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- •Contributors
- •Preface
- •Acknowledgments
- •Contents
- •2 Undifferentiated Problems
- •2.1 Anorexia
- •2.2 Dizziness
- •2.5 Fatigue
- •2.6 Fever
- •2.3 Edema
- •2.4 Falls
- •2.7 Headaches
- •2.8 Hypersomnia
- •2.9 Insomnia
- •2.10 Nausea and Vomiting
- •2.11 Night Sweats
- •2.12 Syncope
- •3 Mental Health Problems
- •3.1 Anxiety
- •3.2 Bipolar Disorder
- •3.3 Depression
- •3.4 Suicide Risk
- •4.1 Ataxia
- •4.2 Coma
- •4.3 Delirium
- •4.4 Dementia
- •4.5 Memory Impairment
- •4.7 Seizures
- •4.8 Stroke
- •4.9 Tremors
- •5 Eye Problems
- •5.1 Blurred Vision
- •5.3 Diplopia
- •5.4 Loss of Vision
- •5.5 Nystagmus
- •5.6 Papilledema
- •5.7 Pupillary Inequality
- •5.8 Red Eye
- •5.9 Scotoma
- •6.1 Halitosis
- •6.2 Hearing Loss
- •6.3 Hoarseness
- •6.4 Nosebleed
- •6.5 Pharyngitis
- •6.6 Rhinitis
- •6.7 Stomatitis
- •6.8 Tinnitus
- •6.9 Vertigo
- •7 Cardiovascular Problems
- •7.1 Atypical Chest Pain
- •7.2 Anticoagulation
- •7.3 Chest Pain
- •7.4 Bradycardia
- •7.5 Cardiomegaly
- •7.6 Congestive Heart Failure
- •7.7 Diastolic Heart Murmurs
- •7.8 Systolic Heart Murmurs
- •7.9 Hypertension
- •7.10 Palpitations
- •7.11 Pericardial Friction Rub
- •7.12 Raynaud’s Disease
- •7.13 Tachycardia
- •8 Respiratory Problems
- •8.1 Cough
- •8.2 Cyanosis
- •8.3 Hemoptysis
- •8.4 Pleural Effusion
- •8.5 Pleuritic Pain
- •8.6 Pneumothorax
- •8.7 Shortness of Breath
- •8.8 Stridor
- •8.9 Wheezing
- •9 Gastrointestinal Problems
- •9.1 Abdominal Pain
- •9.2 Ascites
- •9.3 Constipation
- •9.4 Diarrhea
- •9.5 Dysphagia
- •9.6 Epigastric Distress
- •9.8 Hepatitis
- •9.9 Hepatomegaly
- •9.10 Jaundice
- •9.11 Rectal Bleeding
- •9.12 Steatorrhea
- •10 Renal and Urologic Problems
- •10.1 Dysuria
- •10.2 Hematuria
- •10.4 Urinary Incontinence
- •10.5 Nocturia
- •10.8 Scrotal Mass
- •10.10 Urethral Discharge
- •11.1 Amenorrhea
- •11.2 Breast Mass
- •11.3 Chronic Pelvic Pain
- •11.4 Dysmenorrhea
- •11.5 Dyspareunia
- •11.6 Menorrhagia
- •11.8 Pap Smear Abnormality
- •12 Musculoskeletal Problems
- •12.1 Arthralgia
- •12.2 Calf Pain
- •11.10 Vaginal Discharge
- •12.3 Hip Pain
- •12.4 Knee Pain
- •12.5 Low Back Pain
- •12.6 Monoarticular Joint Pain
- •12.7 Neck Pain
- •12.8 Polymyalgia
- •12.9 Shoulder Pain
- •13 Dermatologic Problems
- •13.1 Alopecia
- •13.2 Erythema Multiforme
- •13.3 Maculopapular Rash
- •13.4 Pigmentation Disorders
- •13.5 Pruritus
- •13.7 Urticaria
- •14.1 Diabetes Mellitus
- •14.2 Gynecomastia
- •14.3 Hirsutism
- •14.4 Hypothyroidism
- •14.5 Polydipsia
- •14.7 Thyroid Nodule
- •15.3 Petechiae and Purpura
- •15.4 Splenomegaly
- •16.1 Anemia
- •16.2 Eosinophilia
- •16.4 Neutropenia
- •16.5 Polycythemia
- •16.6 Proteinuria
- •16.7 Thrombocytopenia
- •17.5 Elevated Creatinine
- •17.6 D-Dimer
- •17.7 Hypercalcemia
- •17.8 Hyperkalemia
- •17.9 Hypokalemia
- •18.1 Abnormal Mammogram
- •18.2 Bone Cyst
- •18.3 Mediastinal Mass
- •18.4 Osteopenia
- •Index

2. Musculoskeletal
a. Inspection. Inspect the contour and shape of the back, looking for scoliosis, lordo-
sis, spasm, and muscle wasting. Assess the range of motion of the spine and lower
