122 PART 2 Cardinal Manifestations and Presentation of Diseases

Normal

Thecal sac Normal

Nerve roots

Normal

Thecal sac Normal

Nerve roots

Facet joints

Compressed Thecal sac

A B

FIGURE 17-5 Spinal stenosis. A. An axial T2-weighted image of the normal lumbar spine shows a

normal thecal sac within the lumbar spinal canal. The thecal sac is bright. The lumbar roots are seen as

dark punctate dots located posteriorly in the thecal sac. B. The thecal sac is not well visualized due to

severe lumbar spinal canal stenosis, partially the result of hypertrophic facet joints.

Severe right L5-S1 foraminal stenosis (*)

Stenotic L5-S1

foramen

Normal lateral

recesses Stenotic L5-S1

foramen Normal L4-5 foramen

A B

Normal L5-S1

foramen

FIGURE 17-6 Foraminal stenosis. A. Sagittal T2-weighted image reveals normal high signal around the exiting right L4 nerve root in the right neural foramen at L4-L5;

effacement of the high signal is noted one level below at L5-S1, due to severe foraminal stenosis. B. Axial T2-weighted image at the L5-S1 level demonstrates normal lateral

recesses bilaterally, a normal intervertebral foramen on the left, but a severely stenotic foramen (*) on the right.

daily living or when focal neurologic signs are present. Most patients

with neurogenic claudication who are treated medically do not

improve over time. Surgical management with laminectomy, which

increases the spinal canal diameter and reduces venous hypertension,

can produce significant relief of exertional back and leg pain, leading

to less disability and improved functional outcomes. Laminectomy and

fusion is usually reserved for patients with LSS and spondylolisthesis.

Predictors of a poor surgical outcome include impaired walking preoperatively, depression, cardiovascular disease, and scoliosis. Up to

one-quarter of surgically treated patients develop recurrent stenosis at

the same or an adjacent spinal level within 7–10 years; recurrent symptoms usually respond to a second surgical decompression.

Neural foraminal narrowing or lateral recess stenosis with radiculopathy is a common consequence of osteoarthritic processes that cause

LSS (Figs. 17-1 and 17-6), including osteophytes, lateral disk protrusion, calcified disk-osteophytes, facet joint hypertrophy, uncovertebral

joint hypertrophy (in the cervical spine), congenitally

shortened pedicles, or, frequently, a combination of

these processes. Neoplasms (primary or metastatic),

fractures, infections (epidural abscess), or hematomas

are less frequent causes. Most common is bony foraminal narrowing leading to nerve root ischemia and

persistent symptoms, in contrast to inflammation that

is associated with a paracentral herniated disk and

radiculopathy. These conditions can produce unilateral nerve root symptoms or signs due to compression

at the intervertebral foramen or in the lateral recess;

symptoms are indistinguishable from disk-related

radiculopathy, but treatment may differ depending on

the etiology. The history and neurologic examination

alone cannot distinguish between these possibilities.

Neuroimaging (CT or MRI) is required to identify the

anatomic cause. Neurologic findings from the examination and EMG can help direct the attention of the

radiologist to specific nerve roots, especially on axial

images. For facet joint hypertrophy with foraminal

stenosis, surgical foraminotomy produces long-term

relief of leg and back pain in 80–90% of patients.

Facet joint or medial branch blocks for back or neck

pain are sometimes used to help determine the anatomic origin of back

pain or for treatment, but there is a lack of clinical data to support their

utility. Medical causes of lumbar or cervical radiculopathy unrelated to

primary spine disease include infections (e.g., herpes zoster and Lyme

disease), carcinomatous meningitis, diabetes, and root avulsion or

traction (trauma).

■ SPONDYLOSIS AND SPONDYLOLISTHESIS

Spondylosis, or osteoarthritic spine disease, typically occurs in later

life and primarily involves the cervical and lumbosacral spine.

Patients often complain of back pain that increases with movement, is associated with stiffness, and is better with inactivity. The

relationship between clinical symptoms and radiologic findings is

usually not straightforward. Pain may be prominent when MRI, CT,

or x-ray findings are minimal, and prominent degenerative spine

disease can be seen in asymptomatic patients. Osteophytes, combined

123Back and Neck Pain CHAPTER 17

disk-osteophytes, or a thickened ligamentum flavum may cause or

contribute to central spinal canal stenosis, lateral recess stenosis, or

neural foraminal narrowing.

Spondylolisthesis is the anterior slippage of the vertebral body, pedicles, and superior articular facets, leaving the posterior elements behind.

Spondylolisthesis can be associated with spondylolysis, congenital

anomalies, degenerative spine disease, or other causes of mechanical

weakness of the pars interarticularis (e.g., infection, osteoporosis, tumor,

trauma, earlier surgery). The slippage may be asymptomatic or may

cause LBP, nerve root injury (the L5 root most frequently), symptomatic

spinal stenosis, or CES in rare severe cases. A “step-off” on palpation

or tenderness may be elicited near the segment that has “slipped” (most

often L4 on L5 or occasionally L5 on S1). Focal anterolisthesis or retrolisthesis can occur at any cervical or lumbar level and be the source of neck

or LBP. Plain x-rays of the low back or neck in flexion and extension will

reveal movement at the abnormal spinal segment. Surgery is performed

for spinal instability (slippage 5–8 mm) and considered for pain symptoms that do not respond to conservative measures (e.g., rest, physical

therapy), cases with a progressive neurologic deficit, or scoliosis.

■ NEOPLASMS

Back pain is the most common neurologic symptom in patients with

systemic cancer and is the presenting symptom in 20%. The cause is

usually vertebral body metastasis (85–90%) but can also result from

spread of cancer through the intervertebral foramen (especially with

lymphoma), carcinomatous meningitis, or metastasis to the spinal

cord. The thoracic spine is most often affected. Cancer-related back

pain tends to be constant, dull, unrelieved by rest, and worse at night.

By contrast, mechanical causes of LBP usually improve with rest. MRI,

CT, and CT myelography are the studies of choice when spinal metastasis is suspected. Once a metastasis is found, imaging of the entire

spine is essential, as it reveals additional tumor deposits in one-third of

patients. MRI is preferred for soft tissue definition, but the most rapidly available imaging modality is best because the patient’s condition

may worsen quickly without intervention. Early diagnosis is crucial. A

strong predictor of outcome is baseline neurologic function prior to

diagnosis. Half to three-quarters of patients are nonambulatory at the

time of diagnosis and few regain the ability to walk. The management

of spinal metastasis is discussed in detail in Chap. 90.

■ INFECTIONS/INFLAMMATION

Vertebral osteomyelitis is most often caused by hematogenous seeding

of staphylococci, but other bacteria or tuberculosis (Pott’s disease) may

be responsible. The primary source of infection is usually the skin or

urinary tract. Other common sources of bacteremia are IV drug use,

poor dentition, endocarditis, lung abscess, IV catheters, or postoperative wound sites. Back pain at rest, tenderness over the involved

vertebra, and an elevated erythrocyte sedimentation rate (ESR) or

C-reactive protein (CRP) are the most common findings in vertebral

osteomyelitis. Fever or an elevated white blood cell count is found in

a minority of patients. MRI and CT are sensitive and specific for early

detection of osteomyelitis. The intervertebral disk can also be affected

by infection (diskitis) and almost never by tumor. Extension of the

infection posteriorly from the vertebral body can produce a spinal

epidural abscess.

Spinal epidural abscess (Chap. 442) presents with back pain (aggravated by movement or palpation of the spinous process), fever, radiculopathy, or signs of spinal cord compression. The subacute development

of two or more of these findings should increase suspicion for spinal

epidural abscess. The abscess is best delineated by spine MRI and may

track over multiple spinal levels.

Lumbar adhesive arachnoiditis with radiculopathy is due to fibrosis

following inflammation within the subarachnoid space. The fibrosis

results in nerve root adhesions and presents as back and leg pain

associated with multifocal motor, sensory, or reflex changes. Causes of

arachnoiditis include multiple lumbar operations (most common in the

United States), chronic spinal infections (especially tuberculosis in the

developing world), spinal cord injury, intrathecal hemorrhage, myelography (rare), intrathecal injections (glucocorticoids, anesthetics, or

other agents), and foreign bodies. The MRI shows clumped nerve

roots on axial views or loculations of cerebrospinal fluid within the

thecal sac. Clumped nerve roots should be distinguished from enlarged

nerve roots seen with demyelinating polyneuropathy or neoplastic

infiltration. Treatment is usually unsatisfactory. Microsurgical lysis of

adhesions, dorsal rhizotomy, dorsal root ganglionectomy, and epidural

glucocorticoids have been tried, but outcomes have been poor. Dorsal

column stimulation for pain relief has produced varying results.

■ TRAUMA

A patient complaining of back pain and an inability to move the legs

may have a spine fracture or dislocation; fractures above L1 place the

spinal cord at risk for compression. Care must be taken to avoid further

damage to the spinal cord or nerve roots by immobilizing the back

or neck pending the results of radiologic studies. Vertebral fractures

frequently occur in the absence of trauma in association with osteoporosis, glucocorticoid use, osteomyelitis, or neoplastic infiltration.

Sprains and Strains The terms low back sprain, strain, and

mechanically induced muscle spasm refer to minor, self-limited injuries

associated with lifting a heavy object, a fall, or a sudden deceleration

such as in an automobile accident. These terms are used loosely and do

not correlate with specific underlying pathologies. The pain is usually

confined to the lower back. Patients with paraspinal muscle spasm

often assume unusual postures.

Traumatic Vertebral Fractures Most traumatic fractures of

the lumbar vertebral bodies result from injuries producing anterior

wedging or compression. With severe trauma, the patient may sustain

a fracture-dislocation or a “burst” fracture involving the vertebral body

and posterior elements. Traumatic vertebral fractures are caused by

falls from a height, sudden deceleration in an automobile accident, or

direct injury. Neurologic impairment is common, and early surgical

treatment is indicated. In victims of blunt trauma, CT scans of the

chest, abdomen, or pelvis can be reformatted to detect associated vertebral fractures. Rules have been developed to avoid unnecessary spine

imaging associated with low-risk trauma, but these studies typically

exclude patients aged >65 years—a group that can sustain fractures

with minor trauma.

■ METABOLIC CAUSES

Osteoporosis and Osteosclerosis Immobilization, osteomalacia, the postmenopausal state, renal disease, multiple myeloma,

hyperparathyroidism, hyperthyroidism, metastatic carcinoma, or glucocorticoid use may accelerate osteoporosis and weaken the vertebral

body, leading to compression fractures and pain. Up to two-thirds of

compression fractures seen on radiologic imaging are asymptomatic.

