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