extremities through flexion, extension, and lateral flexion. Perform the straight leg
raising (SLR) test passively with the patient supine. Note the angle of leg elevation
precipitating pain. A positive test for sciatica is buttock pain radiating to the posterior
thigh and perhaps to the lower leg and foot. The SLR test is usually negative in spinal
stenosis (4).
b. Palpation. Palpation and percussion of the spine and upper pelvis help identify areas of
localized tenderness, as seen in myofascial conditions, fracture, metastatic disease, and
some inflammatory conditions. Include an examination of the hip and sacroiliac joint.
3. Neurologic. Neurologic examination is especially important in the presence of pares-
thesia, weakness, and radiating pain. Assess strength by having the patient walk on their
heels (L5), walk on their toes (S1), and testing for specific nerve root motor, sensory,
and reflex function for each lumbar level. The lower extremity examination includes
motor strength, deep tendon reflexes, sensation, proprioception, and certain functional
maneuvers (see Table 12.5.3). Romberg and Babinski reflexes may also be assessed.
Rectal examination may be done to assess sphincter tone, which can be compromised
in sacral root dysfunction. In the primary care setting, most clinically significant disc
herniations are detected by the following limited examination: dorsiflexion of the great
toe and ankle, Achilles reflex, light touch sensation of the medial (L4), dorsal (L5), and
lateral (S1) aspect of the foot, and the SLR test (1, 3).
C. Testing
1. Clinical Laboratory Tests
a. Testing is influenced by the differential diagnosis after the history and physical
examination. The majority of low back pain evaluations do not require laboratory
or imaging evaluation. In the presence of “red flag” indicators, tests may include
urinary examination, complete blood count, erythrocyte sedimentation rate, elec-
trolytes, including serum calcium, serum alkaline phosphatase, or prostate-specific
antigen. Pain suspected to be caused by a “red flag” condition may also require other
urgent tests (3).
b. Specific tests for inflammatory conditions (such as rheumatoid arthritis or ankylos-
ing spondylitis) or infections may also be needed if indicated from history and
examination.
2. Diagnostic Imaging. In low-risk patients, diagnostic imaging is unlikely to be helpful. A
posteroanterior and lateral radiograph of the lumbosacral spine may be used to delineate
bony structure and alignment but does not provide diagnostic information regarding
many serious causes of back pain. Patients with a potential “red flag” condition, such
TABLE 12.5.3 Neurologic Findings Seen with Disc Herniation
Disc pain/numbness Motor weakness Functional maneuver Reflex
L3–4/anteromedial
thigh and knee
Quadriceps Deep knee bends
↓ Patellar
L4–5/lateral leg, first
three toes
Dorsiflexion of foot or great toe Heel walking
↓ Achilles
L5–S1/posterior leg,
lateral heel
Plantar flexion of foot or
great toe
Toe walking
From Davis S. Low back pain. In: Taylor RB, ed. Musculoskeletal problems. The 10 minute
diagnosis manual. Philadelphia, PA: Lippincott Williams & Wilkins, 2006.
