Introduction
Musculoskeletal (MSK) pain disorders are the second most common cause of disability worldwide and have increased by 45% from 1990 to 2010. This number is expected to continue to rise with an increasingly obese, sedentary, and aging population. In the United States, approximately 8%–10% of both emergency room and primary care visits are related to complaints of MSK pain. ,
The term “musculoskeletal pain disorders” is a broad term that encompasses numerous pain disorders. In order to simplify our discussion, MSK pain disorders are organized into five subcategories: disorders of the (1) bone, (2) joint/bursae, (3) muscle/tendon/ligament, (4) nerve, and (5) systemic processes. This chapter will focus on the most common syndromes in each category ( Table 6.1 ). Explanations of their pathophysiology, diagnostic approaches, and treatment strategies can be applied to less common disease processes that are not discussed in this chapter.
| Bone | Joint/Bursae | Muscle/Tendon/Ligament | Nerve | Systemic Process |
|---|---|---|---|---|
| Vertebral compression fractures | Degenerative joint disease | Muscular sprain/strain | Radiculopathy | Fibromyalgia |
| Bursitis | Tendinopathy | Entrapment neuropathies | ||
| Adhesive capsulitis |
Vertebral Compression Fractures
Vertebral compression fracture is defined as the loss of height of a vertebral body due to the failure of the structural osseous component of the vertebrae. This pathology has a variety of potential causes including osteoporosis, infection, malignancy, and trauma. Individuals who smoke are postmenopausal, and those with a history of chronic or high-dose steroid use are at an increased risk of developing vertebral compression fractures. Approximately 30%–50% of patients on long-term steroid therapy have atraumatic fractures. Evidence suggests that genetics may also place individuals at increased risk. Specifically, vitamin D receptor polymorphisms, among others, lead to decreased bone mineral density thus increasing the risk of a compression fracture.
Trabecular bone is the primary load bearing element in bone. When an axial load on the bone exceeds the vertebral body’s strength, a compression fracture occurs. Reduction in bone density also results in loss of trabecular bone strength. This is most commonly seen in osteoporosis. The risk of developing future compression fractures in the setting of osteoporosis increases after the initial fracture, with up to 19% of patients developing an additional fracture within 1 year. This increased risk is largely due to the altered force vectors that are created by the initial fracture. Compression fractures may also be caused by malignancy or in association with kyphosis or deconditioning.
Many patients with compression fractures are asymptomatic. , Patients who seek medical attention with an acute compression fracture commonly complain of severe localized pain and limited mobility. Pain with palpation and percussion over the injured spinous process and paravertebral structures may be observed on physical exam. Typically, pain is most intense at the fracture level and is exacerbated by movement and alleviated with bedrest.
Suspected acute vertebral body compression fracture can be confirmed by plain radiographs of the spine ( Fig. 6.1 ). Most often, compression fractures occur in the lower thoracic and upper lumbar spine and involve the anterior aspect of the vertebral body, resulting in anterior wedging. Magnetic resonance imaging (MRI) can also be employed to determine the etiology of fractures as well as establish their age ( Fig. 6.2 ). The bone marrow signal on MRI can help determine the acuity of the fracture. Acute compression fractures will have a high signal intensity on T2-weighted scans and low signal on T1-weighted scans. Compression fracture due to osteoporosis may be indistinguishable from those due to metastasis on plain radiographs. Distinguishing the etiology of the fracture impacts management significantly.
The majority of patients can be managed conservatively with pain control and physical therapy. First-line agents for symptom management include oral analgesics such as acetaminophen and ibuprofen. Opioids or a two to four-week course of calcitonin may be used as alternative options if pain persists. Physical activity should be resumed as soon as possible as inactivity may worsen deconditioning. Physical therapy aimed at strengthening the core and improving gait may help patients return to their previous function. Weight-bearing exercises can be used to combat the decrease in bone density seen in osteoporosis. Care must be taken to instruct patients to restrict flexion-based activity as this maneuver loads the anterior vertebral body and thus places them at increased risk for worsening or additional fracture. Bracing, such as thoracic lumbar sacral orthosis, can be considered—however, the efficacy remains inconclusive. Intercostal nerve blocks may also be used for pain management. Lastly, vertebroplasty or kyphoplasty can be used in patients who fail conservative treatment. A surgical consult should be obtained if an unstable fracture is identified on radiographic imaging.
