INTRODUCTION

The actual technique of examination varies according to individual preference. Nevertheless, developing and adhering to a particular routine can be useful. Familiarity with such a routine ensures that an examiner does not overlook any step in the examination.

The part or region under evaluation must be adequately exposed and in good lighting. Many mistakes are made simply because the examiner does not insist on removing enough of the patient’s clothing to allow proper evaluation and inspection (Fig. 2-1). When examining the involved extremity, the uninvolved extremity is always used for comparison.

CARDINAL SYMPTOMS

Wrist Hand Hip Knee Ankle Foot

Adapted from Kelley WN, et al: Textbook of rheumatology, ed 5, Philadelphia, 1997, WB Saunders.

Peripheral Nociceptors

The skin, joint structures, arterial walls, and periosteum are richly supplied with nociceptors that are activated by a variety of mechanical (stretching), thermal (heat and cold), and chemical stimuli. The main neurotransmitters involved in pain inhibitory pathways are serotonin, norepinephrine, and the endogenous opioids.

Weakness

Weakness of limbs or of the whole body can be an important clue. The pattern of asymmetric or symmetric muscle weakness and its central or peripheral distribution may give vital clues to the diagnosis. Weakness may describe the difficulty that the patient has with movement because of joint disease or the feeling of insecurity that is associated with a loss of proprioception that accompanies many forms of joint disease. Patients may also use the term weakness to describe general fatigue rather than loss of muscle power. True generalized muscular weakness often affects gait and stance. Ankle, knee, and hip movements and strength need to be assessed.

Stiffness

Stiffness is a subjective sensation of resistance to movement that probably reflects fluid distension of the limiting boundary of the inflamed tissue. Stiffness resulting from this phenomenon is most noticeable when arising from bed and after inactivity or rest. As normal use resumes, fluid clears from the inflamed structures, and stiffness wears off. The duration and severity of early-morning stiffness (or stiffness after sleep) and inactivity stiffness reflect the degree of local inflammation.

Disability and Handicap

Disability is present when a tissue, organ, or system cannot function adequately. A handicap exists when disability interferes with a patient’s daily activities or social or occupational performance. A marked disability does not necessarily cause a handicap. Conversely, minor disability may produce a major handicap. Both states of disability and handicap require separate assessment, with the evaluation of disability being a purely medical activity, whereas handicap assessment is often a medicolegal function. Patients’ perceptions of their problems is a product of their adaptation to the depreciated tissue, as well as aspirations for recovery (Box 2-1).

SYSTEMIC ILLNESS

Inflammatory musculoskeletal disease may trigger a marked acute-phase response and cause nonspecific symptoms of systemic upset. Symptoms may include fever, reduced appetite, weight loss, fatigue, lethargy, and irritability. The patient might not volunteer specific complaints but might report feeling ill. Florid, acute inflammation may cause confusion, especially in older adults.

Modified from Kelley WN, et al: Textbook of rheumatology, ed 5, Philadelphia, 1997, WB Saunders.

CARDINAL SIGNS

7. Renal disorder 8. Neurologic disorder 9. Hematologic disorders 10. Immunologic disorder 11. Antinuclear antibody An abnormal titer of antinuclear antibody by immunofluorescence or an equivalent assay at any point in time and in the absence of drugs known to be associated with drug-induced lupus syndrome

ECG, Electrocardiogram; LE, lupus erythematosus.

From Tan EM, et al: The 1982 revised criteria for the classification of SLE, Arthritis Rheum 25:1271, 1982.

Features of dermatomyositis rash allow discrimination from lupus. These features include occasional nasolabial fold involvement, prominent heliotrope and extrafacial involvement, erythema following the course of extensor tendons, and scaling and fissuring of lateral aspects of the fingers (mechanic’s hands). A heliotrope rash and Gottron papules are characteristic and possibly pathognomonic cutaneous features of dermatomyositis. The heliotrope rash consists of a violaceous to dusky erythematous rash, with or without edema, in a symmetrical distribution involving periorbital skin.

Tenderness

Precise localization of tenderness is the most useful sign in determining the cause of the problem. Joint line or capsular tenderness signifies arthropathy or capsular disease around the whole margin. Localized joint line tenderness suggests intracapsular pathologic processes. Periarticular point tenderness, away from the joint line, usually signifies bursitis or enthesopathy.

The only reliable finding on examination in fibromyalgia is the presence of multiple tender points. The diagnostic utility of a tender point evaluation has been objectively documented with the use of a dolorimeter or algometer, pressure-loaded gauges that accurately measure force per area, and with manual palpation. The criteria of at least 11 of 18 tender points are recommended for classification purposes but should not be considered essential in individual patient diagnoses. Patients with fewer than 11 tender points can be diagnosed with fibromyalgia, provided other symptoms and signs are present. An investigation must be made to determine whether the fibromyalgia is primary or secondary. The Leeds Assessment of Neuropathic Symptoms and Signs helps differentiate neuropathic pain and fibromyalgic pain (Box 2-2).

