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27 Back and Neck Pain

27 Back and Neck Pain
The Massachusetts General Hospital Handbook of Pain Management

27
Back and Neck Pain

Shihab U. Ahmed

Pain wanders through my bones like a lost fire.
—Theodore Roethke (1908–1963)

I. Definitions
II. Anatomic and pathologic basis of back and neck pain

1. Vertebral bodies

2. Intervertebral discs

3. Ligaments

4. Muscles

5. Joints

6. Nerve roots

7. Meninges
III. Evaluating the patient with back and neck pain

1. History

2. Physical examination

3. Imaging
IV. Causes of back and neck pain

1. Rare causes

2. No clear cause

3. Discogenic pain

4. Facet joint pain

5. Sacroiliac joint pain

6. Spinal stenosis

7. Myofascial pain

8. Failed back syndrome

9. Whiplash injury
V. Conclusion
Selected Readings

One of the most frequent complaints that brings patients to their doctors is low back pain (LBP), which is estimated to afflict 15% to 20% of U.S. adults and is the most common cause of disability in individuals under the age of 45 years. The direct cost of diagnosis and treatment of LBP in the United States is estimated to be in the billions of dollars, and the indirect cost in terms of loss of work is inestimable. Despite its high prevalence in our community, accurate diagnosis and treatment of LBP remains difficult. Neck pain also occurs frequently, having a point prevalence of nearly 13% and a lifetime prevalence of nearly 50%.
I. DEFINITIONS
The International Association for the Study of Pain (IASP) defines lumbar spinal pain as “pain perceived as arising from anywhere within a region bounded superiorly by an imaginary transverse line through the tip of the last thoracic spinous process, inferiorly by an imaginary transverse line through the tip of the first sacral spinous process, and laterally by vertical lines tangential to the lateral borders of the lumbar erectors spinae.”
Sacral spinal pain is defined as “pain perceived as arising from anywhere within a region bounded superiorly by an imaginary transverse line through the tip of the first sacral spinous process, inferiorly by an imaginary transverse line through the sacrococcygeal joints, and laterally by imaginary lines passing through the posterior superior and posterior inferior iliac spines.” LBP is considered to arise from both the lumbar and sacral locations.
Cervical spinal pain is pain perceived as arising from anywhere within the region bounded superiorly by the superior nuchal line, inferiorly by an imaginary transverse line through the tip of the first thoracic spinous process, and laterally by sagittal planes tangential to the lateral borders of the neck.” These definitions are specific to only the location, not to the cause of the pain.
Somatic pain arises from the stimulation of the nerve endings in the skin and musculoskeletal components, such as the bone, ligament, joint or muscle. Referred pain is pain perceived as arising or occurring in a region of the body supplied by nerves other than those that innervate the true source of the pain. Referred pain may be perceived in areas relatively distant from the actual source of pain, but when the true source of pain and area of referred pain are adjacent to each other, they seem to be confluent.
Radicular pain is pain that is evoked by stimulation of the sensory dorsal root of a spinal nerve, or its dorsal root ganglion (DRG), and is not synonymous with radiculopathy. Radiculopathy is a pathologic condition in which the function of the nerve root is compromised, leading to numbness, motor loss, and pain, depending on which fibers of the nerve root are involved.
It may be difficult to distinguish clinically between radicular pain and somatic pain referred from localized pathology of the spine (e.g., discs, facet joints, ligaments, paraspinus muscles), yet it is important to try to make this distinction. In the case of radiculopathy, pain may arise from the deeper structures (e.g., muscle and bone) innervated by the affected nerve root(s) and not in the predicted dermatomal distribution. Likewise, somatic referred pain often presents with a nondermatomal distribution in the proximal limb. It is helpful to remember that radicular pain in the distal limb (forearm and lower leg) is unlikely to be of somatic origin, whereas in the proximal limb (upper arm and leg), somatic pain frequently mimics radicular pain.
II. ANATOMIC AND PATHOLOGIC BASIS OF BACK AND NECK PAIN
The spine consists of the bony vertebral column and cartilaginous discs, supporting ligaments, muscle, joints, soft tissues, and nervous tissue. The spine not only supports the weight of the head and torso but also supports and cushions the spinal cord, the nerve roots, the sensory and autonomic ganglia, and the peripheral nerves. All the tissues of the spine are innervated and sensitive to pain and other sensations. It is not hard to imagine why the tissue diagnosis of spine pain is so difficult. To understand the pathophysiology of back pain, the goal should be to have a thorough knowledge of the different tissue types in the region, their nerve supply (Figure 1), the biomechanics of the various spinal structures, and the various ways they can be injured.

