Download 45 - Neck Pain

PART
6
DIFFERENTIAL DIAGNOSIS OF
REGIONAL AND DIFFUSE
MUSCULOSKELETAL PAIN
45
Neck Pain
JOSEPH S. CHENG • MATTHEW J. MCGIRT • CLINT DEVIN
KEY POINTS
Neck pain is a ubiquitous condition associated with
enormous medical and legal costs in the United States.
Physicians need to differentiate causes of neck pain that can
be managed conservatively from causes that require more
aggressive treatments.
Knowledge of the anatomy helps diagnosis and the
differentiation of symptoms from a musculoskeletal,
neurogenic, or vascular etiology.
The history and clinical examination help focus the
differential diagnosis and help to identify the origin of the
neck pain based on the anatomy and physiology.
Indicated imaging studies, neurophysiologic procedures, and
laboratory studies aid in diagnosis and determining a
treatment plan for the patient’s symptoms.
In the absence of spinal instability, neurologic deficit,
infectious process, or neoplastic process, the patient may
benefit from conservative treatment with expectant recovery
in time.
EPIDEMIOLOGY
Pain is an evolutionary protective mechanism to prevent
further tissue damage. Neck pain is a ubiquitous condition
with a lifetime prevalence of 67% to 71%.1 The point preva­
lence of neck pain ranges between 10% and 15%, with total
annual costs for neck and low back pain corresponding to
1% of the gross national product (GNP) in Sweden, and
direct health service costs representing only a small fraction
of this percentage.2-4 The medical and legal expenses associ­
ated with neck pain can be enormous, as in whiplash inju­
ries, which alone can cost $29 billion annually in the
United States.5
Neck pain may originate from various anatomic sources,
including paraspinal soft tissues, intervertebral joints and
disks, compression of the spinal cord or nerve roots, and
referred visceral pain (Figure 45-1). The origin of neck
pain has a wide differential diagnosis, which can include
trauma, degenerative changes, infection, and autoimmune
disorders such as rheumatoid arthritis and ankylosing
spondylitis.
The perception and resultant reporting of this pain vary
significantly according to cultural and social circumstances.
Honeyman and Jacobs noted that Australian Aborigines
significantly underreport pain and are rarely disabled by
pain.6 Social circumstances also play an important role in
an individual’s ability to cope with and overcome neck pain.
Studies have demonstrated worse outcomes following dis­
kectomy for patients with a workers’ compensation claim or
litigation surrounding their condition.7 These studies indi­
cate nonorganic contributions to neck pain for secondary
gain. Fortunately, most episodes of acute neck pain resolve
with “tincture of time” and patient education.
Physicians need to be able to differentiate causes of neck
pain that can be managed with a conservative approach
from those that require more aggressive treatment. An
understanding of anatomy and physiology and of their asso­
ciation with the pathogenesis of neck pain provides the
basis for obtaining a thorough history, physical examination
findings, and ancillary data with the ultimate goal of effec­
tive treatment.
ANATOMY
The cervical spine consists of seven vertebrae (C1 through
C7). The bony anatomy of the atlas (C1) and axis (C2) is
unique, whereas C3-C7 demonstrates fairly consistent
anatomy (Figure 45-2). The atlas has no vertebral body, and
its lateral masses articulate with the occipital condyles of
the skull, forming the atlanto-occipital joints supported by
anterior and posterior occipital membranes.8 The atlantooccipital joint is responsible for approximately 50% of total
flexion and extension in the neck, and functional implica­
tions are clear when this motion is lost. The axis (C2) has
the dens or an odontoid peg that projects upward and ante­
rior to articulate with the posterior aspect of the anterior
arch of the atlas. The principal stabilizer of the odontoid to
the anterior arch of the atlas is the transverse ligament; alar
and apical ligaments act as secondary stabilizers. This true
synovial joint is susceptible to inflammatory processes such
as those seen with rheumatoid arthritis. No intervertebral
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| PART 6 DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
Neck pain
History
Clinical exam
Axial
neck pain
Conservative care
Soft collar, medications,
PT
Myelopathy
Radiculopathy
No
improvement
Suspected
neoplasm
or infection
Trauma
Radiologic studies
X-ray, CT, MRI, bone
scan
Rigid collar
Spine
precautions
Mild findings
Neural compression
Bone lesion
Deformity
Severe findings
Neural compression
Bone lesion
Deformity
Negative
findings
Continue
conservative
treatments
Neurodiagnostics
EMG, NCS, SSEP
Conservative treatments
with negative results
Request
Evidence of spine surgeon
consult
nerve or cord
compression
Figure 45-1 Algorithm of neck pain. CT, computed tomography; EMG, electromyogram; MRI, magnetic resonance imaging; NCS, nerve conduction
study; PT, physical therapy; SSEP, somatosensory evoked potentials.
disk is present between the atlanto-occipital joint and the
atlantoaxial joint, and without conferred stability from a
disk, destructive inflammatory arthritides may result in
instability.9 The atlantoaxial articulation provides approxi­
mately 50% of rotatory motion of the cervical spine.
The subaxial cervical spine consists of C3 through C7
vertebrae, all demonstrating fairly similar anatomy. Each
vertebra consists of a body, two interconnecting pedicles,
two lateral masses, two transverse processes, two laminae,
and spinous processes. Transverse and spinous processes
External
occipital
protuberance
Foramen for
vertebral
artery
Lambdoid
suture
Atlas
Synovial
joint
Intervertebral
disk
True
transverse
element of
transverse
process
Costotransverse bar
A
Costal
element of
transverse
process
Superior
nuchal line
Axis
3
4
5
6
Foramen
magnum
Odontoid
peg
(dens)
Transverse
process
and
Tubercle on
posterior
arch of atlas
7
B
First rib
Figure 45-2 Cervical spine anatomy. A, Cervical spine. Anterior view of articulated cervical vertebrae. B, Posterior view of the skull, seven cervical
vertebrae, and first thoracic vertebra.
CHAPTER 45 project outward, providing attachment for ligaments and
muscles, and creating a moment arm to facilitate motion.
The spinous processes of C3 through C6 are bifid, whereas
the C7 spinous process usually is not. However, the C7
spinous process is large and is the next most prominent and
most easily palpable spinous process below C2.
Five articulations are present between vertebrae from C2
through C7, including the intervertebral disk, two uncover­
tebral joints, and two facet (zygoapophyseal) joints. Facet
joints are true apophyseal joints with hyaline cartilage artic­
ulations, intervening menisci, synovial lining, and a joint
capsule. This composition makes them susceptible to degen­
erative changes and systemic arthritides. The cartilage and
the synovial lining are aneural, whereas the joint capsule is
highly innervated by the dorsal primary ramus. The facet
joints are angled approximately 45 degrees from the trans­
verse plane, articulating in concert with the uncovertebral
joints and ligaments.
Intervertebral disks increase in size from C2 downward,
giving the cervical spine its characteristic lordotic shape.
Each disk consists of an outer annulus fibrosus and an inner
nucleus pulposus, as well as cephalad and caudad end plates.
The annulus fibrosus consists of type I collagen, which helps
give form to the disk and provides tensile strength. The
annulus fibrosus is innervated by the sinuvertebral nerve,
formed by branches of the ventral nerve root and the sym­
pathetic plexus.10 The nucleus pulposus consists of type II
collagen and proteoglycans, which interact with water to
resist compressive stress. Pressure within the disk is greatest
with flexion, which may explain why those with a disk
herniation find this position most uncomfortable.11 Disk
degeneration with aging includes loss of water content and
resultant loss of height, annular tears, and myxomatous
changes, increasing the risk of disk herniation. This typi­
cally occurs in the posterolateral aspect of the disk, where
the posterior longitudinal ligament is not present and
annulus fibrosus is at its weakest, medial to the uncoverte­
bral joints.
The spinal column is supported by the interplay of liga­
ments and muscles (Figure 45-3). The anterior longitudinal
ligament (ALL) and the posterior longitudinal ligament
(PLL) course along the anterior and posterior aspects of the
vertebral bodies; the anterior longitudinal ligament resists
hyperextension, and the posterior longitudinal ligament
resists hyperflexion. The ligamentum flavum joins the
laminae of adjacent vertebrae and may become thickened,
creating stenosis in the spinal canal. In a similar manner,
the interspinous ligament joins the spinous process of adja­
cent vertebrae. The supraspinous ligament originates as the
nuchal ligament at the occiput and extends caudally as an
aponeurosis until it is attached to the tip of the spinous
processes of C7; it then continues to the lumbar region.
Fourteen paired anterior, lateral, and posterior muscles help
to orchestrate complex movements of the neck.