278
Taylor’s DifferenTial Diagnosis Manual

as spinal trauma, or suspected cauda equina syndrome may require computed tomogra-
phy scanning and/or magnetic resonance imaging (MRI). MRI is usually the preferred
modality if available and the patient is stable. A bone scan may be used when tumor or
infection is suspected. Electromyography may rarely be useful to assess for nerve root
dysfunction when symptoms are questionable. Persistent, chronic pain may require
further diagnostic imaging.
IV. DIAGNOSIS
A.
The most common cause of low back pain in primary care is myofascial dysfunction
with subsequent muscle spasm. The physical examination reveals limitation of motion
of the affected area, with tenderness and increased tone in the affected muscle groups.
Spondylolisthesis (displacement of a vertebra in relation to the vertebra below) typically
presents in adolescence, particularly in athletes. Low back pain, loss of lumbar lordosis,
and a palpable “step off” are classic findings. Lumbar degenerative disc disease may present
in older age groups, with localized or radicular pain due to nerve root compression. Pain
radiating below the knee is more likely to be a true radiculopathy.
B. Aching, throbbing pain of insidious onset that is worse in the morning and is unrelieved by
rest and worse at night suggests an inflammatory origin of the pain. A deep, dull pain, with
intermittent stiffness relieved by rest and worse after activity or the end of the day associated
with a precipitating event or a previous history of back pain suggests mechanical origin.
Increased pain from standing or walking suggests spinal stenosis, whereas pain on sitting is
often due to disc disease. Pain and stiffness in the morning suggest inflammatory disease,
whereas continuous pain is more suggestive of neoplasm or infection. Mechanical disease
often coexists with inflammatory disease, resulting in a more complicated mixed pattern.
REFERENCES
1. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back
pain? JAMA 1992;268:760–765.
2. Van Tudler MW, Assendelft WJ, Koes BW, et al. Spinal radiographic findings and nonspecific low
back pain. A systematic review of observational studies. Spine 1997;22:427–434.
3. Casazza BA. Diagnosis and treatment of acute low back pain. Am Fam Physician 2012;85(4):343–350.
4. McCoy, R. (2007). Low Back Pain. In P. M. Paulman, A. A. Paulman, & J. D. Harrision, Taylor’s
10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter (2nd ed.,
pp. 279–282). Philadelphia: Lippincott Williams & Wilkins.
12.6
Monoarticular Joint Pain
David Patchett
I. BACKGROUND. Pain in a single joint is a common presenting complaint.
II. PATHOPHYSIOLOGY
A. Etiology.
Monoarticular joint pain has many etiologies. Acute monoarticular joint pain
is most commonly due to trauma, infection, osteoarthritis, or crystal-induced conditions.
Other causes of monarticular joint pain are rheumatic diseases and neoplasm. Further,
pain may arise from bursae, ligaments, and tendons or be referred from myofascial trigger
points.
B. Epidemiology. Musculoskeletal complaints account for greater than 315 million outpa-
tient clinic visits per year and 20% of outpatient visits in the United States (1); 49.9 million
(22%) Americans older than age 18 years report having arthritis (2). This is expected to rise
to 67 million (25%) Americans by 2030 (3).
Chapter 12 • Musculoskeletal Problems
279

III. EVALUATION
A. History.
It is important to first determine whether the joint pain is acute or chronic. Acute
monoarthritis is defined as an inflammatory process that develops over the course of a few
days or has been present for less than 2 weeks (4). If the joint pain is acute, then determine
if the pain stems from trauma. A history of trauma or an inability to bear weight indicates
the possibility of fracture, dislocation, or soft tissue injury. Of note, there may be a history
of minimal or no trauma in patients with fractures secondary to osteoporosis (5). Excessive
use of a joint or a rapid increase in physical activity may indicate a stress fracture (6).
Atraumatic acute monoarthritis is most commonly associated with crystals or infection.