The most common nontraumatic vertebral body fractures are due to

a postmenopausal cause, or to osteoporosis in adults >75 years old

(Chap. 411). The risk of an additional vertebral fracture 1 year following a first vertebral fracture is 20%. The presence of fever, weight

loss, fracture at a level above T4, any fracture in a young adult, or the

predisposing conditions described above should increase suspicion

for a cause other than typical osteoporosis. The sole manifestations

of a compression fracture may be localized back or radicular pain

exacerbated by movement and often reproduced by palpation over the

spinous process of the affected vertebra.

Relief of acute pain can often be achieved with acetaminophen,

NSAIDs, opioids, or a combination of these medications. Both pain

and disability are improved with bracing. Antiresorptive drugs are

not recommended in the setting of acute pain but are the preferred

treatment to prevent additional fractures. Less than one-third of

patients with prior compression fractures are adequately treated for

osteoporosis despite the increased risk for future fractures; even fewer

at-risk patients without a history of fracture are adequately treated. The

literature for percutaneous vertebroplasty (PVP) or kyphoplasty for

osteoporotic compression fractures associated with debilitating pain

does not support their use.

124 PART 2 Cardinal Manifestations and Presentation of Diseases

Osteosclerosis, an abnormally increased bone density often due

to Paget’s disease, is readily identifiable on routine x-ray studies and

can sometimes be a source of back pain. It may be associated with

an isolated increase in alkaline phosphatase in an otherwise healthy

older person. Spinal cord or nerve root compression can result from

bony encroachment. The diagnosis of Paget’s disease as the cause of a

patient’s back pain is a diagnosis of exclusion.

For further discussion of these bone disorders, see Chaps. 410,

411, and 412.

■ AUTOIMMUNE INFLAMMATORY ARTHRITIS

Autoimmune inflammatory disease of the spine can present with the

insidious onset of low back, buttock, or neck pain. Examples include

rheumatoid arthritis (RA) (Chap. 358), ankylosing spondylitis, reactive arthritis and psoriatic arthritis (Chap. 355), or inflammatory

bowel disease (Chap. 326).

■ CONGENITAL ANOMALIES OF THE LUMBAR

SPINE

Spondylolysis is a bony defect in the vertebral pars interarticularis (a

segment near the junction of the pedicle with the lamina), a finding present in up to 6% of adolescents. The cause is usually a stress

microfracture in a congenitally abnormal segment. Multislice CT with

multiplanar reformation is the most accurate modality for detecting

spondylolysis in adults. Symptoms may occur in the setting of a single

injury, repeated minor injuries, or during a growth spurt. Spondylolysis

is the most common cause of persistent LBP in adolescents and is often

associated with sports-related activities.

Scoliosis refers to an abnormal curvature in the coronal (lateral)

plane of the spine. With kyphoscoliosis, there is, in addition, a forward

curvature of the spine. The abnormal curvature may be congenital, due

to abnormal spine development, acquired in adulthood due to degenerative spine disease, or progressive due to paraspinal neuromuscular

disease. The deformity can progress until ambulation or pulmonary

function is compromised.

Spina bifida occulta (closed spinal dysraphism) is a failure of closure

of one or several vertebral arches posteriorly; the meninges and spinal

cord are normal. A dimple or small lipoma may overlie the defect, but

the skin is intact. Most cases are asymptomatic and discovered incidentally during a physical examination for back pain.

Tethered cord syndrome usually presents as a progressive cauda

equina disorder (see below), although myelopathy may also be the

initial manifestation. The patient is often a child or young adult who

complains of perineal or perianal pain, sometimes following minor

trauma. MRI studies typically reveal a low-lying conus (below L1 and

L2) and a short and thickened filum terminale. The MRI findings also

occur as incidental findings, sometimes during evaluation of unrelated

LBP in adults.

■ REFERRED PAIN FROM VISCERAL DISEASE

Diseases of the thorax, abdomen, or pelvis may refer pain to the spinal

segment that innervates the diseased organ. Occasionally, back pain

may be the first and only manifestation. Upper abdominal diseases

generally refer pain to the lower thoracic or upper lumbar region

(eighth thoracic to the first and second lumbar vertebrae), lower

abdominal diseases to the midlumbar region (second to fourth lumbar

vertebrae), and pelvic diseases to the sacral region. Local signs (pain

with spine palpation, paraspinal muscle spasm) are absent, and little or

no pain accompanies routine movements.

Low Thoracic or Lumbar Pain with Abdominal Disease Tumors

of the posterior wall of the stomach or duodenum typically produce

epigastric pain (Chaps. 80 and 324), but back pain may occur if retroperitoneal extension is present. Fatty foods occasionally induce back pain

associated with biliary or pancreatic disease. Pathology in retroperitoneal

structures (hemorrhage, tumors, and pyelonephritis) can produce paraspinal pain that radiates to the lower abdomen, groin, or anterior thighs. A

mass in the iliopsoas region can produce unilateral lumbar pain with radiation toward the groin, labia, or testicle. The sudden appearance of lumbar

pain in a patient receiving anticoagulants should prompt consideration of

retroperitoneal hemorrhage.

Isolated LBP occurs in some patients with a contained rupture of

an AAA. The classic clinical triad of abdominal pain, shock, and back

pain occurs in <20% of patients. The diagnosis may be missed because

the symptoms and signs can be nonspecific. Misdiagnoses include

nonspecific back pain, diverticulitis, renal colic, sepsis, and myocardial infarction. A careful abdominal examination revealing a pulsatile

mass (present in 50–75% of patients) is an important physical finding.

Patients with suspected AAA should be evaluated with abdominal

ultrasound, CT, or MRI (Chap. 280).

Sacral Pain with Gynecologic and Urologic Disease Pelvic

organs rarely cause isolated LBP. Uterine malposition (retroversion,

descensus, and prolapse) may cause traction on the uterosacral ligament.

The pain is referred to the sacral region, sometimes appearing after

prolonged standing. Endometriosis or uterine cancers can invade the

uterosacral ligaments. Pain associated with endometriosis is typically

premenstrual and often continues until it merges with menstrual pain.

Menstrual pain with poorly localized, cramping pain can radiate

down the legs. LBP that radiates into one or both thighs is common

in the last weeks of pregnancy. Continuous and worsening pain unrelieved by rest or at night may be due to neoplastic infiltration of nerves

or nerve roots.

Urologic sources of lumbosacral back pain include chronic prostatitis, prostate cancer with spinal metastasis (Chap. 87), and diseases of

the kidney or ureter. Infectious, inflammatory, or neoplastic renal diseases may produce ipsilateral lumbosacral pain, as can renal artery or

vein thrombosis. Paraspinal lumbar pain may be a symptom of ureteral

obstruction due to nephrolithiasis.

■ OTHER CAUSES OF BACK PAIN

Postural Back Pain There is a group of patients with nonspecific

chronic low back pain (CLBP) in whom no specific anatomic lesion can

be found despite exhaustive investigation. Exercises to strengthen the

paraspinal and abdominal muscles are sometimes helpful. CLBP may

be encountered in patients who seek financial compensation; in malingerers; or in those with concurrent substance abuse. Many patients

with CLBP have a history of psychiatric illness (depression, anxiety

states) or childhood trauma (physical or sexual abuse) that antedates

the onset of back pain. Preoperative psychological assessment has been

used to exclude patients with marked psychological impairments that

predict a poor surgical outcome from spine surgery.

Idiopathic The cause of LBP occasionally remains unclear. Some

patients have had multiple operations for disk disease. The original

indications for surgery may have been questionable, with back pain

only, no definite neurologic signs, or a minor disk bulge noted on CT

or MRI. Scoring systems based on neurologic signs, psychological

factors, physiologic studies, and imaging studies have been devised to

minimize the likelihood of unsuccessful surgery.

■ GLOBAL CONSIDERATIONS

While many of the history and examination features described in this

chapter apply to all patients, information regarding the global epidemiology and prevalence of LBP is limited. The Global Burden of Diseases

Study 2019 reported that LBP represented the #1 cause overall for total

years lived with disability (YLD), and #9 overall as a cause of disabilityrelated life years (DALYs). These numbers increased substantially from

1990 estimates, and with the aging of the population worldwide, the

numbers of individuals suffering from LBP are expected to increase

further in the future. Although rankings for LBP generally were higher

in developed regions, a high burden exists in every part of the world.

An area of uncertainty is the degree to which regional differences exist

in terms of the specific etiologies of LBP and how these are managed.

For example, the most common cause of arachnoiditis in developing

countries is a prior spinal infection, but in developed countries the

most frequent cause is multiple lumbar spine surgeries.

125Back and Neck Pain CHAPTER 17

TREATMENT

Back Pain

Management is considered separately for acute and chronic low

back pain syndromes without radiculopathy, and for back pain with

radiculopathy.

ACUTE LOW BACK PAIN WITHOUT RADICULOPATHY

This is defined as pain of <12 weeks duration. Full recovery can

be expected in >85% of adults with ALBP without leg pain. Most

have purely “mechanical” symptoms (i.e., pain that is aggravated by

motion and relieved by rest).

The initial assessment is focused on excluding serious causes

of spine pathology that require urgent intervention, including

infection, cancer, or trauma. Risk factors for a serious cause of

ALBP are shown in Table 17-1. Laboratory and imaging studies are

unnecessary if risk factors are absent. CT, MRI, or plain spine films

are rarely indicated in the first month of symptoms unless a spine

fracture, tumor, or infection is suspected.

The prognosis of ALBP is generally excellent; however, episodes

tend to recur, and as many as two-thirds of patients will experience

a second episode within 1 year. Most patients do not seek medical

care and improve on their own. Even among those seen in primary

care, two-thirds report substantial improvement after 7 weeks. This

high likelihood of spontaneous improvement can mislead clinicians

and patients about the efficacy of treatment interventions, highlighting the importance of rigorous prospective trials. Many treatments commonly used in the past are now known to be ineffective,

including bed rest and lumbar traction.

Clinicians should reassure and educate patients that improvement is very likely and instruct them in self-care. Satisfaction and

the likelihood of follow-up increase when patients are educated

about prognosis, evidence-based treatments, appropriate activity modifications, and strategies to prevent future exacerbations.

Counseling patients about the risks of overtreatment is another

important part of the discussion. Patients who report that they did

not receive an adequate explanation for their symptoms are likely to

request further diagnostic tests.