A brief review of the spinal cord and nerve roots is ben­
eficial for a thorough evaluation. Grossly, the spinal cord is
divided into the posterior column, the lateral column, and
the anterior column. The posterior column mediates pro­
prioceptive, vibratory, and tactile sensation; the lateral
column is a conduit for motor fibers, along with pain and
temperature sensation from the contralateral side of the
body; the anterior column conveys crude touch sensation.
| Neck Pain
627
Spheno-occipital
synchondrosis
Tectorial membrane
Pons
Palate
Apical
ligament
Atlas
Remnant of disk uniting
body and dens of axis
Margins of
foramen
magnum
Dura
Spinal cord
Posterior
longitudinal
ligament
Anterior
longitudinal
ligament
Figure 45-3 Cervical spine anatomy. Sagittal view of the lower head
and neck shows the relationship of the spinal cord and brain stem to the
bones, ligaments, and joints between bodies of the cervical vertebrae.
Cervical lordosis can be seen, as can the relationship of the anterior and
posterior longitudinal ligaments to intervertebral disks and ligaments at
the craniovertebral junction.
Eight total cervical nerve roots are present as the dorsal and
ventral roots converge to form the spinal nerve within the
vertebral foramen. Cervical nerve roots enter the interver­
tebral foramina by passing over the top of the corresponding
pedicle, except the C8 cervical nerve, which lies between
C7 and T1. Therefore, C5-C6 posterolateral disk herniation
will affect the C6 nerve root. The nerve root occupies
approximately one-third of the foramen (Figure 45-4).
Space available for the nerve root is decreased with neck
extension and degenerative changes, and is increased with
neck flexion.
The anterior spinal artery arises from the vertebral arter­
ies and supplies most of the spinal cord, excluding the pos­
terior columns. The posterior columns receive their blood
supply from the two posterior spinal arteries, which origi­
nate from the inferior cerebellar artery or the vertebral
arteries. The vertebral arteries arise from the subclavian
arteries and course through the C6 transverse foramen
cephalad, passing anterior to the emerging cervical nerve
root at each level. They pass behind the lateral mass of C1
and enter the foramen magnum, where they rejoin to form
the basilar artery. Diseases such as dissection of the vessel
can be associated with severe neck pain, and impairment of
blood flow through the vertebral artery can result in poste­
rior circulation signs such as nystagmus, vertigo, drop
attacks, dysarthria, and visual impairment. These symptoms
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PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
Posterior longitudinal ligament
Sinuvertebral nerves
Sympathetic ganglion
Anterior ramus
Rami communicantes
Posterior ramus
Dorsal root ganglion
Ligamentum flavum
are often associated with head position, and a critical reduc­
tion in blood flow can result in a cerebellar infarction.
The cervical spine is the most mobile segment of the
spine; an approximate 90-degree arc of motion occurs in
flexion and extension, three-quarters of which is due to
extension (Table 45-1). The maximal range of motion in
the sagittal plane within the subaxial spine is seen at the
C5-C6 level, making this a common site of disk degenera­
tion. Rotation encompasses approximately 80 to 90 degrees
of motion, and 50% of this occurs at the atlantoaxial joint.
As is seen with extension, rotation reduces the crosssectional area of the spinal canal. The cervical spine dem­
onstrates 30 degrees of lateral mobility in each direction;
this typically occurs with some degree of rotation secondary
to the orientation of the facet joints.
AXIAL NECK PAIN
Axial neck pain may originate from any tissue that receives
innervation, including zygoapophyseal joints, cervical disks,
vertebral periosteum, posterior neck muscles, cervical dura
mater, occipito-atlantoaxial joints, and vertebral arteries.
Sources may include degenerative, traumatic, malignant,
infectious, or systemic inflammatory processes. Zygoapophy­
seal joints and cervical disks have the greatest quantity of
direct supporting data suggesting these sites as the origin of
Table 45-1 Age and Normal Cervical Movement
Age (yr)
<30
31-50
>50
FlexionExtension
(degrees)
Lateral
Rotation
(degrees)
Lateral
Flexion
(degrees)
90
70
60
90
90
90
45
45
30
Figure 45-4 Cervical spine neural elements. Localized
cervical pain is mediated primarily through the posterior
primary ramus and the recurrent meningeal (sinuvertebral) nerves, which supply structures within the spinal
canal. The recurrent meningeal nerves arise from rami
communicantes and enter the spinal canal via intervertebral foramina; branches ascend and descend one or
more levels, interconnecting with recurrent meningeal
nerves from other levels, and innervating, among other
structures, the anterior and posterior longitudinal ligaments, the anterior and posterior portions of the dura,
and blood vessels. (From Levin KH, editor: Neck and back
pain: continuum 7 (no. 1), Philadelphia, 2002, Lippincott
Williams & Wilkins, p 9.)
axial neck pain. Provocative injection into the facet joint
in asymptomatic volunteers invokes a reproducible pattern
of occipital or axial neck pain.12 This pattern of pain can
be accurately diagnosed and treated for at least a short time
with anesthetic injections targeted at the joint capsule
itself, or with blockage of the respective dorsal primary
ramus.13-15 Degenerative arthritis within the upper cervical
spine can manifest as suboccipital headaches denoted as
cervicogenic headaches, which are thought to result from irri­
tation of the greater occipital nerve. Typically, arthritis
within the atlanto-occipital joints is made worse by pro­
vocative neck flexion and extension, whereas atlantoaxial
arthritis is made worse by rotation. This is supported by
investigators who injected asymptomatic volunteers at the
atlanto-occipital and atlantoaxial joints, reproducing this
pattern of pain.16 Relief of suboccipital pain may be attained
with fluoroscopically guided injection of corticosteroid into
the diseased joint, or fusion of these joints in recalcitrant
cases.
The cervical disk is a controversial source of axial neck
pain, which occurs as the result of insult to the highly
innervated annulus fibrosus. This idea is based on provoca­
tive diskography, whereby a diseased disk is fluoroscopically
injected to a given pressure, and pain is reproduced in reli­
able patterns. In a true-positive or concordant study, an adja­
cent normal disk should not produce pain when injected.
Using this method, several studies have implicated cervical
disks as the source of axial neck pain.17-19 Even with careful
technique, a false-positive result can occur, and it is not
unusual to have a nonconcordant study in which multiple
disks elicit a pain response despite being normal.17 Interven­
tions directed at treating the disk for isolated axial neck
pain have been found to be unpredictable, although the
cervical disk is likely to contribute to axial neck pain.
Myofascial pain due to irritation of the muscles about the
neck can contribute to axial neck pain. Patients with
CHAPTER 45 chronic myofascial pain have been shown to have a lower
level of high-energy phosphates in involved muscle tissue.20
Myofascial pain can be the original source of neck pain or,
more commonly, a manifestation of postural adaptations
and compensatory overuse of normal tissue that remains
after the injured structure heals. A more generalized form
of this is fibromyalgia, a widespread disorder defined by
diffuse pain affecting all four quadrants of the body, with at
least 11 of 18 pressure points noted as positive. Patients
have associated symptoms of fatigue, cognitive difficulties,
and irritable bowel syndrome, and a nondermatomal pattern
of dysesthesias, weakness, and paresthesias.21
Systemic inflammatory arthropathies causing neck pain
typically demonstrate the classic pattern of morning stiff­
ness, polyarticular involvement, rigidity, and associated
cutaneous manifestations. Rheumatoid arthritis (RA) often
involves the cervical spine, initially causing stiffness and
later causing pain, potentially leading to instability. After
the hands and feet, the cervical spine is the most common
site of disease involvement in RA.22 The upper cervical
spine is most commonly involved (occiput to C2), followed
by the subaxial cervical spine (C3-C7). The likelihood of
developing cervical spine pathology can be predicted by the
extent of rheumatoid changes that occur in the hands and
feet. Basilar invagination is one such manifestation, whereby
C1 lateral masses erode, allowing the odontoid peg to settle
into the foramen magnum, placing pressure on the brain
stem with potential for instantaneous death. The atlanto­
axial joint can demonstrate instability with potential for
neurologic injury. Because of these potentially catastrophic
complications, dynamic radiographs of the cervical spine
should be obtained before any procedure requiring intuba­
tion is performed. Seronegative spondyloarthropathies that
can manifest with neck pain include ankylosing spondylitis,
psoriatic arthritis, and reactive arthritis. In 70% of patients,
psoriatic arthritis will manifest with skin lesions before
arthritis develops; reactive arthritis rarely involves the cer­
vical spine.
Ankylosing spondylitis often affects the entire axial skel­
eton and is seen as limited lumbar motion and chest expan­
sion with later involvement of the cervical spine. In
progressive patterns, the cervical spine takes on a kyphotic
deformity. As the spine fuses, it biomechanically becomes
similar to a long bone; minor trauma with neck pain should
be taken very seriously in these patients. Even in the face
of negative plain radiographs, patients should be worked up
extensively with strict spine precautions and with neutral
alignment varying with the baseline spinal curvature; fre­
quent neurologic evaluations should be performed to check
for development of an epidural hematoma.
