Industrial Medicine and Acute Musculoskeletal Rehabilitation. 1. Diagnostic Testing in Industrial and Acute Musculoskeletal Injuries

1.1 Educational Activity: To discuss the diagnostic approach in a 40-year-old home improvement warehouse worker who develops heel pain within several weeks of starting a job that entails prolonged walking and standing on concrete floors 

HEEL PAIN IS THE MOST common presenting symptom in the foot, and plantar fasciitis is the most common etiology of that pain.1 The diagnosis can be challenging to clinicians without a familiarity of midfoot and hindfoot anatomy. The midfoot is made up of the navicular, cuboid, and 3 cuneiform bones, and the hindfoot, or heel, is made up of the talus and calcaneus bones. Major soft-tissue regions include the calcaneal fat pad, the plantar fascia, and the Achilles’ tendon insertion. The tendons that cross beneath the medial flexor retinaculum include the posterior tibialis, flexor digitorum longus (FDL), and flexor hallucis longus (FHL) tendons; the peroneal tendons pass beneath the lateral retinaculum.2

Any alteration of normal foot biomechanics can play a role in the development of heel pain through increased plantar fascia stress. The foot dissipates forces and adapts to a surface by increasing flexibility through pronation at initial heel strike. Associated movements include tibial internal rotation, subtalar joint eversion, ankle dorsiflexion, and foot abduction. As the foot rolls forward to toe-off, it stabilizes itself by supinating through the plantar fascia by means of a windlass mechanism.3 The longitudinal arch is then stabilized as the toe hyperextends.

The plantar fascia is composed of fibrous connective tissues that are interwoven into multiple layers to form an aponeurosis. This aponeurosis attaches to the 3 main weight-bearing structures of the foot: the medial calcaneus and first and fifth metatarsal heads, which together form the longitudinal arch.2 It is composed of 3 parts, of which the central portion is referred to as the plantar fascia.3 Underneath the plantar fascia is the insertion of the flexor brevis muscle, where osteophytes can occur.3

Plantar fasciitis most commonly occurs in patients between the ages of 40 and 70 years and in military recruits and runners.3, 4, 5, 6 It affects men and women equally, and risk factors include obesity.3,6 The clinical course is generally favorable, with up to 90% of patients achieving complete resolution with a nonsurgical approach within 11 months; the remaining 5% require surgery.7

The pain is located in the anteromedial or central part of the heel. It has a rapid onset if there has been a rupture of the plantar fascia; otherwise, it gradually worsens. It is exacerbated with toe walking, significant changes in activity, or alterations in footwear.3 The pain tends to be worse in the morning and on standing after prolonged sitting.2 The history typically includes a recent increase in the amount or intensity of walking or running. It may also include a change in footwear or an unyielding walking or running surface.1 The cause is multifactorial and poorly understood, but conditions that increase the tension on the plantar fascia such as pes cavus, pes planus, decreased subtalar motion, and a tight Achilles’ tendon may contribute.2 The repetitive trauma associated with plantar fasciitis is thought to cause a traction injury resulting in microtears. This chronic situation can result in periostitis of the plantar fascia origin on the calcaneus.3

The physical examination routinely shows limited ankle dorsiflexion with maximal tenderness at the anteromedial aspect of the inferior heel.1 Examination should include assessment of the foot during weight bearing and non–weight bearing, with these factors considered: altered arch height, such as pes planus or cavus; passive range of motion of the ankle, subtalar, and midfoot joints; and overall postural assessment. A gap noted with palpation of the plantar fascia may indicate a rupture.3 The bony prominences and tendinous insertions should also be palpated near the heel and midfoot.2 The windlass test is positive if there is plantar fascia pain by forced great toe dorsiflexion.3 Sensation should be evaluated to rule out neurogenic pathology.3

