Diagnosis	Treatment
Diagnosis	Recommended	Not Recommended
D1: Undertake diagnostic triage (serious spinal pathology, nerve root pain/radicular pain, or nonspecific low back pain), consisting of appropriate history and physical examination, at the first assessment.	T1: Give adequate information and reassure the patient.	T2: Prescription of bed rest as a treatment.
D2: Assess for psychosocial risk factors (yellow flags; see Table 1.3) and review them in detail if there is no improvement.	T3: Advise the patient to stay active and to continue normal daily activities, including work if possible.	T4: Specific exercises for acute low back pain.
D3: Diagnostic imaging tests (including radiographs, CT, and MRI) are not routinely indicated for acute low back pain.	T5: Prescribe medication, if necessary, for pain relief.	T6: Epidural corticosteroid injections for acute nonspecific low back pain.
D4: Reassess the patient whose symptoms fail to resolve.	T7: Consider spinal manipulation for patients who are failing to return to normal activities.T13: Consider multidisciplinary treatment programs in occupational settings for workers on sick leave for more than 4-8 weeks.	T8: “Back schools” for treatment of acute low back pain.T9: Behavioral therapy for treatment of acute low back pain.T10: Traction.T11: Massage as a treatment for acute nonspecific low back pain.T12: Transcutaneous electrical nerve stimulation (TENS) as a treatment for acute nonspecific low back pain.

Diagnostic triage of acute LBP consists of the following conditions (see Box 1.1):

▪ Serious spinal pathology

▪ Nerve root pain/radicular pain

▪ Nonspecific LBP

Red flags in the diagnosis of LBP are signs that a serious spinal pathology may be the cause of the LBP; they are listed in Table 1.3:

Table 1.3 Red and Yellow Flags in Diagnosis of Low Back Pain

Red flags (signs of serious pathology)

Patient’s age at onset < 20 years or > 55 years

Recent history of violent trauma

Constant progressive, nonmechanical pain (no relief with bed rest)

Thoracic pain

Past medical history of malignant tumor

Prolonged use of corticosteroids

Drug abuse, immunosuppression, human immunodeficiency virus

Systemic “unwellness”

Unexplained weight loss

Widespread neurologic symptoms (including cauda equina syndrome)

Structural deformity

Fever

Yellow flags (psychosocial risk factors)

Inappropriate attitudes and benefits about back pain (e.g., belief that back pain is potentially harmful or severely disabling, high expectations of passive treatments rather than belief that active participation will help)

Inappropriate pain behavior (e.g., fear-avoidance behavior and reduced activity levels)

Emotional problems (e.g., depression, anxiety, stress, tendency to low mood, withdrawal from social interaction)

Signs or symptoms of neurologic involvement in a patient with LBP are complaint of numbness or weakness in the legs and sciatica with radiation past the knee. The following features apply to possible diagnosis of sciatica:

▪ When pain radiates only to the posterior thigh, it is less likely that the pain is caused by a true radiculopathy.

▪ Sciatica has such a high sensitivity (95%) that its absence makes lumbar disc herniation unlikely.

▪ The likelihood of disc herniation in a patient without sciatica would be 1 in 1000.

Because more than 95% of lumbar disc herniations occur at the L4-L5 or L5-S1 level, the neurologic examination should focus on the L5 and S1 nerve roots; however, upper lumbar nerve root involvement may be suggested when pain conforms to an L2, L3, or L4 dermatomal distribution and is accompanied by anatomically congruent motor weakness or reflex changes.

Psychosocial yellow flags are patient factors that increase the risk for development or perpetuation of chronic pain and long-term disability (including work loss associated with LBP); examples are listed in Table 1.3. Identification of yellow flags should lead to appropriate cognitive and behavioral management.

Considerations for diagnosis

Cauda equina syndrome is a condition requiring emergency evaluation and surgery. A patient with LBP should be referred immediately to the emergency room if any of the following emergency symptoms is present:

▪ Sudden onset of or otherwise unexplained loss of or changes in bowel or bladder control (retention or incontinence)

▪ Sudden onset of or otherwise unexplained bilateral leg weakness

▪ Saddle numbness

A patient should be examined within 24 hours if the patient requests a same-day appointment or any of the following urgent symptoms is present:

▪ Fever (38° C or 100.4° F) for more than 48 hours

▪ Unrelenting night pain or pain at rest

▪ Pain with distal (below the knee) numbness or weakness of leg(s)

▪ Progressive neurologic deficit

Is evaluation indicated? A patient should be offered an appointment within 2 to 7 days if any of the following symptoms or patient factors is present:

▪ Exertion injury (e.g., lifting, digging, reaching)

▪ History of back symptoms—patient has been seen before, at least once

▪ Chronic back pain lasting longer than 6 weeks

▪ Unexplained weight loss (more than 10 pounds in 6 months)

▪ Age more than 50 years

▪ History of cancer

Performance of lumbar spine radiographs should be limited to presence of any of the following red flag indications:

▪ Unrelenting night pain or pain at rest

▪ Fever above 38° C or 100.4° F for more than 48 hours

▪ Progressive neuromotor deficit

▪ Pain with distal numbness or leg weakness

▪ Loss of bowel or bladder control (retention or incontinence)

▪ Clinical suspicion of ankylosing spondylitis

▪ Significant trauma

▪ History or suspicion of cancer

▪ Osteoporosis

▪ Long-term oral steroid therapy

▪ Immunosuppression or immunosuppressive therapy

▪ Drug or alcohol abuse

Advanced imaging studies should be performed only for the patient with the following findings:

▪ Progressive neurologic deficit

▪ Minimal to no improvement of radicular symptoms despite 6 weeks of conservative treatment

▪ Uncontrolled pain

▪ Cauda equina syndrome

Epidemiology of low back pain

The lifetime prevalence of LBP is reported as more than 70% in industrialized countries (1-year prevalence, 15% to 45%; adult incidence, 5% per year). Peak prevalence occurs between ages 35 and 55.

Symptoms, pathology, and radiologic appearances in patients with LBP are poorly correlated. Pain is not attributable to pathology or neurologic encroachment in about 85% of people. About 4% of people seen with LBP in primary care have compression fractures, and about 1% have a neoplasm. Ankylosing spondylitis and spinal infections are even more rare. The prevalence of prolapsed intervertebral disc is about 1% to 3%.

Risk factors for LBP are poorly understood. The most frequently reported are as follows:

1. Heavy physical work.

2. Frequent bending, twisting, lifting, pulling and pushing.

3. Repetitive work.

4. Static postures.

5. Vibrations.

6. Psychosocial risk factors, including stress, distress, anxiety, depression, cognitive dysfunction, pain behavior, job dissatisfaction, and mental stress at work.

Outcomes

The aims of treatment for acute LBP are as follows:

▪ To relieve pain

▪ To improve functional ability

▪ To prevent recurrence and chronicity

Relevant outcomes for acute LBP are as follows:

▪ Overall improvement in pain intensity

▪ Improvement in back pain–specific functional status

▪ Positive impact on employment

▪ Improvement in generic functional status

▪ Decrease in medication use

Intervention-specific outcomes may also be relevant; examples are as follows:

▪ Behavioral treatment may improve coping and pain behavior.

▪ Exercise therapy may improve strength and flexibility.

▪ Antidepressants may decrease the symptoms of depression.

▪ Muscle relaxants may reduce the symptoms of muscle spasm.

Treatment of Acute Low Back Pain in Primary Care

The aims of treatment for acute LBP in primary care are to:

▪ Provide adequate information, reassuring the patient that LBP is usually not a serious disease and that rapid recovery is expected in most cases.

▪ Provide adequate symptom control, if necessary.

▪ Encourage the patient to stay as active as possible and to return to normal activities, including work, as early as possible.

▪ Emphasize patient education and conservative home self-care.

An active approach is the best treatment option for acute LBP. Passive treatment modalities (for example, bed rest, massage, ultrasound, electrotherapy, laser, and traction) should be avoided as monotherapy and should not be routinely be used, because they may increase the risk of illness behavior and chronicity.