Figure 1. Innervation of the lumbar spine. A cross-sectional view incorporating the level of the vertebral body (VB) and its periosteum (p) on the right, and the intervertebral disc (IVD) on the left. PM, psoas major; QL, quadratus lumborum; IL, iliocostalis lumborum; LT, longissimus thoracis; M, multifidus; altlf, anterior layer of thoracolumbar fascia; pltlf, posterior layer of thoracolumbar fascia; esa, erector spinae aponeurosis; ds, dural sac; zj, zygapophysial joint; pll, posterior longitudinal ligament; all, anterior longitudinal ligament; vr, ventral ramus; dr, dorsal ramus; m, medial branch; i, intermediate branch; l, lateral branch; svn, sinuvertebral nerve; grc, gray ramus communicantes; st, sympathetic trunk.

1. Vertebral bodies
The vertebral bodies, like any other bone in the body, are well innervated with nociceptors, especially in the periosteum. The nerve supply comes from adjacent ligaments and muscles. The major innervation comes from the plexus of the anterior and posterior longitudinal ligaments, which supply the periosteum and the deeper structures. Nociceptive markers such as substance P and calcitonin gene-related peptide (CGRP) have been isolated from bone marrow, periosteum, and the cortex of the bones.
Fracture of the vertebral body is often painful and the cause of the pain may be (a) irritation of the nociceptors caused by distention from the local inflammation or hematoma formation, or (b) chemical stimulation from the inflammatory mediators. Fracture may also cause pain because of structural deformity, which can lead to abnormal stress to nearby structures such as joints, ligaments, and muscles.
Metabolic diseases that affect the vertebral body include osteoporosis, Paget’s disease, and osteitis fibrosa. The mechanism of pain in osteoporosis may include microfractures or mechanical irritation of the perivascular sensory nerve within the vertebral spongiosa. The vertebral body can also be affected by primary or secondary tumors. In secondary tumors, multiple vertebral lesions are common, and the tumor usually expands posteriorly. A recently proposed mechanism of vertebral pain is intraosseous hypertension caused by the obstruction and distension of veins, which in turn causes stimulation of the sensory nerves in their adventitia.
The cervical spine in humans consists of seven vertebrae. The first and second vertebrae are modified to provide head movement. Osteoarthrosis of the atlanto-odontoid joint has been found to cause suboccipital pain. Below the C2 level, each vertebra forms an arch with an anterior convexity. One other distinguishing feature of the cervical vertebrae is the uncovertebral joint with its hooklike projections on either side of the superior surface. The uncinate processes are close to the exiting nerves.
2. Intervertebral discs
Intervertebral discs are innervated and a common source of spine pain. Each disc is composed of a central nucleus pulposus surrounded by the peripheral annulus fibrosus and two layers of cartilage, which cover the superior and inferior aspects of the disc.
The nucleus has a semifluid consistency and consists of chondrocytes, collagen fibers, and ground substance. It is avascular and not innervated. The fluid consistency of the nucleus deforms under pressure and transmits pressure in all directions. Thus it works as a shock absorber for vertically applied pressure, and as a semifluid ball bearing during flexion, extension rotation, and lateral bending of the vertebral column.
The annulus fibrosus is composed of concentrically arranged lamellae made of collagen fibers surrounding the nucleus pulposus. The lamellae are thicker in the anterior and lateral portion of the annulus and thinner in the posterior annulus, which is weaker than the rest. The annulus helps to stabilize the interbody joints and acts as a ligament to limit excessive motion. The outer third of the annulus is well innervated. Various studies have documented simple free nerve endings as well as complex sprays, convoluted tangles, and encapsulated nerve endings at the outer annulus. These nerve endings have been found to be immunoreactive to nociceptive neuropeptides such as substance P, CGRP, and vasoactive intestinal polypeptide (VIP). Signals from these nociceptors from the posterolateral segment of the disc travel to the spinal cord via the sinuvertebral nerve.
The anterior disc and part of the lateral disc receive innervation via gray rami communicantes. The vertebral end plate covers the entire nucleus pulposus but does not cover the peripheral annulus fibrosus. The outer annulus inserts by Sharpey’s fibers into the smooth outer rims of the vertebral bodies. The vertebral end plate and the inner annulus together surround the nucleus like a capsule made of collagen fibers.
Lumbar discs have long been known to cause LBP. In patients with symptoms, injection of radiocontrast dye into a diseased disc can mimic the patient’s pain (provocative discography). On the other hand, it appears that in asymptomatic individuals, provocation by injection into the normal disc does not cause LBP. The lumbar disc may be the source of pain in discitis, torsion injury, or internal disc disruption (IDD). Torsion injury to the disc occurs with forceful rotation of the intervertebral joint. The risk of injury increases if rotation occurs while the spine is flexed, which already causes stress at the annulus.
Degradation of the nuclear matrix and disruption of the annulus characterize the clinical entity of IDD. The proposed diagnostic criteria for IDD include a positive provocation discogram and the presence of a radial tear extending to the outer third of the annulus on postdiscogram computed tomography (CT) (Fig. 2). Based on these criteria, Schwarzer et al. (1995) found the prevalence of IDD among the patients with chronic LBP to be at least 39%.