In general, bed rest should be avoided for relief of severe symptoms or limited to a day or two at most. Several randomized trials

suggest that bed rest does not hasten the pace of recovery. In general, early resumption of normal daily physical activity should be

encouraged, avoiding only strenuous manual labor. Advantages of

early ambulation for ALBP also include maintenance of cardiovascular conditioning; improved bone, cartilage, and muscle strength;

and increased endorphin levels. Specific back exercises or early vigorous exercise have not shown benefits for acute back pain. Empiric

use of heating pads or blankets is sometimes helpful.

NSAIDs and Acetaminophen Evidence-based guidelines recommend over-the-counter medicines such as NSAIDs and acetaminophen as first-line options for treatment of ALBP. In otherwise

healthy patients, a trial of NSAIDs can be followed by acetaminophen for time-limited periods. In theory, the anti-inflammatory

effects of NSAIDs might provide an advantage over acetaminophen

to suppress inflammation that accompanies many causes of ALBP,

but in practice there is no clinical evidence to support the superiority of NSAIDs. The risk of renal and gastrointestinal toxicity with

NSAIDs is increased in patients with preexisting medical comorbidities (e.g., renal insufficiency, cirrhosis, prior gastrointestinal

hemorrhage, use of anticoagulants or glucocorticoids, heart failure).

Some patients elect to take acetaminophen and an NSAID together

in hopes of a more rapid benefit.

Muscle Relaxants Skeletal muscle relaxants, such as cyclobenzaprine or methocarbamol, may be useful, but sedation is a common side effect. Limiting the use of muscle relaxants to nighttime

only may be an option for patients with back pain that interferes

with sleep.

Opioids There is no good evidence to support the use of opioid

analgesics or tramadol as first-line therapy for ALBP. Their use is

best reserved for patients who cannot tolerate acetaminophen or

NSAIDs and for those with severe refractory pain. Also, the duration

of opioid treatment for ALBP should be strictly limited to 3–7 days.

As with muscle relaxants, these drugs are often sedating, so it may

be useful to prescribe them at nighttime only. Side effects of shortterm opioid use include nausea, constipation, and pruritus; risks

of long-term opioid use include hypersensitivity to pain, hypogonadism, and dependency. Falls, fractures, driving accidents, and

fecal impaction are other risks. The clinical efficacy of opioids for

chronic pain beyond 16 weeks of use is unproven.

Mounting evidence of morbidity from long-term opioid therapy

(including overdose, dependency, addiction, falls, fractures, accident risk, and sexual dysfunction) has prompted efforts to reduce its

use for chronic pain, including back pain (Chap. 13). When used,

safety may be improved with automated notices for high doses,

early refills, prescriptions from multiple pharmacies, overlapping

opioid and benzodiazepine prescriptions, and in the United States

by state-based prescription drug monitoring programs (PDMPs).

A recent study indicated that most patients with opioid use disorder presenting to emergency departments had no prescriptions

recorded in the PDMP, reflecting other methods used to obtain

opioids. Greater access to alternative treatments for chronic pain,

such as tailored exercise programs and cognitive behavioral therapy

(CBT), may also reduce opioid prescribing.

Other Approaches There is no evidence to support use of oral or

injected glucocorticoids, antiepileptics, antidepressants, or therapies for neuropathic pain such as gabapentin or herbal therapies.

Commonly used nonpharmacologic treatments for ALBP are also

of unproven benefit, including spinal manipulation, physical therapy, massage, acupuncture, laser therapy, therapeutic ultrasound,

corsets, transcutaneous electrical nerve stimulation (TENS), special

mattresses, or lumbar traction. Although important for chronic

pain, use of back exercises for ALBP are generally not supported

by clinical evidence. There is no convincing evidence regarding the

value of ice or heat applications for ABLP; however, many patients

report temporary symptomatic relief from ice or frozen gel packs

just before sleep, and heat may produce a short-term reduction in

pain after the first week. Patients often report improved satisfaction

with the care that they receive when they actively participate in the

selection of symptomatic approaches.

CHRONIC LOW BACK PAIN WITHOUT RADICULOPATHY

Back pain is considered chronic when the symptoms last >12 weeks; it

accounts for 50% of total back pain costs. Risk factors include obesity, female gender, older age, prior history of back pain, restricted

spinal mobility, pain radiating into a leg, high levels of psychological distress, poor self-rated health, minimal physical activity,

smoking, job dissatisfaction, and widespread pain. In general, the

same treatments that are recommended for ALBP can be useful for

patients with CLBP. In this setting, however, the benefit of opioid

therapy or muscle relaxants is less clear. In general, improved activity tolerance is the primary goal, while pain relief is secondary.

Some observers have raised concerns that CLBP may often be

overtreated. For CLBP without radiculopathy, multiple guidelines

explicitly recommend against use of SSRIs, any type of injection,

TENS, lumbar supports, traction, radiofrequency facet joint denervation, intradiskal electrothermal therapy, or intradiskal radiofrequency thermocoagulation. On the other hand, exercise therapy

and treatment of depression appear to be useful and underused.

Exercise Programs Evidence supports the use of exercise therapy

to alleviate pain symptoms and improve function. Exercise can be

one of the mainstays of treatment for CLBP. Effective regimens have

generally included a combination of core-strengthening exercises,

stretching, and gradually increasing aerobic exercise. A program of

supervised exercise can improve compliance. Supervised intensive

126 PART 2 Cardinal Manifestations and Presentation of Diseases

physical exercise or “work hardening” regimens have been effective

in returning some patients to work, improving walking distance,

and reducing pain. In addition, some forms of yoga have been

evaluated in randomized trials and may be helpful for patients who

are interested.

Intensive multidisciplinary rehabilitation programs can include

daily or frequent physical therapy, exercise, CBT, a workplace evaluation, and other interventions. For patients who have not responded

to other approaches, such programs appear to offer some benefit.

Systematic reviews, however, suggest that the evidence and benefits

are limited.

Nonopioid Medications Medications for CLBP may include short

courses of NSAIDs or acetaminophen. Duloxetine is approved for

the treatment of CLBP (60 mg daily) and may also treat coincident

depression. Tricyclic antidepressants can provide modest pain relief

for some patients without evidence of depression. Depression is

common among patients with chronic pain and should be appropriately treated.

Cognitive Behavioral Therapy CBT is based on evidence that

psychological and social factors, as well as somatic pathology, are

important in the genesis of chronic pain and disability; CBT focuses

on efforts to identify and modify patients’ thinking about their condition. In one randomized trial, CBT reduced disability and pain in

patients with CLBP. Such behavioral treatments appear to provide

benefits similar in magnitude to exercise therapy.

Complementary Medicine Back pain is the most frequent reason for seeking complementary and alternative treatments. Spinal

manipulation or massage therapy may provide short-term relief, but

long-term benefit is unproven. Biofeedback has not been studied

rigorously. There is no convincing evidence that either TENS, laser

therapy, or ultrasound are effective in treating CLBP. Rigorous trials of acupuncture suggest that true acupuncture is not superior to

sham acupuncture, but that both may offer an advantage over routine care. Whether this is due entirely to placebo effects provided

even by sham acupuncture is uncertain.

Injections and Other Interventions Various injections, including

epidural glucocorticoid injections, facet joint injections, and trigger

point injections, have been used for treating CLBP. However, in

the absence of radiculopathy, there is no clear evidence that these

approaches are sustainably effective.

Injection studies are sometimes used diagnostically to help determine the anatomic source of back pain. Pain relief following a glucocorticoid and anesthetic injection into a facet or medial branch block

are used as evidence that the facet joint is the pain source; however,

the possibility that the response was a placebo effect or due to systemic absorption of the glucocorticoids is difficult to exclude.

Another category of intervention for CLBP is electrothermal

and radiofrequency therapy. Intradiskal therapy has been proposed

using energy to thermocoagulate and destroy nerves in the intervertebral disk, using specially designed catheters or electrodes.

Current evidence does not support the use of discography to

identify a specific disk as the pain source, or the use of intradiskal

electrothermal or radiofrequency therapy for CLBP.

Radiofrequency denervation is sometimes used to destroy nerves

that are thought to mediate pain, and this technique has been used

for facet joint pain (with the target nerve being the medial branch

of the primary dorsal ramus), for back pain thought to arise from

the intervertebral disk (ramus communicans), and radicular back

pain (dorsal root ganglia). These interventional therapies have not

been studied in sufficient detail to draw firm conclusions regarding

their value for CLBP.

Surgery Surgical intervention for CLBP without radiculopathy

has been evaluated in a number of randomized trials. The case

for fusion surgery for CLBP without radiculopathy is weak. While

some studies have shown modest benefit, there has been no benefit

when compared to an active medical treatment arm, often including

highly structured, rigorous rehabilitation combined with CBT. The

use of bone matrix protein (BMP) instead of iliac crest graft for the

fusion was shown to increase hospital costs and length of stay but

not improve clinical outcomes.

Guidelines suggest that referral for an opinion on spinal fusion

can be considered for patients who have completed an optimal

nonsurgical treatment program (including combined physical and

psychological treatment) and who have persistent severe back pain

for which they would consider surgery. The high cost, wide geographic variations, and rapidly increasing rates of spinal fusion surgery have prompted scrutiny regarding the lack of standardization

of appropriate indications. Some insurance carriers have begun to

limit coverage for the most controversial indications, such as LBP

without radiculopathy.

Lumbar disk replacement with prosthetic disks is US Food and

Drug Administration–approved for uncomplicated patients needing single-level surgery at the L3-S1 levels. The disks are generally

designed as metal plates with a polyethylene cushion sandwiched

in between. The trials that led to approval of these devices were not

blinded. When compared to spinal fusion, the artificial disks were

“not inferior.” Long-term follow-up is needed to determine device failure rates over time. Serious complications are somewhat more likely

with the artificial disk. This treatment remains controversial for CLBP.

LOW BACK PAIN WITH RADICULOPATHY

A common cause of back pain with radiculopathy is a herniated

disk affecting the nerve root and producing back pain with radiation down the leg. The term sciatica is used when the leg pain

radiates posteriorly in a sciatic or L5/S1 distribution. The prognosis

for acute low back and leg pain with radiculopathy due to disk

herniation is generally favorable, with most patients showing substantial improvement over months. Serial imaging studies suggest

spontaneous regression of the herniated portion of the disk in twothirds of patients over 6 months. Nonetheless, several important

treatment options provide symptomatic relief while the healing

process unfolds.