Imaging studies play a limited role. They are used to rule out other causes of heel pain including a calcaneal stress fracture or other bony lesion.1 Plain radiographs, ideally performed in weight bearing, can detect a fracture, dislocation, degenerative joint disease, foreign bodies, tumors, and soft-tissue calcifications.8 A calcaneal osteophyte (heel spur) is often noted, which is often of no value in diagnosis or treatment.1 Wolff’s law of bone remodeling would suggest that the osteophyte is a response to plantar fascia tension rather than a primary etiology of symptoms. A fluffy periostitis may suggest a spondyloarthropathy.1 If a calcaneal stress fracture is suspected and plain radiographs are normal, a bone scan is recommended. A linear fracture line or diffuse calcaneal uptake is consistent with a calcaneal stress fracture compared with increased activity at the calcaneal plantar fascia insertion site associated with plantar fasciitis.1 Avascular necrosis (AVN) is often caused by trauma. Magnetic resonance imaging (MRI) is the most sensitive and specific radiographic test for AVN, because plain radiographs are initially normal.8 MRI of normal plantar fascia is hypointense on all pulse sequences, because the structure is composed mainly of collagen.8 MRI of the foot with plantar fasciitis shows increased tissue thickness and increased signal intensity on T2 and short tau inversion recovery sequences consistent with edema and structural microtears. There is also increased signal in the adjacent subcutaneous tissue and calcaneal insertion site.1 Diagnostic ultrasound is useful but uncommonly used. Under ultrasound, the normal plantar fascia thickness is 2.4 to 4.3mm, whereas abnormal plantar fascia thickness is 4.3 to 8.1mm. There is also a loss of definition at the interface between the plantar fascia and surrounding tissue, as well as calcaneal origin edema.9

The differential diagnosis includes fracture, infection, malignancy, or rheumatologic disorders. The calcaneus is the second most common site of stress fractures in the foot after the metatarsals.2 It occurs with excessive or repetitive weight bearing and is associated with osteoporosis or an increase in occupational or recreational activity.1 It presents with vague pain that is worsened with weight bearing and relieved with rest. A mediolateral calcaneal compression or squeeze may reproduce pain.1 Plain radiographs may be normal initially, but, over time, show a sclerotic area directed inferiorly in an oblique angle from the superior calcaneous.1 A bone bruise may present with similar symptoms but is associated with direct trauma without a cortical fracture on plain radiographs or MRI. The bone bruise is believed to be caused by trabecular microfractures accompanied by hemorrhage, hyperemia, and edema.10

Heel fat pad atrophy presents with symptoms similar to plantar fasciitis and is commonly found in elderly or obese patients. The pain and tenderness is located in the central heel with associated atrophy and is more diffuse than with plantar fasciitis. Unlike plantar fasciitis, pain due to heel pad atrophy does not radiate anteriorly or worsen with great toe dorsiflexion, and it is not worse in the morning.1, 2

Achilles tendinitis develops with overuse or abnormal stresses including jumping or running and may result in Achilles’ insertion tenderness or swelling. The adult Achilles’ tendon is approximately 10 to 15cm in length and is formed by the union of the gastrocnemius and soleus muscle tendons. It inserts on the posterior calcaneus and develops pathology along a critical zone that is 2 to 6cm proximal to the calcaneal insertion.8 A chronic tendonopathy results in thickening associated with microtears that may rupture with a characteristic pop.11

Retrocalcaneal bursitis, also known as a pump bump, is characterized by Achilles’ tendon insertion site pain. It is caused by abrasion and resulting inflammation of the bursa between the Achilles’ tendon insertion site and the calcaneus by shoes with a stiff posterior edge.11 It is also associated with a systemic inflammatory arthritis.2 Haglund’s disease, a bony protuberance of the calcaneal tuberosity, may also result in a retrocalcaneal bursitis.8 A retroachilles’ bursitis presents with similar findings but is caused by inflammation between the Achilles’ tendon and the skin.2

Medial or lateral heel pain may result from a tendonopathy of the posterior tibialis, FDL, or FHL tendons in the medial compartment or a tendonopathy of the peroneus longus and brevis tendons in the lateral compartment. The peroneus brevis tendon ruptures proximally to the insertion site at the base of the fifth metatarsal near or just distal to the lateral malleolus. It is associated with swelling and tenderness after recurrent inversion ankle sprains.11 A pes planus foot predisposes to a posterior tibial tendon rupture.11