Figure 2. Grades of radial fissures in internal disc disruption.
Grade 0: No disruption is evident in the annulus fibrosus
Grade 1: Disruption extends into the inner third of the annulus fibrosus
Grade 2: Disruption extends as far as the inner two thirds of the annulus
Grade 3: Disruption extends into the outer third of the annulus fibrosus, and may spread circumferentially between the lamellae of collagen.

The cause of IDD remains controversial. One possible mechanism is that the end plate fractures as a result of repetitive motion injury. This theory proposes that the end-plate fracture initiates a progressive degradation process of the nuclear matrix. During the process of degradation, the nucleus loses some of its water content and its ability to sustain pressure. This causes a shift of load to the annulus and makes it susceptible to injury. The degradation process may also spread to the annulus in the form of an annular tear. The nociceptors of the outer annulus are now exposed not only to degradation products and enzymes but also to inflammatory chemicals leading to back pain. Standard imaging studies, including magnetic resonance imaging (MRI), CT, myelography, and discography, may not reveal abnormalities of the annulus. However, injecting radiocontrast dye inside the annulus and taking a postcontrast CT may help identify any annular pathology.
3. Ligaments
Anterior and posterior longitudinal ligaments
The lumbar sympathetic trunk, gray rami communicantes, and sinuvertebral nerves innervate the anterior and posterior longitudinal ligaments. These ligaments are attached to the annulus fibrosus and may be difficult to separate from disc (annular) pathology as a source of LBP. Kuslich et al. (1991) found that the posterior longitudinal ligament causes central back pain when stimulated.
Spinous ligaments
The spinous ligaments are less likely to cause pain. The interspinous ligament is innervated by the medial branch of the posterior primary rami, but clinical studies demonstrate that the ligament is responsible for only a small proportion of LBP. Poor innervation of the ligamentum flavum makes it a less likely source of LBP. The supraspinous ligament may not be associated with LBP because it is absent at the lower lumbar region.
4. Muscles
Muscles of the back are supplied by the dorsal rami of the spinal nerves. In normal volunteers, injections of hypertonic saline to the back muscles produced LBP and referred pain in the buttocks. The deeper quadratus lumborum and psoas muscles, on the other hand, are supplied by ventral rami of the lumbar plexus and may potentially be a source of pain in the back itself.
Although the exact mechanism is not well understood, LBP from muscles has been attributed to spasm, to sprain and strain, and to trigger points in myofascial pain. Free nerve endings may be stimulated from direct trauma, stretch, pressure, disruption of the fibers, or accumulated metabolites during anaerobic metabolism. Muscle spasm is probably a common cause of nonspecific back and neck pain (pain with no clear cause), and it may also cause worsening of back and neck pain when spasm is triggered by less painful pathology in other structures.
5. Joints
Facet joints
The facet joints (also known as zygapophysial joints or Z joints) are well innervated by the medial branches from the posterior primary rami. Each joint has a dual innervation, one from the dorsal rami of the same level and one from the level above. The facet joints of the cervical spine, at C2 and below, are located at the lateral edge of the lamina and are richly innervated via the medial branch from the posterior primary rami. The medial branch from the joint above and below innervates each facet joint. The C2-3 facet joints receive innervation from the third occipital nerves and medial branches of the C3 dorsal rami.