Resumption of normal activity is recommended. Randomized

trial evidence suggests that bed rest is ineffective for treating sciatica as well as back pain alone. Acetaminophen and NSAIDs are useful for pain relief, although severe pain may require short courses

(3–7 days) of opioid analgesics. Opioids are superior for acute pain

relief in the emergency department.

Epidural glucocorticoid injections have a role in providing symptom relief for acute lumbar radiculopathy due to a herniated disk,

but do not reduce the use of subsequent surgical intervention. A

brief course of high-dose oral glucocorticoids (methylprednisolone

dose pack) for 3 days followed by a rapid taper over 4 more days can

be helpful for some patients with acute disk-related radiculopathy,

although this specific regimen has not been studied rigorously.

Diagnostic nerve root blocks have been advocated to determine

if pain originates from a specific nerve root. However, improvement

may result even when the nerve root is not responsible for the pain;

this may occur as a placebo effect, from a pain-generating lesion

located distally along the peripheral nerve, or from effects of systemic absorption.

Urgent surgery is recommended for patients who have evidence

of CES or spinal cord compression, generally manifesting as combinations of bowel or bladder dysfunction, diminished sensation in

a saddle distribution, a sensory level on the trunk, and bilateral leg

weakness or spasticity. Surgical intervention is also indicated for

patients with progressive motor weakness due to nerve root injury

demonstrated on clinical examination or EMG.

Surgery is also an important option for patients who have

disabling radicular pain despite optimal conservative treatment.

Because patients with a herniated disk and sciatica generally experience rapid improvement over weeks, most experts do not recommend considering surgery unless the patient has failed to respond to

a minimum of 6–8 weeks of nonsurgical management. For patients

who have not improved, randomized trials show that surgery results

in more rapid pain relief than nonsurgical treatment. However, after

127Back and Neck Pain CHAPTER 17

2 years of follow-up, patients appear to have similar pain relief and

functional improvement with or without surgery. Thus, both treatment approaches are reasonable, and patient preferences and needs

(e.g., rapid return to employment) strongly influence decisionmaking. Some patients will want the fastest possible relief and find

surgical risks acceptable. Others will be more risk-averse and more

tolerant of symptoms and will choose watchful waiting, especially if

they understand that improvement is likely in the end.

The usual surgical procedure is a partial hemilaminectomy with

excision of the prolapsed disk (diskectomy). Minimally invasive

techniques have gained in popularity in recent years, but some

evidence suggests they may be less effective than standard surgical

techniques, with more residual back pain, leg pain, and higher rates

of rehospitalization. Fusion of the involved lumbar segments should

be considered only if significant spinal instability is present (i.e.,

degenerative spondylolisthesis). The costs associated with lumbar

interbody fusion have increased dramatically in recent years. There

are no large prospective, randomized trials comparing fusion to

other types of surgical intervention. In one study, patients with

persistent LBP despite an initial diskectomy fared no better with

spine fusion than with a conservative regimen of cognitive intervention and exercise. Artificial disks, as discussed above, are used

in Europe; their utility remains controversial in the United States.

PAIN IN THE NECK AND SHOULDER

Neck pain, which usually arises from diseases of the cervical spine and

soft tissues of the neck, is common, typically precipitated by movement, and may be accompanied by focal tenderness and limitation

of motion. Many of the earlier comments made regarding causes of

LBP also apply to disorders of the cervical spine. The text below will

emphasize differences. Pain arising from the brachial plexus, shoulder,

or peripheral nerves can be confused with cervical spine disease

(Table 17-4), but the history and examination usually identify a

more distal origin for the pain. When the site of nerve tissue injury is

unclear, EMG studies can localize the lesion. Cervical spine trauma,

disk disease, or spondylosis with intervertebral foraminal narrowing

may be asymptomatic or painful and can produce a myelopathy, radiculopathy, or both. The same risk factors for serious causes of LBP also

apply to neck pain with the additional feature that neurologic signs of

myelopathy (incontinence, sensory level, spastic legs) may also occur.

Lhermitte’s sign, an electrical shock down the spine with neck flexion,

suggests involvement of the cervical spinal cord.

■ TRAUMA TO THE CERVICAL SPINE

Trauma (fractures, subluxation) places the spinal cord at risk for compression. Motor vehicle accidents, violent crimes, or falls account for

87% of cervical spinal cord injuries (Chap. 442). Immediate immobilization of the neck is essential to minimize further spinal cord injury

from movement of unstable cervical spine segments. A CT scan is the

diagnostic procedure of choice for detection of acute fractures following severe trauma; plain x-rays are used for lesser degrees of trauma

or in settings where CT is unavailable. When traumatic injury to the

vertebral arteries or cervical spinal cord is suspected, visualization by

MRI with magnetic resonance angiography is preferred.

The decision to obtain imaging should be based on the clinical

context of the injury. The National Emergency X-Radiography Utilization Study (NEXUS) low-risk criteria established that normally alert

patients without palpation tenderness in the midline; intoxication;

neurologic deficits; or painful distracting injuries were very unlikely to

have sustained a clinically significant traumatic injury to the cervical

spine. The Canadian C-spine rule recommends that imaging should

be obtained following neck region trauma if the patient is >65 years

old or has limb paresthesias or if there was a dangerous mechanism

for the injury (e.g., bicycle collision with tree or parked car, fall from

height >3 ft or five stairs, diving accident). These guidelines are helpful

but must be tailored to individual circumstances; for example, patients

with advanced osteoporosis, glucocorticoid use, or cancer may warrant

imaging after even mild trauma.

Whiplash injury is due to rapid flexion and extension of the neck,

usually from automobile accidents. The likely mechanism involves

injury to the facet joints. This diagnosis should not be applied to

patients with fractures, disk herniation, head injury, focal neurologic

findings, or altered consciousness. Up to 50% of persons reporting

whiplash injury acutely have persistent neck pain 1 year later. When

personal compensation for pain and suffering was removed from the

Australian health care system, the prognosis for recovery at 1 year

improved. Imaging of the cervical spine is not cost-effective acutely but

is useful to detect disk herniations when symptoms persist for >6 weeks

following the injury. Severe initial symptoms have been associated with

a poor long-term outcome.

■ CERVICAL DISK DISEASE

Degenerative cervical disk disease is very common and usually asymptomatic. Herniation of a lower cervical disk is a common cause of pain

or tingling in the neck, shoulder, arm, or hand. Neck pain, stiffness,

and a range of motion limited by pain are the usual manifestations.

TABLE 17-4 Cervical Radiculopathy: Neurologic Features

CERVICAL

NERVE ROOT 

EXAMINATION FINDINGS

REFLEX SENSORY MOTOR PAIN DISTRIBUTION 

C5 Biceps Lateral deltoid Rhomboidsa

 (elbow extends backward with hand on

hip)

Lateral arm, medial scapula

Infraspinatusa

 (arm rotates externally with elbow flexed

at the side)

Deltoida

 (arm raised laterally 30°–45° from the side)

C6 Biceps Palmar thumb/index finger Bicepsa

 (arm flexed at the elbow in supination) Lateral forearm, thumb/index fingers

Dorsal hand/lateral forearm Pronator teres (forearm pronated)

C7 Triceps Middle finger Tricepsa

 (forearm extension, flexed at elbow) Posterior arm, dorsal forearm, dorsal

hand

Dorsal forearm Wrist/finger extensorsa

C8 Finger flexors Palmar surface of little finger Abductor pollicis brevis (abduction of thumb) Fourth and fifth fingers, medial hand

and forearm

Medial hand and forearm First dorsal interosseous (abduction of index finger)

Abductor digiti minimi (abduction of little finger)

T1 Finger flexors Axilla, medial arm, anteromedial

forearm

Abductor pollicis brevis (abduction of thumb) Medial arm, axilla

First dorsal interosseous (abduction of index finger)

Abductor digiti minimi (abduction of little finger)

a

These muscles receive the majority of innervation from this root.

 

114 PART 2 Cardinal Manifestations and Presentation of Diseases

TABLE 16-3 Classification of Daily or Near-Daily Headache

Primary

>4 H DAILY <4 H DAILY SECONDARY

Chronic migrainea Chronic cluster

headacheb

Posttraumatic

Head injury

Iatrogenic

Postinfectious

Chronic tension-type

headachea

Chronic paroxysmal

hemicrania

Inflammatory, such as

Giant cell arteritis

Sarcoidosis

Behçet’s syndrome

Hemicrania continuaa SUNCT/SUNA Chronic CNS infection

New daily persistent

headachea

Hypnic headache Medication-overuse

headachea

a

May be complicated by medication overuse. b

Some patients may have headache

>4 h/d.

Abbreviations: CNS, central nervous system; SUNA, short-lasting unilateral

neuralgiform headache attacks with cranial autonomic symptoms; SUNCT, shortlasting unilateral neuralgiform headache attacks with conjunctival injection and

tearing.

is the dominant symptom and often appears in association with malaise and muscle aches. Head pain may be unilateral or bilateral and

is located temporally in 50% of patients but may involve any and all

aspects of the cranium. Pain usually appears gradually over a few hours

before peak intensity is reached; occasionally, it is explosive in onset.

The quality of pain is infrequently throbbing; it is almost invariably

described as dull and boring, with superimposed episodic stabbing

pains similar to the sharp pains that appear in migraine. Most patients

can recognize that the origin of their head pain is superficial, external

to the skull, rather than originating deep within the cranium (the pain

site usually identified by migraineurs). Scalp tenderness is present,

often to a marked degree; brushing the hair or resting the head on a

pillow may be impossible because of pain. Headache is usually worse

at night and often aggravated by exposure to cold. Additional findings

may include reddened, tender nodules or red streaking of the skin

overlying the temporal arteries, and tenderness of the temporal or, less

commonly, the occipital arteries.

The erythrocyte sedimentation rate (ESR) is often, although not

always, elevated; a normal ESR does not exclude giant cell arteritis. A

temporal artery biopsy followed by immediate treatment with prednisone 80 mg daily for the first 4–6 weeks should be initiated when

clinical suspicion is high; treatment should not be unreasonably delayed

to obtain a biopsy. The prevalence of migraine among the elderly is substantial, considerably higher than that of giant cell arteritis. Migraineurs

often report amelioration of their headache with prednisone; thus, caution must be used when interpreting the therapeutic response.

■ GLAUCOMA

Glaucoma may present with a prostrating headache associated with

nausea and vomiting. The headache often starts with severe eye pain.

On physical examination, the eye is often red with a fixed, moderately

dilated pupil.

Glaucoma is discussed in Chap. 32.