Infection and neoplasms can cause axial neck pain
through bone destruction with irritation of vertebral body
periosteal nerves and altered biomechanics of the facet
joints and cervical disks. The onus is upon the clinician to
identify these patients at the initial visit because a delay in
diagnosis can have catastrophic consequences. Red flags for
axial neck pain that require further workup at the initial
presentation include elderly patients, patients with a history
of malignancy, immunocompromised patients, and those
with fever, chills, unexplained weight loss, fatigue, night­
time awakening, recent antecedent bacteremia, and severe
nonmechanical neck pain.21
| Neck Pain
629
Patients who have undergone previous cervical spine
surgery should be evaluated for the presence of pseudoar­
throsis or iatrogenic instability. Pseudoarthrosis is failure of
an attempted arthrodesis or fracture to fully heal with bridg­
ing bone. Patients will describe a “honeymoon” period,
whereby they did well for 3 to 6 months following surgery.
Patients then develop worsening axial neck and interscapu­
lar pain with associated headaches. This can be diagnosed
on plain radiographs with evidence of hardware loosening
or movement on dynamic images. Computed tomography
(CT) scanning with coronal and sagittal reconstructions
should be done to more definitively diagnose a pseudoar­
throsis. Once pseudoarthrosis has been diagnosed, a surgical
consult should be obtained, the patient should be counseled
on smoking cessation given the deleterious effects of nico­
tine and carbon monoxide on bone healing, and a bone
metabolic workup should be undertaken. An additional
cause of neck pain following surgery is iatrogenic instability,
whereby the surgery itself creates pathologic motion. This
requires a surgical consultation to determine whether stabi­
lization is warranted.
RADICULOPATHY AND MYELOPATHY
The clinician must determine whether there is evidence of
nerve root compression, termed radiculopathy, versus spinal
cord compression, termed myelopathy. Cervical spondylosis
with changes within the disk may cause loss of height with
posterior bulging of the disk into the spinal canal and
foramen. As the disk collapses, the posterior soft tissue
structures, including the ligamentum flavum and the facet
joint capsule, fold inward, further compromising the spinal
canal and neural foramen. Pressure that once was dispersed
throughout the disk is transferred to the facet joints and
uncinate processes, resulting in the development of bone
overgrowth or osteophytes and causing extrinsic pressure on
the nerve root or spinal cord.
In radiculopathy, mechanical distortion of the nerve
leads to increased vascular permeability, resulting in chronic
edema and eventually fibrosis. This causes hypersensitivity
of the nerve root with an inflammatory response mediated
by chemicals released from the cell bodies of sensory neurons
and cervical disks.23 Compression of the dorsal root gan­
glion is felt to be especially important in producing radicular
pain.24 Clinically, this presents with pain in a dermatomal
distribution; dermatomes for the higher cervical nerve roots,
including C3 and C4, are found along the posterior scapula,
and the pain should not be confused with isolated axial neck
pain.25 Minor symptoms that are tolerable may be treated
with conservative care, but persistent compression on a
nerve root can lead to sensory loss and weakness. Disabling
deficits should be treated operatively given that prolonged
nerve compression can result in irreversible changes. In
patients without a neurologic deficit, it is reasonable to
expect a good outcome with conservative care.26
Myelopathy has a clinical presentation of long tract signs
resulting from compression of the spinal cord. Factors that
contribute to the development of myelopathy include a
congenitally narrow spinal canal, dynamic cord compres­
sion, dynamic thickening of the spinal cord, and vascular
changes. The anterior-posterior diameter in the subaxial
spine for a normal adult measures 17 to 18 mm. The cord
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PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
measures 10 mm, and diameters less than 13 mm are con­
sidered to be congenitally stenotic. The shape of the spinal
cord deformity has a strong association with the develop­
ment of myelopathy; patients with a banana-shaped cord on
axial views had evidence of myelopathy 98% of the time.27
Ono and associates described a ratio whereby the anteriorposterior diameter of the spinal cord is divided by the trans­
verse diameter of the cord. Patients with a ratio of less than
0.40 tended to have severe neurologic deficits.28 Patients
may have dynamic cord compression with signs and symp­
toms of myelopathy only during neck flexion and extension.
The space available for the cord is decreased during neck
extension owing to infolding of the ligamentum flavum and
overlapping of the lamina. In addition, the spinal cord
shortens during neck extension, effectively increasing the
diameter and making it more prone to compression by pos­
terior structures. In flexion, the cord lengthens and drapes
over anterior degenerated disks and osteophytes.29
Myelopathy can be exacerbated by altered biomechanics
from degenerated segments, as when a given level stiffens,
the level above can become hypermobile.30 A certain subset
of patients can develop myelopathy in the absence of
mechanical compression; this has been attributed to isch­
emic insult.31 It has been shown in a canine model that in
the setting of spinal cord compression, additive ischemia
results in significantly worse outcomes, because over time
the spinal cord demonstrates permanent irreversible
changes.32 Patients with mild cases of myelopathy that does
not affect activities of daily living can be closely followed.33
Those with more severe deficits or progressive deficits tend
to deteriorate over time with conservative care, and it is
recommended these patients should undergo surgery to
decompress the spinal cord.34
CLINICAL FEATURES
In terms of functional anatomic pathways, neck pain is
mediated via somatic or autonomic pathways.35 Somatic
pain is the most common, being perceived in dermatomes,
myotomes, or sclerotomes. Pain originating in the auto­
nomic pathway, or in the sympathetic nervous system, may
fall into somatic segmental distributions, vascular supply
distributions, peripheral nerve distributions, or noncon­
forming patterns. Because pain mediation pathways may
have significant overlap, additional clinical information
regarding characteristics of neck pain, along with diagnostic
studies, complements the determination of pain origin
when localization based on functional anatomy is not
sufficient.
Patient History
Neck pain is the most common symptom of cervical spine
pathology; correctly characterizing it helps to identify con­
ditions requiring immediate treatment. Important charac­
teristics to note include onset, distribution, frequency,
duration, quality, and aggravating factors, as well as the
presence of neurologic symptoms other than pain. In
general, pain that is present only intermittently may be
indicative of instability or motion, whereas constant and
increasing pain evokes concern regarding a mass effect.
New-onset and relatively short duration generalized neck
pain is likely related to benign pathology such as muscle
strain, whereas a longer duration of symptoms indicates
significant or progressive pathology. Well-localized pain
indicates specific nerve root irritation, whereas poorly
defined pain may derive from irritation of deep connective
tissue structures such as muscle, joint, bone, or disk. Aggra­
vating and relieving factors may help elucidate biomechani­
cal changes in the cervical spine that are contributing to
the symptoms.
Localized axial neck pain is commonly reported as origi­
nating posteriorly with extension into the shoulder or
occiput. Localized pain of myofascial origin may worsen
with neck flexion, whereas diskogenic neck pain will worsen
with neck extension or rotation. Pain referred to the occiput
usually indicates pathologic changes in the upper cervical
spine and may radiate down the neck and to the ear. Shoul­
der girdle pain develops secondary to postural adaptations
from initial neck pain symptoms. It is not uncommon for
pain to be referred from the shoulder, heart, lungs, viscera,
or temporomandibular joint to the neck region as the result
of overlapping nerve distribution. Symptoms may arise
owing to irritation or activation of receptors directly, as is
seen in articular pain, pseudoarticular pain, vascular and
cervicogenic headaches, pseudo–angina pectoris, eye and
ear symptoms, and throat symptoms.
Articular symptoms arise from innervation to the facet
and uncovertebral joints causing local pain and stiffness.
Patients often state that their symptoms are made worse
with inactivity and describe feelings of clicking, grating, or
“sand” in the neck. Pseudoarticular pain may be felt in the
shoulder and elbow, with true pathology originating from
the neck. Vascular symptoms result from compression of the
vertebral artery by osteophytes or a protruding disk. Symp­
toms may intensify with neck movement or with certain
postures. Tenosynovitis and tendinitis may involve the
rotator cuff and tendons about the elbow, wrist, or hand.
Stenosis or fibrosis of tendon sheaths or palmar fascia may
be present, along with trigger points over the affected joints,
giving a false impression of local pathology.36
Localization of Pain Generators
Pain may be somatic or autonomic and is not always felt in
precise anatomic zones. Overlapping sensory supplies may
be present, as well as radiation in spinal segments by recruit­
ment within the spinal column, causing difficulty in local­
ization. Somatic pain is caused by cervical nerve root
irritation. It is the most common type of pain, and diabetic
patients are more susceptible to this nerve root irritation.
Neurologic deficits correspond with the offending disk level
in 80% of patients.37 Neuralgic and myalgic pain describes
symptoms related to compression of different areas of the
nerve root. Neuralgic pain originates from irritation of the
dorsal sensory root and has a “lightning” or “electric” sensa­
tion, which tends to be dermatomal and associated with
numbness and paresthesia. Pain tends to present more prox­
imally and paresthesia more distally. Myalgic pain occurs
with irritation of the ventral motor root. This pain is
described as a deep, boring, unpleasant sensation that tends
to be poorly localized because of its referral to sclerotomal
areas. These sensations conform to the areas of muscles
present that are innervated by the compressed nerve root.