Patient education and conservative home self-care consist of the following activities and medications:

▪ Anti-inflammatory and analgesic over-the-counter medications

▪ Early return to work or activities

Patients with acute LBP should be advised to stay active and continue ordinary and daily activity within the limits permitted by the pain. For chronic back pain, there is evidence that exercise therapy is effective.

Natural History of Low Back Pain

Acute LBP is usually self-limiting (the recovery rate is 90% within 6 weeks), but chronic pain develops in 2% to 7% of people. Recurrent LBP and chronic LBP account for 75% to 85% of total worker absenteeism. Most patients will experience partial improvement in 4 to 6 weeks and have a recurrence of LBP in 12 months.

A General Assessment of Patients Reporting Low Back Pain

The patient presenting for low back pain should undergo assessment that establishes answers to the following questions:

▪ Has the patient had any recent back procedure or epidural anesthesia?

▪ What is the location of pain—simple LBP (does not radiate past the knee) versus sciatica (LBP with radiation past the knee)?

▪ What is the duration of symptoms, including date of injury or onset of symptoms? LBP for 6 weeks or less is acute; LBP for more than 6 weeks is chronic.

▪ If the pain is a result of an injury, how did the injury occur?

▪ Is the patient experiencing unrelenting or severe pain—rated on a scale of 0 to 10, with 10 indicating most severe pain?

▪ Are other medical conditions present?

▪ Does the patient have a history of previous back pain or surgery?

▪ Are any psychosocial factors present?

Psychosocial Factors to consider include the following:

▪ Belief that pain and activity are harmful

▪ “Sickness behavior” such as extended rest

▪ Depressed or negative moods, social withdrawal

▪ Self-treatment that does not fit best practice

▪ Problems with disability claim and compensation

▪ History of back pain, time off, or other claim

▪ Problems at work or low job satisfaction

▪ Heavy work, unsociable hours

▪ Overprotective family or lack of support

▪ Other factors, such as fear, financial problems, anger, depression, job dissatisfaction, family problems, and stress, that can contribute to prolonged disability

Relevant Medical History

Key elements of the patient’s medical history when symptoms of spinal pain are present (Boxes 1.2 to 1.4 and Table 1.4) are as follows:

▪ Chief complaint

▪ History of present illness: location, character, severity, duration and timing, context, modifying factors, and associated signs and symptoms

▪ Review of systems

▪ Past history of interventional pain management: history of past pain problems, motor vehicle accidents, and occupational or nonoccupational injuries

▪ Family history: history of pain problems in the family, degenerative disorders, familial disorders, drug dependency, alcoholism, and drug abuse

▪ Psychological disorders: depression, anxiety, schizophrenia, and suicidal tendencies

▪ Social history: environmental information, education, marital status, children, habits, hobbies, and occupational history

BOX 1.2 Waddell Embellishment Tests That Indicate Nonorganic Pathology For Low Back Pain

Modified from Waddell G: 1987 Volvo award in clinical sciences: A new clinical model for the treatment of low-back pain. Spine 1987;12:632-644.

Tests

1. Tenderness: Subcutaneous (or less) pressure reproduces symptoms.

2. Stimulation of symptoms:

a. Loading the spine with the weight of the examiner’s hands on top of the patient’s head (to reproduce back symptoms).

b. Simulation of twisting the trunk when rotating the shoulders and hips in unison to reproduce back pain (can physiologically reproduce sciatica).

3. Distraction: Sitting knee extension to rest sciatic tension while distracting the patient with knee or foot examination as the reason for extending the knee. (If the patient is comfortable during sitting knee extension, the straight-leg raising test result should not be positive; a positive result of that test is of questionable significance.)

4. Nonanatomic distribution of pain: As seen on a pain drawing (total body or outside the body) or demonstrated on muscle testing (intermittent efforts).

5. Overreaction: Grimacing, complaints, or suffering displays are inappropriate for the situation or maneuver.

Scoring

A score of 0 to 2 (up to two positive responses) is normal. Three to five positive responses (score of 3 to 5) warn the clinician that nonphysical interference may render the history and physical findings somewhat confusing (identifying a need for a greater focus on objective measures). The more positive Waddell test responses, the greater the chance that nonphysical factors may alter the patient’s response to the physician’s care and potentially lower the clinical expectations for an excellent outcome from both surgical and nonsurgical treatments.

BOX 1.3 Referral Guidelines For Presurgical Psychological Screening

Guidelines for Referral

Presence of no or 1 item: Referral not needed unless desired by patient.

Presence of 2-4 items: Referral should be considered.

Presence of 4 or more items: Referral should be strongly considered.

BOX 1.4 Preoperative Psychological Screening Risk Factors For Poor Surgical Outcome

MMPI, Minnesota Multiphasic Personality Inventory.

Preoperative Psychological Screening Prognosis

Good: 0-4 risk factors

Fair: 5-8 risk factors

Poor: 9-14 risk factors

Table 1.4 History Taking for Spinal Pain

Question/Subject	Answer	Diagnostic Significance
Age	Young	Disc injuries, spondylolisthesis
	Middle age	Sprain/strain, herniated disc, degenerative disc disease
	Elderly	Spinal stenosis, herniated disc, degenerative disc disease, arthritis
Pain:
Character	Radiating (shooting)	Radiculopathy (herniated disc, spondylosis)
Character	Diffuse, dull, nonradiating	Cervical or lumbar strain (soft tissue injury)
Location	Unilateral vs. bilateral	Unilateral: herniated disc Bilateral: systemic or metabolic disease, space-occupying lesion

Neck Cervical spondylosis, neck sprain, muscle strain Arm (± radiation) Cervical spondylosis (± myelopathy), neck sprain, muscle strain Lower back Degenerative disc disease, back sprain, muscle strain Legs (± radiation) Herniated disc, spinal stenosis Occurrence Night pain Tumor With activity Usually mechanical etiology Alleviated by Arm elevation Herniated cervical disc Sitting down Spinal stenosis (stenosis relieved) Exacerbated by Back extension Spinal stenosis (e.g., going down stairs) Trauma Motor vehicle accident (seatbelt?) Cervical strain (whiplash), cervical fractures, ligamentous injury Activity Sports (stretching injury) “Burners/stingers” (especially in football) Neurologic symptoms Pain, numbness, tingling Radiculopathy, neuropathy Spasticity, clumsiness Myelopathy Bowel or bladder symptoms Cauda equina syndrome Systemic complaints Fever, weight loss Infection, tumor

Physical Examination

A physical examination for patients with symptoms of spinal pain would include palpation for spinal tenderness, neuromuscular testing, and the straight-leg raise (SLR) test. Table 1.5 summarizes the examination, techniques, and their clinical application in the patient with a complaint of low back pain.

Table 1.5 Physical Examination of the Spine

Neuromuscular testing should be performed to evaluate the following aspects:

▪ Motor: ankle and greater toe dorsiflexion strength

▪ Reflex: ankle and knee reflexes

▪ Sensory: pinprick sensation in the medial, dorsal, and lateral aspect of the foot

Significant or progressive neuromotor deficit requires surgical consultation.

The SLR test should be performed bilaterally to evaluate for nerve root impingement including, but not limited to, disc herniation. A positive SLR test result is defined as the presence of pain in the posterior leg that radiates below the knee when the patient is lying supine and the hip is flexed 60 degrees or less; it is suggestive of disc herniation. A negative SLR test result rules out surgically significant disc herniation in 95% of cases.

Related anatomy and physiology

The spinal muscles on the neck and back are described in Tables 1.6 through 1.9. The spinal nerves are described in Tables 1.10 through 1.15 and shown in Figures 1-1 and 1-2. The spinal blood supply is shown in Figures 1-3 and 1-4 and described in Table 1.16. The intervertebral foraminal ligaments of the lumbar spine are shown in Figure 1-5.