PRIMARY HEADACHE DISORDERS

Primary headaches are disorders in which headache and associated features occur in the absence of any exogenous cause. The most common

are migraine, tension-type headache, and the TACs, notably cluster

headache. These entities are discussed in detail in Chap. 430.

■ CHRONIC DAILY OR NEAR-DAILY HEADACHE

The broad description of chronic daily headache (CDH) can be

applied when a patient experiences headache on 15 days or more per

month. CDH is neither a single entity nor a diagnosis; it encompasses

a number of different headache syndromes, both primary and secondary (Table 16-3). In aggregate, this group presents considerable

disability and is thus specially mentioned here. Population-based

estimates suggest that about 4% of adults have daily or near-daily

headache.

APPROACH TO THE PATIENT

Chronic Daily Headache

The first step in the management of patients with CDH is to diagnose any secondary headache and treat that problem (Table 16-3).

This can sometimes be a challenge when the underlying cause

triggers worsening of a primary headache. For patients with primary headaches, diagnosis of the headache type will guide therapy.

Preventive treatments such as tricyclics, either amitriptyline or

nortriptyline, at doses up to 1 mg/kg, are very useful in patients

with CDH arising from migraine or tension-type headache or

where the secondary cause has activated the underlying primary

headache. Tricyclics are started in low doses (10–25 mg daily)

and may be given 12 h before the expected time of awakening in

order to avoid excessive morning sleepiness. Medicines including

topiramate, valproate, propranolol, flunarizine (not available in

the United States), candesartan, and the newer calcitonin generelated peptide (CGRP) pathway monoclonal antibodies, or gepantsCGRP receptor antagonists (see Chap. 430) are also useful when

the underlying issue is migraine.

MANAGEMENT OF MEDICALLY INTRACTABLE DISABLING

PRIMARY HEADACHE

The management of medically intractable headache is difficult,

although recent developments in therapy are at hand. Monoclonal

antibodies to CGRP or its receptor have been reported to be effective and well tolerated in chronic migraine and are now licensed for

use in clinical practice. Noninvasive neuromodulatory approaches,

such as single-pulse transcranial magnetic stimulation and noninvasive vagal nerve stimulation, which appear to modulate thalamic

processing or brainstem mechanisms, respectively, in migraine

have been used in clinical practice with success. Noninvasive vagal

nerve stimulation has also shown promise particularly in chronic

cluster headache, chronic paroxysmal hemicrania, and hemicrania continua, and possibly in short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)

and short-lasting unilateral neuralgiform headache attacks with

conjunctival injection and tearing (SUNCT) (Chap. 430). Other

modalities are discussed in Chap. 430.

MEDICATION-RELATED AND MEDICATION-OVERUSE HEADACHE

Overuse of analgesic medication for headache can aggravate headache frequency, markedly impair the effect of preventive medicines,

and induce a state of refractory daily or near-daily headache called

medication-overuse headache. A proportion of patients who stop taking analgesics will experience substantial improvement in the severity and frequency of their headache. However, even after cessation

of analgesic use, many patients continue to have headache, although

they may feel clinically improved in some way, especially if they have

been using opioids or barbiturates regularly. The residual symptoms

probably represent the underlying primary headache disorder, and

most commonly this issue occurs in patients prone to migraine.

Management of Medication Overuse: Outpatients For patients

who overuse analgesic medications, it is often helpful to reduce

and eliminate the medications, although this approach is far from

universally effective. One approach is to reduce the medication

dose by 10% every 1–2 weeks. Immediate cessation of analgesic

use is possible for some patients, provided there is no contraindication. Both approaches are facilitated by use of a medication diary

maintained during the month or two before cessation; this helps to

identify the scope of the problem. A small dose of a nonsteroidal

anti-inflammatory drug (NSAID) such as naproxen, 500 mg bid, if

tolerated, will help relieve residual pain as analgesic use is reduced.

115Headache CHAPTER 16

TABLE 16-4 Differential Diagnosis of New Daily Persistent Headache

PRIMARY SECONDARY

Migrainous-type Subarachnoid hemorrhage

Featureless (tension-type) Low cerebrospinal fluid (CSF) volume headache

Raised CSF pressure headache

Posttraumatic headachea

Chronic meningitis

a

Includes postinfectious forms.

NSAID overuse is not usually a problem for patients with daily

headache when an NSAID with a longer half-life is taken once or

twice daily; however, overuse problems may develop with shorteracting NSAIDS. Once the patient has substantially reduced analgesic use, a preventive medication should be introduced. Another

widely used approach is to commence the preventive at the same

time the analgesic reduction is started. It must be emphasized that

preventives may not work in the presence of analgesic overuse, particularly with opioids. The most common cause of unresponsiveness to

treatment is the use of a preventive when analgesics continue to be

used regularly. For some patients, discontinuing analgesics is very

difficult; often the best approach is to inform the patient that some

degree of headache is inevitable during this initial period.

Management of Medication Overuse: Inpatients Some patients

will require hospitalization for detoxification. Such patients have

typically failed efforts at outpatient withdrawal or have a significant

medical condition, such as diabetes mellitus or epilepsy, which

would complicate withdrawal as an outpatient. Following admission

to the hospital, medications are withdrawn completely on the first

day, in the absence of a contraindication. Antiemetics and fluids are

administered as required; clonidine is used for opioid withdrawal

symptoms. For acute intolerable pain during the waking hours,

aspirin, 1 g IV (not approved in the United States), is useful. IM

chlorpromazine can be helpful at night; patients must be adequately

hydrated. Three to five days into the admission, as the effect of the

withdrawn substance wears off, a course of IV dihydroergotamine

(DHE) can be used. DHE, administered every 8 h for 5 consecutive

days, a treatment that is not stopped short if headache settles, can

induce a significant remission that allows a preventive treatment

to be established. Serotonin 5-HT3

 receptor antagonists, such as

ondansetron or granisetron, or the neurokinin receptor antagonist,

aprepitant, may be required with DHE to prevent significant nausea, and domperidone (not approved in the United States) orally or

by suppository can be very helpful. Avoiding sedating or otherwise

side effect–prone antiemetics is helpful.

NEW DAILY PERSISTENT HEADACHE

New daily persistent headache (NDPH) is a clinically distinct syndrome with important secondary causes; these are listed in Table 16-4.

Clinical Presentation NDPH presents with headache on most if

not all days, and the patient can clearly, and often vividly, recall the

moment of onset. The headache usually begins abruptly, but onset

may be more gradual; evolution over 3 days has been proposed as

the upper limit for this syndrome. Patients typically recall the exact

day and circumstances of the onset of headache; the new, persistent head pain does not remit. The first priority is to distinguish

between a primary and a secondary cause of this syndrome. Subarachnoid hemorrhage is the most serious of the secondary causes

and must be excluded either by history or appropriate investigation

(Chap. 429).

Secondary NDPH  •  Low CSF Volume Headache In these

syndromes, head pain is positional: it begins when the patient sits

or stands upright and resolves upon reclining. The pain, which is

occipitofrontal, is usually a dull ache but may be throbbing. Patients

with chronic low CSF volume headache typically present with a

history of headache from one day to the next that is generally not

present on waking but worsens during the day. Recumbency usually

improves the headache within minutes, and it can take only minutes to

an hour for the pain to return when the patient resumes an upright

position.

The most common cause of headache due to persistent low CSF

volume is CSF leak following LP (Chap. S9). Post-LP headache

usually begins within 48 h but may be delayed for up to 12 days.

Its incidence is between 10% and 30%. Beverages with caffeine

may provide temporary relief. Besides LP, index events may include

epidural injection or a vigorous Valsalva maneuver, such as from

lifting, straining, coughing, clearing the eustachian tubes in an

airplane, or multiple orgasms. Spontaneous CSF leaks are well

recognized, and the diagnosis should be considered whenever the

headache history is typical, even when there is no obvious index

event. As time passes from the index event, the postural nature

may become less apparent; cases in which the index event occurred

several years before the eventual diagnosis have been recognized.

Symptoms appear to result from low volume rather than low

pressure: although low CSF pressures, typically 0–50 mm CSF, are

usually identified, a pressure as high as 140 mm CSF has been noted

with a documented leak.

Postural orthostatic tachycardia syndrome (POTS; Chap. 440)

can present with orthostatic headache similar to low CSF volume

headache and is a diagnosis that needs consideration in this setting.

When imaging is indicated to identify the source of a presumed leak, an MRI with gadolinium is the initial study of choice

(Fig. 16-1). A striking pattern of diffuse meningeal enhancement

is so typical that in the appropriate clinical context the diagnosis

is established. Chiari malformations may sometimes be noted on

MRI; in such cases, surgery to decompress the posterior fossa is not

indicated and usually worsens the headache. Spinal MRI with T2

weighting may reveal a leak, and spinal MRI may demonstrate spinal meningeal cysts whose role in these syndromes is yet to be elucidated. The source of CSF leakage may be identified by spinal MRI

with appropriate sequences, or by CT, preferably digital subtraction,

myelography. In the absence of a directly identified site of leakage,

111In-DTPA CSF studies may demonstrate early emptying of the

tracer into the bladder or slow progress of tracer across the brain

suggesting a CSF leak; this procedure is now only rarely employed.

POST CONTRAST

FIGURE 16-1 Magnetic resonance image showing diffuse meningeal enhancement

after gadolinium administration in a patient with low cerebrospinal fluid (CSF)

volume headache.

116 PART 2 Cardinal Manifestations and Presentation of Diseases

Initial treatment for low CSF volume headache is bed rest. For

patients with persistent pain, IV caffeine (500 mg in 500 mL of

saline administered over 2 h) can be very effective. An electrocardiogram (ECG) to screen for arrhythmia should be performed

before administration. It is reasonable to administer at least two

infusions of caffeine before embarking on additional tests to identify the source of the CSF leak. Because IV caffeine is safe and can

be curative, it spares many patients the need for further investigations. If unsuccessful, an abdominal binder may be helpful. If a leak

can be identified, an autologous blood patch is usually curative. A

blood patch is also effective for post-LP headache; in this setting,

the location is empirically determined to be the site of the LP. In

patients with intractable headache, oral theophylline is a useful

alternative that can take some months to be effective.

Raised CSF Pressure Headache Raised CSF pressure is well recognized as a cause of headache. Brain imaging can often reveal the

cause, such as a space-occupying lesion.

Idiopathic intracranial hypertension (pseudotumor cerebri)

NDPH due to raised CSF pressure can be the presenting symptom

for patients with idiopathic intracranial hypertension, a disorder

associated with obesity, female gender, and, on occasion, pregnancy.