CHAPTER 45 | Neck Pain
631
Table 45-2 Cervical Nerve Root Segments and Corresponding Clinical Signs and Symptoms
Nerve Root
Symptom
Correlate
C3
C4
Suboccipital pain with extension to the back of the ear
Pain from caudad aspect of the neck to superior aspect of the
shoulder
Numbness over shoulder and down lateral aspect of arm to
midportion. Deltoid muscle may be weak, and biceps reflex,
which is innervated by C5-C6, may be affected.
Radiating pain and numbness down the lateral aspect of arm and
forearm to the thumb and IF (“six shooter”). Weakness in wrist
extension, elbow flexion, and supination. Diminished
brachioradialis and biceps reflex.
Numbness and pain down the posterior aspect of arm and forearm
to LF. Weakness in the triceps, wrist flexion, and finger extensors.
If C3, C4, and C5 are all involved, may cause
paradoxical breathing
C5
C6
C7
C8
T1
Pain and numbness down the medial aspect of arm and forearm
into the small ring finger. Weakness in the FDP to IF and LF and
FPL.
Sensory component can mimic carpal tunnel
syndrome
Most frequent. Entrapment of posterior interosseous
nerve can mimic motor component; however, no
sensory deficits are present.
AIN entrapment can mimic motor component of C8
or T1; however, sensory changes and involvement
of thenar muscles will not be present.
Ulnar nerve entrapment will spare short thenar
muscles with exception of ADP. Does not involve
FPL or FDP to IF and LF.
ADP, adductor pollicis; AIN, anterior interosseous nerve; FDP, flexor digitorum profundus; FPL, flexor pollicis longus; IF, index finger; LF, long finger..
Autonomically mediated symptoms result in dizziness, blur­
ring of vision, tinnitus, retro-ocular pain, and facial and
jaw pain.
It is important to determine whether axial neck pain is
isolated, or if radiating pain, weakness, changes in sensa­
tion, or alterations in proprioception are associated. Com­
pression of a nerve root often can be localized by identifying
the distribution of pain, paresthesias, or weakness as they
follow the segmental distribution of that respective nerve
root (Table 45-2). Sensory loss may be characterized by the
patient in precise terms with a description of numbness, or
alternatively may consist of vague symptoms of swelling or
bogginess to the skin. If the face, head, or tongue is involved,
the upper three nerve roots of the cervical plexus may be
affected. Numbness of the neck, shoulder, arm, forearm, or
fingers indicates involvement of C5-T1. Weakness, as
occurs with sensory changes, appears in a graded fashion,
depending on the amount of compression upon the nerve
root. This event will present clinically with an obvious
functional deficit or more subtle findings, made obvious
only by repetitive testing. The clinician must be attuned to
these subtle complaints of weakness, which may be described
by the patient as a feeling of heaviness of the limbs, early
fatigue, or insufficient power grip. If obvious atrophy is
present in a muscle, more than one nerve root is affected as
a result of the evolutionary benefit of multiple levels of
innervation for a given muscle. Alterations in propriocep­
tion are due to compression of the dorsal column of the
spinal cord. This will be described by the patient as symp­
toms of clumsiness, with complaints of tripping or dropping
objects. This is a matter of concern for the more ominous
condition of myelopathy, which may occur secondary to
spinal cord compression.
Cervical spinal disease classically causes isolated axial
neck pain or radicular pain that radiates to the shoulder or
down the upper extremity (Table 45-3). However, less com­
monly, it can be the cause of headache, pseudo–angina
pectoris, and otolaryngologic sensations. Cervicogenic
occipital headaches can be compounded by adaptive
changes in the posterior occipital muscles, often spreading
to the eye region and manifesting as dull rather than pulsat­
ing pain. These headaches are unique in that they
are aggravated by neck movements. Patients typically
have migraine-like symptoms such as phonophobia or
photophobia.
Pseudo–angina pectoris has been reported as the result
of cervical spinal disease and may be confused with angina
pectoris or breast pain in women (Figure 45-5). In the pres­
ence of a C6-C7 lesion, neuralgic or myalgic pain may be
noted, along with tenderness in the precordium or scapular
region. Heart disease is differentiated from symptoms associ­
ated with C6-C7 dysfunction on the basis of muscle weak­
ness, fasciculations, or sensory or reflex changes.
Differentiation of these two pathologies may be difficult
when true angina and pseudoangina coexist in the same
patient.38
Cervical spinal disease may manifest in the form of eye,
ear, and throat symptoms (see Figure 45-5). Eye and ear
symptoms may arise from irritation of the plexuses surround­
ing the vertebral and internal carotid arteries. Eye symp­
toms can present as blurring of vision relieved by changing
neck position, increased tearing, orbital and retro-orbital
pain, or descriptions of eyes being “pulled backward” or
“pushed forward.” Altered equilibrium with associated gait
disturbances may result from irritation of the surrounding
sympathetic plexus or from vertebral insufficiency. Hearing
can be affected, with tinnitus and altered auditory acuity
Table 45-3 Cervical Pain Referral Pathways
Location of Pain
Upper posterolateral cervical region
Occipital region
Upper posterior cervical region
Middle posterior cervical region
Lower posterior cervical region
Suprascapular region
Superior angle of scapula
Midscapular region
Source
C0-C1, C1-C2, C2-C3
C2-C3, C3
C2-C3, C3-C4, C3
C3-C4, C4-C5, C4
C4-C5, C5-C6, C4, C5
C4-C5, C5-C6, C4
C6-C7, C6, C7
C7-T1, C7
632
PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
Temporomandibular
joint
Chondrosternal
joint
Hiatal hernia
with complications
Cardiac
disease
Cystic duct stone
Pancreatic disease
Esophageal
hernia
Gastric ulcer
Gallbladder
disease
A
Duodenal ulcer
with or without
perforation
Gastric ulcer
Duodenal ulcer
Tail of pancreas
B
Gallbladder;
common duct
stone
Lesions of
mediastinum
and lung
Perforated
peptic ulcer
involving
pancreas
Hiatal hernia
Costochondral
junction
separation
Temporomandibular joint
Gallbladder Pancreas
Head of pancreas
Gallbladder
Figure 45-5 Patterns of referred pain. Patterns of reflex-referred pain from visceral and somatic structures. A, Anterior distribution. B, Posterior
distribution.
reported. Throat symptoms, including dysphagia, may be
related to anterior vertebral osteophytes causing direct com­
pression, as well as to cranial nerve and sympathetic nerve
communications.
Symptoms of dyspnea and cardiac arrhythmia and drop
attacks may have a cervical spinal origin. Dyspnea can be
related to a deficit in C3-C5 innervation of the diaphragm.
Cardiac palpitations and tachycardia secondary to cervical
spine pathology can be differentiated from those associated
with other causes by the fact that these symptoms are associ­
ated with unusual positions or hyperextension of the neck.
This is caused by irritation of C4 innervation of the dia­
phragm and pericardium, or by irritation of the cardiac
sympathetic nerve supply. Drop attacks suggest posterior
circulation insufficiency, resulting in an abrupt loss of pro­
prioception without loss of consciousness.
Myelopathy, or spinal cord compression, initially pre­
sents with subtle complaints of hand clumsiness or difficulty
with balance. Patients will report worsening handwriting in
the past few months or difficulty buttoning shirts. Patients
may have nausea and emesis caused by equilibrium dysfunc­
tion. Paresthesias and dysesthesias may be present, often
involving bilateral upper extremities and not following a
dermatomal distribution. This is often mistaken for periph­
eral neuropathy or carpal tunnel syndrome but should be
considered when bilateral extremity symptoms are present.
As the disease progresses over time, more advanced mani­
festations include weakness in the triceps, hand intrinsics,
and hip flexors most commonly. Late manifestations include
spasticity, as well as bowel and bladder dysfunction.
Finally, neck pain may present concomitant with sys­
temic disease with varied symptoms requiring further inves­
tigation. Examples include inflammatory arthritides,
infection or tumor, multiple sclerosis, subacute combined
degeneration, and syrinx. Inflammatory arthritides often
present with morning stiffness, polyarticular involvement,
or cutaneous manifestations. Fever, weight loss, or night
pain points to an infectious or neoplastic origin. A Pancoast
tumor is a neoplastic process of the apical portion of the
lung that can cause a mass effect on the caudad cervical
nerve roots. This should always be considered in a person
with radicular symptoms and a history of smoking, with
workup including a chest x-ray. Idiopathic brachial plexus
neuritis, formerly known as Parsonage-Turner syndrome, is
caused by viral infection of the brachial plexus presenting
with severe arm pain involving multiple nerve roots. Once
the acute phase resolves, patients are left with variable defi­
cits. Subacute combined degeneration from vitamin B12
deficiency is a consideration when sensory deficit is greater
in the lower extremities.
Clinical Examination
A careful clinical examination provides additional focus to
the differential diagnosis. The clinical examination begins
broadly with observation of the patient’s gait, as well as head
and neck posture. Further palpation, range-of-motion
testing, and neurologic examination for motor signs, reflexes,
sensory signs, autonomic signs, and articular signs are per­
formed (Table 45-4).
