is due to self-limiting degenerative conditions that seldom cause neurologic compromise. LBP emanating from benign spinal degenerative conditions has been termed lumbago, mechanical LBP, or spondylosis. The common spinal syndromes causing benign LBP include:

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  Musculoligamentous strain or sprain

  
  
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  Herniated disc

  
  
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  Foraminal stenosis causing symptoms from nerve root compression

  
  
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  Spinal canal stenosis causing neurogenic claudication or myelopathic symptoms

  
  
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  Facet joint dysfunction and arthropathy

  
  
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  Sacroiliac joint dysfunction and arthropathy

  
  
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  Myofascial pain syndrome

  
  
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  Degenerative disc disease, discogenic pain, internal disc disruption

  
  
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  Spondylolisthesis (displacement of a VB compared to the adjacent)

  
  
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  Spondylolysis (defect in pars interarticularis without vertebral slippage)

  
  
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  Spinal instability (anomalous movement between the contiguous VBs)

  
  
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  Spinal conditions causing misalignment such as kyphosis or scoliosis

Infrequently, LBP of spinal origin is from nondegenerative conditions. Such nonmechanical LBP may result from widely diverse pathologic conditions such as:

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  Primary or metastatic neoplasm of the spine or its neural contents

  
  
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  Infections, such as osteomyelitis of the VBs, septic discitis, paraspinal, or epidural abscess

  
  
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  Noninfectious inflammatory spinal disorders such as ankylosing spondylitis, Reiter syndrome, psoriatic spondylitis, inflammatory bowel disease

  
  
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  Traumatic or pathologic fractures such as VB compression fractures and dislocations

  
  
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  Metabolic disorders of the spine such as Paget disease

  
  
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  Miscellaneous conditions such as Scheuermann disease, osteochondrosis and hemangiomas

LBP can also be referred from adjacent or even distant organs, particularly retroperitoneal structures. Chronic LBP of extraspinal and visceral etiology, however, is uncommon, and is easily distinguished from the common spinal sources of LBP by other associated symptoms related to the various disease processes and lack of local tenderness or pain with active ROM of the spine. The diverse etiology of LBP of visceral origin includes:

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  Pelvic visceral disorders such as prostatitis, endometriosis, or pelvic inflammatory disease

  
  
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  Renal disease such as nephrolithiasis, pyelonephritis, or perinephric abscess

  
  
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  Vascular disease such as abdominal aortic aneurysm

  
  
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  Gastrointestinal disease such as pancreatitis, cholecystitis, or perforated bowel

Overall, the relatively less common causes of LBP that are nondegenerative and nonspinal, also referred to as secondary or nonmechanical LBP, are typically rapidly progressive, often cause neurologic compromise, and may be life-threatening.

LBP has also conventionally been labeled as either specific or nonspecific LBP ( Table 24.1 ). As one might infer, specific LBP can be attributed to a definite cause, but nonspecific LBP lacks a clear etiology. Unfortunately, approximately 90% of all LBP patients have at times been diagnosed with nonspecific LBP. Reasons for this elevated incidence include concomitant presence of various LBP syndromes, similar and vague topographic localization of the pain originating from spinal structures and diagnostic imaging techniques that may demonstrate similar abnormalities in symptomatic and asymptomatic individuals.

LBP is divided into three categories based on duration of symptoms. LBP is classified as acute when present for less than 4 weeks, subacute when it persists for over 12 weeks, and chronic when the patient is symptomatic for greater than 3 months. The majority of acute LBP episodes are self-limited and resolve spontaneously within a few days to weeks. Subacute LBP is also generally caused by degenerative conditions such as disc herniations or exacerbations of facet arthropathy, which also tend to be self-limiting but may require treatment to ease symptoms. Chronic LBP, however, can be further categorized as persistent or recurrent and is often refractory to treatment. By some estimates, almost 30% of patients with acute LBP progress to develop chronic LBP. In addition, chronic LBP may be accompanied by a myriad of comorbidities such as depression, behavioral disorders, substance abuse, disability, and secondary gain issues, which can make chronic LBP difficult to treat. The likelihood of return to work diminishes with increased duration of LBP. Patients on medical leave for greater than 6 months due to LBP had lifetime return to work rate of only 50%; this rate decreased to 25% if leave was over a year in duration and to less than 5% if they were off work for greater than 2 years. Chronic LBP, therefore, poses substantial challenges to suffering individuals, their families, and the community as a whole.