Tarsal tunnel syndrome (TTS) is caused by posterior tibial nerve irritation and/or compression as it dives beneath the medial retinaculum behind the medial malleolus.11 The posterior tibial nerve separates into medial and lateral calcaneal sensory nerves and into the medial and lateral plantar nerves, which have sensory and motor components. Increased tibial nerve tension may be caused by increased forefoot abduction and hindfoot valgus deviation.2 Nerve compression may be caused by trauma or degenerative bony conditions. It may present with numbness, tingling, or burning pain or tenderness along the path of the nerve that may radiate along the plantar aspect of the foot to the toes.1 It is worsened with prolonged weight bearing and ambulation on hard surfaces. A Tinel sign may be found at the medial heel. Foot dorsiflexion and eversion stretches the nerve and can reproduce symptoms.2 Nerve conduction studies (NCS) for TTS should include the distal tibial motor, medial, and lateral plantar orthodromic sensory nerve studies and electromyography of the abductor hallucis longus and abductor digiti quinti. The NCS results may be compared with those of the asymptomatic side. Other causes of neurogenic heel pain include a medial calcaneal neuroma, S1 radiculopathy, or a neuropathy of the nerve to the abductor digiti quinti.1

1.2 Clinical Activity: To review the etiology and diagnostic assessment in a Department of Transportation worker who presents with neck pain after a rear-end collision while stopped at the side of the road 

The cervical spine is composed of 7 vertebrae that permit greater motion compared with the lumbar spine. The term whiplash describes the transfer of energy to the neck through sagittal acceleration–deceleration leading to bony and/or soft-tissue injury. It is most commonly associated with rear-end motor vehicle collisions (MVCs). It has been associated with chronic somatic and psychologic problems.

A constellation of symptoms and signs has been named whiplash-associated disorders. These disorders are associated with disability, increased health care costs, and decreased income, social functioning, and overall well-being.12 In 1994, the estimated incidence of whiplash-associated disorders in the United States was 3.8 per 1000.13 Many people who are involved in rear-end collisions do not suffer permanent injury, and symptoms usually resolve within 4 to 6 weeks. However, up to 33% have chronic symptoms.14 Chronic pain does not represent persistent acute pain but results from adaptations of peripheral and central pain modulation. Symptoms associated with whiplash-associated disorder include neck pain and stiffness, arm pain, paresthesias, temporal mandibular joint dysfunction, headache, dizziness, visual disturbances, and difficulty with memory and concentration.15

The Quebec Task Force on Whiplash-Associated Disorders developed a classification system grading severity from 0 to IV by stratifying patients on anatomic-clinical determinants (table 1).16 Not surprisingly, increased severity in the acute stage leads to increased risk of whiplash-associated disorders at follow-up.12

Table 1. Classification of Whiplash-Associated Disorders16

	Grade	Description
	0	A patient without subjective complaints or objective signs
	I	Neck complaints of pain, stiffness, or tenderness without physical signs
	II	Neck complaints with musculoskeletal signs including decreased range of motion and point tenderness without neurologic dysfunction
	III	Neck complaints with neurologic dysfunction including changes in upper-extremity strength, deep tendon reflexes, or sensation
	IV	Patients with neck complaints associated with fractures or dislocations

Whiplash was first identified in World War I pilots after emergency ejection, but the prevalence decreased with the development of the shoulder harness and headrest.12 Significant risk factors for whiplash after MVC include older age, higher acceleration and deceleration forces, seat belt use, poor headrest positioning, poor car seat energy absorption, and improper car design and construction.12, 17

Cadavers exposed to rear-end collisions show tears in the ligamentum flavum, disruption of the annulus of the intervertebral disk and anterior longitudinal ligament, capsular strains, and fractures of the zygapophyseal joints.18 These injuries often do not show up on imaging studies.18 Lord et al19 used controlled diagnostic blocks to show zygapophyseal pain generators in 60% of patients with chronic whiplash-associated disorders.