Degenerative Joint Disease
Degenerative joint disease (DJD), often called osteoarthritis, is one of the most common causes of disability due to pain and dysfunction of the joint. It most often involves the knees, hips, spine, and small hand joints and is characterized by deterioration of joint structures and remodeling of subchondral bone. ,
DJD is commonly thought of as a progressive “wear and tear” process but the pathophysiology is multifaceted ( Fig. 6.3 ). While the exact pathway leading to the disease varies between individuals, commonly the same pathological findings are observed in articular cartilage, bone, synovium, and surrounding soft tissues. Excess shear forces placed on the joint can lead to repetitive trauma and inflammation. This inflammation then leads to the production of proteolytic enzymes which degrade the extracellular matrix and ultimately compounds to lead to accelerated chondrocyte death and injure the articular cartilage of the joint and synovium. Over time, this process leads to loss of joint space, eburnation of the subchondral bone, and hypertrophic repair of cartilage. Risk factors for the disease include age, joint injury, genetics, repetitive joint trauma or stress, neuromuscular weakness, obesity, occupation, biomechanics, and anatomical factors, as well as gender.
Typically, patients presenting with symptoms of DJD are older than 45 years, complain of activity-related joint pain, and may have morning joint stiffness lasting less than 30 min. The quality of the pain varies, ranging from aching joint pain to less localized radiating pain. Joint locking and instability may also be observed. On exam, patients may present with pain on range of motion (ROM) and swelling of the affected joint. In hip DJD, pain may radiate to the groin, anterior thigh, and knee.
A comprehensive history and physical exam is essential to the diagnosis of DJD. Plain radiographs can be utilized to confirm the diagnosis and rule out other conditions. In the earliest stages of the disease, X-ray findings may be benign. As the underlying process advances, subchondral bony sclerosis, formation of osteophytes, and joint space narrowing are commonly seen. In the knee, narrowing tends to be seen at the medial joint space, whereas in the hip the superior lateral joint space is narrowed. Additional laboratory testing may be appropriate in younger patients, those with atypical symptoms, or those with constitutional symptoms. Inflammatory markers are typically normal in DJD and may exclude other diagnoses. If the diagnosis is unclear, imaging modalities such as MRI can be used to identify the disease at earlier stages before radiographic evidence is present. The use of MRI occurs most often when evaluating knee pathology to assess for pathology in other structures which may be contributing to patient presentation.
Goals of treatment include pain relief and improvement of joint dysfunction. Nonpharmacologic treatment is first line of treatment and includes patient counseling focused on encouraging patients to exercise and strengthen local muscles. , Weight loss is essential if the patient is overweight or obese. Physical therapy can be utilized to improve function and reduce pain in patients with mild to moderate symptoms. First-line pharmacological management includes the use of acetaminophen and/or topical nonsteroidal antiinflammatory drugs (NSAIDs). If further pain control is necessary, substitution with oral NSAIDs or COX-2 inhibitors may be used. Tramadol can also be considered for initial management of hand, knee, or hip DJD. Intraarticular corticosteroid injections may be beneficial for short-term relief of symptoms. The role of hyaluronic acid or platelet-rich plasma remains unclear. Surgical referral for joint replacement can be made if conservative treatment fails or if quality of life is significantly impaired. Opioid analgesics are not indicated in the management of chronic osteoarthritic pain.
Trochanteric Pain Syndrome
Trochanteric bursitis is one of the most common causes of lateral hip pain in adults. The condition results from gluteus medius or minimus insertional tendinopathy along the greater trochanter and often involves the regional bursae. Recently, the term “greater trochanteric pain syndrome” has gained wider use as the bursae are not always the source of pain. Risk factors for the disease include female gender, obesity, and hip and knee arthritis.
Bursae are designed to reduce friction as soft tissues move over bony prominences. In the hip, a proximal bursa exists between the iliotibial band and the greater trochanter ( Fig. 6.4 ). It may become inflamed as a result of trauma but often abnormal biomechanics lead to gradual inflammation. An imbalance in strength of the hip muscles may also contribute to development. The medial aspect of the greater trochanter serves as the insertion point of the short external rotators of the hip. These muscles along with the abductors work to maintain pelvic stability while walking. An imbalance or weakness of these muscles may contribute to development of greater trochanteric pain syndrome.