In the lumbar region, intra-articular injection of hypertonic saline and contrast medium in volunteers has shown to cause LBP and referred pain. Although facet joints can be affected when disc disease or spondylosis is present, facet joints have also been shown to cause LBP. Among the suggested causes of facet joint pain are trauma, inflammation, synovial impingement, meniscoid entrapment, and chondromalacia. Hyperextension and rotation of the lumbar spine can cause a capsular tear and avulsion, subchondral fracture, or fracture of the articular process or intra-articular hemorrhage. Pain from facet joints tends to be localized to the back with radiation to the buttock and posterior thigh and, occasionally, below the knee joints. Plain radiographs, CT scans, and MRI are usually not useful in the diagnosis of facet joint pain. Diagnosis can be made only by diagnostic blockade with local anesthetic. To avoid a high false-positive response, controlled diagnostic block techniques are recommended. In one study, the estimated prevalence of LBP from facet joint origins among injured workers was found to be 15%.
Sacroiliac joint
The sacroiliac (SI) joint is a synovial joint, and a portion of it contains a synovial lining. Posteriorly, it receives innervation from dorsal rami of L4–5, and S1–2, and there is some controversy about whether it also receives ventral innervation. Sacroiliac joints have been found to cause localized pain over the joint and referred pain to the lower extremity when stressed with contrast medium in healthy volunteers. Various systemic illnesses including ankylosing spondylitis, metabolic derangements, and infectious disease can affect the SI joint and cause pain. Most cases of suspected SI joint pain are considered mechanical in origin, although the exact mechanism remains unclear. The diagnosis of SI joint pain can be made by an injection of local anesthetic intra-articularly. Its prevalence among chronic LBP sufferers is estimated to be 15%.
6. Nerve roots
Nerve roots and DRG, when compressed, can be the source of axial spine pain and extremity pain. It is important to separate radicular pain, which is pain along the distribution of a spinal nerve, from radiculopathy, in which sensory or motor deficits of a spinal nerve distribution are associated with the pain symptoms. Although acute compression of a normal nerve root will cause paresthesia or numbness, it will not generate persistent pain. In contrast, compression of the normal DRG can cause sustained discharge and may provoke radicular pain and radiculopathy.
Chronic compression of the nerve root can cause pain by sensitizing the nerve to both mechanical and chemical irritation. The underlying neural pathology in chronic compression may include focal demyelination, partial axonal damage, or intraneuronal edema. Nuclear material from a disrupted disc can cause chemical irritation with nerve root inflammation (radiculitis), radicular pain, or radiculopathy.
7. Meninges
The dura mater is a well-innervated structure. The nerve supply is more abundant on the ventral aspect and around the nerve root sleeves. Back pain can arise in a patient with a dura mater inflamed by infection or the presence of intrathecal blood. Clinical studies have shown that LBP and referred gluteal pain are associated with stimulation of the dura by both mechanical and chemical irritation. Chemical irritation from the herniated disc material can cause an inflammatory reaction around the dural sleeve and is believed to be the cause of LBP and somatic referred pain. This is distinct from the radicular pain resulting from radiculitis secondary to chemical or mechanical irritation from the herniated disc materials.
III. EVALUATING THE PATIENT WITH BACK AND NECK PAIN
Important principles in the evaluation of back and neck pain are the following:

Rule out the serious causes of pain (e.g., infection, tumor, trauma).

The etiology of pain in a significant number of patients with back and neck pain may remain unknown. Nonspecific back or neck pain is a legitimate diagnosis.

History and physical examination have a limited role in the diagnosis of back and neck pain but are important in ruling out serious pathology.

It is important to distinguish somatic referred pain from radicular pain and radiculopathy.

Reassure patients that the vast majority of patients with acute back and neck pain recover within weeks.

Diagnostic local anesthetic blocks may be the key for making an anatomic diagnosis.

IDD is the most common cause of axial LBP with or without somatic referred pain.