Two causes hypothesized for the cognitive impairment seen with these disorders are (1) disruption of the central homeostatic regulatory system resulting in neural, hormonal, and behavioral changes in response to stress12 and (2) a coup–contrecoup traumatic brain injury.14

The center of the automobile headrest should be at ear level to limit the amount of head and neck flexion and extension at impact. The more reclined the car seat is during a rear-end collision, the larger the arc that the head and neck travel in relation to the chest.14 From the 1980s to mid-1990s, the proper use of seat belts would have been expected to decrease the prevalence of whiplash injuries, yet whiplash injuries increased between 1989 and 1995 although seat belt use remained stable.20

There is no specific historical or physical examination finding for the diagnosis of whiplash-associated disorders. To gauge the force of impact it is very important to review the details, including speed at the time of the collision, possible head injury with associated loss of consciousness, and condition of the vehicle. Symptoms may be initially mild after the accident but may increase over the following 2 to 3 days.14 Although the physical examination shows stiffness and decreased cervical spine range of motion, neurologic deficits are rare. The mechanism of injury in combination with the presenting symptoms and signs on physical examination allows the diagnosis of whiplash-associated disorders to be made. Imaging is useful to rule out bony or soft-tissue injury, including fractures and injuries to the disk and ligamentous structures. Plain radiographs often show decreased lordosis and possible widening of adjacent soft tissues.14 Flexion and extension films should be ordered to rule out instability. MRI and computed tomography seldom show structural abnormalities related to the injury and are often unnecessary.

1.3 Clinical Activity: To advise an executive secretary who supervises a large secretarial pool about the pathogenesis of job-related wrist and elbow pain 

Work-related musculoskeletal disorders that result from repetitive motions have had various names, including cumulative trauma disorders and repetitive strain injuries. Repetitive movements in occupational and avocational settings may result in these conditions21; however, debate exists concerning the actual existence of these injuries.22 The biomechanic risk factors associated with tissue damage include the extent of tissue damage caused by repetitive or prolonged activities, forceful exertion, awkward or static postures, vibration, localized mechanical stress, and cold temperatures.23 Individual risk factors include older age, obesity, diabetes, smoking, pregnancy, rheumatoid arthritis, and psychologic stress.21 In 2002, there were 96,500 cases of repetitive strain injury reported in the United States, resulting in a median of 23 days lost from work.24 Causation is often difficult to identify.

Repetitive strain injuries are often attributed to musculotendinous unit disorders.23 Tendons and ligaments require mechanical stress to maintain function. When the load exceeds the ability to adapt, injury occurs, with resultant inflammation. This is associated with subsequent healing, scarring, and tissue remodeling. If the injury is not allowed to heal completely, continued high–muscle-effort levels can result in further disability.21 Several theories exist to explain such injuries, including (1) temporary lengthening of collagenous structures in response to prolonged loading,25 (2) intramuscular pressure rise with resulting ischemia caused by prolonged loading,26 and (3) inconsistent afferent information including visual and proprioceptive resulting motor responses.27 Some have termed repetitive strain injuries to be tendonopathy or tendonosis, because histopathology has not shown inflammatory mediators.28

The history should include questions assessing occupational and avocational activities that include high repetition rates and prolonged abnormal postures. The history may also identify obstacles to recovery such as “catastrophizing,” histrionic behavior, job monotony, high work demands, and financial reliance on disability payments.29 The cardinal complaint is pain at the site of muscle or tendon insertion associated with tenderness during palpation or resisted motion. Often there is associated swelling and warmth. Evaluation for upper-extremity complaints begins at the cervical spine and proceeds to the digits; it includes a screen of the unaffected contralateral side. The patient should be assured that there is no evidence that continued activity will increase the damage, although work activities must be modified, with minimal time off from work taken.29 Treatment should include physical and/or occupational therapy with work modifications.

De Quervain’s disease results in pain of the first dorsal compartment (fig 1) through which pass the tendons of the abductor pollicis longus and extensor pollicis brevis muscles. Symptoms can also include tenderness and swelling over the radial styloid at the anatomic snuffbox.23 The Finkelstein’s test is accomplished by having the patient place his/her thumb in the palm and closing the fingers around it, followed by ulnar deviation of the wrist. Increased pain on palpation of the site confirms the clinical diagnosis. Other tendinous disorders at the wrist may present as pain in the region of the involved tendon reproduced with resisted motion.

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Fig 1. Wrist extensor compartments (labeled 1 through 6), dorsal view. Adapted from Jenkins.44(p187) Reprinted with permission.

