Introduction

The musculoskeletal system is designed primarily for locomotion, movement, and performance of functional physical tasks and to mechanically support and protect the body’s organs. The system consists of muscles and tendons, ligaments, bones, joints, intervertebral discs, and their associated tissues such as synovial capsule, cartilage, fascia, and other fibrous tissues. However, these tissues should not be considered in isolation—their function depends on complex neurologic, biomechanical, and physiologic interactions. This chapter will discuss the biology of musculoskeletal tissues and their responses to injury and rehabilitation, and will introduce the complex interactions between the musculoskeletal system and the rest of the body as whole. Finally, an overview of common musculoskeletal ailments from a variety of body parts will be presented as examples of these principles.

A more detailed review will be provided in “Section III: Ambulatory Care: Sports, Musculoskeletal, and Pain Medicine” of this textbook.

Skeletal muscle comprises 40 to 45% of the total body mass, converting chemical energy derived from food intake into generation of mechanical force.¹ Muscles also contribute to essential body functions such as generation of heat; blood glucose regulation; and storage of lipids, carbohydrates, and amino acids.² Muscles typically attach to bones with strong tendons, the fibers of which branch deep within the muscle bellies. Tendons consist of bundles of collagen that form sequentially larger fascicles. These are often covered by synovial tissues that bathe the tendon in a thin layer of tenosynovial fluid for lubrication and nutrient delivery. Others are covered only by muscular tissue or a dense sheath of connective tissue known as peritenon. Most muscular strain injuries occur at the muscle–tendon junctions. These can be toward the end of the muscle belly where it tapers to become predominantly tendon tissue or deep within the muscle along the tendon fibers. Tendons themselves are also commonly injured at the bony attachments (entheses) and within areas of particular high stress (i.e., where they wrap around bony prominences) or in areas of low vascularity such as the mid-substance of the Achilles tendon.

Ligamentous tissues connect bone to bone. In the process, they form joint capsules, provide stability, and assist with energy conservation. Examples include knee collaterals, which are firm and minimally elastic, providing structure stability, and the shoulder capsular (glenohumeral) ligaments, which are thin and pliable and allow for a large range of motion. The iliofemoral (“Y”) ligament provides support in standing and therefore allows reduced muscular activity. It controls external rotation in flexion and both internal and external rotation in extension; this stores energy as the hip goes into extension, allowing for more efficient gait.³

Cartilaginous tissue cushions the spaces between bones and provides a smooth surface to reduce friction within joints. Two major cartilage types are hyaline and fibrocartilage. Both are matrices consisting of living cells (chondrocytes); a nonliving framework supports the chondrocytes and provides for the tissue’s mechanical properties. In response to injury, fibrocartilage can be formed and fills in gaps created within hyaline cartilage, but is without the ideal mechanical properties of the native tissue. Articular cartilage is particularly good at cushioning against impact forces, but is susceptible to injury from shear forces. Therefore, biomechanical abnormalities that result in shear forces across joints (i.e., malalignment, ligament laxity, and underlying bony injury) predispose joints to loss of cartilage and degenerative joint disease.

Dysfunction due to disuse is also common as flexibility and strength diminish rapidly with immobilization. Deconditioning also affects the cardiovascular, respiratory, neurologic, and skeletal systems. Lack of mobility and pain with movements may also result in decreased community ambulation and therefore more social isolation. Social isolation, sleep deprivation, or even pain itself may lead to psychological stress and depression, potentiating chronic pain syndromes. Decreased effectiveness of the cardiopulmonary system as a result of deconditioning leads to decreased exercise tolerance, potentiating muscular atrophy and osteopenia. The human body is thus dependent on the musculoskeletal system to not only provide a functional capacity, but also plays a significant role in maintenance of physiological and neuropsychological homeostasis.

Kinetic Chain

The body is a linked system of interdependent segments, often working in a proximal-to-distal sequence to perform a desired action at the distal segment.⁴ Hence biomechanical dysfunction in one body region is capable of causing injury at a distance, a concept otherwise known as kinetic chain.⁵ The concept of kinetic chain should be considered when assessing many of the common musculoskeletal syndromes encountered in clinical settings. Assessment of shoulder impingement syndrome would be incomplete without additional consideration of scapular stability, cervical and upper torso posture, and even lower extremity dysfunction, especially for overuse or repetitive stress injuries.