In young adults, disseminated gonococcal infection is the most common cause (5). Gout
occurs most commonly in males, affects the first metatarsophalangeal joint, ankle, mid foot,
or knee (5). Pseudogout is most common in the elderly and is indistinguishable in presenta-
tion to gout in the acute setting (7). Both present with joint pain, erythema, and decreased
joint range of motion (ROM).
Risk factors for septic arthritis include intravenous drug use, immunosuppression, and
sexual activity (8). Constitutional symptoms such as fevers, chills, and rigors present in
57%, 27%, and 19% of patients, respectively (9). These symptoms may also be present in
acute crystal joint disease.
Other atraumatic causes of monoarticular joint pain include degenerative joint disease,
rheumatic disease, and malignancy (see Table 12.6.2).
B. Physical Examination
1. A general physical examination is important. Vital sign abnormalities can point to
infection or systemic disease as the cause of joint pain. Elements of the musculoskeletal
physical examination should always include inspection, palpation, ROM, and special
tests. When evaluating an individual for joint pain, you must first determine if the source
is articular or arising from the periarticular soft tissue. Joint pain commonly results from
TABLE 12.6.1 Diagnoses Consistent with Findings from Synovial Fluid
Analysis
Condition Appearance
White blood
cells/mm
Polymor-
ph onuclear
neutrophils
(%)
Glucose
(% serum
level)
Crystals under
polarized light
Normal Clear
<200 <25
95–100 None
Noninflammatory
(e.g.,
Degenerative
joint disease
(DJD))
Clear
<400 <25
95–100 None
Acute gout Turbid 2,000–5,000
>75
80–100 Negative birefringence;
needle-like crystals
Pseudogout Turbid 5,000–50,000
>75
80–1,000 Positive birefringence;
rhomboid crystals
Septic arthritis Purulent/
turbid
>50,000 >75 <50
None
Inflammatory
(e.g., rheuma-
toid arthritis)
Turbid 5,000–50,000 50–75
∙75
None
Adapted from Roberts JR, Hedges JR, eds. Clinical procedures in emergency medicine, 3rd ed.
Philadelphia, PA: WB Saunders, 1998.
280
Taylor’s DifferenTial Diagnosis Manual

tendonitis or bursitis. Pain may also be referred from myofascial trigger points (10).
Asking the patient to point with one finger to the exact site of pain can be helpful.
Intra-articular problems cause restriction in both active and passive ROM, whereas
periarticular problems favor restrictions in active ROM. In tendonitis or bursitis, pain is
elicited with joint motion against resistance (5).
2. Erythema, edema, and warmth signal inflammation of a joint. This can be due to infec-
tion, crystal-induced disease, trauma, or rheumatic conditions (11). Crepitus of a joint
indicates a derangement of bone, cartilage, or menisci (12).
C. Testing. Laboratory testing with a complete blood count, sedimentation rate, or C-reactive
protein can help to distinguish inflammatory from noninflammatory disorders. Uric acid
levels may be helpful in diagnosing and monitoring gout (1). Other lab tests such as anti-
nuclear antibody and rheumatoid factor are useful if there is a high degree of suspicion of a
specific diagnosis.
1. Arthrocentesis is indicated when there is a warm, red joint with effusion, especially when
there is no history of trauma (13). Absence of fever does not exclude the presence of a
septic joint and should not influence this decision (14). Synovial fluid should be sent
for the “3 Cs”: cell count, culture (Gram’s stain), and crystals. Table 12.6.1 reviews the
diagnoses consistent with findings on synovial fluid analysis.
2. Plain radiographs remain the initial imaging of choice in most bone and joint disorders.
X-rays should be ordered for patients with chronic pain, suspected arthritits, chondro-
calcinosis, fractures, or dislocations. Computed tomography is helpful at detecting occult
fractures and other bony abnormalities (15). Magnetic resonance imaging (MRI) is
superior at detecting septic arthritis and meniscal, tendinous, and ligamentous injuries.
3. MRI with gadolinium injection (MRI arthrography) can visualize intra-articular struc-
tures. This modality is used commonly to detect labral tears of the hip and shoulder.