Patients with trochanteric pain syndrome complain of lateral gluteal pain especially while lying on their affected side and will have difficulty tolerating weight bearing on the affected side. On examination, maximal tenderness occurs over the posterior corner of the trochanter , and commonly extends along the length of the iliotibial band. Motor testing often reveals weakness in hip abduction and external rotation. Tensor fascia lata inflexibility is also commonly seen. There are no established criteria for diagnosing trochanteric pain syndrome. There is commonly no cardinal sign of inflammations such as erythema, edema, or rubor along the lateral buttock. Concurrent intraarticular hip and lumbar spine pathology should be ruled out prior to making the diagnosis of primary trochanteric pain syndrome. Findings on plain radiography are highly variable and thus are not recommended.
There are no established treatment protocols for trochanteric bursitis. Initial management may include oral NSAIDs. If more immediate relief is required, local glucocorticoid injections may be considered. , Physical therapy or home exercises focused on isometric loading of the gluteus medius, minimus, and quadriceps should be a mainstay of treatment as it will both improve patient symptoms and treat the underlying cause of their symptoms. Additional conservative therapies include platelet-rich plasma injection, shock wave therapy, and weight reduction. It is estimated that over 90% of cases will resolve with conservative therapy. Trochanteric bursitis may also be self-limiting in many patients. If symptom relief is not obtained after several months, investigation of a tear of the gluteus medius tendon should be performed using MRI. Refractory cases may also be managed with bursectomy, iliotibial band lengthening techniques, or gluteal tendon repair. ,
Adhesive Capsulitis
Adhesive capsulitis (AC), often called frozen shoulder, has been defined as a condition characterized by the progressive development of global limitation of active and passive shoulder motion without radiographic findings other than osteopenia.
AC can be primary or secondary to various conditions such as diabetes mellitus, thyroid pathology, or following trauma or surgery. This condition commonly presents unilaterally, more often in women, and affecting the nondominant shoulder. The exact pathophysiology of the condition is unclear. A commonly cited hypothesis is that inflammation occurs in the joint capsule and leads to the development of adhesions and fibrosis in the synovial lining of the joint. This leads to loss of joint volume due to thickening and contracture of the joint capsule and surrounding tissues. There is considerable debate as to whether the underlying pathology is predominantly inflammatory or fibrosing in nature. The thickened glenohumeral joint capsule can form adhesions to itself and/or to the anatomic neck of the humerus. The joint volume is subsequently decreased as there is minimal synovial fluid present.
Patients with frozen shoulder complain of severe shoulder pain and progressively worsening limited mobility. AC is described as progressive, and patients may present at any of the three distinct phases of the disease. During the initial or freezing stage, the patient will complain of diffuse shoulder pain that is worse at night. Physical exam reveals limited active and passive ROM in two or more planes of motion. Often external rotation and abduction are most greatly affected. Loss of external rotation ROM more than internal rotation can be helpful in differentiating AC from rotator cuff pathology. The initial/freezing phase can last anywhere from 3 to 9 months. During the subsequent “frozen stage,” which can last 4–12 months, pain does not necessarily worsen but limited use of the limb can lead to deconditioning. , ROM improves and pain improves during the final thawing phase which lasts 12–24 months , ( Fig. 6.5 ).
The diagnosis of AC is based on an appropriate history and physical examination. Plain radiographs may be utilized to rule out other conditions such as osteoarthritis. MRI or ultrasound may also be used to rule out other pathologies and can be especially helpful in diagnostically challenging clinical situations. These include patients with concomitant osteoarthritis or rotator cuff pathology. An injection of anesthetic into the subacromial space can be employed to help differentiate AC from subacromial pathology. Symptoms will not improve in patients with AC but should improve in patients with subacromial impingement/rotator cuff dysfunction.
There is little high-level evidence supporting any specific treatment for AC. Rest and shoulder mobility exercises are recommended. Adequate pain control can usually be achieved with activity modification and acetaminophen or NSAIDs early in the disease course. Physical therapy should be initiated as mobility improves. An intraarticular injection of a combination of anesthetic and glucocorticoid can be considered in patient with severe symptoms for short-term relief. Surgical referral for manipulation under anesthesia or arthroscopy and capsular release may be warranted if patients fail to find relief from conservative measures. Future treatments in the development stage are aimed at targeting inflammatory cytokines in early disease and decreasing fibrosis and capsular remodeling in later stages.