Tissue Repair

The musculoskeletal system is a multicomponent system composed of muscle, connective tissue, tendon, ligament, and bone vessels.⁶ Damage to tissues initiates a cascade of events leading to the inflammatory and repair process. If tissue injury is severe or chronic, healing may not be accomplished with natural regeneration. Chronic inflammation stimulates scar formation and is the predominant healing process that occurs with severe injury (extensive damage to the extracellular matrix). Fibrosis is characterized by the extensive deposition of collagen that occurs under these conditions. Adequacy of tissue healing may be affected by both systemic and local factors. Systemic factors include age, psychological stress, alcohol consumption, smoking, nutrition status, obesity, metabolic status (e.g., diabetes mellitus), medications, circulatory status, and hormones (e.g., glucocorticoids inhibit collagen synthesis).⁷ Local factors include vascular supply/oxygenation, infection, mechanical factors (early or excessive motion of injuries may delay healing), location, and type of injury. Even after completion of the healing process, ongoing pain and dysfunction commonly persist. For example, the fibrosis that occurs after a hamstring strain leads to changes in muscle length, altering optimal relationships and decreasing ability for maximal muscle contraction. This has been postulated as a mechanism for recurrent muscular strains.^8,9

Extrinsic and Intrinsic Risk Factors of Injury

A variety of risk factors are associated with musculoskeletal injuries and may be categorized as either extrinsic or intrinsic. Extrinsic risk factors are external or environmental characteristics outside of the immediate anatomic/biological system that influence a person’s injury risk.¹⁰ Extrinsic risk factors include use or misuse of protective equipment, skill level, work tasks, or weather conditions. Intrinsic risk factors are characteristic of a biological or psychological nature that may predispose an individual to injury. A nonexhaustive list of intrinsic risk factors includes age, sex, previous injury and adequacy of rehabilitation, aerobic fitness, body size, limb dominance, flexibility and laxity, muscle strength, imbalance and reaction time, central motor control, psychological and psychosocial factors, mental ability, postural stability, and anatomic alignment/morphology. Extrinsic factors may interact with predisposing intrinsic factors to increase likelihood of injury.¹¹

Risk factors can be further subdivided into modifiable and nonmodifiable factors. Although it is important to acknowledge and study the presence of nonmodifiable risk factors, it is also important for the clinician to identify modifiable ones, and a complete understanding of mechanism of injury is required, including the concept of kinetic chain. Identifying and addressing modifiable risk factors is key to prevention and treatment of musculoskeletal injury.

Shoulder

The shoulder is a complex joint that sacrifices stability for mobility. The rotator cuff musculature contributes to dynamic stability of the glenohumeral joint. The other main articulations are the acromioclavicular (AC) joint and the scapulothoracic joint.

Due to its complexity, as well as possible referred pain from the cervical spine, identification of the pain-generating structure in the shoulder may prove challenging. Fortunately, treatment of the various syndromes often overlaps. Goals of a physical therapy program are to normalize scapular stability, posture, and strengthening/stabilization. Treatment of pain is often necessary to facilitate therapy. This is usually possible with analgesic (including nonsteroidal anti-inflammatory medications) and intra-articular steroid/anesthetic injection (which also may aid with diagnosis).

Acromioclavicular Joint Pain

AC joint pain commonly localizes onto the superior aspect of the shoulder. Symptomatic AC joint pain will demonstrate focal tenderness on the joint itself and a positive “scarf test” (cross-arm adduction test). Imaging may also demonstrate degenerative changes or traumatic osteolysis of the clavicle, especially in individuals who do excessive overhead lifting.

Subacromial Bursitis

This bursa provides cushioning and lubrication within the confines of the subacromial space. Pain and inflammation may result from impingement of the bursa and rotator cuff underneath the acromion. Surgical intervention with acromioplasty and repair of associated rotator cuff tears may be warranted.

Rotator Cuff Injury

Chronic overuse or direct injury to the rotator cuff musculature may result in varying degrees of injury and functional deficit. The supraspinatus, followed by the infraspinatus tendon, are most commonly affected. Patients typically present with weakness on active abduction and/or external rotation. Small rotator cuff tears often can be managed conservatively. Full-thickness injuries should be addressed with surgical repair promptly to avoid tendon retraction. Severe chronic full-thickness tears with retraction may also be managed conservatively, depending on the patient’s functional needs. In some instances, radiographic imaging of the shoulder may demonstrate superior migration of the humeral head as a result of the absence of the supraspinatus tendon (Fig. 4–1).

Adhesive Capsulitis (Aka Frozen Shoulder)

Presents after rotator cuff injury, periods of immobilization, or idiopathically. Diabetic patients, particularly with poor glucose control, are more likely to develop this condition. It initially presents with severe pain and progressive stiffness over a 9-month period followed by a “frozen” phase for 9 to 15 months and a “thawing” phase over a period of up to 2 years.¹²

Elbow

There are three articulations within the elbow: humeroulnar, humeroradial, and proximal radioulnar joints, which aid in flexion, extension, supination, and pronation. When the arm is fully extended, there is normally an anatomic valgus alignment (carrying angle), which is greater in women. The common extensor tendon origin is located at the lateral epicondyle, while the common flexor tendon origin is located at the medial condyle.