Careful palpation with knowledge of key anatomic bony
and soft tissue landmarks in the cervical spine may localize
pain to a particular cervical level and location. Anteriorly
or anterolaterally, the transverse process of C1 is palpated
between the angle of the jaw and the styloid process. C3 is
identified by palpation of the hyoid bone. C4-C5 is at the
level of the thyroid cartilage, and C6 is at the level of the
cricoid ring and the carotid tubercle. In the process of exam­
ining the neck, also note the sagittal balance with retention
or loss of normal cervical lordosis. Posteriorly and
CHAPTER 45 | Neck Pain
633
Table 45-4 Nerves and Tests of Principal Muscles
Nerve
Nerve Roots
Muscle
Test
Accessory
Spinal
Trapezius
Spinal
Sternocleidomastoid
Pectoralis major
Clavicular part
Sternocostal part
Serratus anterior
Rhomboid
Supraspinatus
Infraspinatus
Latissimus dorsi
Deltoid
Biceps
Brachialis
Triceps
Brachioradialis
Extensor carpi radialis longus
Supinator
Extensor digitorum
Extensor carpi ulnaris
Extensor indicis
Abductor pollicis longus
Extensor pollicis longus
Extensor pollicis brevis
Pronator teres
Flexor carpi radialis
Flexor digitorum superficialis
Flexor digitorum profundus
(lateral part)
Flexor pollicis longus (anterior
interosseous nerve)
Abductor pollicis brevis
Flexor pollicis brevis
Opponens pollicis
1st and 2nd lumbricals
Elevation of shoulders
Abduction of scapula
Tilting of head to same side with rotation to opposite side
Brachial plexus
Axillary
Musculocutaneous
Radial
Posterior
interosseous
Median
C5, C6
C7, C8, T1
C5, C6, C7
C4, C5
C4, C5, C6
(C4), C5, C6
C6, C7, C8
C5, C6
C5, C6
C6, C7, C8
C5, C6
C6, C7
C5, C6
C7, C8
C7, C8
C7, C8
C7, C8
C7, C8
C7, C8
C6, C7
C6, C7
C7, C8, T1
C8, T1
C8, T1
C8, T1
C8, T1
C8, T1
C8, T1
Ulnar
C7, C8
C8, T1
C8, T1
C8, T1
Flexor carpi ulnaris
Flexor digitorum profundus
(medial part)
Hypothenar muscles
3rd and 4th lumbricals
C8, T1
C8, T1
C8, T1
Adductor pollicis
Flexor pollicis brevis
Interossei
posterolaterally, the occiput, inion, superior nuchal line,
mastoid processes, and spinous processes of C2 and C7-T1
are palpable.
Soft tissues about the anterior and posterior triangles of
the neck, occipital region, and posterior paraspinal muscles
are examined. The sternocleidomastoid muscle is involved
with whiplash injury, whereby abrupt hyperextension of the
neck occurs. The muscle may be tender to palpation, or the
patient may be splinting the neck with the head turned
away from the injured muscle. This posturing of the neck is
termed torticollis, and the clinician should remember that
the head is turned away from the side of the involved ster­
nocleidomastoid. Flexion injury may traumatize the trape­
zius muscle. Midline cervical tenderness is more of a concern
with ligament injury, whereas paraspinal muscle tenderness
typically is a more benign process.39 The greater occipital
nerves are located lateral to the inion and may be involved
in traumatic inflammation associated with flexion or
Adduction of arm
Adduction, forward depression of arm
Fixation of scapula during forward thrusting of the arm
Elevation and fixation of scapula
Abduction of arm initiated
External rotation of arm
Adduction of horizontal, externally rotated arm, coughing
Lateral and forward elevation of arm to horizontal
Flexion of supinated forearm
Extension of forearm
Flexion of semiprone forearm
Extension of wrist to radial side
Supination of extended forearm
Extension of proximal phalanges
Extension of wrist to ulnar side
Extension of proximal phalanx of index finger
Abduction of first metacarpal in plane at right angle to palm
Extension of first interphalangeal joint
Extension of first metacarpophalangeal joint
Pronation of extended forearm
Flexion of wrist to radial side
Flexion of middle phalanges
Flexion of terminal phalanges, index and middle fingers
Flexion of distal phalanx, thumb
Abduction of first metacarpal in plane at right angle to palm
Flexion of proximal phalanx, thumb
Opposition of thumb against 5th finger
Extension of middle phalanges while proximal phalanges are
fixed in extension
Observation of tendons during testing of abductor digiti minimi
Flexion of distal phalanges of ring and little fingers
Abduction and opposition of little finger
Extension of middle phalanges while proximal phalanges are
fixed in extension
Adduction of thumb against palmar surface of index finger
Flexion of proximal phalanx, thumb
Abduction and adduction of fingers
extension injury resulting in suboccipital headaches. Skin
markings or visible trauma should be noted at this time.
Range-of-motion examination may reveal pain or limita­
tions in flexion-extension, lateral bending, and rotation.
Flexion limitation may be assessed by the examiner placing
fingers between the patient’s chin and sternum at maximum
flexion with 50% of the motion occurring at the occiput-C1
joint and the remaining 50% distributed over C2-C7. If the
patient is unable to place the chin on the chest, the interval
should be measured. One fingerwidth shows a limitation of
10 degrees, whereas three fingerwidths indicates a 30-degree
limitation in flexion. On extension, the distance between
the base of the occiput and the spinous process of T1 should
be measured. Lateral flexion should allow the ear to touch
the shoulder with motion being shared across all cervical
vertebrae. On rotation, the chin should touch the shoulder
with 50% of rotation occurring at C1-C2, and the remain­
ing 50% distributed in the subaxial spine between C3 and
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PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
C7. A natural decrease in range of motion occurs with age,
even in the healthy individual.40
Range-of-motion tests the ligaments, capsules, and fascia;
this motion will be reduced in the presence of cervical
spinal muscular spasm or pain. Patients with degenerative
changes in the cervical spine will have pain with decreased
range of motion of the cervical spine without resistance.
The most common findings due to changes in cervical spine
articulations are as follows (in order): restriction of move­
ment with or without pain, pain on movement, and local
tenderness. Lateral flexion is the earliest and most impaired
movement in degenerative diseases; rotation is first impaired
in rheumatoid arthritis owing to involvement of the odon­
toid peg. A uniformly stiff neck may be caused by diffuse
idiopathic skeletal hyperostosis (DISH), present in a quarter
of elderly patients, but also may be due to ankylosing spon­
dylosis or recent trauma to the neck.41 If articular signs are
found, the examiner must evaluate the entire vertebral
column and peripheral joints for evidence of further arthri­
tis and to search for extra-articular manifestations.
Motion against resistance testing is performed after
active and passive range of motion is established. Muscle
groups tested include the flexors and extensors of the neck.
In testing flexor muscles, a hand is placed between the
forehead and the chest. The primary flexor is the sterno­
cleidomastoid muscle; secondary flexors include the three
scalene muscles and the small prevertebral muscles. Exten­
sors are tested by placing a hand on the shoulder and head
for resistance. Primary extensors include the paravertebral
extensor mass, splenius, semispinalis capitis, and trapezius.
Secondary flexors include the small intrinsic muscles of the
neck. Rotators are examined by placing a hand on the
shoulder and chin for resistance. The sternocleidomastoid
muscle and the intrinsic muscles of the neck provide rota­
tional force. Motion against resistance testing should
include active maximum effort strength testing to the
extremes of flexion, extension, and rotation to assess muscle
Ophthalmic
Mandibular
C6
V
V
Maxillary
C2
V
V
C3
C4
T2
T3
T4
T5
C5
strength. Causes of decreased range of motion of the cervi­
cal spine include joint locking and bony ankylosis resulting
from degenerative changes or arthritides, fibrous contrac­
tures, muscle spasm, splinting over painful joints, and nerve
root or spinal cord compression or irritation. Decreased
range of motion in the presence of pain or weakness war­
rants further investigation.
Sensation for light touch, pin prick, temperature, and
proprioception should be performed. These tests are admit­
tedly subjective; therefore both extremities should be com­
pared to assess differences in sensation. Comparing an
unaffected area such as the face with the area of decreased
sensation can also be helpful. Pin prick can be performed
by using a sterile needle and temperature by using an alcohol
pad to assess the function of the spinothalamic tract that
traverses the anterolateral aspect of the spinal cord. Light
touch and proprioception assess the function of the poste­
rior spinal column.
Dermatomes are anatomically distributed as noted in
Figure 45-6. The lower extremities demonstrate a unique
dermatomal map that correlates with embryologic develop­
ment, whereby the limb starts in a supinated position and
pronates with longitudinal growth. Perineal sensation and
rectal tone are important to examine because an abnormal­
ity may indicate compression of the spinal cord or cauda
equina, requiring immediate surgical intervention. Isolating
the level of pathology at times can be challenging. Nerve
roots with proximal compression are more susceptible to
distal compression in a phenomenon termed double crush.