Table 1.6 Anterior Neck Muscles: Origins, Insertions, Actions, and Related Innervations

Table 1.7 Posterior Neck Muscles (Suboccipital Triangle): Origins, Insertions, Actions, and Related Innervations

Table 1.8 Superficial (Extrinsic) Posterior Neck and Back Neck Muscles: Origins, Insertions, Actions, and Related Innervations

Table 1.9 Deep (Intrinsic) Posterior Neck and Back Neck Muscles: Origins, Insertions, Actions, and Related Innervations

Table 1.10 Anterior and Posterior Branches of the Spinal Nerves

Table 1.11 Cervical Plexus (C1-C4 Ventral Rami) behind Internal Jugular Vein and Sternocleidomastoid (SCM) Muscles

Table 1.12 Brachial Plexus

Table 1.13 Lumbar Plexus

Table 1.14 Sacral Plexus and Coccygeal Nerves

Table 1.15 Spinal Nerve Branches and the Territories They Supply

Spinal nerve branch	Motor visceromotor territory	Sensory territory
Ventral ramus	All somatic muscles except for the intrinsic back muscles	Skin of the lateral and naterior trunk wall and of the upper and lower limbs
Dorsal ramus	Intrinsic back muscles	Posterior skin of the head and neck, skin of the back and buttock
Menigeal ramus	–	Spinal meniges, ligaments of the spinal column, capsules of the facet joints
White ramus communicans	Carries preganglionic fibers from the spinal nerve to the sympathetic trunk (‘White’ because the preganglionic fibers are myelinated)	–
Gray ramus communicans*	Carrries postganglionic fibers from the sympahetic trunk back to the spinal nerve (‘Gray’ because the fibers are unmyelinated)	–

* Strictly speaking, the gray ramus communicans is not a spinal nerve branch but a branch passing from the sympathetic trunk to the spinal nerve.

Figure 1–1 Anterior view of the nerves of the trunk wall.

Figure 1–2 Branches of the spinal nerves. Formed by the union of the dorsal (sensory) and ventral (motor) roots, the approximately 1 cm–long spinal nerve courses through the intervertebral foramen and divides into five branches after exiting the vertebral canal (see Table 1.15).

Figure 1–3 Composite schema of blood supply to the spinal cord and nerve roots showing two regions of the cord. Note the distribution between medullary arteries and true radicular arteries and that the medullary arteries usually run a course that is independent of the roots. 1, Dorsolateral longitudinal artery; 2, proximal radicular artery (of dorsal root); 3, dorsal medullary artery; 4, dorsal root of the thoracic spinal nerve; 5, distal radicular artery (of dorsal root); 6, sinuvertebral nerve; 7, dorsal ramus of spinal nerve; 8, segmental artery; 9, dorsal central artery; 10, dorsal root ganglion; 11, anterior laminar artery; 12, ventral ramus of spinal nerve; 13, rami communicantes; 14, ventral root of spinal nerve; 15, proximal radicular artery of ventral root; 16, periradicular theca of dura; 17, dorsal meningeal branch of vertebromedullary artery; 18, dura; 19, ventral meningeal plexus; 20, great ventral medullar artery (great “radicular” artery of Adamkiewicz); 21, anterior (ventral) spinal artery; 22, vasa corona of spinal cord; 23, spinal nerve; 24, ventral medullary artery of thoracic cord.

Figure 1–4 Schema showing the venous relations of a lumbar vertebra. The divisions of the network are the internal vertebral plexus, which surrounds the dura and is drained by veins in the intervertebral foramina; the basivertebral veins on the back of the vertebral bodies, which drain a network in the marrow spaces of the vertebrae; and the external vertebral plexus, which lies on the anterior and lateral sides of the vertebral bodies and on the vertebral arches. 1, Dorsal external vertebral plexus; 2, dorsal epidural plexus; 3, ascending lumbar veins; 4, basivertebral vein; 5, anterior ventral external vertebral plexus; 6, lumbar segmental vein; 7, muscular vein from posterior abdominal wall; 8, circumferential channels (sinuses) of epidural plexus; 9, ventral epidural plexus; 10, internal ventral and dorsal venous plexus; 11, lateral ventral external vertebral plexus.

Table 1.16 Spinal Arteris^*

Figure 1–5 Intervertebral foraminal ligaments of the lumbar spine: A, corporo-transverse superior and corporo-transverse inferior; B, superior transforaminal ligament ; C, mid- transforaminal ligament; D, inferior transforaminal ligament; E, posterior transforaminal ligament. Enlarged image shows all ligaments in context.

(Modified from Park HK, Rudrappa S, Dujovny M, Diaz FG: Intervertebral foraminal ligaments of the lumbar spine: Anatomy and biomechanics. Childs Nerv Syst 2001;17:275-282.)

Imaging studies

The indications for and advantages of magnetic resonance imaging (MRI) and computed tomography (CT) in the evaluation of low back pain are summarized in Table 1.17.

Table 1.17 Magnetic Resonance Imaging (MRI) and Computed Tomography (CT): Indications and Advantages in the Evaluation of Low Back Pain

	MRI	CT
Indications
Major or progressive neurologic deficit (e.g., foot drop or functionally limiting weakness such as hip flexion or knee extension)	Yes	Yes
Cauda equina syndrome (loss of bowel or bladder control or saddle anesthesia)	Yes	Yes
Progressively severe pain and debility despite conservative therapy	Yes	Yes
Severe or incapacitating back or leg pain (e.g., requiring hospitalization, precluding walking, or significantly limiting the activities of daily living)	Yes	Yes
Clinical or radiologic suspicion of neoplasm (e.g., lytic or sclerotic lesion on plain radiographs, history of cancer, unexplained weight loss, or systemic symptoms)	Yes	Yes
Clinical or radiologic suspicion of infection (e.g., end plate destruction on plain radiographs, history of drug or alcohol abuse, or systemic symptoms)	Yes	No
Severe low back pain or radicular pain that is unresponsive to conservative therapy and with indications for surgical intervention	Yes	No
Bone tumors (to detect or characterize)	No	Yes
Advantages	Better visualization of soft tissue pathology Better soft tissue contrast Better visualization of neurologic structures Improved sensitivity for cord pathology and for intrathecal masses Improved sensitivity for infection and neoplasm No radiation exposure; therefore safer for women who are pregnant, especially in the first trimester

Better visualization of calcified structures

Direct visualization of fractures

Direct visualization of fracture healing and fusion mass

More accurate in the assessment of certain borderline or active benign tumors

More available and less costly

Better accommodation for patients weighing > 300 lbs and for patients with claustrophobia

Less sensitive to patient motion; particularly useful for patients who cannot lie still or for patients who cannot cooperate for MRI

Diagnostic interventional techniques

Evidence-based interventional diagnostic techniques for low back pain are as follows:

▪ Facet joint blocks

▪ Discography

▪ Transforaminal epidural injections or selective nerve root blocks

▪ Sacroiliac joint injections

Pain provocation in any structure is an unreliable criterion, except in provocative discography. Relief of pain is an essential criterion in almost all structures. Most pain-provocative or pain-relieving tests used to diagnose painful conditions of the spine are more closely related to a physical examination than to a laboratory test.

For an anatomic structure to be deemed a potential cause of back pain it must fulfill the following four criteria developed by Bogduk [2]:

▪ It must have a nerve supply.

▪ It should be capable of causing pain similar to that seen clinically in normal volunteers.

▪ It must be susceptible to painful diseases or injuries.

▪ It must be demonstrated as a source of pain by diagnostic techniques of known reliability and validity.

The following three assumptions related to diagnostic use of neural blockade were developed by Hildebrandt [3]:

▪ The pathology causing pain is located in an exact peripheral location, and impulses from this site travel via unique and consistent neural routes.

▪ The injection of local anesthetic totally abolishes the sensory function of intended nerves.

▪ The relief of pain after local anesthetic block is attributable solely to the block of the target afferent neural pathway.

