After a peripheral nerve lesion, muscle denervation and sensory loss contribute to upper extremity prehensile limitations, leading to incoordination and maladaptive strategies.
The key to successful rehabilitation is to adhere to precautions initially to protect the nerve after repair, then provide carefully designed therapeutic activity and exercise as the individual progresses through the phases of recovery.
Greater emphasis placed on fostering neural reorganization and recovery of sensorimotor control may enhance achievement of flexible and efficient prehensile skill following nerve injury and repair.
Prehensile skill is often taken for granted until it is lost or diminished, as in the case of peripheral nerve injury (PNI). After a peripheral nerve lesion, muscle denervation and sensory loss contribute to prehensile limitations, leading to incoordination and maladaptive strategies. To effectively foster neural recovery and prehension following injury, clinicians should address not only impairments and function but motor control through the provision of specific sensory and motor experiences.
This chapter (1) considers adaptations to injury; (2) reviews the clinical presentation following injury; (3) discusses evaluations to establish a baseline and monitor neural recovery; and (4) reviews rehabilitation tactics used to prevent deformity and enhance recovery and prehensile skill.
Adaptation to Injury
Immediately after PNI the central (CNS) and peripheral nervous systems (PNS) adapt to a reduction in sensory input. Neural adaptation to changes in input, or plasticity, ranges from axonal degeneration to topographic reorganization. , The residual effects of PNI depend on the degree of axon and connective tissue involvement (see Chapters 42 and 43 ). Table 45-1 (online) shows the relationship between injury classification schemes by Seddon and Sunderland. , An appreciation of postinjury adaptations may aid in the design of effective interventions.
|Neurapraxia (Sunderland I)||Interruption of nerve conduction, some segmental demyelization; axon continuity intact||Reversible|
|Axonotmesis (Sunderland II)||Axon continuity disrupted; neural tube intact||Wallerian degeneration, intact endoneurial tubes, may have incomplete recovery|
|Neurotmesis (Sunderland III–V)||Complete disruption of nerve continuity; loss of axons with select loss of neural tubes and other neural elements||No spontaneous recovery, surgical repair required|
Early Peripheral Changes
Postinjury peripheral changes include the onset of Wallerian degeneration and initiation of neural recovery. Wallerian degeneration involves axonal disintegration and demyelination distal to the lesion site, and phagocytic macrophages interact with Schwann cells to remove debris. With long-standing nerve injury, the endoneurial tubes shrink and collapse due to a reduction in cross-sectional area and the end-organs often degenerate.
Following a PNI, nerve function diminishes in the largest diameter fibers first and later the smallest. Large-diameter fibers (group A and B) are myelinated with a fast conduction rate, and small fibers (C or IV) are unmyelinated with a slower conduction rate. After a nerve lesion, functional loss may proceed in the following sequence: motor, proprioception/vibration, touch, pain, and sudomotor function. Large-diameter fibers carrying motor, proprioceptive, and vibration information may be lost first, yet may be the last to return. Because pain information is primarily carried by the smallest diameter fibers, it is usually one of the last sensations to be lost and the first to return.
Recovery from PNI involves remyelination, collateral sprouting of axons, and axonal regeneration. Regeneration following neurapraxia or axonotmesis begins immediately, whereas a neurotmesis usually requires nerve repair. After a 2- to 3-week latency period, a repaired nerve begins to regenerate. For the nerve to regenerate, the central axon must survive, the environment must support axonal growth, the axon must make timely contact with receptors, and the CNS must integrate signals from the PNS. Axonal regeneration is guided by Schwann cells. In a favorable environment, the axon sprouts a “finger-like” growth cone initiating the process, and the Schwann cells provide a source of neurotrophic factors, which diffuse across the distal to proximal stump. The regrowth rate in adults is 1 to 3 mm a day or more for a nerve laceration and repair , and about 3 to 4 mm a day after a crush. The timing for axon regrowth after relief from nerve compression is more variable.
Factors that influence nerve recovery include (1) the lesion type (e.g., crush, stretch, laceration); (2) distance from the cell body; (3) age; (4) time since injury; (5) health; and (6) genetic factors. Genetic factors include muscle fiber type, density, motor unit number, height, and weight. Constraints that influence recovery include the ability of the axon to cross the repair site, a slow rate of axon regrowth, and mismatching of sensory and motor fibers. Research examining methods to overcome constraints has included the use of neurotrophic factors, electrical stimulation, and exercise. These methods are reviewed later in the chapter.