IV. DIAGNOSIS
A. Differential Diagnosis.
Table 12.6.2 illustrates the differential diagnosis for monoarticular
joint pain (16).
TABLE 12.6.2 Differential Diagnosis of Joint Pain
Trauma Infection Other
Sprain Gonococcal Reflex sympathetic dystrophy
Strain Nongonococcal: viral,
mycobacterial, or fungal
Sjögren’s syndrome
Fracture Lyme disease Polymyositis
Dislocation Subacute bacterial endocarditis Scleroderma
Tear of ligament, tendon, or
meniscus
Secondary to enteric and
urogenital infections
Sarcoidosis
Tendinitis Fibromyalgia
Erythema nodosum
Sickle cell disease
Aseptic necrosis
Charcot’s disease
Drug reaction
Hypothyroidism
Irritable bowel syndrome
Osteochondritis dissecans
(Continued)
Chapter 12 • Musculoskeletal Problems
281

B. Clinical Manifestations
1. Osteoarthritis is a common cause of monoarticular joint pain in older patients. It occurs
most commonly in large weight-bearing joints or joints used repetitively. It may manifest
initially or during flares as monoarticular joint pain and is usually worse at the end of
the day or after prolonged weight-bearing. There may be some swelling, usually without
erythema or warmth in the affected joint.
3. Gout occurs rapidly over hours to days and often during the night. An affected great toe
may be tender, swollen, and erythematous. Affected joints are often exquisitely tender.
4. Septic arthritis typically presents with fever, joint pain, swelling, and erythema. Absence
of fever should not preclude joint aspiration. Infants may present atypically with non-
specific symptoms such as irritability, fever, crying with movement of the hip (as with
diaper changes), or refusal to bear weight.
REFERENCES
1. Longo DL, Fauci AS, Kasper DL, et al., eds. Harrison’s principles of internal medicine, 18th ed. New
York, NY: McGraw-Hill, 2012.
2. Bolen J, Schieb L, Hootman JM, et al. Differences in the prevalence and impact of arthritis among
racial/ethnic groups in the United States, National Health Interview Survey, 2002, 2003, and 2006.
Prev Chronic Dis 2010;7(3):A64.
3. Hootman JM, Helmick CG. Projections of U.S. prevalence of arthritis and associated activity limita-
tions. Arthritis Rheum 2006;54(1):226–229.
4. Sack K. Monarthritis: differential diagnosis. Am J Med 1997;102:30S.
5. Civa C, Valazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical
approach for the family physician. Am Fam Physician 2003;68:83–90.
6. Reeder M, Dick B, Atkins J, et al. Stress fractures. Current concepts of diagnosis and treatment. Sports
Med 1996;22(3):198–212.
7. Rosenthal, AK. Pseudogout: presentation, natural history, and associated conditions. In: Wortmann
RL, Schumacher HR Jr, Becker MA, Ryan LM, eds. Crystal-induced arthropathies. Gout, pseudogout
and apatite-associated syndromes. New York, NY: Taylor & Francis Group, 2006:99.
8. Horowitz D, Katzap E, Horowitz S, Barilla-Labarca M. Approach to septic arthritis. Am Fam
Physician 2011;84(6):653–660.
9. Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA
2007;297(13):1478–1488.
10. Simons DG, Travell JG, Simons LS, Cummings BD. Travell and Simons’ myofascial pain and dysfunc-
tion: the trigger point manual, 2nd ed. Baltimore, MD: Lippincott Williams and Wilkins, 1998.
TABLE 12.6.2 Differential Diagnosis of Joint Pain
Crystal-induced arthropathy Degenerative joint disease Malignant
Gout Osteoarthritis Tumor
Pseudogout Metastases
Leukemia
Rheumatic
Rheumatoid arthritis
Reiter’s syndrome
Psoriatic arthritis
Lupus erythematosus
Ankylosing spondylitis
(Continued)
282
Taylor’s DifferenTial Diagnosis Manual

11. Sarwark JF. Essentials of musculoskeletal care, 4th ed. Rosemont, IL: American Academy of Orthopaedic
Surgeons, 2010.