The limitations of the validity of these assumptions are (1) the complexities of anatomy, physiology, and the psychology of pain perception and (2) the effect of local anesthetics on impulse conduction

Ideally, a diagnostic block achieves block of the same structure three times as described below:

▪ All controlled blocks should include placebo injections of normal saline, but it may be neither logical nor ethical to use placebo injection of normal saline in conventional practice in each and every patient.

▪ As an alternative, the use of comparative local anesthetic block, on two separate occasions, during which the same structure is anesthetized using two local anesthetics with different durations of action, has been proposed.

The minimum requirements for performance of diagnostic interventional techniques are as follows:

▪ History and physical examination

▪ Informed consent

▪ Appropriate documentation of the procedure

▪ Correct environment, including a sterile operating room or procedure room, appropriate monitoring equipment, radiology equipment, sterile preparation, resuscitative equipment, needles, gowns, injectable drugs, intravenous fluids, anxiolytic medications, and trained personnel for preparation and monitoring of patients

Contraindications to the performance of a diagnostic interventional technique are as follows:

▪ Ongoing bacterial infection

▪ Possible pregnancy

▪ Bleeding diathesis and anticoagulant therapy

The reliability and validity of any diagnostic technique are determined by the following factors:

False-positive rate: The rate at which patients without a condition nonetheless have a positive test result.

False-negative rate: The rate at which patients with a condition nonetheless show a negative test result.

Placebo response: A remarkable phenomenon in which a placebo – a fake treatment, an inactive substance – can sometimes improve a patient’s condition simply because the person has the expectation that it will be helpful.

Sensitivity: A description of the diagnostic technique in relation to the prevalence of false-positive results; the most sensitive test yields a positive result for all cases in which the disease is present.

Specificity: A description of the diagnostic technique in relation to the prevalence of the false-negative results; the specificity is greatest when there is a positive test result only when the disease is present.

Facet or Zygapophyseal Joint Block

Diagnostic blocks of facet or zygapophyseal joint can be performed by anesthetizing the joint itself or the medial branches which supply the target joint with injections of local anesthetic, to test whether the joint is the source of pain (Table 1.18). If pain is not relieved, the joint cannot be considered the source of pain. If pain is relieved, the joint may be considered the primary source of the pain.

Table 1.18 Possible Results of Diagnostic Block of Facet Joints

False-positive rates for diagnostic block of facet joints are shown in Table 1.19, in comparison with rates at which facet joints are actually the source of chronic spinal pain. The false-negative rate, which is 8% at all spine levels, is due to unrecognized intravascular injection of local anesthetic.

Table 1.19 Accuracy of Diagnostic Block of Facet Joints: False-Positive Rate versus Rate of Facet Joint–Caused Chronic Spinal Pain

Region of Spine	Reported False-Positive Rates (%)	Rate for Confirmed Facet Joint–Caused Chronic Spinal Pain (%)
Cervical	27-63	54-67
Thoracic	55-58	42-48
Lumbar	17-47	15-45

Modified from Manchikanti L, Boswell MV, Singh V, Pampati V, Damron KS, Beyer CD. Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions. BMC Musculoskelet Disord 2004;5:15.

The prevalence of facet joints as the source of chronic spinal pain is 30% in individuals younger than 65 years and 52% in older individuals, 38% in men, and 43% in women

The rationale for using facet joint blocks for diagnosis is based on the following findings in normal volunteers (Figs 1-6):

▪ Cervical facet joints have been shown to be capable of being a source of neck pain and referred pain in the head or upper limb girdle.

▪ Thoracic facet joints have been shown to be capable of being a source of thoracic pain and referred pain over the chest wall.

▪ Lumbar facet joints have been shown to be capable of being a source of LBP and referred pain in the lower limb.

Figure 1–6 The main distribution of referred pain from each joint and the dorsal rami, as explained in the table. 1, occipital region; 2, upper posterolateral cervical region; 3, upper posterior cervical region; 4, middle posterior cervical region; 5, lower posterior cervical region; 6, suprascapular region; 7, superior angle of the scapula; 8, midscapular region; 9, shoulder joint; 10, upper arm.

Source	Region
Joint	Main Region(s) of Pain Distribution
C0-C1	2
C1-C2	2
C2-C3	3
C3-C4	3, 4
C4-C5	4, 5, 6
C5-C6	5, 6
C6-C7	7, 8
C7-T1	7, 8
Dorsal Ramus	Region(s) to which Pain is Referred with Electrical Stimulation
C3	1, 3
C4	4
C5	5
C6	7
C7	7,8

(Modified from Fukui S, Ohseto K, Shiotani M, Ohno K, Karasawa H, Naganuma Y, Yuda Y. Referred pain distribution of the cervical zygapophyseal joints and cervical dorsal rami. Pain 1996;68:79-83.)

Facet joint pain is neither an articular disorder nor a neurologic disorder. It does not meet the criteria for pain from other joints, which is typically diagnosed on the grounds of swelling, tenderness, and restricted motion. The referral patterns described for various joints are not only variable but also restricted. Other structures in the same segment, such as the disc, may produce the same pattern of pain. Most maneuvers used in physical examination are likely to stress several structures simultaneously, especially the disc, muscles, and facet joints, thus failing to provide any reasonable diagnostic criteria.

Most published studies have not found a correlation between facet joint–caused pain and imaging findings, including findings of MRI, CT, dynamic bending films, single-photon emission computed tomography (SPECT), and radionuclide bone scanning. Thus, controlled diagnostic blocks using two separate local anesthetics (or with placebo control) are the only means of confirming diagnosis of facet joint pain.

Safety and Complications

Complications of diagnostic block of the facet or zygapophyseal joint that are related to needle placement and drug administration are as follows:

▪ Dural puncture

▪ Spinal cord trauma

▪ Infection

▪ Intravascular injection

▪ Spinal anesthesia

▪ Chemical meningitis

▪ Neural trauma

▪ Pneumothorax

▪ Hematoma formation

Complications related to administration of steroids are as follows:

▪ Radiation exposure

▪ Facet capsule rupture

▪ Vertebral artery damage

▪ Local anesthetic leakage out of the joint into spinal canal

Another potential complication is an incidental block of the third occipital nerve, which may result in transient ataxia and unsteadiness due to partial blockade of the upper cervical proprioceptive afferents and the righting response, and phrenic nerve block, which can result from diagnostic block at the C3-C4, C4-C5, or C5-C6 facet joint block.

Provocative Discography

Provocative discography is a diagnostic procedure designed to determine whether a disc is intrinsically painful. It involves making the nucleus pulposus of an intervertebral disc opaque to render it visible on radiographs. The procedure involves disc puncture, disc stimulation, assessment of disc morphology, and assessment of the patient’s pain response.

The overall accuracy of the various modalities of provocative discography is as follows [4]:

▪ CT discography: 87%

▪ CT/myelography: 77%

▪ CT: 74%

▪ Myelography: 70%

▪ Discography alone: 58%

Safety and Complications

Complications of provocative discography are as follows:

▪ Infection: acute epidural abscess, subdural empyema, prevertebral abscess, and discitis

▪ Neural and spinal cord trauma

▪ Intravascular penetration, which may lead to post-injection hematoma

▪ Headache

The incidence of discitis is 2% to 3% for a single-open-needle technique but only 0.7% for a double-open-needle technique [4].

Therapeutic interventional techniques

The rationale for therapeutic interventional techniques in the spine is based on the following considerations:

▪ Cardinal sources of chronic spinal pain, namely discs and joints, are accessible to neural blockade.

▪ Removal or correction of structural abnormalities of the spine may fail to cure and may even worsen painful conditions.

▪ Degenerative processes of the spine and the origin of the spine pain are complex.

▪ The effectiveness of a large variety of the therapeutic interventions in managing chronic spinal pain has not been demonstrated conclusively.