The syndrome can also occur without visual problems, particularly

when the fundi are normal. These patients typically present with

a history of generalized headache that is present on waking and

improves as the day goes on. It is generally present on awakening

in the morning and is worse with recumbency. Transient visual

obscurations are frequent and may occur when the headaches

are most severe. The diagnosis is relatively straightforward when

papilledema is present, but the possibility must be considered even

in patients without funduscopic changes. Formal visual field testing should be performed even in the absence of overt ophthalmic

involvement. Partial obstructions of the cerebral venous sinuses are

found in a small number of cases. In addition, persistently raised

intracranial pressure can trigger a syndrome of chronic migraine.

Other conditions that characteristically produce headache on rising

in the morning or nocturnal headache are obstructive sleep apnea

or poorly controlled hypertension.

Evaluation of patients suspected to have raised CSF pressure

requires brain imaging. It is most efficient to obtain an MRI, including an MR venogram, as the initial study. If there are no contraindications, the CSF pressure should be measured by LP; this should be

done when the patient is symptomatic so that both the pressure and

the response to removal of 20–30 mL of CSF can be determined. An

elevated opening pressure and improvement in headache following

removal of CSF are diagnostic in the absence of fundal changes.

Initial treatment is with acetazolamide (250–500 mg bid); the

headache may improve within weeks. If ineffective, topiramate is

the next treatment of choice; it has many actions that may be useful

in this setting, including carbonic anhydrase inhibition, weight loss,

and neuronal membrane stabilization, likely mediated via effects on

phosphorylation pathways. Severely disabled patients who do not

respond to medical treatment require intracranial pressure monitoring and may require shunting. If appropriate, weight loss should

be encouraged.

Posttraumatic Headache A traumatic event can trigger a headache process that lasts for many months or years after the event.

The term trauma is used here in a very broad sense: headache can

develop following an injury to the head, but it can also develop

after an infectious episode, typically viral meningitis; a flulike illness; or a parasitic infection. Complaints of dizziness, vertigo, and

impaired memory can accompany the headache. Symptoms may

remit after several weeks or persist for months and even years after

the injury. Typically, the neurologic examination is normal and CT

or MRI studies are unrevealing. Chronic subdural hematoma may

on occasion mimic this disorder. Posttraumatic headache may also

be seen after carotid dissection and subarachnoid hemorrhage and

after intracranial surgery. The underlying theme appears to be that

a traumatic event involving the pain-producing meninges can trigger a headache process that lasts for many years.

Other Causes In one series, one-third of patients with NDPH

reported headache beginning after a transient flulike illness characterized by fever, neck stiffness, photophobia, and marked malaise.

Evaluation typically reveals no apparent cause for the headache.

There is no convincing evidence that persistent Epstein-Barr virus

infection plays a role in NDPH. A complicating factor is that many

patients undergo LP during the acute illness; iatrogenic low CSF

volume headache must be considered in these cases.

Treatment Treatment is largely empirical and directed at the

headache phenotype. Tricyclic antidepressants, notably amitriptyline, and anticonvulsants, such as topiramate, valproate, candesartan, and gabapentin, have been used with reported benefit. The

monoamine oxidase inhibitor phenelzine may also be useful in

carefully selected patients. The headache usually resolves within

3–5 years, but it can be quite disabling.

PRIMARY CARE AND HEADACHE

MANAGEMENT

Most patients with headache will be seen first in a primary care setting.

The challenging task of the primary care physician is to identify the

very few worrisome secondary headaches from the very great majority

of primary and less dangerous secondary headaches (Table 16-2).

Absent any warning signs, a reasonable approach is to treat when a

diagnosis is established. As a general rule, the investigation should focus

on identifying worrisome causes of headache or on helping the patient

to gain confidence if no primary headache diagnosis can be made.

After treatment has been initiated, follow-up care is essential to

identify whether progress has been made against the headache complaint. Not all headaches will respond to treatment, but, in general,

worrisome headaches will progress and will be easier to identify.

When a primary care physician feels the diagnosis is a primary

headache disorder, it is worth noting that >90% of patients who present to primary care with a complaint of headache will have migraine

(Chap. 430).

In general, patients who do not have a clear diagnosis, have a primary headache disorder other than migraine or tension-type headache,

or are unresponsive to two or more standard therapies for the considered headache type, should be considered for referral to a specialist. In

a practical sense, the threshold for referral is also determined by the

experience of the primary care physician in headache medicine and the

availability of secondary care options.

Acknowledgment

The editors acknowledge the contributions of Neil H. Raskin to earlier

editions of this chapter.

■ FURTHER READING

Headache Classification Committee of the International

Headache Society: The International Classification of Headache

Disorders, 3rd ed. Cephalalgia 33:629, 2018.

Kernick D, Goadsby PJ: Headache: A Practical Manual. Oxford:

Oxford University Press, 2008.

Lance JW, Goadsby PJ: Mechanism and Management of Headache,

7th ed. New York, Elsevier, 2005.

Olesen J et al: The Headaches. Philadelphia, Lippincott, Williams &

Wilkins, 2005.

Silberstein SD, Lipton RB, Dodick DW: Wolff’s Headache and Other

Head Pain, 9th ed. New York, Oxford University Press, 2021.

117Back and Neck Pain CHAPTER 17

The importance of back and neck pain in our society is underscored

by the following: (1) the cost of chronic back pain in the United States

is estimated at more than $200 billion annually; approximately onethird of this cost is due to direct health care expenses and two-thirds

are indirect costs resulting from loss of wages and productivity; (2)

back symptoms are the most common cause of disability in individuals

<45 years of age; (3) low back pain (LBP) is the second most common

reason for visiting a physician in the United States; and (4) more than

four out of five people will experience significant back pain at some

point in their lives.

ANATOMY OF THE SPINE

The anterior spine consists of cylindrical vertebral bodies separated by

intervertebral disks and stabilized by the anterior and posterior longitudinal ligaments. The intervertebral disks are composed of a central gelatinous nucleus pulposus surrounded by a tough cartilaginous ring, the

annulus fibrosis. Disks are responsible for 25% of spinal column length

and allow the bony vertebrae to move easily upon each other (Figs. 17-1

and 17-2). Desiccation of the nucleus pulposus and degeneration of the

annulus fibrosus worsen with age, resulting in loss of disk height. The

disks are largest in the cervical and lumbar regions where movements

of the spine are greatest. The anterior spine absorbs the shock of bodily

movements such as walking and running, and with the posterior spine

protects the spinal cord and nerve roots in the spinal canal.

The posterior spine consists of the vertebral arches and processes.

Each arch consists of paired cylindrical pedicles anteriorly and paired

lamina posteriorly. The vertebral arch also gives rise to two transverse

processes laterally, one spinous process posteriorly, plus two superior

and two inferior articular facets. The apposition of a superior and

inferior facet constitutes a facet joint. The posterior spine provides an

anchor for the attachment of muscles and ligaments. The contraction

of muscles attached to the spinous and transverse processes and lamina

works like a system of pulleys and levers producing flexion, extension,

rotation, and lateral bending movements of the spine.

Nerve root injury (radiculopathy) is a common cause of pain in the

neck and arm, or low back and buttock, or leg (see dermatomes in

Figs. 25-2 and 25-3). Each nerve root exits just above its corresponding vertebral body in the cervical region (e.g., the C7 nerve root exits

17 Back and Neck Pain

John W. Engstrom

at the C6-C7 level), and just below the vertebral body in the thoracic

and lumbar spine (e.g., the T1 nerve root exits at the T1-T2 level). The

cervical nerve roots follow a short intraspinal course before exiting. In

contrast, because the spinal cord ends at the L1 or L2 vertebral level,

the lumbar nerve roots follow a long intraspinal course and can be

injured anywhere along its path. For example, disk herniation at the

L4-L5 level can produce L4 root compression laterally, but more often

compression of the traversing L5 nerve root occurs (Fig. 17-3). The

lumbar nerve roots are mobile in the spinal canal, but eventually pass

through the narrow lateral recess of the spinal canal and intervertebral

Posterior Posterior Anterior

Superior articular

process

Superior vertebral

notch

Transverse

process

Inferior vertebral

notch

Inferior articular

process (facet)

Intervertebral

foramen

Intervertebral

disk

Body

Spinous

process

Superior

articular

process

Spinal canal

Body

Lamina

Pedicle

Lateral

recess

A Anterior B

FIGURE 17-1 Vertebral anatomy. A. Vertebral body—axial view; B. vertebral column—sagittal view. (Reproduced with permission from AG Cornuelle, DH Gronefeld:

Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998.)

Sacrum

Coccyx

Lumbar (5)

Thoracic (12)

Cervical (7)

Anterior view Right lateral view

1

2

3

4

5

6

7

1

2

3

4

5

6

7

8

9

10

11

12

1

2

3

4

5

Sacral

curvature

(Kyphosis)

Thoracic

curvature

(Kyphosis)

Cervical

curvature

(Lordosis)

Lumbar

 curvature

(Lordosis)

FIGURE 17-2 Spinal column. (Reproduced with permission from AG Cornuelle, DH

Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998.)

118 PART 2 Cardinal Manifestations and Presentation of Diseases

4th Lumbar

vertebral body

Lateral

recess

5th Lumbar

vertebral body

4th Lumbar

pedicle

L4 root

Intervertebral

foramen

Protruded

L4-L5 disk

L5 Root

S1 Root

S2 Root

Protruded

L5-S1 disk

FIGURE 17-3 Compression of L5 and S1 roots by herniated disks. (Reproduced with permission from AH Ropper, MA Samuels: Adams and Victor’s Principles of Neurology, 9th ed.

New York, McGraw-Hill, 2009.)

TABLE 17-1 Acute Low Back Pain: Risk Factors for an Important

Structural Cause

History

Pain worse at rest or at night

Prior history of cancer

History of chronic infection (especially lung, urinary tract, skin, poor dentition)

History of trauma

Incontinence

Age >70 years

Intravenous drug use

Glucocorticoid use

History of a rapidly progressive neurologic deficit

Examination

Unexplained fever

Unexplained weight loss

Focal palpation/percussion tenderness over the midline spine

Abdominal, rectal, or pelvic mass

Internal/external rotation of the leg at the hip

Straight-leg or reverse straight-leg raising signs

Progressive focal neurologic deficit

foramen (Figs. 17-2 and 17-3). When imaging the spine, both sagittal

and axial views are needed to assess possible compression at these sites.