Muscle Strain
Ninety percent of all muscle injuries are either contusions or sprains. Contusions are caused by blunt extrinsic compressive trauma to the muscle, while strains are caused by intrinsic muscle tearing. Strains most commonly affect muscles spanning two joints, such as the semitendinosus or gastrocnemius.
Excessive tensile forces and tearing of the myofibers at the myotendinous junction commonly leads to disruption of intramuscular vessels and necrosis. This muscle trauma results in release of adenosine triphosphate and protons which activate nociceptors (unmyelinated C or thinly myelinated Aδ nerves) in the muscle belly. Subsequently nociceptors transmit to the central nervous system where the depolarization is perceived as pain. Skeletal muscle healing occurs with regeneration of the myofibers and remodeling of scar tissue.
Patients who sustain a muscle strain typically develop immediate sharp pain in the muscle and exhibit a decrease in ROM acutely. The pain develops into a cramping or pressure-like sensation throughout the muscle. On physical exam, point tenderness is noted along the injured muscle with possible concurrent warmth or edema in the area. ROM is expected to be decreased within the muscle and joint movement it contributes to. Muscle injury is a clinical diagnosis based on patient’s history and physical exam, with findings described above. Imaging with ultrasound and/or MRI can be helpful in identifying small hematomas or muscular tears, but are not recommended unless a patient fails to exhibit expected symptomatic improvement with conservative care.
There is limited research on the treatment of “muscle strain” due to the high variability in presentation and severity. The current treatment regimen is based on the underlying pathophysiology and expert recommendations. Immediate treatment should utilize the RICE protocol-rest, ice, compression, and elevation, which targets the initial bleeding and inflammation after injury. Temporary immobility prevents further damage to the muscle and vasculature, reduces excessive scar formation, and minimizes risk of rerupture. Cryotherapy with ice packs or cold compresses decrease pain and intramuscular blood flow. Compression and elevation minimize edema and bleeding, which interfere with healing and regeneration. NSAIDS are recommended for the acute phase and have been shown to reduce strength loss and soreness after injury.
No specific duration for relative immobility has been formally recommended. Studies have demonstrated scar tissue approximating the ruptured muscle fibers achieves sufficient tensile strength for muscle contraction by day 10. It is essential that patients return to graduated activity within the limits of pain. Early mobilization induces vasculature regrowth, aligns myofibers for faster recovery of preinjury strength, and prevents extensive scarring. , A graduated exercise program should be initiated after rest. The injured muscle should be progressed through isometric, isotonic, and finally dynamic training. Surgery is reserved for severe injuries, including complete thickness muscle tear or tears with significant loss of function. In full thickness muscle strains, injury recovery time can range from 4 to 6 weeks.
Tendinopathy
Tendinopathy is a degenerative overuse tendon injury and describes both tendinitis and tendinosis. Upper extremity tendinopathies frequently involve the biceps, supraspinatus, and medial and lateral elbow tendons. Lower extremity tendinopathies more commonly affect the gluteal, patellar, and Achilles tendons.
Tendinopathies occur with high stress, repeated strains, compression, or shearing forces. Injured tendons exhibit changes in tenocytes, extracellular matrix, and increased inflammation. Biopsies of painful tendon have demonstrated disorganized collagen fibers, increased vascularity, and changes in cellularity and extracellular matrix. Pain from tendon injuries is multifactorial in nature. Studies have shown that local elevations in substance P, prostaglandins, glutamate, and neovascularization with new innervation , , may all contribute to stimulating nociceptors.
Patients with tendon-related pain present with localized tendon pain typically at the enthesis. Local swelling and warmth is commonly seen. Pain is exacerbated with tendon loading, short duration-high force movements, and focal pressure applied to the area.
Ultrasound with color doppler is a highly sensitive tool to visualize neovascularization, tendon thickening, and hypoechoic intratendinous which are changes suggestive of tendinopathy , ( Fig. 6.6 ). MRI is a more specific imaging modality compared with ultrasound and is superior in evaluating degenerative changes. ,
NSAIDs can provide acute pain relief and have been proven to improve the biomechanical properties of injured tendons in animal studies. , NSAID use should be limited to the acute period after injury as it may impair enthesis healing with prolonged use. Similarly, local corticosteroid injections can provide short-term pain relief particularly in upper extremity tendinopathies but there are conflicting studies. Eccentric strengthening exercises may improve pain, function, and strength, by stimulating mechanotransduction for healing, but has not been proven superior or inferior to other isometric or isotonic exercises for pain relief. Exercise is most beneficial when used in conjunction with other physical therapy modalities such as ice, heat, or ultrasound. , There is limited evidence for iontophoresis, phonophoresis, or deep friction massage. Refractory tendinopathy can be treated surgically with tendon debridement, repair, or augmentation.