Warmth

Warmth is one of the cardinal signs of inflammation. The back of the examiner’s hand is a sensitive area for comparing skin temperature above, over, and below an inflamed structure.

Painful Arc of Movement

Ligament injuries are detected by eliciting tenderness over the damaged portion of the affected tendon. Injuries are also detected in attempting to distract the bony structures held together by the ligament of interest.

When the tendon is subjected to disease or excessive load, it may rupture. In tendon disease or injury less than rupture, tendon inflammation usually results. Tendinopathy is detected by eliciting a painful arc of active movement in the plane of action of the affected tendon. Passive movement in the same plane is almost pain free (Table 2-6).

Fixed Deformity

Although articular deformity may be observed at rest, most become more apparent when the limb is bearing weight or being used. The examiner should determine whether the deformity is correctable or noncorrectable. Many conditions are associated with characteristic deformities, but no deformity is pathognomonic of any single disease (Table 2-7). Shorthand terms are used for combined deformities, such as swan-neck finger deformity for hyperextension at the proximal and fixed flexion at the distal interphalangeal joints.

TABLE 2-7 SPECIFIC MUSCULOSKELETAL DEFORMITIES

Lower Limb	Upper Limb
Hallux abductovalgus Genu varum Genu valgum Dislocation of the patella Valgus deformity of the heel Coxa vara Pes planovalgus Fixed flexion of the knee Fixed flexion of the hip

DIPs, Distal interphalangeal joints; MCPs, metacarpophalangeal joints; PIP, proximal interphalangeal joints.

Movement

Every joint has a normal range of motion. The range of motion for any joint varies with age, gender, and ethnic origin. A range of movement that is beyond the upper limit represents hypermobility. Ranges below the lower limit represent hypomobility. The normal joint range of motion is diminished by joint inflammation or by irreversible damage to the joint structures. In trauma or disease, movement is first lost from the extreme end ranges. Increasing joint damage results in more profound loss of range of motion. The complete loss of movement of a joint is known as fixation ankylosis or joint ankylosis, depending on soft-tissue versus bony involvement, respectively. Fixation or joint ankylosis is further complicated by the involvement or loss of multiple planes of motion (Table 2-8).

TABLE 2-8 JOINT PLANE MOTION CHARACTERISTICS

Type	Planes	Joints
Hinge	One	Elbow, knee, ankle, MCP, PIP, DIP, MTP
Two-way hinge	Two (circumduction)	Wrist, trapeziometacarpal
Ball and socket	All planes	Shoulder, hip

DIP, Distal interphalangeal; MCP, metacarpophalangeal; MTP, metatarsophalangeal; PIP, proximal interphalangeal.

Hypermobility is recognized by a series of passive maneuvers collectively known as the 9-point scale of Beighton (Box 2-3). The Beighton modification of the Carter and Wilkinson scoring system has been used for many years as an indicator of widespread hypermobility. A high Beighton score by itself does not mean that an individual has HMS. It simply means that the individual has widespread hypermobility. Diagnosis of Hypermobility Syndrome or HMS should be made using the Brighton Criteria. The Beighton score is an easy to administer 9-point scale where points are given for the performance of five maneuvers. It is generally considered that hypermobility is present if 4 out of 9 points are scored. The scale was not designed for clinical use and has been criticized because it only samples a few joints and gives no indication of the degree of hypermobility.

Stability

The stability of a joint depends partly on the integrity of its articulating surfaces and partly on its intact ligaments. When a joint is unstable, mobility is abnormal. When testing for abnormal mobility, the examiner must ensure that the muscles controlling the joint are relaxed. A muscle in strong contraction can often conceal ligamentous instability (Table 2-9).

TABLE 2-9 JOINT INSTABILITY FINDINGS

Passive side-to-side movement of the tibia on the femur (collateral knee ligaments) Passive anteroposterior movement of the tibia on the femur (cruciate ligaments) Gross genu recurvatum Positive Trendelenburg sign Arthritis mutilans—flail interphalangeal joints Spontaneous dislocation of the shoulder or patella Pes planus (collapse of the longitudinal arch)

Crepitation

Crepitation is a palpable crunching sensation present throughout the movement of the involved joint or enthesis structure. Fine crepitation may be audible only by stethoscope and is not transmitted through the adjacent bone. Fine crepitation may accompany inflammation of the tendon sheath, bursa, or synovium. Coarse crepitation may be audible at a distance and is palpable through the bone. Coarse crepitation usually reflects cartilage or bone damage (Table 2-10).