The cervical spine should always be considered as the
potential source in patients who present with symptoms of
carpal or cubital tunnel syndrome and peripheral neuropa­
thy. Ancillary imaging and nerve conduction studies can
help elucidate the origin.
After palpation, range-of-motion testing, and assessment
of sensation, muscle strength testing is continued for local­
ization of any positive findings. Lower motor neuron disease
C2,C3
V
C2
V
C2
C4 C3
C5
C3
C6
T1
T2
T2
T3
T3
T4
T4
T5
T5
C5
T2
C6
T1
C3
T1
C4
T2
T3
T4
T5
V
C2,C3
C5
C6
C5
T2
T1
T1
C7
C6
C7
C8
C7
C6
C8
C8
C6
C7
Figure 45-6 Dermatome distributions. Dermatome distribution of nerve fibers from C1 through T5, carrying senses of pain, heat, cold, vibration, and
touch to the head, neck, arm, hand, and thoracic area. The sclerotomes and myotomes are similar but show some overlap. Pain arising from structures
deep to the deep fascia (myotome and sclerotome) does not precisely follow the dermatome distribution.
CHAPTER 45 Table 45-5 Strength Grading in Motor Examination
0
1
2
3
4
5
No function with total paralysis
Trace movement with palpable or visible contraction
Full range of joint motion with gravity eliminated
Active movement against gravity
Active movement against slight resistance
Normal strength
is indicated by weakness, hypotonia, and fasciculations.
Upper motor neuron disease is indicated by spasticity. Motor
function should be graded using the standard 0 to 5 nomen­
clature, with grade 0 having no function, 1 having trace, 2
having full range of joint motion with gravity eliminated, 3
having antigravity function, 4 having function against
slight resistance, and 5 having normal strength against resis­
tance (Table 45-5). If weakness is present, a more focused
examination should be performed to look at other muscles
innervated by that same nerve root.
Deep tendon stretch reflexes should be performed and
graded 0 to 3 with 0 being no response, 1 being hyporeflex­
ive, 2 being normal, and 3 being hyperreflexive. C5 is tested
by striking the biceps tendon; C6, brachioradialis; C7,
triceps; L4, patellar tendon; and S1, Achilles tendon. To
facilitate reflex testing, it may be helpful to use muscle
loading or Jendrassik’s maneuver (performed by having the
patient flex both sets of fingers into a hook-like form, inter­
locking the hands, and pulling apart). This creates a diver­
sion to help relax the patient and better assess lower
extremity reflexes. If difficulty with reflex testing persists,
ensure that no peripheral neuropathy is present. In addition
to deep tendon reflex testing, the abdominal reflex, the
Babinski test, and the bulbocavernosus test should be
assessed.
Provocative tests that can be helpful in confirming com­
pressive extradural monoradiculopathy include Spurling’s
test, the arm abduction test, and the axial compression and
traction test. All of these tests are meant to change the
diameter of the neural foramen, thus increasing or decreas­
ing the symptoms, respectively. Spurling’s test is performed
by having the patient extend his or her neck and rotate
toward the side of pain. The test is positive if radicular pain
is made worse in this position; this indicates foraminal ste­
nosis with potential compression of a nerve root. The arm
abduction sign is positive if the patient’s pain is relieved by
placing the hand on the affected side, on top of the head.42
The axial compression test is performed by pressing on top
of the patient’s head with the neck in neutral position; the
result is positive if radicular symptoms are exacerbated by
this maneuver and are relieved by placing traction on the
head and opening up the foramina.
Provocative tests that are helpful in diagnosing myelopa­
thy include the presence of Hoffmann’s sign, the finger
escape sign, the abnormal grip-release test, and Lhermitte’s
sign. Hoffmann’s sign is performed by holding the middle
finger extended and suddenly extending the distal interpha­
langeal joint, leading to flexion of the index finger and
thumb if pathologic. A positive finger escape sign occurs
when an individual cannot hold all fingers in an adducted
and extended position without the ulnar two digits falling
into flexion and abduction over time. The grip-release test
is an inability to rapidly open and close a fist caused by
weakness and spasticity of the hand. Lhermitte’s sign
| Neck Pain
635
evaluates for changes in the spinal cord itself and occurs
when the patient’s neck is forcefully flexed, resulting in
electric-like shocks that travel down the arms and legs. This
indicates changes in the white matter of the spinal cord and
may occur secondary to cervical myelopathy or multiple
sclerosis.
DIAGNOSTIC EVALUATION
After the history and clinical examination are completed,
imaging studies, neurophysiologic procedures, and labora­
tory studies may aid in completing the differential diagnosis
and building a treatment plan for the patient’s neck pain.
Cervical radiographs often show degenerative changes in
asymptomatic individuals in their 60s.43 In the absence of
trauma, constitutional symptoms, or worsening neurologic
deficit, 4 to 6 weeks of conservative care is indicated before
radiographs are obtained.44 Dynamic radiographs should
also be used for screening patients with rheumatoid arthritis
before endotracheal intubation, given the risk of cervical
instability. One study demonstrated that 61% of patients
with RA had evidence of instability defined by at least
3 mm of atlantoaxial subluxation on preoperative screening
x-rays.45
In the presence of significant degenerative changes and
end plate osteophytes, CT myelography can be helpful in
further characterizing bony involvement. CT myelography
should be thought of as a complementary test to magnetic
resonance imaging (MRI).46 It should be used as the primary
test to evaluate neural involvement only when MRI is con­
traindicated, because MRI is superior for evaluating spinal
cord changes such as syringomyelia, myelomalacia, or neo­
plasm.47 MRI scanning is indicated for progressive neuro­
logic deficit, disabling weakness, or long tract signs and is
recommended for patients with persistent cervical radicu­
lopathy after 6 weeks of conservative care.44 The addition
of gadolinium contrast enhancement is helpful in evaluat­
ing infection and neoplasm, and in differentiating scar from
recurrent disk herniation in patients who have undergone
previous spinal surgery. MRI results must be correlated with
physical examination findings given that asymptomatic vol­
unteers have been found to have abnormal cervical spine
MRI.48 Increased signal on T2 sequence can be representa­
tive of a spectrum of disease from edema to myelomalacia
and syrinx formation. Therefore the presence of increased
signal within the spinal cord warrants a surgical consulta­
tion, and operative intervention, or close follow-up at a
minimum, is provided if examination and history correlate.
If MRI findings do not correlate with the history and physi­
cal examination findings, additional studies such as CT
myelography may be required. CT myelography is superior
for detecting bony foraminal stenosis. Nuclear bone scan­
ning techniques, including single-photon emission com­
puted tomography (SPECT) scans, have been used to
identify and characterize acuity in occult fracture, periosteal
injury, and posttraumatic osteoarthritis in the absence of
positive radiograph findings.49
Neurophysiologic procedures are indicated when the
clinical examination and imaging studies fail to correlate,
or when there is conflicting information. Electromyography
(EMG), nerve conduction studies (NCSs), and somatosen­
sory evoked responses (SERs) help differentiate cervical
636
PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
spine disorders from peripheral nerve entrapment syndromes
and help in differentiating intrinsic joint pathology from a
radiculopathy. These tests are complementary to plain
radiographs and an MRI or CT myelogram.
Neck pain typically occurs secondary to mechanical
causes, and laboratory studies generally are not helpful in
its diagnosis. However, laboratory studies can be critical in
ruling out infection, neoplasm, and systemic arthritides.
Erythrocyte sedimentation rate (ESR) indirectly measures
the acute phase response with high sensitivity but low speci­
ficity. Patients younger than age 50 should have an ESR less
than 20 mm/hr, with the accepted normal range increasing
as the patient ages. Values above 100 are seen with infection
and neoplasm, whereas less dramatic elevations are seen
with rheumatoid arthritis and following surgery.50 C-reactive
protein (CRP) is an acute phase reactant synthesized by the
liver; elevations peak by day 2 of the inciting event and
return to normal within 3 to 7 days of removal of the
insult.51 Complete blood count (CBC) with differential and
spinal tap can be helpful if meningitis is a concern.