Early Central Changes
Lost or diminished sensory input induces CNS changes, including remodeling of cortical and subcortical structures and alterations at the spinal cord level. Neural reorganization may stem from any one of the following mechanisms:
Removal or unmasking of inhibitory controls in the affected region. , For example, changes in excitatory and inhibitory mechanisms in the spinal cord may alter tonic inhibition, causing tactile hypersensitivity.
Migration of cells that serve other body parts into deafferented cortical regions ,
Strengthening of existing connections and subthreshold excitatory inputs based on postinjury experience
Reorganization of subcortical regions that project to the cortex such as the basal ganglia, brainstem, or thalamus ,
Neurogenesis and sprouting of new pathways ,
Feedback and Anticipatory Control
Somatosensory feedback and anticipatory control are essential components of grasp and manipulation. Current visual information and memories from past sensorimotor experiences are used to preshape the hand ( Fig. 45-1 ) in advance of contact to accommodate object size and shape, aiding the acquisition of stable grasp points. Visual and somatosensory information are also used to anticipate the frictional conditions at the digit–object interface and estimate object weight to adequately grade fingertip forces (grip and load) used to grasp and lift objects. , If anticipatory control is sufficient, the peak rate of increase in grip (normal or squeeze) and load (tangential or lift) force will be higher for heavier or more slippery objects.
Performance during reach-to-grasp tasks, including the movement path, velocity, and finger width (aperture), and exhibited during grip formation can be examined using kinematic (spatial–temporal) analysis. Kinetic (force) information on fingertip force scaling can be obtained from multiaxial force transducers shown in Figure 45-2A and documented as shown in Figure 45-2B . Kinematic and kinetic analyses allow for close examination of alterations in the spatiotemporal features of the movement and force control as occurs when sensory input is distorted or absent, as in cases of denervation, , focal hand dystonia, and large-fiber neuropathy.
Previous kinematic and kinetic analyses indicate there is a strong relationship between impaired visual skills or somatosensation and anticipatory control. Visual or somatosensory deficits may lead to insufficient finger opening, object grasp at incorrect contact points, slips at object contact, temporal delays, and the use of excessive fingertip forces during fine-motor tasks. PNI can impair the sebaceous glands in the fingertips, causing objects to seem more slippery. If somatosensory input is diminished, grip force and movement time may increase to prevent slips and ensure success. To examine the effect of injury on fingertip force scaling, Cole and colleagues induced median nerve compression and then generated sensory nerve action potentials via electric stimulation proximal to the carpal canal. It was not until the compression caused a 50% reduction in sensory nerve action potentials that sensibility began to diminish and subjects began to use greater than 50% increase in grip force to secure objects.
Secondary to diminished sensation and muscle denervation experienced after PNI, the number of motor units and joint motion available is reduced. Thus, altered sensory and motor function reduces the degrees of freedom or the number of ways the involved hand and arm can move, necessitating the use of alternative prehensile patterns. For example, after a radial nerve injury there is little active wrist and finger–thumb extension. Thus, it may be difficult to preshape the hand in preparation for object contact. After median nerve injury, thenar muscle denervation may require a shift from precision to power grips or the use of bilateral versus unilateral grip patterns. With a low ulnar nerve injury, a visible Froment’s sign (excess thumb interphalangeal [IP] joint flexion during lateral pinch) suggests that the adductor pollicis is affected, resulting in overpowering from the flexor pollicis longus to pinch. Fingertip force generation is significantly affected by median and ulnar nerve injuries, influencing dexterity and handedness. Although activation of intact muscles aids function, coordination is compromised, increasing the effort used, and, therefore, the cost of engaging in prehensile tasks.
Presentation of Specific Nerve Injuries
Radial Nerve Injury
Injury to the radial nerve can stem from humeral shaft fractures (middle and distal third), elbow dislocations, fractures, and compression between the head of the radius and the supinator (radial tunnel syndrome). Nerve compression in the axilla from the incorrect use of crutches or awkward sleeping postures (Saturday night palsy) can also lead to a radial nerve injury. The effect of injury on function depends on the level of the injury ( Fig. 45-3 ). A “wrist drop” is the classic deformity associated with a radial nerve injury characterized by forearm pronation, wrist flexion, thumb flexion and abduction, slight metacarpophalangeal (MCP) joint flexion, and IP joint extension ( Fig. 45-4 ). The individual is unable to extend the wrist and fingers simultaneously or abduct the extended thumb. Depending on the level of the injury, there may be atrophy of the dorsal forearm due to involvement of the finger and thumb extensors and the extensor carpi ulnaris. With higher level injuries there may be atrophy of the extensor muscle mass near the lateral epicondyle due to involvement of the brachioradialis, extensor carpi radialis longus and brevis, or the triceps.