12.
Richie A, Francis M. Diagnostic approach to polyarticular joint pain. Am Fam Physician
2003;68(6):1151–1160.
13.
Till SH, Snaith ML. Assessment, investigation, and management of acute monoarthritis. J Accid
Emerg Med 1999;16(5):355–361.
14. Learch TJ. Imaging of infectious arthritis. Semin Musculoskelet Radiol 2003;7(2):137–142.
15. Conway WF, Totty WG, McEnery KW. CT and MR imaging of the hip. Radiology 1996;198:297.
16. Paulman PM, Paulman AA, Harrison JD, et al., eds. Taylor’s 10-minute diagnosis manual, 2nd ed.
Baltimore, MD: Lippincott Williams and Wilkins, 2006.
12.7
Neck Pain
Richard L. Engle
I. BACKGROUND. Neck pain is defined as pain occurring anywhere between the base of the skull
and thorax. This pain can occur anteriorly, posteriorly, or laterally. The cervical spine is one of
the most mobile and complex joints in the body. Considering that, on average, the neck moves
over 600 times an hour (1), it is no wonder that it is a common source of pain. Most episodes
of neck pain are short lived and resolve spontaneously. The examiner must be cautious about
ascribing the etiology of pain as intrinsic to the neck without evaluating the patient for risk fac-
tors and conditions that cause pain referred to the neck region such as angina, aortic dissection,
or other mediastinal pathology.
II. PATHOPHYSIOLOGY
A. Etiology
1. Trauma, job-related causes (e.g., manual labor, driving for long periods, head forward
positioning while typing), smoking, and a previous history of low back pain are consid-
ered risk factors for neck pain. Often, no specific cause can be elicited.
2. Symptoms due to cervical pathology can be referred to other areas of the body, most
commonly the upper back, chest, and arms. Likewise, pain from shoulder or chest
pathology can be referred to the neck.
B. Epidemiology. Neck pain is extremely common in the general population, with a
40–70% lifetime prevalence. Cervical arthritis is seen in 80% of individuals over 50 years
of age and cervical radiculopathy in 83.2/100,000 of the general population, with most of
them in the C6–7 distribution (2).
III. EVALUATION
A. History.
Characterizing the location, quality, intensity, radiation, duration, and associated
symptoms helps determine the likely cause of neck pain.
1. Key associated neck complaints are radicular symptoms, such as paresthesias, sensory
loss, muscle weakness, which can indicate nerve root compression; lower extremity
symptoms, such as lower extremity paresthesias, bowel/bladder dysfunction, which can
indicate cauda equina syndrome; and fever, weight loss, and other joint involvement that
can indicate inflammatory arthritis, infection, or neoplasm.
2. Unusual symptoms can be related to neck pathology and should not be discounted.
Sympathetic nervous system activation can cause eye pain, increased tearing, and blurry
vision. Irritation of the C3–5 nerve root (due to phrenic nerve involvement) can cause
respiratory symptoms such as shortness of breath (3).
Chapter 12 • Musculoskeletal Problems
283

B. Physical Examination. Examination should include inspection, palpation for tender-
ness in both midline and paraspinous areas, range of motion, neurovascular examination,
and special tests. Inspection of the neck should evaluate for loss of normal lordosis, rash,
or other abnormalities. Active range of motion is observed. Reduction of active range
of motion may be associated with underlying bony pathology such as arthritis or may
be due to muscle spasm. Loss of passive range of motion is usually due to underlying
bony pathology. Neurovascular examination includes the evaluation of motor strength,
sensation, and deep tendon reflexes. Special tests for cervical pathology are reviewed in
Table 12.7.1.
C. Testing. Laboratory tests are rarely needed in patients with neck pain. Suspicion of a
malignancy or inflammatory arthritis, such as rheumatoid arthritis or ankylosing spondyli-
tis, may prompt tests such as rheumatoid factor, sedimentation rate, complete blood count,
and/or HLA B27.