DIFFERENTIAL DIAGNOSIS AND
TREATMENT
By using the history, physical examination findings, and
diagnostic studies, it is helpful to divide the differential
diagnosis into benign axial neck pain, radiculopathy,
myelopathy, infection, neoplasm, systemic arthritides, and
referred pain. Most axial neck pain is self-limiting and will
resolve with appropriate conservative care.52 Axial neck
pain with associated radiculopathy has a fairly benign
course; 75% of patients have only one recurrence or mild
symptoms at 19 years’ follow-up with conservative treat­
ment.53 Patients with isolated neck pain and a negative
radiographic and laboratory workup are best treated with a
multimodal approach. During the acute phase, patients can
be treated with a soft collar to reduce inflammation, but this
should not be worn for longer than 2 weeks so as to avoid
deconditioning. Multimodal treatments, including proprio­
ceptive training, exercise with resisted strengthening,
muscle relaxers during the acute period, and nonsteroidal
anti-inflammatory drugs (NSAIDs), have been found to be
most effective in treating axial neck pain.54-59 Evidence is
inconclusive as to the effectiveness of radiofrequency dener­
vation of facet joints, acupuncture, transcutaneous electri­
cal nerve stimulation (TENS) treatment, iontophoresis,
EMG biofeedback, or local injections for treatment of axial
neck pain.60-63
Cervical traction may be prescribed; a typical regimen
includes 8 to 10 pounds for sessions of 15 to 20 minutes with
the device at 20 to 25 degrees of flexion. However, this has
resulted in only short-term relief of radicular symptoms.64
Fluoroscopically guided interlaminar and transforaminal
epidural steroids have been shown to be effective in treating
lumbar radiculopathy, but this has not been shown in the
cervical spine.65 Cervical injections carry a higher risk, with
complications, including neurologic deficits, reported in up
to 16% of patients.66,67 Given these increased risks with
epidural steroid injections in the cervical spine, a more
conservative approach should be taken in prescribing this
treatment modality. Atlantoaxial facet joint osteoarthritis
may be treated successfully with a facet block and nonste­
roidal anti-inflammatory medications. If conservative
therapy with NSAIDs fails, a fusion may be indicated.
In addition to degenerative changes to the cervical spine,
trauma, and acute disk herniation, more insidious causes of
neck pain include schwannoma, Pancoast tumor, brachial
plexus neuritis, and complex regional pain syndrome.
Schwannomas, if intradural, may involve a sensory nerve
root, causing dermatomal pain in addition to a myelopathy
or radiculopathy from compression. Pancoast tumor involv­
ing the lung apex may cause caudal cervical nerve root and
sympathetic changes, in addition to nerve root or brachial
plexus compression. Brachial plexus neuritis (ParsonageTurner syndrome) is of viral origin, causing severe arm pain
followed by weakness and then pain resolution; return of
arm strength follows. This condition may progress to
complex regional pain syndrome, along with autonomic
changes such as discoloration of the skin, in a small number
of cases associated with diffuse burning pain.
Follow-up and vigilance are in order because a progres­
sive neurologic deficit, segmental instability, or persistent
radicular symptoms for at least 6 weeks may be indications
for surgical intervention. In a prospective randomized study
comparing surgery, physical therapy, and cervical collar use
for long-standing cervical radiculopathy, no difference was
found between the three groups at 12 months.68 Cervical
myelopathy with very mild deficits can be followed closely;
however, the natural course of the illness consists of long
periods of stability with episodes of deterioration. Definitive
indications for surgery include the presence of myelopathy
for 6 months or longer, progression of signs or symptoms,
difficulty walking, or changes in bowel or bladder function.
Surgery is directed at decompressing the spinal cord and
preventing further deterioration, rather than improving
neurologic deficits.
Systemic arthritides, infection, and tumors can affect the
cervical spine with variable neurologic and constitutional
symptoms. Rheumatoid arthritis typically causes atlanto­
axial subluxation, atlantoaxial impaction, and subaxial sub­
luxation (Table 45-6). Surgical stabilization is indicated
Table 45-6 Rheumatologic Disorders Causing
Neck Pain
Rheumatoid arthritis
Without disease of the C1-C2 joint
With structural cervical abnormalities
C1-C2 subluxation
C1-C2 facet involvement
Spondyloarthropathies
Ankylosing spondylitis
Reactive arthritis
Psoriatic arthritis
Enteropathic arthritis
Polymyalgia rheumatica
Osteoarthritis
Fibromyalgia
Nonspecific musculoskeletal pain
Miscellaneous spondyloarthropathies
Whipple’s disease
Behçet’s disease
Paget’s disease
Acromegaly
Ossification of the posterior longitudinal ligament
Diffuse idiopathic skeletal hyperostosis
CHAPTER 45 with progressive neurologic deficit, persistent axial neck
pain with radiographic evidence of instability, canal diam­
eter of 14 mm or less (posterior atlanto-dens interval), and
odontoid migration of 5 mm or greater above McGregor’s
line. In the setting of atlantoaxial subluxation or subaxial
subluxation, the involved levels are fused posteriorly, and
atlantoaxial impaction should be treated with occipitocer­
vical fusion.9 Rheumatoid patients with evidence of insta­
bility demonstrate radiographic progression over time, but
this correlates poorly with neurologic outcome.69 Regard­
less, these patients require close follow-up given that once
myelopathy develops, most patients die within 1 year.70
Ankylosing spondylitis commonly affects the cervical
spine, resulting in a kyphotic deformity over time with
altered biomechanics; this has implications in the setting of
trauma. The kyphotic deformity can have significant func­
tional implications because the person’s gaze moves toward
the floor, making interaction with the surrounding world
difficult. Corrective osteotomies are available, but risks
include neurologic deficit and intraoperative bleeding.
Hopefully, earlier diagnosis with the use of MRI and treat­
ment with tumor necrosis factor–blocking agents will help
make cervical deformity a thing of the past.71
Both infection and neoplastic processes can cause
destruction with mechanical or nonmechanical neck pain,
constitutional symptoms, and variable neurologic deficit.
The goals of treatment are similar in both with eradication
of the infection or tumor, decompression if a neurologic
deficit exists, and stabilization of the spinal column.
In summary, a careful history and physical examination
and ancillary studies will help one arrive at a fairly narrow
differential diagnosis. In the absence of spinal instability,
neurologic deficit, and infectious or neoplastic processes,
the patient may benefit from conservative treatment with
expectant recovery with a “tincture of time.”
References
1. Nachemson AL, Waddell G, Norhlund AI: Neck and back pain: the
scientific evidence of causes, diagnosis, and treatment, Baltimore, 2000,
Lippincott Williams & Wilkins, pp 172–173.
2. Andersson HI, Ejlertsson G, Leden I, Rosenberg C: Chronic pain in
a geographically defined general population: studies of differences in
age, gender, social class, and pain localization, Clin J Pain 9:174–182,
1993.
3. Hansson EK, Hansson TH: The costs for persons sick-listed more
than one month because of low back or neck problems: a two-year
prospective study of Swedish patients, Eur Spine J 14:337–345,
2005.
4. Mäkelä M, Heliövaara M, Sievers K, et al: Prevalence, determinants,
and consequences of chronic neck pain in Finland, Am J Epidemiol
134:1356–1367, 1991.
5. Freeman MD, Croft AC, Rossignol AM, et al: A review and methodo­
logic critique of the literature refuting whiplash syndrome, Spine
24:86–96, 1999.
6. Honeyman PT, Jacobs EA: Effects of culture on back pain in Austra­
lian Aboriginals, Spine 21:841–843, 1996.
7. Klekamp J, McCarty E, Spengler DM: Results of elective lumbar dis­
cectomy for patients involved in the workers’ compensation system,
J Spinal Disord 11:277–282, 1998.
8. Daniels DL, Williams AL, Haughton VM: Computed tomography of
the articulations and ligaments at the occipito-atlantoaxial region,
Radiology 146:709–716, 1983.
9. Kim DH, Hilibrand AS: Rheumatoid arthritis in the cervical spine,
J Am Acad Orthop Surg 13:463–474, 2005.
10. Bogduk N, Windsor M, Inglis A: The innervation of the cervical
intervertebral discs, Spine 13:2–8, 1988.
11. Nachemson AL: Disc pressure measurements, Spine 6:93–97, 1981.
| Neck Pain
637
12. Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain pat­
terns. I. A study in normal volunteers, Spine 15:453–457, 1990.
13. Bogduk N, Marsland A: The cervical zygapophyseal joints as a source
of neck pain, Spine 13:610–617, 1988.
14. Aprill C, Dwyer A, Bogduk N: Cervical zygapophyseal joint pain pat­
terns. II. A clinical evaluation, Spine 15:458–461, 1990.
15. Cavanaugh JM, Lu Y, Chen C, Kallakuri S: Pain generation in lumbar
and cervical facet joints, J Bone Joint Surg Am 88:63–67, 2006.
16. Dreyfuss P, Michaelsen M, Fletcher D: Atlantooccipital and lateral
atlanto-axial joint pain patterns, Spine 19:1125–1131, 1994.
17. Bogduk N, Aprill C: On the nature of neck pain, discography and
cervical zygapophysial joint pain, Pain 54:213–217, 1993.
18. Grubb SA, Kelly KC: Cervical discography: clinical implications from
12 years of experience, Spine 25:1382–1389, 2000.
19. Schellhas KP, Smith MD, Gundry CR, Pollei SR: Cervical discogenic
pain: prospective correlation of magnetic resonance imaging and dis­
cography in asymptomatic subjects and pain sufferers, Spine 21:
300–312, 1996.
20. Bengtsson A, Henriksson KG, Larsson J: Reduced high-energy phos­
phate levels in the painful muscles of patients with primary fibromy­
algia, Arthritis Rheum 29:817–821, 1986.
21. Dryer SJ: Laboratory evaluation in neck pain, Phys Med Rehabil Clin
North Am 14:589–604, 2003.