Lateral Epicondylitis (Tennis Elbow)

The name implies an inflammatory process and is thus a misnomer, as the pathology is tendinosis, most commonly resulting from microtears of the extensor carpi radialis brevis tendon. Pain over the epicondyle and weak grip strength are common complaints and are reproduced on examination with resisted wrist extension. Conservative treatment may include rest; a tennis elbow brace, which unloads the common extensor origin; anti-inflammatory medications; and modalities such as strengthening. Corticosteroid injections may prolong healing and result in worse long-term outcomes.¹³ Other treatments such as dry needling, prolotherapy, and platelet-rich plasma (PRP) are showing promise; however, further studies are needed to establish efficacy. Surgical intervention may be required if conservative treatments fail.

Medial Epicondylitis (Golfer’s Elbow)

With medial epicondylitis, the most prominently affected tendons are the origins of the flexor carpi radialis and pronator teres (in contrast to lateral epicondylitis in which the extensor tendons are affected). Mild ulnar neuropathy may also develop. Treatment is similar to that of lateral epicondylitis, and surgical intervention is rarely indicated.

Ulnar Nerve Entrapment Neuropathy (Cubital Tunnel Syndrome)

Cubital tunnel syndrome is the second most common peripheral nerve entrapment syndrome after carpal tunnel syndrome. Patients present with weakness in the ulnar nerve–innervated muscles of the hand, as well as with sensory deficit in the ulnar nerve distribution. Electrophysiologic studies may be helpful with diagnosis. Cervical nerve root compression should also be considered.

Wrist/Hand

There are eight carpal bones arranged in two rows (Fig. 4–2A and B). The articulation between the rows is referred to as the midcarpal joint. There are five carpometacarpal (CMC) joints, five metacarpophalangeal (MCP) joints, four proximal interphalangeal (PIP) joints, four distal interphalangeal (DIP) joints, one interphalangeal joint (IP) in the thumb, and a distal radial ulnar joint (DRUJ). The triangular fibrocartilage complex (TFCC) is located between the distal ulna and carpal bones and acts as the primary stabilizer of the DRUJ. Normally the wrist functions in flexion, extension, and radial and ulnar deviation.

Carpal Tunnel Syndrome

This is syndrome is the most common peripheral mononeuropathy.

The carpal tunnel is a fixed space surrounded by the flexor retinaculum and contains nine flexor tendons and the median nerve. Being a fixed space, any inflammatory or mechanical process leads to median nerve compression and furthers the cycle of inflammation. Patients typically present with pain and paresthesia in the median nerve distribution (radial three and a half digits of the hand), with symptoms most prominent at night. Electrophysiologic studies are diagnostic and helpful in determining severity of nerve damage. Risk factors include female gender, pregnancy, metabolic disorders, repetitive stress, and prior wrist fracture. Conservative treatment includes activity modification, night splinting, anti-inflammatory medications/modalities, nerve-stabilizing medications, and corticosteroid injections. Surgical intervention with carpal tunnel release is indicated for cases unresponsive to conservative measures or those with neural deficits.

Carpal Metacarpal Joint (CMC) Osteoarthritis

Osteoarthritis (OA) at the first CMC joint (base of the thumb) is the most common arthropathy of the wrist/hand. Diagnosis is established by symptom location, grind test (pain with axial loading of thumb CMC joint), and correlation with x-ray. De Quervain’s (first extensor compartment) tenosynovitis should be included in the differential diagnosis. Treatment includes anti-inflammatory medications and modalities, thumb splinting, and corticosteroid injection. Surgical reconstruction or fusion may be necessary.

Wrist/Hand Arthritis

The wrist and hand can be affected by both rheumatoid and osteoarthritis. In rheumatoid arthritis symmetrical swelling of the MCP and PIP joints occurs. Long-standing disease results in ulnar deviation of the fingers, dorsal subluxation of the ulna, ulnar styloid erosion, and finger deformities. X-rays demonstrate periarticular osteopenia and erosions. Conversely, osteoarthritis is a noninflammatory process that results in articular cartilage deterioration and osteophytes at the bone margins. Patients can exhibit Heberden’s nodules at the DIP joints and Bouchard’s nodules at the PIP joints (Fig. 4–3). There is usually tenderness over the affected joint and crepitus with range of motion, but stiffness often improves with 10 to 15 minutes of motion. Plain films aid in diagnosis, but are often not necessary. Treatment for all forms of hand arthritis includes lifestyle modification, nonsteroidal anti-inflammatory drugs (NSAIDs), bracings, and therapy. For inflammatory (rheumatoid) arthritis disease-modifying antirheumatic drugs (DMARDs)/biologic agents and joint replacement are common treatments.