Beginning at the C3 level, each cervical (and the first thoracic)

vertebral body projects a lateral bony process upward—the uncinate

process. The uncinate process articulates with the cervical vertebral

body above via the uncovertebral joint. The uncovertebral joint can

hypertrophy with age and contribute to neural foraminal narrowing

and cervical radiculopathy.

Pain-sensitive structures of the spine include the periosteum of the

vertebrae, dura, facet joints, annulus fibrosus of the intervertebral disk,

epidural veins and arteries, and the longitudinal ligaments. Disease of

these diverse structures may explain many cases of back pain without

nerve root compression. Under normal circumstances, the nucleus

pulposus of the intervertebral disk is not pain sensitive.

APPROACH TO THE PATIENT

Back Pain

TYPES OF BACK PAIN

Delineating the type of pain reported by the patient is the essential

first step. Attention is also focused on identifying risk factors for a

serious underlying etiology. The most frequent serious causes of

back pain are radiculopathy, fracture, tumor, infection, or referred

pain from visceral structures (Table 17-1).

Local pain is caused by injury to pain-sensitive structures that

compress or irritate sensory nerve endings. The site of the pain is

near the affected part of the back.

Pain referred to the back may arise from abdominal or pelvic viscera. The pain is usually described as primarily abdominal or pelvic,

accompanied by back pain, and usually unaffected by posture. The

patient may occasionally complain of back pain only.

Pain of spine origin may be located in the back or referred to the

buttocks or legs. Diseases affecting the upper lumbar spine tend to

refer pain to the lumbar region, groin, or anterior thighs. Diseases

affecting the lower lumbar spine tend to produce pain referred to

the buttocks, posterior thighs, calves, or feet. Referred pain often

explains pain syndromes that cross multiple dermatomes without

evidence of nerve or nerve root injury.

119Back and Neck Pain CHAPTER 17

Radicular pain is typically sharp and radiates from the low back

to a leg within the territory of a nerve root (see “Lumbar Disk

Disease,” below). Coughing, sneezing, or voluntary contraction of

abdominal muscles (lifting heavy objects or straining at stool) may

elicit or worsen the radiating pain. The pain may also increase in

postures that stretch the nerves and nerve roots. Sitting with the leg

outstretched places traction on the sciatic nerve and L5 and S1 roots

because the sciatic nerve passes posterior to the hip. The femoral

nerve (L2, L3, and L4 roots) passes anterior to the hip and is not

stretched by sitting. The description of the pain alone often fails

to distinguish between referred pain and radiculopathy, although a

burning or electric quality favors radiculopathy.

Pain associated with muscle spasm is commonly associated with

many spine disorders. The spasms may be accompanied by an

abnormal posture, tense paraspinal muscles, and dull or achy pain

in the paraspinal region.

Knowledge of the circumstances associated with the onset of

back pain is important when weighing possible serious underlying

causes for the pain. Some patients involved in accidents or workrelated injuries may exaggerate their pain for the purpose of compensation or for psychological reasons.

EXAMINATION

A complete physical examination including vital signs, heart and

lungs, abdomen and rectum, and limbs is advisable. Back pain

referred from visceral organs may be reproduced during palpation

of the abdomen (pancreatitis, abdominal aortic aneurysm [AAA])

or percussion over the costovertebral angles (pyelonephritis).

The normal spine has a cervical and lumbar lordosis and a

thoracic kyphosis. Exaggeration of these normal alignments may

result in hyperkyphosis of the thoracic spine or hyperlordosis of the

lumbar spine. Inspection of the back may reveal a lateral curvature

of the spine (scoliosis). A midline hair tuft, skin dimpling or pigmentation, or a sinus tract may indicate a congenital spine anomaly.

Asymmetry in the prominence of the paraspinal muscles suggests

muscle spasm. Palpation over the spinous process transmits force to

the entire vertebrae and suggests vertebral pathology.

Flexion at the hips is normal in patients with lumbar spine disease, but flexion of the lumbar spine is limited and sometimes painful. Lateral bending to the side opposite the injured spinal element

may stretch the damaged tissues, worsen pain, and limit motion.

Hyperextension of the spine (with the patient prone or standing)

is limited when nerve root compression, facet joint pathology, or

other bony spine disease is present.

Pain from hip disease may mimic the pain of lumbar spine disease. Hip pain can be reproduced by passive internal and external

rotation at the hip with the knee and hip in flexion or by percussing

the heel with the examiner’s palm with the leg extended (heel percussion sign).

The straight-leg raising (SLR) maneuver is a simple bedside test

for nerve root disease. With the patient supine, passive straightleg flexion at the hip stretches the L5 and S1 nerve roots and the

sciatic nerve; dorsiflexion of the foot during the maneuver adds

to the stretch. In healthy individuals, flexion to at least 80° is normally possible without causing pain, although a tight, stretching

sensation in the hamstring muscles is common. The SLR test is

positive if the maneuver reproduces the patient’s usual back or

limb pain. Eliciting the SLR sign in both the supine and sitting

positions can help determine if the finding is reproducible. The

patient may describe pain in the low back, buttocks, posterior

thigh, or lower leg, but the key feature is reproduction of the

patient’s usual pain. The crossed SLR sign is present when flexion

of one leg reproduces the usual pain in the opposite leg or buttocks. In disk herniation, the crossed SLR sign is less sensitive but

more specific than the SLR sign. The reverse SLR sign is elicited by

standing the patient next to the examination table and passively

extending each leg with the knee fully extended. This maneuver,

which stretches the L2-L4 nerve roots, lumbosacral plexus, and

femoral nerve, is considered positive if the patient’s usual back or

limb pain is reproduced. For all of these tests, the nerve or nerve

root lesion is always on the side of the pain. Examination of the

unaffected leg first provides a control test, ensures mutual understanding of test parameters, and enhances test utility.

The neurologic examination includes a search for focal weakness

or muscle atrophy, localized reflex changes, diminished sensation in

the legs, or signs of spinal cord injury. The examiner should be alert

to the possibility of breakaway weakness, defined as fluctuations in

the maximum power generated during muscle testing. Breakaway

weakness may be due to pain, inattention, or a combination of pain

and underlying true weakness. Breakaway weakness without pain is

usually due to a lack of effort. In uncertain cases, electromyography

(EMG) can determine if true weakness due to nerve tissue injury is

present. Findings with specific lumbosacral nerve root lesions are

shown in Table 17-2 and are discussed below.

LABORATORY, IMAGING, AND EMG STUDIES

Laboratory studies are rarely needed for the initial evaluation of

nonspecific acute (<3 months duration) low back pain (ALBP).

TABLE 17-2 Lumbosacral Radiculopathy: Neurologic Features

LUMBOSACRAL

NERVE ROOT 

EXAMINATION FINDINGS

REFLEX SENSORY MOTOR PAIN DISTRIBUTION 

L2a — Upper anterior thigh Psoas (hip flexors) Anterior thigh

L3a — Lower anterior thigh Psoas (hip flexors) Anterior thigh, knee

Anterior knee Quadriceps (knee extensors)

Thigh adductors

L4a Quadriceps (knee) Medial calf Quadriceps (knee extensors)b Knee, medial calf

Thigh adductors Anterolateral thigh

L5c — Dorsal surface—foot Peronei (foot evertors)b Lateral calf, dorsal foot,

posterolateral thigh, buttocks

Lateral calf Tibialis anterior (foot dorsiflexors)

Gluteus medius (leg abductors)

Toe dorsiflexors

S1c Gastrocnemius/

soleus (ankle)

Plantar surface—foot Gastrocnemius/soleus (foot plantar flexors)b Bottom foot, posterior calf,

posterior thigh, buttocks

Lateral aspect—foot Abductor hallucis (toe flexors)b

Gluteus maximus (leg extensors)

a

Reverse straight-leg raising sign may be present—see “Examination of the Back.” b

These muscles receive the majority of innervation from this root. c

Straight-leg raising

sign may be present—see “Examination of the Back.”

120 PART 2 Cardinal Manifestations and Presentation of Diseases

TABLE 17-3 Causes of Back or Neck Pain

Lumbar or Cervical Disk Disease

Degenerative Spine Disease

Lumbar spinal stenosis without or with neurogenic claudication

Intervertebral foraminal or lateral recess narrowing

Disk-osteophyte complex

Facet or uncovertebral joint hypertrophy

Lateral disk protrusion

Spondylosis (osteoarthritis), spondylolisthesis, or spondylolysis

Spine Infection

Vertebral osteomyelitis

Spinal epidural abscess

Septic disk (diskitis)

Meningitis

Lumbar arachnoiditis

Neoplasms

Metastatic with/without pathologic fracture

Primary Nervous System: Meningioma, neurofibroma, schwannoma

Primary Bone: chordoma, osteoma

Trauma

Strain or sprain

Whiplash injury

Trauma/falls, motor vehicle accidents

Metabolic Spine Disease

Osteoporosis with/without pathologic fracture—hyperparathyroidism, immobility

Osteosclerosis (e.g., Paget’s disease)

Congenital/Developmental

Spondylolysis

Kyphoscoliosis

Spina bifida occulta

Tethered spinal cord

Autoimmune Inflammatory Arthritis

Other Causes of Back Pain

Referred pain from visceral disease (e.g., abdominal aortic aneurysm)

Postural

Psychiatric, malingering, chronic pain syndromes

Risk factors for a serious underlying cause and for infection, tumor,

or fracture in particular should be sought by history and examination. If risk factors are present (Table 17-1), then laboratory

studies (complete blood count [CBC], erythrocyte sedimentation

rate [ESR], urinalysis) are indicated. If risk factors are absent, then

management is conservative (see “Treatment,” below).

CT scanning is used as a primary screening modality for acute

trauma that is moderate to severe. CT is superior to x-rays for

detection of fractures involving posterior spine structures, craniocervical and cervicothoracic junctions, C1 and C2 vertebrae, bone

fragments in the spinal canal, or misalignment. MRI or CT myelography is the radiologic test of choice for evaluation of most serious

diseases involving the spine. MRI is superior for the definition of

soft tissue structures, whereas CT myelography provides optimal

imaging of the lateral recess of the spinal canal, defines bony abnormalities, and is tolerated by claustrophobic patients.

Population surveys in the United States suggest that patients

with back pain report greater functional limitations in recent years,

despite rapid increases in spine imaging, opioid prescribing, injections, and spine surgery. This suggests that more selective use of

diagnostic and treatment modalities may be reasonable for many

patients. One prospective case-control study found that older adults

with back pain of less than 6 weeks duration who received spine

imaging as part of a primary care visit had no better outcomes than

the control group.