22. Crockard HA: Surgical management of cervical rheumatoid problems,
Spine 20:2584–2590, 1995.
23. Cooper RG, Freemont AJ, Hoyland JA, et al: Herniated intervertebral
disc-associated periradicular fibrosis and vascular abnormalities occur
without inflammatory cell infiltration, Spine 20:591–598, 1995.
24. Chabot MC: The pathophysiology of axial and radicular neck pain,
Semin Spine Surg 7:2–8, 1995.
25. An HS, editor: An atlas of surgery of the spine: anterior cervical spine
procedures, London, 1998, Martin Dunitz Ltd.
26. Truumees E, Herkowitz HN: Cervical spondylotic myelopathy and
radiculopathy, Am Acad Orthop Surg Instruct Course Lect 29:339–360,
2000.
27. Houser OW, Onofrio BM, Miller GM, et al: Cervical spondylotic
stenosis and myelopathy: evaluation with computed tomographic
myelography, Mayo Clin Proc 69:557–563, 1994.
28. Ono K, Tada K, Yamamoto T: Cervical myelopathy secondary to mul­
tiple spondylotic protrusions: a clinicopathologic study, Spine 2:
109–125, 1977.
29. Breig A, Turnbull I, Hassler O: Effects of mechanical stresses on the
spinal cord in cervical spondylosis, J Neurosurg 25:45–56, 1966.
30. Mihara H, Ohnari K, Hachiya M, et al: Cervical myelopathy caused
by C3-C4 spondylosis in elderly patients: a radiographic analysis of
pathogenesis, Spine 25:796–800, 2000.
31. Ferguson RJ, Caplan LR: Cervical spondylotic myelopathy, Neurol Clin
3:373–382, 1985.
32. Gooding MR, Hoff WC: Experimental cervical myelopathy: effect of
ischemia and compression of the canine cervical spinal cord, J Neurosurg 43:9–17, 1975.
33. Nurick S: The pathogenesis of the spinal cord disorder associated with
cervical spondylosis, Brain 95:87–100, 1972.
34. Sampath P, Bendebba M, Davis JD, Ducker TB: Outcome of patients
treated for cervical myelopathy: a prospective, multicenter study with
independent clinical review, Spine 25:670–676, 2000.
35. Romanelli P, Esposito V: The functional anatomy of neuropathic pain,
Neurosurg Clin N Am 15:257–268, 2004.
36. Mackley RJ: Role of trigger points in the management of head, neck,
and face pain, Funct Orthod 7:4–14, 1990.
37. Henderson CM, Hennessy RG, Shuey HM Jr, Shackelford EG:
Posterior-lateral foraminotomy as an exclusive operative technique for
cervical radiculopathy: a review of 846 consecutively operated cases,
Neurosurgery 13:504–512, 1983.
38. Frøbert O, Fossgreen J, Søndergaard-Petersen J, et al: Musculo-skeletal
pathology in patients with angina pectoris and normal coronary angio­
grams, J Intern Med 245:237–246, 1999.
39. Hoffman JR, Mower WR, Wolfson AB, et al: National emergency
x-radiography utilization study group validity of a set of clinical criteria
to rule out injury to the cervical spine in patients with blunt trauma,
N Engl J Med 343:94–99, 2000.
40. Sforza C, Grassi G, Fragnito N, et al: Three-dimensional analysis of
active head and cervical spine range of motion: effect of age in healthy
male subjects, Clin Biomech 17:611–614, 2002.
41. Weinfeld RM, Olson PN, Maki DD, Griffiths HJ: The prevalence of
diffuse idiopathic skeletal hyperostosis (DISH) in two large American
638
PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
Midwest metropolitan hospital populations, Skeletal Radiol 26:222–
225, 1997.
42. Davidson RI, Dunn EJ, Metzmaker JN: The shoulder abduction test
in the diagnosis of radicular pain in cervical extradural compressive
monoradiculopathies, Spine 6:441–446, 1981.
43. Gore DR, Sepic SB, Gardner GM: Roentgenographic findings of the
cervical spine in asymptomatic people, Spine 11:521–524, 1986.
44. Levine MJ, Albert TJ, Smith MD: Cervical radiculopathy: diagnosis
and nonoperative management, J Am Acad Orthop Surg 4:305–316,
1996.
45. Collings DN, Fitz Randolph RL: Cervical spine instability in rheuma­
toid patients having total hip or knee arthroplasty, Clin Orthop
272:127–135, 1991.
46. Modic MT, Masaryk TJ, Mulopulos GP, et al: Cervical radiculopathy:
prospective evaluation with surface coil MR imaging, CT with metri­
zamide, and metrizamide myelography, Radiology 161:753–759, 1986.
47. Modic MT, Ross JS, Masaryk TJ: Imaging of degenerative disease of
the cervical spine, Clin Orthop Relat Res (239):109–120, 1989.
48. Boden SD, McCowin PR, Davis DO, et al: Abnormal magneticresonance scans of the cervical spine in asymptomatic subjects, J Bone
Joint Surg Am 72:1178–1184, 1990.
49. Seitz JP, Unguez CE, Corbus HF, Wooten WW: SPECT of the cervical
spine in the evaluation of neck pain after trauma, Clin Nucl Med
20:667–673, 1995.
50. Waddell G: An approach to backache, Br J Hosp Med 28:187–190,
1982.
51. Kushner HL: Acute phase response, Clin Aspects Autoimmunity 3:20–
30, 1989.
52. Gore DR, Sepic SB, Gardner GM, Murray MP: Neck pain: a long-term
follow-up of 205 patients, Spine 12:1–5, 1987.
53. Saal JS, Saal JA, Yurth EF: Nonoperative management of herniated
cervical intervertebral disc with radiculopathy, Spine 21:1877–1883,
1996.
54. Beebe FA, Barkin RL, Barkin S: A clinical and pharmacologic review
of skeletal muscle relaxants for musculoskeletal conditions, Am J Ther
12:151–171, 2005.
55. Bronfort G, Evans R, Nelson B, et al: A randomized clinical trial of
exercise and spinal manipulation for patients with chronic neck pain,
Spine 26:788–799, 2001.
56. Gross AR, Kay T, Hondras M, et al: Manual therapy for mechanical
neck disorders: a systematic review, Man Ther 7:131–149, 2002.
57. Kay TM, Gross A, Goldsmith C, et al: Exercises for mechanical neck
disorders, Cochrane Database Syst Rev (3):CD004250, 2005.
58. Taimela S, Takala EP, Asklöf T, et al: Active treatment of chronic neck
pain, Spine 25:1021–1027, 2000.
59. Waling K, Sundelin G, Ahlgren C, Jarvholm B: Perceived pain before
and after three exercise programs: a controlled clinical trial of women
with work-related trapezius myalgia, Pain 85:201–207, 2000.
60. Dagenais S, Haldeman S, Wooley JR: Intraligamentous injection of
sclerosing solutions (prolotherapy) for spinal pain: a critical review of
the literature, Spine J 5:310–328, 2005.
61. Irnich D, Behrens N, Molzen H, et al: Randomised trial of acupuncture
compared with conventional massage and “sham” laser acupuncture
for treatment of chronic neck pain, Br Med J 322:1574–1578, 2001.
62. Kroeling P, Gross AR, Goldsmith CH: A Cochrane review of
electrotherapy for mechanical neck disorders, Spine 30:E641–E648,
2005.
63. Niemisto L, Kalso E, Malmivaara A, et al: Radiofrequency denervation
for neck and back pain: a systematic review of randomized controlled
trials, Cochrane Database Syst Rev (1):CD004058, 2003.
64. Carette S, Fehlings MG: Clinical practice: cervical radiculopathy, N
Engl J Med 353:392–399, 2005.
65. Riew KD, Yin Y, Gilula L, et al: The effect of nerve-root injections on
the need for operative treatment of lumbar radicular pain: a prospec­
tive, randomized, controlled, double-blind study, J Bone Joint Surg Am
82:1589–1593, 2000.
66. Abbasi A, Malhotra G, Malanga G, et al: Complications of interlami­
nar cervical epidural steroid injections: a review of the literature
[Review], Spine 32:2144–2151, 2007.
67. Malhotra G, Abbasi A, Rhee M: Complications of transforaminal
cervical epidural steroid injections, Spine 34:731–739, 2009.
68. Persson LC, Carlsson CA, Carlsson JY: Long-lasting cervical radicular
pain managed with surgery, physiotherapy, or cervical collar, Spine
22:751–758, 1997.
69. Pellicci PM, Tsairis P, Bryan WJ: A prospective study of the progression
of rheumatoid arthritis of the cervical spine, J Bone Joint Surg Am
63:342–350, 1981.
70. Marks JS: Rheumatoid cervical myelopathy, Q J Med 50:301–319,
1989.
71. Mansour M, Cheema GS, Naquwa SM, et al: Ankylosing spondylitis:
a contemporary perspective on diagnosis and treatment, Semin Arthritis
Rheum 36:210–223, 2006.
The references for this chapter can also be found on www.expertconsult.com.