Cervical facet joints are by far the most common cause of neck pain.
1. History
General medical history
The first responsibility of the physician presented with a patient with back or neck pain is to seek signs and symptoms that indicate a serious underlying cause for the pain. A careful medical history should include any history of cancer, recent weight loss, immunosuppression, recent back or neck surgery, intravenous drug abuse, anticoagulation, metabolic bone diseases, abdominal aortic aneurysm, and history of trauma. It is also important to ask questions about associated symptoms including bilateral lower extremity pain, numbness, weakness, bowel and bladder incontinence, and perineal numbness, which could suggest a spinal cord or nerve root compression. Worsening pain at night, inability to get relief at rest, and increased pain in the supine position suggest epidural spinal metastasis. It is important to include a social and family history to assess the psychosocial support needed to cope with the chronic pain condition.
Pain history
The pain history should document events surrounding the onset of pain. If a motor vehicle accident is the cause of pain, a thorough history including the use of a seat belt, single or multiple car involvement, and whether impact was from the rear or side of the vehicle can be useful in formulating a differential diagnosis. Cervical facet joint pain has been found to be a common source of pain after acceleration–deceleration (whiplash) injury.
The pain history should also focus on the location of pain, its duration, radiation, character (e.g., deep, superficial, sharp, achy, burning, shooting, pins and needles) and worsening or relieving factors. When more then one site is involved, each pain complaint should be documented separately. Pain history also includes previous interventions for pain symptoms including medications, nerve blocks, surgery, physical therapy, and behavioral therapy. If another pain physician saw the patient, a review of those medical records is quite useful. A brief history of the patient’s activities of daily living and limitations resulting from the pain should be documented. This will be helpful in assessing the benefits of future interventions.
2. Physical examination
Comprehensive physical examination
The initial focus of the physical examination should be to determine if there are signs of serious pathology such as fever, spine tenderness, and signs of myelopathy, perineal numbness, loss of anal tone, and pulsatile abdominal mass. If infection or neoplasia is present and there are symptoms of neurologic compromise, an MRI (if available) should be ordered. This will delineate the spread of infection or tumor in the soft tissues. Routine radiographs can help identify bony fractures or destructive bony lesions. A bone scan delineates infection or tumor in bone, although it does not differentiate between the two. In patients with osteoporosis, minor trauma can lead to fracture presenting with significant pain and neurologic deficits.
Examination of the spine
Examination of the spine begins with inspection. The patient’s gait, posture, and any obvious deformity of the spine can be examined very easily. The next step should include a closer examination of the entire length of the spine for scars, rash, or swelling. Palpation should begin gently to detect any sensitivity of the skin. Firmer palpation is then used to detect any midline tenderness or mass, paraspinous tenderness, or muscle tightness. Range of motion of the spine should be examined (flexion, extension, and lateral bending). During the range of motion examination, pain with flexion of the spine can be related to disc pathology, whereas pain with extension can indicate facet arthropathy or spinal stenosis. Pain with lateral bending can be a sign of ipsilateral facet disease.
A thorough neurologic examination, including sensory, motor and deep tendon reflexes, helps to rule out associated spinal cord or nerve root pathology. A positive straight leg raising (SLR) test with the patient in a supine or sitting position can point to nerve root irritation. However, nerve root irritation is not always present in patients with LBP or posterior thigh discomfort. In patients with nerve root irritation, a clear bandlike distribution of pain along a dermatomal distribution is typical in the SLR test. Tenderness over the SI joint should raise the suspicion of SI joint etiology. One compression test to detect SI pathology is Patrick’s test: the supine patient with flexed leg rests an ankle on the opposite knee, and the examiner presses over the flexed knee to elicit the patient’s LBP.
3. Imaging
Radiologic studies for the anatomic diagnosis of neck and back pain have a limited role. A plain film of the spine is indicated when a fracture is suspected, as in the case of trauma, a history of bony metastasis, or the presence of osteoporosis. An urgent MRI is recommended for patients with axial back pain and evidence of neurologic deficit when spinal cord pathology is suspected. If tumor or infection is thought to be the cause of pain, MRI is the imaging study of choice because it delineates the extent of the disease, including epidural spinal compression. Although routine use of MRI for nonspecific axial neck and LBP is controversial, many physicians consider this after initial conservative therapy fails. Provocative intradiscal dye injection (discography) is the most effective way to identify the pathologic disc disease. A postdiscography CT scan is recommended to delineate the anatomic distortion, which may not be seen by routine fluoroscopy.
Further descriptions of history taking, physical examination, and radiologic testing for pain patients can be found in Chapter 4 and Chapter 5. Table 1 summarizes the differentiating features of LBP.