Interventional techniques in the management of chronic spinal pain include neural blockade and minimally invasive surgical procedures such as:

▪ Epidural injections

▪ Facet joint injections

▪ Neuroablation techniques

▪ Intradiscal neural therapy

▪ Disc decompression

▪ Morphine pump implantation

▪ Spinal cord stimulation

The requirements for the performance of therapeutic interventional techniques in the spine include:

▪ A sterile operating room or a procedure room

▪ Monitoring equipment

▪ Radiographic equipment

▪ Special equipment specific to technique

▪ Sterile preparation with all of the following available: resuscitative equipment, needles, gowns, agents for injection, intravenous fluids, sedative agents, and trained personnel for preparation and monitoring of the patient

Minimum requirements in preparation for these procedures are as follows:

▪ History and physical examination

▪ Informed consent

▪ Appropriate documentation of the procedure

Contraindications to therapeutic interventional techniques in the spine are as follows:

▪ Bacterial infection

▪ Possible pregnancy

▪ Bleeding diathesis and anticoagulant therapy

Facet Joint Injections

The effectiveness of intra-articular injections, medial branch blocks, and neurolysis of medial branches for pain relief over the short or long term is shown in Table 1.20.

Table 1.20 Duration of Effectiveness of Therapeutic Interventional Techniques in Facet Joint Pain

Modality	Short-Term	Long-Term
Intra-articular injection	≤ 3 months	3 to 6 months
Medial branch block	≤ 3 months	3 to 6 months
Neurolysis of medial branches	3 to 6 months	> 6 months

Epidural Injections

The three approaches for the epidural space are interlaminar, caudal, and transforaminal. The advantages and disadvantages of the three approaches are listed in Table 1.21. The known evidence for the short-term or long-term effectiveness of epidural injections is summarized in Table 1.22.

Table 1.21 Advantages and Disadvantages of the Three Approaches to Injection of the Epidural Space

Table 1.22 Known Evidence for Effectiveness of Epidural Injections

Type of Injection	Short-Term Effect (Significant Relief ≤ 3 Months)	Long-Term Effect (Significant Relief > 3 Months)
Interlaminar	Moderate evidence	Limited evidence
Caudal	Strong evidence	Moderate evidence
Transforaminal	Strong evidence	Strong evidence

Epidural Adhesiolysis

The purpose and goals of percutaneous epidural lysis of adhesions are:

▪ To eliminate the deleterious effects of scar formation, which can physically prevent direct application of drugs to nerves or other tissues for treatment of chronic back pain.

▪ To ensure delivery of high concentrations of injected drugs to the target areas.

▪ To achieve epidural lysis of adhesions and direct deposition of corticosteroids in the spinal canal with the three-dimensional view provided by epiduroscopy or spinal endoscopy.

The known evidence for short-term or long-term effects of percutaneous epidural adhesions and spinal endoscopic adhesiolysis is summarized in Table 1.23.

Table 1.23 Known Evidence for Effectiveness of Percutaneous Epidural Adhesions and Spinal Endoscopic Adhesiolysis

Percutaneous epidural adhesions

Moderate evidence for short-term effect (≤ 3 months)

Moderate evidence for long-term effect (3 to 6 months) with repeat interventions

Spinal endoscopic adhesiolysis

Moderate evidence for short-term effect (3 to 6 months)

Limited evidence for long-term effect (> 6 months)

Safety and Complications

The complications of percutaneous epidural lysis of adhesions are as follows:

▪ Dural puncture, spinal cord compression, infection, steroids, hypertonic saline, hyaluronidase, and damage by the endoscope

▪ Administration of high volumes of fluids, potentially resulting in excessive epidural hydrostatic pressures (which may cause spinal cord compression, excessive intraspinal and intracranial pressure, epidural hematoma, bleeding, infection, increased intraocular pressure with resultant visual deficiencies, and even blindness and dural puncture)

▪ Unintended subarachnoid or subdural puncture with injection of local or hypertonic saline

▪ Catheter shearing and retention in the epidural space

▪ Excessive intraspinal pressure development with potential to affect both local and distant profusion, resulting in visual changes, even blindness

▪ A combination of high volumes of fluid and generation of high hydrostatic pressures (spinal endoscopic adhesiolysis > percutaneous epidural catheter adhesiolysis)

▪ Spinal cord trauma or spinal cord or epidural hematoma formation

Intradiscal Therapies

The known evidence for the short-term or long-term effects of epidural injections is described in Table 1.24.

Table 1.24 Evidence for Effectiveness of Intradiscal Therapies

Intradiscal electrothermal therapy

Moderate evidence for short-term relief

Limited evidence for long-term relief

Percutaneous disc decompression (PDD) Limited evidence for the effectiveness Nucleoplasty Limited evidence for the effectiveness

Implantable Therapies

Spinal Cord Stimulation

Brief history related to spinal cord stimulation

▪ The gate control theory by Melzack and Wall (1965) [9]

▪ Shealy’s the first spinal cord stimulator device for the treatment of chronic pain (1967) [8]

The mechanism of action of spinal cord stimulation occurs (1) at the local and supraspinal levels and (2) through dorsal horn interneuronal and neurochemical mechanisms. The indications for and contraindications to spinal cord stimulation are listed in Table 1.25. There is moderate evidence for long-term relief with spinal cord stimulation in a properly selected population with neuropathic pain.

Table 1.25 Indications for and Contraindications to Spinal Cord Stimulation

Indications (for patients with chronic pain of predominantly neuropathic origin and topographical distribution involving the extremities)

In United States:

Failed back surgery syndrome

Complex regional pain syndrome type I and II

In Europe:

Chronic intractable angina and pain

Disability due to peripheral vascular disease

Contraindications (such asprimary nociceptive conditions)

Degenerative disc disease

Sacroiliac dysfunction

Arthritis

Cancer

Acute tissue injury

Falowski S, Celii A, Sharan A. Spinal cord stimulation: an update. Neurotherapeutics 2008; 5: 86-99.

Complications

Complications of spinal cord stimulation range from simple, easily correctable problems, such as lack of appropriate paresthesia coverage, to devastating complications, such as paralysis, nerve injury, and death. Possible infections range from simple infections at the surface of a wound to epidural abscess and concomitant meningitis. Mechanical complications of the procedure are malposition, migration, breakage, and failure of the electrode lead.

Implantable Intrathecal Drug Administration Systems

The advantages and disadvantages of implantable intrathecal drug administration systems are listed in Table 1.26. There is moderate evidence for long-term effectiveness of intrathecal infusion systems.

Table 1.26 Advantages and Disadvantages of Implantable Intrathecal Drug Administration Systems

Advantages

More powerful analgesia at a significantly lower dose of administered drug

More consistent analgesia with a lower incidence of somnolence, mental clouding, constipation, and euphoria

Theoretically better for treatment of the chemically dependent patient with an intractable nociceptive and/or neuropathic pain condition (the intrathecal medication does not produce euphoria and cannot be manipulated by the patient)

Disadvantages

Surgical risks involved with any implanted device

Risk of spinal injury from the catheter or infused medications

Risk of side effects specific to intrathecal drug delivery

High cost

Medical decision-making – spinal pain

The key components for establishing a diagnosis and/or selecting a management option (medical decision-making) in the patient with spinal pain are as follows:

1. Consider all of the many options for diagnosis and management.

2. Obtain, review, and analyze all medical records, diagnostic tests, and other information.

3. Consider the risk of significant complications as well as the morbidity and mortality of diagnostic procedures and/or possible management options; also consider the risks of any comorbidities in patients presenting with spinal pain.

Treatment for spinal pain is medically necessary when the following conditions are met:

▪ Suspected organic problem

▪ Nonresponsiveness to less invasive modalities of treatments

▪ Pain and disability of moderate to severe degree

▪ No evidence of contraindications, such as severe spinal stenosis resulting in intraspinal obstruction, infection, and predominantly psychogenic pain

▪ Responsiveness to prior interventions with improvement in physical and functional status

Activity recommendations for acute lower back pain

Patients with acute LBP should be advised to stay active and continue ordinary activity within limits permitted by the pain. Compared with bed rest and back-mobilizing exercises, remaining active leads to:

▪ More rapid recovery

▪ Less chronic disability

▪ Fewer recurrent problems

Activity Modification

▪ Patients should be advised to continue routine activity while paying attention to correct posture.