The sensory branch of the radial nerve can be injured at the wrist as it resurfaces in the anatomic snuff box. Injury mechanisms may include a radioulnar joint dislocation or nerve compression (wrist-band injury). A lesion at this level only affects sensibility on the dorsal thumb, index, middle, and radial side of the ring finger to the PIP joint (excluding the nail beds), with some variation.
Forearm- or Elbow-Level Injury
Forearm-level injury can result in full or partial denervation of the following muscles: extensor carpi ulnaris (ECU), extensor digitorum communis (EDC), extensor digiti minimi (EDM), abductor pollicis longus (APL), extensor pollicis longus (EPL), extensor pollicis brevis (EPB), and extensor indicis proprius (EIP). Forearm-level injuries can result in lost or diminished ulnar wrist extension, MCP joint extension of all digits, and thumb abduction or extension. As described for low-level injuries, sensibility through the dorsoradial aspect of the hand is affected.
Elbow-level lesions result in diminished sensibility to the dorsoradial portion of the hand and full or partial denervation of the muscles described earlier with the addition of the supinator, extensor carpi radialis longus (ECRL), and extensor carpi radialis brevis (ECRB). With injury at this level, radial wrist extension is lost or weakened, and supination is weakened. Lesions proximal to the elbow also involve the brachioradialis and triceps, resulting in the addition of slightly weakened elbow flexion and lost or weakened elbow extension.
Lost or diminished sensibility on the dorsoradial aspect of the hand from a wrist-level injury (or higher) has little effect on hand function because the volar surface continues to obtain the sensory input needed for prehension. However, the injured individual should remain vigilant during daily tasks to prevent superficial injury or scalds and burns to the dorsum of the hand. Forearm- or elbow-level lesions limit the ability to turn the hand over and extend the wrist to receive objects. Inadequate wrist stabilization may prevent the formation of stable prehension patterns, such as a spherical grip or radial digital grasp used to open jars or bottles and to perform manipulative tasks such as buttoning. Limited finger and thumb extension will hinder grip formation and object release and may lead to hand asymmetries as found in other populations. To compensate for poor grip formation, the wrist may flex to passively extend the fingers or objects may be transferred to the involved hand by the noninvolved hand. Object release may be accomplished by wrist flexion, shaking objects free, or through use of the noninvolved hand to retrieve them. Reach-to-grasp activities and tasks such as writing or typing are difficult to complete with the wrist in flexion and the fingers and thumb in extension, limiting the use of adequate grip force.
Median Nerve Injury
Injuries to the median nerve can result from lacerations, humeral fractures, elbow dislocations, distal radius fractures, and lunate dislocations into the carpal tunnel. Nerve compression can occur between the two heads of the pronator teres (pronator syndrome), when it branches off as the anterior interosseous nerve and in the carpal tunnel. Functional changes associated with median nerve injury depend on the level of injury ( Fig. 45-5 ). The classic deformity associated with a median nerve injury is the sign of “benediction” with the thumb resting in adduction and the index and long fingers in extension and adduction. With higher-level lesions there may be atrophy of the pronator teres and flexor carpi radialis resulting in loss of volar muscle mass near the medial epicondyles. Thenar muscle atrophy is often visible with long-standing injury ( Fig. 45-6 ).
Wrist-level injuries result in full or partial denervation of the opponens pollicis (OP), abductor pollicis brevis (APB), flexor pollicis brevis-superficial head (FPB), and the first and second lumbricals. Thumb flexion, palmar abduction, and opposition are lost or weakened with wrist-level lesions. Sensibility may be impaired through the volar thumb, index, long, and the radial half of the ring finger and the nail beds. If the injury occurs in the carpal tunnel, sensibility to the thenar eminence is spared because the cutaneous branch travels outside of the carpal tunnel.
Forearm- or Elbow-Level Injury
Forearm- or elbow-level lesions result in full or partial denervation of the muscles previously mentioned with the addition of the pronator teres (PT), flexor carpi radialis (FCR), flexor digitorum superficialis (FDS), palmaris longus (PL), flexor pollicis longus (FPL), flexor digitorum profundus (FDP) to the index and long fingers, and the pronator quadratus (PQ). Motions lost or weakened include pronation, wrist flexion and radial deviation, thumb IP joint flexion, and flexion of the index and middle fingers at the PIP and DIP joints. MCP joint hyperextension may be observed due to the overpowering activation of the EDC.