Table 1. Differentiating features of low back pain

IV. CAUSES OF BACK AND NECK PAIN
1. Rare causes
Infection, tumor, aortic aneurysm, sickle cell crisis, retroperitoneal mass, and chronic pancreatitis are among the rare causes of axial spine pain with or without extremity pain. A thorough medical history is critical. Pain often starts suddenly, and it is severe, unrelenting, and not relieved by rest. MRI in most cases is the imaging study of choice, and treatment of the underlying pathology (e.g., surgery, radiation) usually helps to alleviate the pain.
2. No clear cause
In most cases of LBP or neck pain, the anatomic or pathologic diagnosis remains unclear. A thorough history and physical examination is essential to exclude some of the rare but serious causes. LBP and neck pain of unclear etiology is a legitimate diagnosis. In the absence of neurologic symptoms, analgesics such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) can be provided.
Patients should be encouraged to continue their usual activity. If no improvement is seen within 3 weeks, physical therapy may be helpful. If axial neck pain or LBP lasts for more then 12 weeks, an attempt should be made to establish an anatomic diagnosis. The etiology of pain can be established in many cases with controlled invasive diagnostic tests with local anesthetics. Schwarzer et al. found that among patients suffering from chronic LBP, 40% have discogenic pain, 15% to 20% have SI joint pain, and 5% to 10% have facet joint pain.
3. Discogenic pain
The patient with LBP or neck pain originating from the vertebral disc often presents with deep, achy, axial midline pain. Pain can be referred to shoulder or scapular regions for cervical discs, and to buttocks and posterior thigh for lumbar discs. Patients with discogenic pain are often young, are otherwise healthy, and may have jobs that require repetitive motion of the affected spine segment (such as package handlers). Onset of symptoms is usually gradual. Pain is experienced while sitting, standing, and bending forward. The referred pain usually remains in the proximal part of the extremity. Results of physical examination are usually nonspecific, with limited range of motion at the affected segment, or pain with movement, particularly on flexion. MRI and CT scans are not usually helpful. The presence of a high-intensity zone on MRI at the posterior aspect of the disc on sagittal plane may indicate the radial fissure of IDD. Provocative discography by injection of radiocontrast dye is utilized to rule out axial disc pathology. Discography is usually done with fluoroscopic guidance, with a second disc as a control. A postdiscography CT scan can provide more detailed information concerning the anatomic abnormality. Treatment for discogenic pain starts with conservative therapy, including physical therapy and oral NSAIDs. Refractory patients may be considered for intradiscal electrothermal therapy (IDET) (see Chapter 13). This is a relatively new technique with some encouraging data suggesting efficacy. Surgical fusion of the spine remains an option, usually as a last resort.
4. Facet joint pain
Axial spine pain originating from the facet joints has a presentation similar to that of discogenic pain. In most cases, the pain starts gradually and is deep, achy, and localized around the midline; there may be some standing and sitting intolerance. Extension and lateral bending of the affected spine are usually painful.Referred pain to the shoulder, buttock, and proximal extremities is common. Most commonly, pain is the result of stress of the facet joint capsule secondary to loss of disc or vertebral height. It can be caused by degenerative change or osteoporosis, and it is also seen after decompression surgery. When pain is secondary to osteoarthritis of the facet joints, it tends to be less severe and is often described as morning stiffness. In rare cases, facet joint pain may originate from fracture or hemarthrosis following trauma.
Physical examination is usually nonspecific, and sensory and motor examination is usually benign. Some patients have paraspinal tenderness and pain on extension and lateral bending. Imaging studies may help identify pathology such as loss of disc or vertebral height, spondylolisthesis, or other degenerative changes. Diagnostic local anesthetic block under fluoroscopic guidance is the most accurate way to isolate the facet joint as the source of axial spine pain (see Chapter 12). Currently, radiofrequency lesioning of the medial branches is considered the most effective long-term therapy for axial spine pain originating from the facet joints.
5. Sacroiliac joint pain
Localized lower back or upper buttock pain is the common presentation of SI joint pain. Pain referred to the posterior thigh and below the knee is rare. In most cases, the cause is unclear. Trauma, infection, and tumor are uncommon causes of SI joint pain. Physical examination may reveal localized tenderness over the joint, and Patrick’s test may be positive (see preceding section, “Examination of the Spine”). Degenerative change of the joint on a radiograph is extremely common and nonspecific and not helpful in making a diagnosis. Intra-articular injection of local anesthetic under fluoroscopic guidance with complete pain relief indicates that the SI joint is the probable source of the pain. Treatment for SI joint pain remains controversial. Currently, an intra-articular injection of steroid with local anesthetics is the most common therapy (see Chapter 12).
6. Spinal stenosis
Spinal stenosis includes both central canal narrowing and foraminal narrowing. Symptoms from central canal narrowing tend to be diffuse compared to foraminal narrowing (when the exiting nerve root often produces symptoms in a dermatomal distribution). The clinical presentation of central canal narrowing includes axial spine pain (e.g., LBP) and extremity pain. The degree of axial and extremity pain varies between individuals; pain tends to start at the spine and gradually involve the extremities. The pain tends to be diffuse (nondermatomal) and is usually characterized as achy. It commonly worsens with walking (neurogenic claudication), especially downhill walking, and with extension of the spine. Rest and flexion of the spine usually provide temporary relief. A simple way to distinguish neurogenic from vascular claudication is to exercise patients on a bike. Patients with neurogenic claudication usually have no pain, whereas those with vascular claudication have pain while biking.