Risk Factors

The risk factors associated with LBP have been classified into three broad categories: biomechanical, psychosocial, and personal. Biomechanical risk factors are determined by spinal loading, and typically include parameters such as physical stress and the asymmetry of physical tasks the patient is required to perform. The psychosocial risk factors pertain to psychogenic stress and are often related to job satisfaction, responsibility, and variety. Personal risk factors have been acknowledged as physical, familial, psychologic, anthropometric (e.g., obesity), and gender-related. The following risk factors have also been associated with the development of LBP:

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  An occupation with elevated physical or emotional stress

  
  
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  Cigarette smoking

  
  
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  Spinal deformities

  
  
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  VB endplate injury

  
  
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  Genetic predisposition

  
  
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  Peripheral vascular disease

  
  
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  Obesity

Clinical Evaluation

Despite the diagnostic complexities and the daunting list of causal conditions, the majority of LBP is caused by benign self-limiting conditions and symptoms typically resolve in 1–3 months. A comprehensive history and physical examination are important components in the diagnosis of various LBP syndromes.

“Red Flags” in Patient’s Clinical Evaluation ( Table 24.3 )

Due to the high prevalence of LBP, its frequent spontaneous resolution, the rarity of serious causes, and the frequent presence of abnormal findings in asymptomatic individuals, performing exhaustive diagnostic testing is not recommended. This practice would lead to inappropriate diagnosis, excessive fiscal impact, and poor treatment results. Therefore, in the United States, the Agency for Health Care Policy and Research (AHCPR) developed guidelines to recognize clinical features that would signify the presence of conditions such as fractures, tumors, and infections that can pose significant threat to life or neurologic function and termed these “red flags.” Recognition of these notable clinical signs is essential, as their existence would require further diagnostic testing to either exclude a serious condition or confirm the presence of a benign diagnosis. However, it is possible that a malignant spinal condition may go undetected despite a careful appraisal for these characteristic “red flags.” In general, patients with benign mechanical LBP should have pain mainly with spinal movements such as sitting, bending, lifting, or twisting, and the pain should improve while lying down and at night and it should diminish over the course of days to weeks. Benign diagnoses of exclusion, such as muscle sprain or ligamentous strain, should be made with caution in the presence of “red flags.” If the clinician hastily arrives at a benign diagnosis, this could delay appropriate workup of LBP due to malignant etiology, leading to increased morbidity and mortality. The characteristic “red flags” are as follows:

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  Age: Patients less than 20 or over 50 years of age. Younger patients have a higher incidence of congenital and developmental anomalies, while older patients have a greater likelihood of neoplasms, pathologic fractures, serious infections, and life-threatening extraspinal pathologic conditions.

  
  
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  Duration of symptoms: Symptoms lasting over 3 months without any other associated red flag symptoms arising indicate a less serious etiology.

  
  
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  History of trauma: History of significant traumatic injury or mild trauma in an elderly patient or in a patient with a serious medical condition may indicate traumatic spinal injury.

  
  
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  Presence of constitutional symptoms: Examples such as a history of fever, chills, malaise, night sweats, and unexplained weight loss indicate a more ominous etiology of LBP.

  
  
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  Presence of systemic illness: Patients with a history of cancer, recent bacterial infections, intravenous drug abuse, immunosuppression, organ transplantation, and corticosteroid use are at higher risk for pathologic fractures, epidural and VB abscesses, and spinal metastasis.

  
  
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  Unrelenting pain: Pain of a benign etiology is typically relieved with rest and supine position, especially at night, while pain from a serious pathologic condition is typically unrelenting, may worsen at night, and is not responsive to rest and analgesics.

  
  
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  Presence of cauda equina syndrome (CES): This syndrome is caused by acute compression of the spinal cord or the nerve roots of the cauda equina. CES is characteristically caused by a massive midline IVD herniation or a smaller disc herniation in a patient with preexisting spinal stenosis. Rarely, CES may be caused by spinal metastases, hematoma, epidural abscess, traumatic compression, acute transverse myelitis, or abdominal aortic dissection. Typical symptoms include bilateral, but often unequal, lower extremity radicular pain and weakness, gait disturbances, and urinary retention causing abdominal pain or overflow incontinence. In addition to the positive findings on neurologic examination, the patient’s physical examination typically reveals saddle anesthesia, diminished sensation in the buttocks and perineum, diminished anal sphincter tone, and evidence of urinary retention. Given the similar constellation of symptoms regardless of the vertebral level of insult, CES must be evaluated by imaging the entire spine. CES is one of the rare neurosurgical emergencies that may require urgent decompressive surgery to reduce permanent neurologic disability.

TABLE 24.3

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