Carpal tunnel syndrome (CTS) can result in short- and/or long-term work absence, so early management and treatment are essential. Classically, it causes pain, numbness, or tingling at the thumb, index, and long fingers. It can cause wasting of the thenar muscles and significant loss of oppositional function in advanced cases. It is caused by increased carpal tunnel pressure impairing neurovascular flow and causing direct median nerve compression. Repetitive or sustained flexed or extended wrist positions, as well as finger flexion, can increase carpal tunnel pressure, leading to demyelination or Wallerian degeneration over months to years. The history should assess work factors associated with repetitive wrist motions.

The Phalen test is accomplished by wrist flexion for about 1 minute to reproduce dysesthesias and numbness in the median nerve distribution. The Tinel sign involves tapping over the wrist crease to reproduce median nerve dysesthesias. However, the sensitivity of these tests is poor.30 Electrodiagnostic studies have been found to provide a high degree of sensitivity (>85%) and specificity (95%) for diagnosing CTS.31 At the least, a 14-cm median sensory NCS across the wrist should be performed and compared with a sensory NCS of an adjacent nerve in the symptomatic limb followed by an 8-cm median motor NCS to the abductor pollicis brevis (APB).31 Needle electromyography of the APB muscle can determine the severity of the CTS and exclude other conditions. Ultrasound of the carpal tunnel is viewed as a new and promising diagnostic method.32

1.4 Clinical Activity: To formulate a diagnostic plan for a loading dock worker who has lower back pain 

Diagnosis and treatment of low back pain (LBP) in an injured worker can present formidable tasks for clinicians because of the interactive anatomic, functional, medical, and psychologic factors. The workers’ compensation system adds an additional layer of complexity, occasionally promoting additional pain behaviors and disability. An early and accurate diagnosis is essential for the patient to return to work safely and effectively.

The peak prevalence of LBP is age 25 to 60 years, yet the age group that results in the highest costs is the 31- to 40-year-old subgroup.33 LBP is associated with lifting, carrying, material handling, and lower job performance ratings.33 Accidental onset has also been found to result in higher total treatment costs.33

The objective of the history and physical examination is to direct the patient toward diagnostic tests of greatest yield, to formulate the most specific treatment, and to return the patient to the highest functional level. Failure to do this can lead to treatment failure and recurrence. It is important to recognize psychologic factors that may impede recovery yet be unbiased so that one does not inadvertently attribute a treatment failure to psychologic factors when diagnostic errors may possibly have occurred.34

The first step in assessing an occupational injury is to determine whether it is indeed work related or is related to an underlying illness. This step consists of reviewing the mechanism of injury to clarify its association with work. Reviewing the consistency of the injury report with witnesses may also help complete the sequence of events. Occasionally, an association with a work injury remains elusive despite diligent information gathering. Possible litigation associated with the injury either in the workplace or after an MVC can alert the physician to possible counterproductive incentives.34 The physician should not communicate a message of disbelief; otherwise, treatment of the patient may become more difficult.34

Pain localization often can be difficult for patients and physicians. Localized point tenderness that is easily identifiable and reproducible denotes localized injury. Dermatomal pain patterns caused by nerve lesions are not as easy to localize but follow established distribution patterns. Sclerotomal and myotomal referral patterns of non–nervous system tissues such as muscles and ligaments are not as well established. They can be diffuse and overlap with dermatomal patterns. To further understand a patient’s pain experience, additional information about intensity, frequency, quality, and aggravating and relieving factors also must be articulated. A family history of spondyloarthopathies and connective tissue disorders should be clarified.

Fractures, infection, and cauda equina syndrome also must be excluded. Cauda equina syndrome can be a serious condition; therefore, inquiries regarding bowel or bladder function must be made even in the absence of limb nerve root involvment.34 A patient with a cancer history must have malignancy excluded, especially if his/her pain has persisted longer than 1 month, is not relieved with bedrest, or is associated with unplanned weight loss. Intravenous drug use, persistent fevers, and/or night sweats suggest a spinal infection.

Detailed information on past treatments gives the physician a unique view of the patient’s compliance and response. A review of medications, physical modalities, and exercise regimens, as well as surgical and nonsurgical procedures, provides a clue to previous diagnoses. Detailed inquiry needs to be made about medication names and doses, what nonsurgical invasive interventions were performed, and the responses to these treatments.