▪ Those with acute LBP problems may be more comfortable if they temporarily limit or avoid specific activities known to increase mechanical stress on the spine, especially prolonged unsupported sitting, heavy lifting, and bending or twisting the back, particularly while lifting.

▪ Activity recommendations for the employed patient with acute low back symptoms must take into consideration the patient’s age and general health and the physical demands of the patient’s job.

▪ Patients should discontinue any activity or exercise that causes spread of symptoms (peripheralization).

Bed Rest

▪ Bed rest is not recommended. If the patient must rest, bed rest should be limited to no more than 2 days and should be regarded as an option only for patients with severe initial symptoms of primarily leg pain [6].

▪ A gradual return to normal activities is more effective and leads to more rapid improvement with less chronic disability than prolonged bed rest for treatment of acute low back problems.

▪ Prolonged bed rest—4 days or longer—may lead to debilitation and is not recommended for treatment of acute low back problems.

Exercise

Patients should discontinue any activity or exercise that causes spread of symptoms (peripheralization). Low-stress aerobic and flexibility exercises can prevent debilitation due to inactivity during the first month of symptoms and thereafter may help return patients to the highest level of functioning appropriate to their circumstances. Recommendations that involve gradually increasing exercise quotas have better outcomes than telling patients to stop exercising if pain occurs. Most patients with acute low back problems can begin aerobic (endurance) programs that minimally stress the back (walking, biking, or swimming) during the first 2 weeks.

Strengthening exercises for trunk muscles (especially back extensors), with gradual increase, are helpful for patients with low back problems. During the first 2 weeks, however, strengthening exercises may aggravate symptoms because they mechanically stress the back more than endurance exercise. It is important for patients to consult with a medical specialist such as a qualified spine specialist, who can evaluate individual symptoms and recommend a safe and effective program. Self-treatment with an exercise program not specifically designed for the patient may aggravate the symptoms.

A self-care brochure can be given to the patient to emphasize the following issues:

▪ It is likely that the patient does not have serious disease if the doctor found no “red flag” symptoms.

▪ Hurt does not equal harm.

▪ There is a good prognosis for LBP. The majority of patients experience significant improvement in 2 to 4 weeks.

▪ Bed rest is not recommended and should be limited to no more than 2 days.

▪ Light activity will not further injure the spine and typically helps speed recovery.

▪ A progressive resumption of work and activity levels leads to better short-term and long-term outcomes.

▪ Information and advice regarding any specific potentially painful activities, such as sitting, lifting, and getting up from bed should be included.

▪ No specific exercise type can be recommended as more effective than any other.

Examples of specific advice are:

1. Exercise as soon as back pain allows.

2. Minimize bed rest, keep mobile, and increase walking time each day.

3. Some of the easier activities to resume or begin after an episode of back pain are walking and swimming.

Follow-up Visit for Acute Lower Back Pain

Because most patients with acute pain improve by 2 weeks, a conservative treatment approach, as previously described, is recommended. Patients whose LBP is not improving or who experience significant limitation of daily activity at home or work should contact their provider within 1 to 3 weeks of the initial evaluation. Patients who are improving should continue home self-care.

Red flags and psychosocial indicators (yellow flags) should be reviewed and evaluated for at each contact or visit. Indications for referral to superior hospital or institution include:

▪ Failure to make improvement with home self-care after 2 weeks

▪ Severe incapacitating and disabling back or leg pain

▪ Significant limitation of functional or job activities

General decision-making process for chronic low back pain and sciatica

Chronic Low Back Pain

Reevaluation, including a general assessment, should be performed for patients not improving after 6 weeks (chronic LBP). The assessment should include a subjective pain rating, a functional assessment, and a clinician’s objective assessment. Psychosocial screening and assessment tools should be used to rule out major depression in adults in primary care.

Of the 10% of patients with chronic symptoms, 90% have chronic LBP and only 10% have chronic sciatica. For patients not improving after 6 weeks, lumbar spine radiographs, as described later, should be obtained.

Physical factors that may lead to delayed recovery or prolonged disability include malignancy, infection, metabolic, and biomechanical conditions (e.g., sacroiliac joint dysfunction). Blood testing, including a complete blood count and measurement of the erythrocyte sedimentation rate, should be ordered if there is suspicion of cancer or infection.

The patient should be evaluated for sacroiliac joint dysfunction. Clinical indicators of the disorder include delayed recovery with unilateral pain below L5, pain near the posterior-superior iliac spine, and, sometimes, radicular or referred pain to the groin or thigh, or below the knee. Pain from the sacroiliac joint can often be referred into the lower extremity, even below the knee or into the foot. The most reliable locations are below L5, in the region of the posterior-superior iliac spine, and into the groin. Diagnostic maneuvers for this condition are the Patrick test, the gapping test, the compression test, and the Gaenslen test. Appropriate treatment of sacroiliac joint dysfunction by a trained spine professional involves manual therapy, instruction on self-corrective maneuvers, and strengthening exercises. There is at least some theoretical support for active rehabilitation of the abdominal musculature to stabilize the joint in the treatment of sacroiliac joint dysfunction.

Lumbar spine radiographs (anteroposterior and lateral views) should be obtained if indicated. Oblique views are not recommended; they add only minimal information in a small percentage of cases, and they more than double the radiation exposure for the patient. Several radiographic findings are of questionable clinical significance and may be unrelated to back pain; they include the following [7]:

▪ Single disc space narrowing

▪ Spinal bifida occulta

▪ Disk calcification

▪ Mild to moderate scoliosis

Chronic Sciatica

MRI and CT are not useful during acute sciatica unless there are red flag indications and the patient is a potential surgical candidate. In isolated cases of LBP without radicular symptoms, MRI is the preferred diagnostic procedure. However, in an otherwise healthy adult suffering LBP with radicular symptoms who has not undergone a previous back surgery, a CT scan may be as sensitive as an MR image (see Table 1.17).

Treatment of the painful motion segment

Diagnosis of radiographic cervical instability requires either of the following findings:

▪ Sagittal displacement greater than 3 mm or relative sagittal plane displacement greater than 11% on a plain film of the spine in the neutral position

▪ Sagittal plane translation greater than 3.5 mm or rotation greater than 20% on a flexion-extension film

Indications for fusion of the degenerative spine are listed in Table 1.27:

Table 1.27 Indications for Fusion Procedures of the Degenerative Spine

Procedure	Absolute Indications	Controversial Indications
Cervical spine:
Anterior infusion Posterior fusion	Unstable > 3 mm movement > 11° range of motion Kyphosis After laminectomy in the kyphotic spine Bilateral facetectomy

Straightening of the spine

Axial neck pain

After discectomy

After laminectomy in straightened spine

Sustained axial pain after laminectomy

Lumbar spine

Decompression with grade II or greater spondylolisthesis

After repeated (> 2) discectomies

Radiographically documented instability (defined as > 3 mm movement and translational movement and/or movement > 10 degrees on flexion-extension radiographs)

After bilateral facetectomy

Decompression with grade I spondylolisthesis

Suggestive mechanical pain

After unilateral facetectomy

Bambakidis NC, Feiz-Erfan I, Klopfenstein JD, Sonntag VK. Indications for surgical fusion of the cervical and lumbar motion segment. Spine 2005; 30 (16 Suppl): S2-S6.

Indications for surgical decompression and fusion in the cervical spine are as follows:

▪ Radiographic evidence of instability with progressive neurologic deterioration

▪ Mild disabling myelopathy

▪ Moderate to severe myelopathy

Fusion is universally indicated if an anterior approach is used. Fusion after posterior laminectomy is controversial but is indicated in the presence of a deformity or preoperative reversal of the lordotic curvature.