Several novel treatments are being investigated for tendinopathies. Transdermal and topical nitric oxide has been shown in randomized, double-blind, placebo-controlled trials to improve pain in some chronic tendinopathies. Extracorporeal shock wave therapy (EWST) applies low-energy shock waves to stimulate tenocyte proliferation for repair. EWST is approved by US Food and Drug Administration for lateral epicondylitis and may be promising for other tendinopathies. , , Sclerotherapy ablates neovascularization and potential pain-generating adjacent nerve fibers and has been shown to reduce pain in several small studies. , Regenerative therapies including plasma-rich plasma have shown promise for pain relief and functional improvement. , Gene therapy for altering the inappropriate remodeling pathways in tendinopathy and tissue engineering is currently limited to animal studies.
Radiculopathy
Radiculopathy is dysfunction of a spinal nerve root, caused by mechanical compression and/or chemical irritation. , Degenerative changes of the spine and intervertebral disc protrusions are the most common causes for both cervical and lumbar radiculopathy.
The pathophysiology of pain in radiculopathy is dependent on the underlying etiology. Nerve compression upregulates pain pathways. In radiculopathy caused by herniated discs, proinflammatory cytokines are released by the discs which may stimulate nociceptive fibers causing sensitization and pain. In facet injury, spinal hyperexcitability may cause and perpetuate pain. ,
Radicular pain is commonly described as radiating electric or shooting pain in a dermatomal distribution ( Fig. 6.7 ). In clinical practice, pain characterization is highly variable and can be dull or aching in character with a nondermatomal distribution. If related to mechanical nerve root compression from a disc herniation, symptoms may be exacerbated by coughing or Valsalva. Corresponding sensory, motor, or reflex changes should be noted on neurologic testing. Neurodynamic tests can also aid in diagnosis. The slump test is more sensitive (84%) than the straight leg test, but the straight leg test is more specific (89%) for lumbar radiculopathy secondary to herniated lumbar disc. The Spurling’s maneuver is 89%–100% specific for cervical radiculopathy.
The diagnosis of radiculopathy can be made clinically with a comprehensive history and physical exam. MRI can be utilized to confirm the specific causes of the underlying nerve root dysfunction ( Fig. 6.8 ). One obvious drawback to MRI is its high false-positive rate for discogenic radiculopathy. Electrodiagnostic testing, nerve conduction studies/electromyography (NCS/EMG), is also helpful in confirming the underlying diagnosis and excluding concurrent diagnoses such as peripheral neuropathy, mononeuropathy, or plexopathy.
Most cervical and lumbar radiculopathies resolve spontaneously. , 50% of patients with a lumbar radiculopathy will obtain symptom resolution by 2 weeks and 90% of patients will obtain symptom resolution within 12 weeks. NSAIDs are the mainstay treatment for radicular pain. For an acute inflammatory episode due to herniated disc, oral corticosteroids can be effective in improving function, but may not improve pain. Common adjunctive therapy include opioids for severe pain, short courses of muscle relaxants for concurrent spasms, anticonvulsants (gabapentin, pregabalin), tricyclic antidepressants, or serotonin and norepinephrine reuptake inhibitors (SNRIs) for neuropathic pain relief. , With adequate pain control, physical therapy should be utilized for both cervical and lumbar radiculopathies. Traction and spinal manipulation are controversial manual therapies, but may provide relief in select patients. , ,
Epidural steroid injections can provide both short- and long-term symptomatic relief but responses vary based on the underlying etiology. Patients with symptoms of a cervical radiculopathy due to a disc herniation obtain more relief from an epidural steroid injection compared with those with radicular pain due to underlying spinal stenosis. Operative management is commonly reserved for patients with at least 6 weeks of persistent symptoms and failed nonsurgical treatments. Surgery is indicated on a more accelerated timeline in the setting of progressive weakness, bowel or bladder incontinence ( Fig. 6.9 ).