The focused physical examination helps to confirm or exclude diagnoses suggested by the history. This examination involves inspection, range of motion, flexibility, palpation, neurovascular testing, and performance of provocative maneuvers.34 Inspection includes assessing for symmetry of the shoulders, iliac crests, and greater trochanteric areas and checking for muscle bulk symmetry and tone of the paraspinal muscles, for excessive or reduced kyphosis and lordosis, or for a fixed or functional scoliosis. A functional scoliosis is reduced with forward flexion, whereas a fixed scoliosis does not change. Lumbar range of motion is checked in the 6 cardinal planes including forward flexion, extension, and right- and left-side bending and rotation. Forward flexion involves a reversal of the normal lumbar lordosis and pelvic rotation. It can be measured with an inclinometer or the modified Schober test, in which a horizontal line is drawn between the posterior superior iliac spines at approximately the S2 level. At the midline, a perpendicular line is drawn to 5cm below and 10cm above. An increase of more than 5cm is normal.34

Lower-limb joints are screened using the Quick test, in which a patient squats 2 or 3 times and returns to standing. This grossly tests the sacrum, hips, knees, and ankles to rule out pathology. This should not be performed by pregnant women and should be used cautiously in elderly patients. Palpation is used to assess side-to-side differences in tenderness and tissue quality in the muscular, osseous, and ligamentous structures. Trigger points are noted by their characteristic band-like quality and palpation-induced twitch response. Myotomal screening should include strength assessments of the hip flexors (L1-3), knee extensors (L2-4), ankle dorsiflexors (L4-5), great toe extension (L5), and ankle plantarflexors (S1). The ankle plantarflexors should provocatively be tested with toe-walking or 10 toe raises. Sensation should be tested at the knee (L3), medial malleolus (L4), dorsum of the foot (L5), and the lateral malleolus (S1). Muscle stretch reflexes are assessed at the patella (L4), medial hamstring (L5), and the Achilles’ tendon (S1). Because 98% of all lumbar disk herniations occur at the L4-5 and L5-S1 levels affecting the L5 and S1 nerve roots, it is important to screen the strength of the ankle dorsiflexors and great toe extensors as well as the ankle reflexes and sensation at the medial, dorsal, and lateral foot.35 Peripheral vascular disease should be assessed by checking lower-extremity pulses and looking for signs of vascular insufficiency.

Hamstring and gluteus maximus inflexibility can cause a posterior pelvic tilt, decreasing lumbar lordosis, whereas a tight rectus femoris and iliopsoas can increase anterior pelvic tilt, thereby increasing lumbar lordosis—both of which may increase forces across the lumbar spine.36 The Ely test, which tests for a tight rectus femoris, is accomplished by maximally flexing the knee toward the buttock while the patient is prone. Elevation of the buttocks constitutes a positive test. In the Thomas test, which assesses the iliopsoas muscle, the contralateral leg is maximally flexed toward the chest while the patient is supine. A positive sign is elevation of the nonflexed thigh off the table. The straight-leg raise (SLR) test assesses hamstring flexibility and is also a dural tension sign. A person tests positive if posterior leg pain occurs below the knee with a straight leg raise between 30° and 70° of hip flexion. Sacroiliac dysfunction is uncovered at greater than 70°. The positive crossed SLR suggests a large disk protrusion. The femoral stretch test to assess pathology at the L4 nerve root and above is accomplished with the patient in the prone position by lifting the thigh off the table while flexing the knee to 90°. Finally, it is also important to review the condition of the bone and soft-tissue structures above and below the lumbar spine. These structures include the thoracic spine, the sacroiliac joint (SIJ), and the pelvic girdle muscles.34