Spine imaging often reveals abnormalities of dubious clinical

relevance that may alarm clinicians and patients alike and prompt

further testing and unnecessary therapy. When imaging tests are

reviewed, it is important to remember that degenerative findings

are common in normal, pain-free individuals. Randomized trials

and observational studies have suggested that imaging can have

a “cascade effect,” creating a gateway to other unnecessary care.

Interventions have included physician education and computerized

decision support within the electronic medical record to require

specific indications for approval of imaging tests. Other strategies

have included audit and feedback of individual practitioners’ rates

of ordering, more rapid access to physical therapy, or consultation

with spine experts for patients without imaging indications.

Educational tools created by the America College of Physicians

for patients and the public have included “Five Things Physicians

and Patients Should Question”: (1) Do not recommend advanced

imaging (e.g., MRI) of the spine within the first 6 weeks in

patients with nonspecific ALBP in the absence of red flags. (2) Do

not perform elective spinal injections without imaging guidance,

unless contraindicated. (3) Do not use bone morphogenetic protein

(BMP) for routine anterior cervical spine fusion surgery. (4) Do

not use EMG and nerve conduction studies (NCSs) to determine

the cause of purely midline lumbar, thoracic, or cervical spine pain.

(5) Do not recommend bed rest for >48 h when treating LBP. In an

observational study, application of this strategy was associated with

lower rates of repeat imaging, opioid use, and referrals for physical

therapy.

Electrodiagnostic studies can be used to assess the functional

integrity of the peripheral nervous system (Chap. 446). Sensory

NCSs are normal when focal sensory loss confirmed by examination

is due to nerve root damage because the nerve roots are proximal

to the nerve cell bodies in the dorsal root ganglia. Injury to nerve

tissue distal to the dorsal root ganglion (e.g., plexus or peripheral

nerve) results in reduced sensory nerve signals. Needle EMG complements NCSs by detecting denervation or reinnervation changes

in a myotomal (segmental) distribution. Multiple muscles supplied

by different nerve roots and nerves are sampled; the pattern of

muscle involvement indicates the nerve root(s) responsible for the

injury. Needle EMG provides objective information about motor

nerve fiber injury when clinical evaluation of weakness is limited by

pain or poor effort. EMG and NCSs will be normal when sensory

nerve root injury or irritation is the pain source.

The COVID-19 pandemic has disrupted and complicated the care

of patients with LBP. Paraspinal myalgias may result in LBP. The sedentary lifestyle resulting from quarantine is associated with an increased

frequency or severity of LBP. Fear of infection risk has also prevented

many patients from seeking needed care. Video-telemedicine visits

can help identify patients with underlying risks for a serious cause and

inform appropriate next steps in management.

CAUSES OF BACK PAIN (TABLE 17-3)

■ LUMBAR DISK DISEASE

Lumbar disk disease is a common cause of acute, chronic, or recurrent

low back and leg pain (Figs. 17-3 and 17-4). Disk disease is most likely

to occur at the L4-L5 or L5-S1 levels, but upper lumbar levels can also

be involved. The cause is often unknown, but the risk is increased in

overweight individuals. Disk herniation is unusual prior to age 20 years

and is rare in the fibrotic disks of the elderly. Complex genetic factors

may play a role in predisposition. The pain may be located in the low

back only or referred to a leg, buttock, or hip. A sneeze, cough, or

trivial movement may cause the nucleus pulposus to prolapse, pushing

the frayed and weakened annulus posteriorly. With severe disk disease,

the nucleus can protrude through the annulus (herniation) or become

extruded to lie as a free fragment in the spinal canal.

121Back and Neck Pain CHAPTER 17

Herniated L4 disk

Herniated L4 disk

A B

Compressed

Thecal Sac

Compressed

L5 root Compressed

Thecal Sac

Compressed

L5 root

Normal

L5 root

FIGURE 17-4 Disk herniation. A. Sagittal T2-weighted image on the left side of the spinal canal

reveals disk herniation at the L4-L5 level. B. Axial T1-weighted image shows paracentral disk

herniation with displacement of the thecal sac medially and the left L5 nerve root posteriorly in the

left lateral recess.

The mechanism by which intervertebral disk injury causes back

pain is uncertain. The inner annulus fibrosus and nucleus pulposus

are normally devoid of innervation. Inflammation and production of

proinflammatory cytokines within a ruptured nucleus pulposus may

trigger or perpetuate back pain. Ingrowth of nociceptive (pain) nerve

fibers into the nucleus pulposus of a diseased disk may be responsible

for some cases of chronic “diskogenic” pain. Nerve root injury (radiculopathy) from disk herniation is usually due to inflammation, but

lateral herniation may produce compression in the lateral recess or

intervertebral foramen.

A ruptured disk may be asymptomatic or cause back pain, limited spine motion (particularly flexion), a focal neurologic deficit, or

radicular pain. A dermatomal pattern of sensory loss or a reduced or

absent deep tendon reflex is more suggestive of a specific root lesion

than is the pattern of pain. Motor findings (focal weakness, muscle

atrophy, or fasciculations) occur less frequently than focal sensory or

reflex changes. Symptoms and signs are usually unilateral, but bilateral

involvement does occur with large central disk herniations that involve

roots bilaterally or cause inflammation of nerve roots within the spinal

canal. Clinical manifestations of specific nerve root lesions are summarized in Table 17-2.

The differential diagnosis covers a variety of serious and treatable

conditions, including epidural abscess, hematoma, fracture, or tumor.

Fever, constant pain uninfluenced by position, sphincter abnormalities, or signs of myelopathy suggest an etiology other than lumbar

disk disease. Absent ankle reflexes can be a normal finding in persons

>60 years or a sign of bilateral S1 radiculopathies. An absent deep tendon reflex or focal sensory loss may indicate injury to a nerve root, but

other sites of injury along the nerve must also be considered. As examples, an absent knee reflex may be due to a femoral neuropathy or an L4

nerve root injury; loss of sensation over the foot and lateral lower calf

may result from a peroneal or lateral sciatic neuropathy, or an L5 nerve

root injury. Focal muscle atrophy may reflect injury to the anterior

horn cells of the spinal cord, a nerve root, peripheral nerve, or disuse.

A lumbar spine MRI scan or CT myelogram can often confirm the

location and type of pathology. Spine MRIs yield exquisite views of

intraspinal and adjacent soft tissue anatomy, whereas bony lesions of

the lateral recess or intervertebral foramen are optimally visualized

by CT myelography. The correlation of neuroradiologic findings to

clinical symptoms, particularly pain, is not simple. Contrast-enhancing

tears in the annulus fibrosus or disk protrusions are widely accepted as

common sources of back pain; however, studies have found that many

asymptomatic adults have similar radiologic findings. Entirely asymptomatic disk protrusions are also common, occurring in up to onethird of adults, and these may also enhance with contrast. Furthermore,

in patients with known disk herniation treated either

medically or surgically, persistence of the herniation 10

years later had no relationship to the clinical outcome.

In summary, MRI findings of disk protrusion, tears in

the annulus fibrosus, or hypertrophic facet joints are

common incidental findings that, by themselves, should

not dictate management decisions for patients with back

pain.

The diagnosis of nerve root injury is most secure when

the history, examination, results of imaging studies, and

the EMG are concordant. There is often good correlation

between CT and EMG findings for localization of nerve

root injury.

Management of lumbar disk disease is discussed below.

Cauda equina syndrome (CES) signifies an injury of

multiple lumbosacral nerve roots within the spinal canal

distal to the termination of the spinal cord at L1-L2. LBP,

weakness and areflexia in the legs, saddle anesthesia, or

loss of bladder function may occur. The problem must

be distinguished from disorders of the lower spinal cord

(conus medullaris syndrome), acute transverse myelitis

(Chap. 442), and Guillain-Barré syndrome (Chap. 447).

Combined involvement of the conus medullaris and

cauda equina can occur. CES is most commonly due to a large ruptured

lumbosacral intervertebral disk, but other causes include lumbosacral

spine fracture, hematoma within the spinal canal (sometimes following

lumbar puncture in patients with coagulopathy), and tumor or other

compressive mass lesions. Treatment is usually surgical decompression, sometimes on an urgent basis in an attempt to restore or preserve

motor or sphincter function, or radiotherapy for metastatic tumors

(Chap. 90).

■ DEGENERATIVE CONDITIONS

Lumbar spinal stenosis (LSS) describes a narrowed lumbar spinal canal.

Neurogenic claudication consists of pain, typically in the back and buttocks or legs, that is brought on by walking or standing and relieved

by sitting. Unlike vascular claudication, symptoms are often provoked

by standing without walking. Unlike lumbar disk disease, symptoms

are usually relieved by sitting. Patients with neurogenic claudication

can often walk much farther when leaning over a shopping cart and

can pedal a stationary bike with ease while sitting. These flexed positions increase the anteroposterior spinal canal diameter and reduce

intraspinal venous hypertension, producing pain relief. Focal weakness, sensory loss, or reflex changes may occur when spinal stenosis is

associated with neural foraminal narrowing and radiculopathy. Severe

neurologic deficits, including paralysis and urinary incontinence,

occur only rarely.

LSS by itself is common (6–7% of adults) and is usually asymptomatic. Symptoms are correlated with severe spinal canal stenosis.

LSS is most often acquired (75%) but can also be congenital or due to

a mixture of both etiologies. Congenital forms (achondroplasia and

idiopathic) are characterized by short, thick pedicles that produce

both spinal canal and lateral recess stenosis. Acquired factors that contribute to spinal stenosis include degenerative diseases (spondylosis,

spondylolisthesis, and scoliosis), trauma, spine surgery, metabolic or

endocrine disorders (epidural lipomatosis, osteoporosis, acromegaly,

renal osteodystrophy, and hypoparathyroidism), and Paget’s disease.

MRI provides the best definition of the abnormal anatomy (Fig. 17-5).

LSS accompanied by neurogenic claudication responds to surgical

decompression of the stenotic segments. The same processes leading to

LSS may cause lumbar foraminal or lateral recess narrowing resulting

in coincident lumbar radiculopathy that may require treatment as well.

Conservative treatment of symptomatic LSS can include nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, exercise

programs, and symptomatic treatment of acute pain episodes. There is

insufficient evidence to support the routine use of epidural glucocorticoid injections. Surgery is considered when medical therapy does not

relieve symptoms sufficiently to allow for resumption of activities of