1. Radiographs are frequently helpful in cases of trauma, radicular symptoms, or prolonged
(3–6 weeks) symptoms. Typical views include anteroposterior, odontoid (open-mouth
view), and lateral radiographs of the cervical spine. All seven cervical vertebrae should be
visualized in the lateral radiograph. Oblique views assist in the evaluation of the neural
foramina and posterior elements. Flexion and extension views are obtained when insta-
bility of the cervical spine is suspected. It is important to remember that radiographic
abnormalities are common in the general population and may not be the cause of the
symptoms.
2. Computerized tomography is best used for identifying bony pathology such as subtle
fractures, whereas magnetic resonance imaging is ideal for soft tissue pathology, such as
disc disease and spinal stenosis. The use of discography to localize the exact disc causing
pain is controversial (1). Nerve conduction velocity and electromyogram may be helpful
in differentiating the nerve root from peripheral nerve pathology.
D. Genetics. Cervical degenerative disc disease may have a genetic component (4). Genetic
predisposition to inflammatory disorders such as rheumatoid arthritis, ankylosing spondyli-
tis, and osteoarthritis is well established (1).
TABLE 12.7.1 Special Physical Examination Tests of Cervical Spine
Test Evaluation for How performed Positive test
Spurling’s test Nerve root
compression
(disc herniation)
Head in mild extension
and flexion toward side of
radicular symptoms
Pain in dermatomal
pattern on affected
side
Distraction test Nerve root
compression
(disc herniation)
Head lifted axially with
one hand under chin
and other hand around
occiput
Pain relief with lifting
head
Adson’s maneuvers Thoracic outlet
syndrome
Extend patient’s symptomatic
shoulder while patient
rotates neck toward
affected side. Pulse is
checked during deep
inspiration
Loss of pulse in
affected extremity
Lhermitte’s sign Spinal canal
narrowing (spinal
stenosis),
multiple sclerosis
Patient sitting with legs
extended; ask patient to
flex neck forward
Shock-like sensation
into lower back and/
or extremities
284
Taylor’s DifferenTial Diagnosis Manual

IV. DIAGNOSIS
A. Differential Diagnosis.
See Table 12.7.2.
B. Clinical Manifestations. See Table 12.7.3.
TABLE 12.7.2 Differential Diagnosis of Neck Pain
Musculoskeletal Neurologic Infectious Neoplastic Referred
Cervical strain or
sprain
Thoracic outlet
syndrome
Discitis Spinal cord
tumor
Rotator cuff
tendinopathy
Disc herniation Peripheral
neuropathy
Osteomyelitis Primary neck
neoplasm
Myocardial
ischemia
Degenerative disc
disease
Myelopathy Meningitis Malignant
neoplasm
Pneumonia
Inflammatory
arthritis
( rheumatoid,
ankylosing
spondylitis)
Radiculopathy Cervical
lymphadenitis
Cervical fracture
Cervical instability
Cervical stenosis
Fibromyalgia
Whiplash
Diffuse idiopathic
skeletal
hyperostosis
Torticollis
TABLE 12.7.3 Most Common Causes of Neck Pain
Etiology Typical history Key physical examination
findings
Key lab findings
Spondylosis Dull neck ache Tender to palpation midline Radiograph (X-ray)
shows degenerative
changes that can
include narrowing
of disc space,
sclerosis of posterior
elements, and
osteophytes
Older age group Decreased active and
passive ROMs
Occipital headache and/
or radicular symptoms
(Continued)
Chapter 12 • Musculoskeletal Problems
285

TABLE 12.7.3 Most Common Causes of Neck Pain
Etiology Typical history Key physical examination
findings
Key lab findings
Cervical disc
herniation
Sharp neck pain Decreased active ROM MRI shows disc
protrusion or
extrusion into spinal
canal
Burning or tingling in
upper extremities
Reduced deep tendon
reflexes