Spinal stenosis is more common in older individuals and may be associated with age-related changes of the spine. The pathophysiology includes osteophytes, facet capsular hypertrophy, and diffuse broad-based disc bulge. Foraminal narrowing can be caused by these changes as well as by loss of disc height and by spondylolisthesis. MRI can be useful in delineating the extent and the causes of the narrowing.
In mild to moderate cases, a translaminar epidural steroid injection may be therapeutic. Most patients feel their extremity pain improve sooner then their axial pain. The injection can be repeated for a cumulative benefit. If there is no improvement from epidural steroid injections, a surgical consultation may be sought to evaluate possible decompression surgery. Cervical spinal stenosis symptoms can involve both upper and lower extremities, and an early surgical consultation should be sought.
7. Myofascial pain
Neck pain and low back pain of myofascial origin are fairly common, especially after trauma and repetitive motion injury. Myofascial pain around the neck and low back presents as deep, achy, localized discomfort worsening with activity. Pain is thought to be caused by strain or sprain injury to the muscle. Patients are sometimes able to feel a focal area of tight muscle knot and tenderness on palpation. Patients may complain only of paraspinal muscle discomfort, or the pain may extend to the occiput, scapular, and shoulder areas, or to the buttocks and upper thigh areas. It is important to distinguish somatic referred pain (from disc or facet joint pathology) from pain of muscular origin. Physical examination may reveal a tight muscle band, tender to palpation, and may have a characteristic radiation pattern (trigger point).
Various physiotherapy techniques (e.g., stretching and strengthening exercise, massage, iontophoresis) remain the initial therapy of choice (see Chapter 16). Injection of local anesthetics into the tender points may be very useful, especially if a coordinated physiotherapy program immediately follows the injection. Some physicians add steroid with local anesthetics for this injection. There is a risk of local muscle atrophy with repeated steroid injection. Myofascial pain is described in detail in Chapter 17.
8. Failed back syndrome
The diagnosis of failed back syndrome is given to patients who suffer from chronic pain after spine surgery. The surgery may have been performed only for the purpose of relieving pain, or it may have been done for other reasons including stabilization or decompression to relieve neurologic deficit. Pain may vary significantly, and it may be accompanied by neurologic deficits. The pain is often different in quality and in distribution from the patient’s presurgical pain. Epidural scarring is thought to be the primary cause of persistent pain. A thorough history and physical examination are critical to distinguish the nociceptive and neuropathic components of pain. Pain along the distribution of one or more nerve roots may indicate epidural fibrosis. Nociceptive pain from facet or disc disease should be also considered. Up to 40% of postlaminectomy (lumbosacral) patients have LBP originating from facet joints. Scar tissue, early-onset arthritic change, and osteophytes may cause spinal stenosis.
Therapy for failed back syndrome remains controversial. Repeat surgery may not provide the desired pain relief. For patients with neuropathic pain, epidural steroid injection via the foraminal or caudal route can be a useful and relatively benign initial intervention. Other interventional modalities, such as epidural lysis of adhesions via epiduroscopy or by catheter technique (Racz procedure), are not widely practiced because of limited evidence of efficacy. Spinal cord stimulation has been shown to be an effective mode of therapy for neuropathic pain from failed back surgery (see Chapter 13).
9. Whiplash injury
Acceleration–deceleration injury from motor vehicle accidents, commonly known as whiplash injury, frequently causes neck pain. Whiplash is estimated to occur in 1% of the general population, and the pain may become chronic in 10% to 25% of the patients. A controlled study found cervical facet joints to be the most common cause of neck pain after whiplash injury. The authors estimated that in at least 50% (possibly as high as 80%) of high-speed injuries, cervical facet joints are the source of neck pain. The most common cervical segments involved are C5-6 and C2-3. The neck has a large number of muscles, including the neck extensor, flexor, rotator, and lateral flexors. They are well innervated and a common source of neck pain.
The initial office visit should include a history of injury or risk factors for serious pathology. Physical examination has a limited role because of poor reliability and validity of identifying specific causes of pain. It may show limited range of motion, pain with movement, or tenderness over the articular pillars or paraspinous muscles. These signs are nonspecific for making pathoanatomic diagnoses. In the case of trauma, plain films may show fracture or dislocation. MRI and CT are not indicated unless there is a suggestion of impending neurologic compromise. Ronnen et al. (1996) showed that MRI is not useful for diagnosing whiplash-related injury.
Facet joints are the most common cause of neck pain. To formulate an accurate diagnosis of cervical facet joint pain, a control joint block is recommended because of the high rate of false-positive responses from a single diagnostic block. The prevalence of cervical discogenic pain is unknown. Provocative discography may help to identify discogenic pain, although cervical discography has a fairly high level of false-positive responses. A high degree of vigilance and expertise are required when using this technique to avoid infection and injury to vital structures.
V. CONCLUSION
The vast majority of the patients with back and neck pain recover within weeks. The cause of the acute pain remains undetermined in the majority of cases. Neoplasms and infections account for less than 0.7% and 0.01% cases of acute LBP, respectively. History and physical examination should focus on identifying the warning signs of serious underlying pathology. In routine cases, findings include a limited range of motion, pain with activity, and back tenderness; these signs and symptoms are nonspecific and do not help in making a definitive diagnosis. Furthermore, if serious pathology is not suspected, special investigations do not help to make a specific diagnosis. Initial treatment for acute nonspecific back and neck pain should focus on providing reassurance and encouragement, as well as adequate analgesia using simple analgesics and physical treatments, allowing patients to remain active and continue to work.
SELECTED READINGS