The SIJ has been found to contribute to LBP. Several tests have been characterized, yet none are very sensitive or specific.37 The Patrick or FABER test is accomplished by flexing, abducting, and externally rotating the hip while applying pressure to the contralateral anterior superior iliac spine. Ipsilateral groin pain is of hip origin, whereas contralateral buttock pain often originates from the SIJ.34 The Gaenslen test is performed with the patient supine by flexing the contralateral leg while dropping the ipsilateral leg off the table. A positive response is pain in the region of the SIJ of the ipsilateral leg. The Gillet test is performed by palpating the posterior superior iliac spine while the patient is standing and asking the patient to flex the ipsilateral hip to 90°. A positive finding is the failure of the posterior superior iliac spine to descend. The 5 Waddell signs of nonorganic pathology include nonanatomic regional tenderness, overreaction, nonanatomic regionalization, distraction (using a seated SLR), and stimulation (with axial loading). If 3 of the 5 findings are positive, the Waddell signs suggest the neurotic triad of hysteria, depression, and hypochondriasis on the Minnesota Multiphasic Personality Inventory.38

Diagnostic testing is based on history and physical examination findings. If there are no red flags noted it is often prudent to refrain from ordering imaging studies. The dogmatic reliance on plain radiographs predates the understanding of lumbar pathology, recent surgical observations, and imaging techniques; therefore, minimal critical review has been done.39 The routine use of plain radiographs has been controversial, because radiographic abnormalities are not necessarily related to symptoms. Criteria have been established for the early use of plain radiographs. They include age greater than 50 years, significant trauma, neurologic deficits, unplanned weight loss for longer than 6 months, and assessing for possible ankylosing spondylitis. Plain radiographs should also be considered if there is drug or alcohol abuse, a history of carcinoma, corticosteroid use, fever, lack of improvement with conservative care, litigation, and no improvement after 7 weeks.39, 40 They are optimal for checking spinal segment alignment during weight bearing in the anteroposterior and lateral views to rule out spondylolisthesis and to assess for hypermobility using flexion and extension films.39 Although oblique views significantly increase the radiation dose, they help assess the posterior elements for fractures or other lesions. The presence of spondylolysis, spondylolisthesis, or posterior element hypertrophy can have a significant influence on the specific exercise prescription.

Computed tomography (CT) is an excellent means of assessing bony architecture—specifically, foraminal bony narrowing and lateral recess stenosis. It is most often used to assess fractures, especially stress fractures, or disk lesions in patients who cannot have an MRI scan. CT myelography allows improved visualization of compression by soft tissues or bone. The major limitation of CT is radiation exposure, restricted field of view, and poor delineation of intrathecal anatomy.41

MRI provides excellent osseous and soft-tissue detail. Disk degeneration is clearly shown through the state of hydration of the disk complex. High-intensity zones, which may represent an annular tear as well as various stages of a herniated nucleus pulposus, are clearly delineated. It is the study of choice to detect sequestered disk fragments and vertebral body endplate changes,41 to assess for inflammatory processes and neoplastic conditions, and to assess structures in the retroperitoneal space. The addition of gadolinium contrast helps differentiate postsurgical granulation tissue from disk material and increases the sensitivity of detecting pathologic fractures, neoplasms, and demyelinating conditions. MRI clearly delineates the zygapophyseal joints and eliminates the need for contrast in the evaluation of spinal stenosis. However, abnormal MRI findings have been noted in asymptomatic people. Boden et al42 noted that their 20- to 39-year-old subgroup had a 35% prevalence of at least 1 level of degenerative disk disease and that the chance of abnormal findings increased with age. Asymptomatic people older than 60 years had a 36% prevalence of a herniated disk and a 21% prevalence of spinal stenosis in addition to a near 100% prevalence of degenerative disk disease. Open MRIs are available for obese or claustrophobic patients but may compromise image quality. Recently developed weight-bearing MRIs allow assessment of loaded axial structures to identify occult nerve root compression.43

Bone scans assess function and tissue metabolism through the emission of absorbed technetium-99m. These scans can detect localized or systemic bony abnormalities caused by disturbances in the normally balanced activity of osteoblasts and osteoclasts. Single photon emission computed tomography increases the sensitivity for bony abnormality detection and permits better lesion localization. This modality is useful for localizing posterior element fractures or degenerative changes and also helps identify neoplastic conditions and infections.

Electrodiagnostic studies are the only physiologic test of muscle and nerve function and are useful in several ways: for differentiating objective weakness from weakness resulting from pain, for ruling out a peripheral neuropathy or neuromuscular diseases, to localize the level of the lesion, to differentiate between neuropraxic and axonal injuries, and to assist in prognosis.