Muscular Atrophy

Muscle atrophy is a common sign but can be difficult to detect, particularly in older adults. Synovitis quickly produces local spinal reflex inhibition of muscles acting across the joint. Atrophy can be rapid (within several days) in septic arthritis. Severe arthropathy produces widespread periarticular wasting. Localized atrophy is more characteristic of a mechanical tendon or muscle problem or nerve entrapment. Disuse atrophy is complex and highly regulated biochemical process (Table 2-11).

TABLE 2-11 SIGNALS INVOLVED IN DISUSE-INDUCED MUSCLE ATROPHY

Signals	Finding	Function
PI3K, Akt	Decreased	Promotes protein degradation Inhibits protein synthesis

FOXO1, FOXO3 Increased mTOR, p70S6K, eIF4B Decreased Inhibits protein synthesis PHAS-I Increased Inhibits protein synthesis p50, c-Rel, Bcl-3 Increased Promotes protein degradation Myostatin, ActIIB Increased Inhibits protein synthesis? p38 Increased Promotes protein degradation Erk Increased Promotes glucose uptake? JNK Increased Increases insulin resistance Calcineurin Increased Compensatory mechanism? ROS Increased Promotes protein degradation MAFbx, MuRF1 Increased Promotes protein degradation

Signal abbreviations: ACTIIB, Myostatin receptor; Akt, serine/threonine kinase; Bcl-3, transcriptional coactivtor; Calcineurin, serine/threonine phosphatase; c-REL, NF-kB family transcription factor; E1F4B, eukaryotic translation initiation factor 4B (homo sapiens); ERK, extracellular signal-regulated kinase; FOXO, Forkhead family of transcription factor; JNK, c-JUN N-terminal kinase; MAFbx, muscle atrophy f-box ubiquitin ligase; mTOR, mammalian target of rapamycin; MuRF1, muscle ring finger 1 ubiquitin ligase; Myostatin, inhibitor of skeletal muscle mass; p38, p38 isoform mitogen activated protein; p50, NF-kB family transcription factor; p70S6K, 70-kDa ribosomal protein s6 kinase; PHAS-I, eukaryotic initiation factor 4E-binding protein; PI3K, phosphatidylinositol 3-OH kinase; ROS, reactive oxygen species.

Adapted from Zhang P, Chen X, Fan M: Signaling mechanisms involved in disuse muscle atrophy, Med Hypoth 70(2):314–316, 2008.

Fasciculations

Fasciculations are visible, spontaneous contractions of muscle fibers supplied by a single motor nerve filament. Visible dimpling or twitching may occur. Fasciculations occurring during muscular contraction (twitching) are associated with conditions of irritability, resulting in poorly coordinated contraction of small and large motor units (spasmophilia). Benign fasciculation occurs in normal individuals and in muscle of normal strength and size. Fascicular twitches noted during rest, with exaggerated muscular weakness and atrophy, are characteristic of peripheral motor neuron disorders. Acute denervation of skeletal muscles results in spontaneous contractions of muscle fibers.

Cramps and Spasm

Muscular spasm, or tremor (Table 2-12), may occur at rest or with movement. Spasms and tremors occur in the normal individual with metabolic and electrolyte alterations. Cramping is a common complaint after excessive sweating and subsequent hyponatremia, hypocalcemia, hypomagnesemia, or hyperuricemia (electrolyte imbalance).

TABLE 2-12 TREMOR CLASSIFICATION

Cause	Type and Rate of Movement	Description
Anxiety	Fine, rapid, 10 to 12/sec	Irregular, variable Increased by attempts to move part; decreased by relaxation of part

Parkinsonism Fine, regular, or coarse, 2 to 5/sec Cerebellar tremor Variable rate Essential or senile Coarse, 3 to 7/sec Involves the jaw, sometimes the tongue, and sometimes the entire head Metabolic  

From Barkauskas VH et al: Health & physical assessment, ed 2, St Louis, 1998, Mosby.

Tetany

Hypocalcemia and hypomagnesemia often cause the involuntary spasms of skeletal muscle, which resemble cramping. Tetanic cramps can be elicited by repeatedly percussing the motor nerve that leads to a muscle group contraction-cramp-spasm at frequencies of 15 to 20 per second. Chvostek sign is the spasm of facial muscles produced by tapping over the facial nerve near its foraminal exit. Chvostek sign may also occur with normocalcemia, as well as with hypocalcemia.

Impairment of Gait

Finding a spinal or lower extremity orthopedic or neurologic disorder that does not produce abnormalities of gait at some time during its course can be difficult.

Bladder Control

Incontinence and other disturbances of urinary bladder function are occasionally the first manifestation of disease of the spinal cord, as well as the rest of the nervous system. The physiologic mechanism of micturition is complex. The terms atonic bladder and spastic bladder are no longer useful in describing different levels of neurologic involvement because they are related mainly to local factors in the bladder wall.