1.
Barnsley L, Lord S, Wallis B, Bogduk N. False positive rates of cervical zygapophysial-joint blocks. Clin J Pain 1993;9:124–130.

2.
Bogduk N. Low back pain. In: Bogduk N. The Clinical anatomy of the lumbar spine and sacrum,3rd ed. Edinburgh: Churchill Livingstone, 1999:188–189.

3.
Bogduk N. Acute lumbar radicular pain, chap 3, p 5. Newcastle, Australia: Cambridge Press, 1999.

4.
Bogduk N, Aprill C. On the nature of neck pain, discography and cervical zygapophysial-joint pain Pain 1993;54:213–217.

5.
Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: A report of pain response to tissue stimulation during operation on the lumbar spine using local anesthesia. Orthop Clin North Am 1991;22: 181–187.

6.
Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996;21:1889–1892.

7.
Merskey H, Bogduk N, eds. Classification of chronic pain, 2nd ed. Seattle, WA: IASP Press, 1994.

8.
Ronnen HR, de Korte PJ, Brink PR, vander Bijl HR. Acute whiplash injury: Is there a role for MR imaging? A prospective study of 100 patients. Radiology 1996;201: 93—96.

9.
Schwarzer AC, Wang SC, Bogduk N, et al. The false positive rate of uncontrolled diagnostic blocks of the lumbar Z-joints. Pain 1994;58:195–200.

10.
Schwarzer AC, Aprill CN, Derby R, Fortin J. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995;20:1878–1883.

12.
Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. J Bone Joint Surg 1990;72A:1081–1088.

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