Pain with neck motion Decreased strength in
upper extremities
Upper extremity
weakness
Positive Spurling’s test
Cervical
strain/sprain
Intermittent dull neck
pain
Normal ROM X-ray is normal or
shows loss of
lordosis
And/or occupational
related (postural)
Loss of lordosis Consider computed
tomography to rule
out bony injury in
trauma
And/or trauma his-
tory (motor vehicle
accident, fall)
Palpable tightness
Muscle spasm Occasional acute edema
Muscle spasms
Fibromyalgia Diffuse axial skeletal
pain
Normal passive ROM No laboratory test to
confirm
Sleep disturbance Trigger points
Fatigue
Inflammatory
arthritis such
as RA or AS
Dull ache Decreased active and
passive ROMs
RA: increased
rheumatoid factor
anderythrocyte
sedimentation rate
Morning stiffness >1 h
Other joint inflammation AS: positive HLA B27
Other joint involvement
Referred pain Symptoms from other
sites (e.g., chest pain,
shoulder pain)
Normal ROM of neck X-ray of other sites,
electrocardiogram,
MRI potentially
helpful
Physical examination find-
ings at other sites (e.g.,
shoulder strength loss,
chest rales)
AS, ankylosing spondylitis; MRI, magnetic resonance imaging; RA, rheumatoid arthritis; ROM, range
of motion.
(Continued)
286
Taylor’s DifferenTial Diagnosis Manual

REFERENCES
1. Nankano KK. Neck pain. In: Harris E, Budd R, Firestein G, et al., eds. Kelley’s textbook of rheumatology,
7th ed. Philadelphia, PA: Elsevier Saunders, 2005:537–554.
2. Devereaux MW. Neck pain. Prim Care Clin Office Pract 2004;31:19–31.
3. Bland JH. Disorders of the cervical spine. In: Noble J, ed. Textbook of primary care medicine, 3rd ed.
St Louis, MO: Mosby, 2001:1125–1137.
4. MacGregor AJ, Andrew T, Sambrook PN, et al. Structural, psychological, and genetic influences on
low back and neck pain: a study of adult female twins. Arthritis Rheum 2004;51:160–167.
12.8
Polymyalgia
Shannon C. Scott
I. BACKGROUND. Multiple (poly) muscle aches (myalgia) are a common presentation in primary
care with a broad differential diagnosis. The challenge for the physician lies in distinguishing
benign and self-limiting causes, such as a benign viral infection, from more serious illnesses. In
most cases, diagnosis remains primarily a clinical one.
II. PATHOPHYSIOLOGY. A number of conditions can result in polymyalgia (see Table 12.8.1).
The most common causes are polymyalgia rheumatica and inflammatory conditions (e.g.,
polymyositis/dermatomyositis and fibromyalgia). Table 12.8.2 summarizes how these may be
distinguished. The etiology and epidemiology are dependent upon the cause. In many cases,
the precise etiology is unknown.
III. EVALUATION. The key to the evaluation of this condition lies in a careful history and physical
examination (1). Frequently, laboratory investigations are inconclusive, and there is a danger
that patients may be overinvestigated.
A. History
1. Ask about onset (acute or insidious) and the muscles affected (diffuse, proximal muscles
of shoulder/hip girdle). To assess proximal muscle weakness, ask about difficulty going
up stairs, getting up from chairs, and raising hands above the head.
2. Inquire about the presence of systemic symptoms; such as fever, weight loss, and fatigue.
Is there joint involvement? If so, which ones?
TABLE 12.8.1 Differential Diagnosis of Polymyalgia
Systemic rheumatic disease Infection Endocrine
Polymyalgia rheumatica Viral or bacterial Hypothyroid
Polymyositis/dermatomyositis Spirochetal Adrenal insufficiency
Rheumatoid arthritis
Systemic lupus erythematosus Noninflammatory Medications
Spondyloarthropathy Fibromyalgia Statins
Vasculitis Chronic fatigue syndrome
Metabolic
Osteomalacia (7)
Chapter 12 • Musculoskeletal Problems
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