Indications for cervical arthroplasty are as follows:

▪ Radiculopathy caused by disc herniation

▪ Radiculopathy caused by foraminal osteophytes

▪ Myelopathy caused by disc herniation

The advantages of lumbar interbody fusion over posterolateral fusion are as follows:

▪ Interbody grafts are compressed by 80% of spinal loads, whereas posterolateral grafts are compressed by 20% of spinal loads (Fig. 1-7).

▪ Interbody grafts occupy 90% of intervertebral body surface area, whereas posterolateral grafts occupy 10% of intervertebral bony surface area.

▪ The interbody space is more vascular than the posterolateral space, thereby promoting the chances for fusion.

▪ Interbody grafts can better restore coronal and sagittal balance.

▪ Interbody fusions may be promoted by the use of recombinant human bone morphogenetic hormone type 2 (rhBMP-2) in the disc space.

▪ Differentiation of fusion and pseudarthrosis is easier with an interbody fusion than with a posterolateral fusion.

Figure 1–7 Illustration of spinal loads and articular surface area across the lumbar spinal column.

Potential indications for posterolateral lumbar fusion are as follows:

1. Clinical or radiographic spinal instability due to:

f. Deformity correction.

2. Spondylolisthesis demonstrating:

a. Documented progression.

b. Symptomatic grade I/II slip refractory to conservative therapy.

c. Grade III/IV slip.

3. Degenerative disc disease causing discogenic LBP.

4. Recurrent lumbar disc herniation with significant mechanical back pain.

5. Third or greater recurrence of lumbar disc herniation with radiculopathy (with or without back pain).

6. Treatment of pseudoarthrosis.

Potential indications for lumbar interbody fusion are as follows:

▪ Spondylolisthesis with documented progression and/or symptomatic grade I/II slip refractory to conservative therapy

▪ Degenerative disc disease causing discogenic LBP

▪ Recurrent lumbar disc herniation with significant mechanical LBP

▪ Postdiscectomy collapse with neuroforaminal stenosis and secondary radiculopathy

▪ Third or greater recurrence of lumbar disc herniation with radiculopathy (with without back pain)

▪ Pseudoarthrosis

▪ Postlaminectomy kyphosis

▪ Lumbar deformity with coronal and/or sagittal plane imbalance

Table 1.28 compares posterolateral fusion with lumbar interbody fusion.

Table 1.28 Indications for the Selection of Posterolateral Fusion versus Lumbar Interbody Fusion

Posterolateral fusion	No risk factors for pseudoarthrosis Osteopenia Grade III/IV spondylolisthesis Alignment/balance preserved
Lumbar interbody fusion	Risk factors for pseudoarthrosis (e.g., tobacco use, rheumatologic disease, diabetes) Axial load-bearing pain Need to correct coronal/sagittal imbalance

Table 1.29 lists the relative contraindications to lumbar fusion procedures.

Table 1.29 Relative Contraindications to Lumbar Fusion Surgery

Contraindication	To Posterolateral Fusion	To Lumbar Interbody Fusion
Multilevel (> 3 levels) degenerative disc disease (except in cases of spinal deformity)	x	x
Single-level disc disease causing radiculopathy without symptoms of mechanical low back pain or instability	x	x
Severe osteoporosis (possible subsidence of interbody grafts through the end plates)		x

Table 1.30 lists the appropriate uses for interbody grafts (spacers).

Table 1.30 Uses for Interbody Grafts

Type	Shape
PEEK (polyetheretherketone) interbody spacer	One boomerang spacer
Carbon fiber cage	One boomerang spacer
Titanium cages	Two small circular cages
	One small circular cage
	One boomerang cage
	One elliptical cage
Allograft	One “kidney bean–shaped” allograft
Allograft	Two circular allografts
Macropore spacer	One boomerang spacerOne or two circular or rectangular shaped spacers

Wang JC, Mummaneni PV, Haid RW. Current treatment strategies for the painful lumbar motion segment: posterolateral fusion versus interbody fusion. Spine. 200; 30(16 Suppl): S33-43.

Table 1.31 summarizes the inclusion and exclusion criterias for lumbar disc arthroplasty.

Table 1.31 Inclusion and Exclusion Criteria for Lumbar Disc Arthroplasty Trials

Type of implant	Inclusion Criteria	Exclusion Criteria
SB Charité III	Age 18-60 years Failed nonoperative treatment of at least 6 months’ duration Single-level degenerative disc disease at L4-L5 or L5-S1 confirmed by MRI and provocative discography Oswestry Disability Index ≥ 30 Back pain Visual Analog Score ≥ 40	Previous thoracic or lumbar fusion Multilevel degenerative disc disease Facet joint arthrosis Noncontained herniated nucleus pulposus Osteoporosis Spondylolisthesis > 3 mm Midsagittal stenosis < 8 mm
Prodisc II	Age 18-60 years At least 6 months of failed nonoperative therapy Degenerative disc disease (DDD) at one or two adjacent vertebral levels between L3 and S1, where a diagnosis of DDD requires 1. primary back and/or radicular pain 2. Radiographic confirmation of any one of the following by CT, MRI, discography, plain film, myelography and/or flexion/extension films: 1) lack of instability (defined as > 3mm of translation or > 5° of angulation) 2) Decreased disc height > 2mm 3) Scarring/thickening of the annulus fibrosus 4) herniated nucleus pulposus or 5) vacuum phenomenon Oswestry Disability Index ≥ 40 Psychosocially, mentally, or physically able to fully comply with this protocol, including adhering to the follow-up schedule and requirements and the filling out of forms	> 2 degenerative levels End plate dimensions < 34.5 mm in the coronal plane and/or < 27 mm in the sagittal plane Known allergy to titanium, polyethylene, cobalt, chromium, or molybdenum Prior lumbar fusion Post-traumatic vertebral body compromise/deformity Facet degeneration Lytic spondylolisthesis or spinal stenosis Degenerative spondylolisthesis of grade > 1 Back or leg pain of unknown etiology Osteoporosis Metabolic bone disease (excluding osteoporosis, e.g., Paget’s disease) Morbid obesity (BMI > 40 or weight > 100 lb over ideal body weight) Pregnant or interested in becoming pregnant in the next 3 years Active systemic/local infection Medications or drugs known to potentially interfere with bone/soft tissue healing, excluding smoking Rheumatoid arthritis or other autoimmune spondyloarthropathies Systemic disease, including but limited to acquired immunodeficiency syndrome, human immunodeficiency virus, hepatitis Active malignancy: a patient with a history of any invasive malignancy (except non-melanoma skin cancer), unless he/she has been treated with curative intent and there has been no clinical signs or symptoms of the malignancy for at least 5 yr

Issues to be considered in the selection of lumbar spinal fusion for the treatment of disc herniation and radiculopathy are as follows:

▪ Lumbar spinal fusion is not recommended as routine treatment after primary disc excision in the patient with a herniated lumbar disc that was causing radiculopathy.

▪ Lumbar spinal fusion is recommended as a potential surgical adjunct in the patient with a herniated disc in whom there is evidence of preoperative lumbar spinal deformity or instability and in the patient with significant chronic axial LBP associated with radiculopathy due to a herniated lumbar disc.

▪ Reoperative discectomy is recommended as treatment option in the patient with a recurrent lumbar disc herniation.

▪ Reoperative discectomy combined with fusion is recommended as a treatment option in the patient with a recurrent disc herniation associated with lumbar instability, deformity, or chronic axial LBP.

▪ Pedicle screw fixation may be used as an adjunct to lumbar posterolateral fusion (see below). Considerations in the selection of fusion after decompression to treat patients with stenosis without spondylolisthesis are as follows:

▪ In situ posterolateral lumbar fusion is not recommended as a treatment option in the patient with lumbar stenosis in whom there is no evidence of preexisting spinal instability or likely iatrogenic instability after facetectomy.

▪ In situ lumbar posterolateral lumbar fusion is recommended as a treatment option in addition to decompression in patients with lumbar stenosis without deformity in whom there is evidence of spinal instability.

▪ The addition of pedicle screw instrumentation is not recommended in conjunction with posterolateral lumbar fusion after decompression for lumbar stenosis in the patient without spinal deformity or instability.

Issues to be considered in the selection of interbody techniques for lumbar fusion to treat degenerative disease of the lumbar spine are as follows:

▪ Placement of an interbody graft is recommended as a treatment option to improve fusion rates and functional outcome in patients undergoing surgery for LBP due to degenerative disk disease at one or two levels. The surgeon is cautioned that the marginal improvement in fusion rates and functional outcome with these techniques is associated with higher complication rates, particularly when combined approaches are used.

▪ The use of multiple approaches (anterior or and posterior) to accomplish lumbar fusion is not recommended as a routine option for the treatment of patients with LBP without deformity.

Considerations in the selection of pedicle screw fixation as an adjunct to posterolateral fusion for treatment of LBP are as follows:

▪ Pedicle screw fixation is recommended as a treatment option for patients with LBP treated with posterolateral fusion who are at high risk for fusion failure, because the use of pedicle screw fixation improves fusion success rates.

▪ Pedicle screw fixation is not recommended as a routine adjunct to posterolateral fusion in the treatment of patients with chronic LBP due to degenerative disk disease, because there is conflicting evidence that the use of pedicle screw fixation is associated with high costs and complications.

The issues to be considered in the use of lumbar facet joint injections related to lumbar fusion surgery are as follows:

▪ The use of lumbar facet joint injection is recommended as a diagnostic tool for predicting the response to lumbar facet radiofrequency ablation.

▪ The use of lumbar facet joint injection is not recommended as a diagnostic tool to predict the response to lumbar fusion surgery.

Considerations for the use of brace therapy as an adjunct to or substitute for lumbar fusion are as follows:

▪ Lumbar braces are recommended as a means of decreasing the number of sick days lost due to LBP among workers with previous lumbar injury.

▪ Lumbar braces are not recommended as a means of decreasing LBP in the general working population.

▪ The use of lumbar brace therapy as a preoperative diagnostic tool to predict the outcome of lumbar fusion surgery is not recommended.

▪ The use of transpedicular external fixation as a tool to predict the outcome of lumbar fusion surgery is not recommended.

Issues to be considered for the use of electrophysiologic monitoring during fusion procedures for degenerative disease of lumbar spine are as follows:

▪ Intraoperative evoked electromyography (EMG) response recording is recommended as an option during lumbar spinal fusion surgery when the operating surgeon desires immediate information about the integrity of the pedicle wall, because an intact pedicle wall produces a normal evoked EMG response.

▪ Intraoperative monitoring of somatosensory or dermatomal somatosensory evoked potentials, EMG, and/or evoked EMG responses are recommended only as adjunctive options during instrumented lumbosacral fusion procedures for degenerative spinal disease. The use of any of these modalities has not been convincingly demonstrated to influence patient outcome favorably.

Considerations for the use of autologous bone or rhBMP-2 bone graft substitute in fusion procedures for the degenerative disease of the lumbar spine are as follows:

▪ Recombinant human bone morphogenetic protein type 2 (rhBMP-2) in combination with hydroxylapatite and tricalcium phosphate may be used as a substitute for autograft bone in some cases of posterior lumbar fusion.

▪ Several formulations of calcium phosphate are recommended as bone graft extenders, especially when used in combination with autologous bone.

Treatment guidelines for bone growth stimulators and lumbar fusion are as follows:

▪ Either direct current stimulation or capacitative coupled stimulation is recommended as an adjunct to spinal fusion to increase fusion rates in patients who are at high risk for arthrodesis failure after posterior lumbar fusion.

▪ Pulsed electromagnetic field stimulation is recommended as an adjunct to increase fusion rates in similar patients treated with lumbar interbody fusion procedures.

Cancer-related spinal pain

Figure 1-8 shows an algorithm for management of metastatic cancer–related spinal pain and the locations of primary neoplasms producing metastatic bone lesions are described in Table 1.32.

Figure 1–8 Algorithm for management of metastatic cancer–related spinal pain.

Table 1.32 Location of Primary Neoplasms Producing Metastatic Bone Lesions

Primary Site	Number of Lesions (%)
Breast	2020 (40)
Lung	646 (13)
Prostate	296 (6)
Kidney	284 (6)
Gastrointestinal tract	255 (5)
Bladder	160 (3)
Thyroid	110 (2)
Total	5006

From Herkowitz, HN, Garfin SR, Eismont FJ, et al : Rothman-Simeone: The Spine, 5th ed. Philadelphia, Saunders, 2006, p. 1284.

Other information for cancer-related spinal pain is summarized such as incidence and prognosis of bone metastasis (Table 1.33), radiologic appearance of metastatic bone lesions (Table 1.34), predicting the risk of pathologic fracture (Table 1.35), Karnofsky’s performance status (Table 1.36), signs of spinal compression (Table 1.37), categories of skeletal spinal metastasis (Table 1.38), and Tokuhashi’s scoring system for spinal metastasis (Table 1.39).

Table 1.33 Incidence and Prognosis of Bone Metastasis

Table 1.34 Radiologic Appearance of Metastatic Bone Lesions

Radiologic Appearance	Primary Lesion
Osteolytic	Lung, thyroid, kidney, colon
Osteoblastic	Prostate, bladder, stomach
Mixed	Breast

Table 1.35 Predicting the Risk of Pathologic Fracture

Table 1.36 Karnofsky Performance Status

Grade	Performance Level
100	Normal, no complaints, no evidence of disease
90	Able to carry on normal activity; minor signs or symptoms of disease
80	Normal activity with effect; some signs symptoms
70	Cares for self; unable to carry on normal activity or to do active work
60	Requires occasional assistance, but is able to care for most of his or her needs
50	Requires considerable assistances and frequent medical care
40	Disabled, requires special care and assistance
30	Severely disabled, hospitalization indicated; death not imminent
20	Very sick, hospitalization necessary, active supportive treatment necessary
10	Moribund, fatal processes, progressing rapidly
0	Dead

Table 1.37 Signs of Spinal Compression

Table 1.38 Categories of Skeletal Spinal Metastasis

Category	Severity of Skeletal Involvement by Metastasis
I	No major neurologic involvement
II	Involvement of bone without collapse and instability
III	Major neurologic involvement (sensory or motor) without significant bone involvement
IV	Vertebral collapse with pain caused by mechanical causes or instability but without significant neurologic impairment
V	Vertebral collapse or instability combined with major neurologic impairment

Modified from Herrington KD: Metastatic disease of the spine. J Bone Joint Surg Am 1986;68:1110-1115.

Table 1.39 Tokuhashi’s Scoring System for Spinal Metastasis

Characteristic	Point(s)
General condition (performance status, PS):
Poor (PS 10-40%)	0
Moderate (PS 50-70%)	1
Good (PS 80-100%)	2
Number of extraspinal bone metastases foci:
≥ 3	0
1-2	1
0	2
Number of metastases in the vertebral body:
≥ 3	0
1-2	1
0	2
Metastases to the major internal organs:
Irremovable	0
Removable	1
No metastases	2
Primary site of cancer:
Lung, osteosarcoma, stomach, bladder, esophagus, pancreas	0
Liver, gallbladder, unidentified	1
Other Primary Sites	2
Kidney, uterus	3
Rectum	4
Thyroid, breast, prostate, carcinoid tumor	5
Palsy:
Complete (Frankel A, B)	0
Incomplete (Frankel C, D)	1
None (Frankel E)	2

Current Trend In Treatment According to Total Score
0-8: ≥ 6-8 months (actual survival period)	Conservative treatment or palliative surgery
9-11: ≤ 6 months (actual survival period)	Palliative or excisional surgery
12-15: ≤ 1 year (actual survival period)	Excisional surgery

Modified from Tokuhashi Y, Matsuzaki H, Oda H, et al: A revised scoring system for preoperative evaluation of metastatic spine tumour prognosis. Spine 2005;30:2186-2191.