Prehensile skill is compromised after median nerve injury. Lost or diminished finger flexion, thumb flexion, palmar abduction, and opposition impedes grip formation during reach-to-grasp tasks. The ability to stabilize opposing forces between the radial fingers to grasp, and to use the intrinsic muscles for in-hand manipulation, is lost or diminished. Insufficient activation of lumbricals I and II prevents finger-to-thumb-pad approximation used for precision grip, resulting in a raking pattern or a weak lateral pinch. Inadequate thumb mobility prevents in-hand manipulation of small objects, thus, compensatory patterns are often used such as two-handed manipulation or stabilizing items against the body. In-hand manipulation used to rotate (turn), translate (move palm to fingertips or fingertips to palm), and shift (move along fingertips) coins, pegs, or a key in one hand is affected. A complete median nerve injury may also result in a 60% loss of lateral pinch strength and 32% loss of power grasp strength.
Lost or diminished sensation in the volar–radial side of the hand impairs somatosensory feedback needed for object recognition, coordination, and grading of movement. If feedback is impaired, excess grip force is often employed to prevent object slippage and drops. Premature fatigue from the use of excess grip force may limit endurance during writing and related tasks as shown in other groups. Reach-to-grasp and pointing movements are less accurate with diminished tactile feedback. Furthermore, insufficient tactile feedback makes it difficult to determine the start and end position in tasks such as typing, text messaging, and calculator use. Median nerve injury significantly limits the ability to complete activities of daily living (ADL), often requiring individuals to change hand dominance if the dominant hand is injured.
Ulnar Nerve Injury
Causes of ulnar nerve injury include direct lacerations and fracture of the medial epicondyle of the humerus or olecranon of the ulna. , Compression may occur at the cubital or Guyon’s canal. The effect of injury on function depends on the individual’s age and level of the lesion ( Fig. 45-7 ). High-level lesions in young individuals recover fairly well after repair, whereas adults rarely regain motor function. The classic deformity associated with an ulnar nerve injury is a “partial intrinsic minus” deformity ( Fig. 45-8 ) due to loss of the interossei and lumbricals III and IV with less posturing in the index and long fingers (lumbricals intact). Yet, as reinnervation occurs, the posturing often increases. This deformity is noted for MCP joint hyperextension with PIP joint flexion at the ring and small fingers. With long-standing injury the hypothenar eminence and intrinsics between the IV and V metacarpals may be atrophied. After high-level injuries, there may be medial forearm atrophy.
Low-level lesions result in full or partial denervation of: abductor digiti minimi (ADM), flexor digiti minimi (FDM), opponens digiti minimi (ODM), III and IV lumbricals, dorsal interossei (DI), palmar interossei (PI), flexor pollicis brevis (deep head) (FPB-deep), and adductor pollicis (AP). Due to partial or full denervation of the intrinsics, finger abduction and adduction, thumb adduction, and opposition of the small finger are lost or weakened. Also, MCP joint flexion at the small and ring finger with simultaneous extension of the IP joints is lost or weakened. Because FDS and FDP function remain intact and the EDC can contract, ulnar-sided “intrinsic minus,” or claw, posturing is more pronounced than in individuals with high ulnar nerve lesions. With a wrist-level injury, sensibility is lost or diminished through the volar–ulnar aspect of the palm distally and the small and ulnar half of the ring finger.
Forearm- or Elbow-Level Injury
Lesions at the elbow and above result in full or partial denervation of the muscles listed earlier plus the flexor carpi ulnaris (FCU) and FDP to the ring and small fingers, resulting in lost or weakened ulnar deviation and distal interphalangeal (DIP) joint flexion. Without the FDP and FDS, the “intrinsic minus” position through the ring and small fingers is less severe but noticeable due to contraction of the EDC. Sensibility is now lost or diminished through the dorsal and volar surface of the small and ulnar half of the ring fingers and the ulnar aspect of the proximal palm.
During many daily tasks the ulnar border of the hand interfaces with a contact surface area. Therefore, lost or diminished sensation through the ulnar side of the hand increases the risk for burns, lacerations, and skin breakdown. To prevent injury, it is vital that the injured individual remains vigilant. Individuals should be advised to wear gloves when exposed to extreme temperature, sharp or rough surfaces, or friction during repetitive physical labor tasks.
The ulnar side of the hand acts as a point of stability for powerful grip and pinch as well as manipulation. Weakness after ulnar nerve injury affects gross grasp needed for opening jars and carrying heavy objects. Lost or weakened intrinsic muscle function restricts active grasp and release and reduces strength. Following an ulnar nerve block, Kozin and colleagues found a mean decrease of 38% gross grasp strength and 77% key pinch strength. Limited key pinch strength makes it difficult to secure fasteners and open doors. Froment’s sign is an inefficient substitution for weak key pinch. Posturing into intrinsic minus prevents ulnar digit extension to accommodate large objects during grasping or attempts to catch a football or basketball. Quarterbacks and pitchers with ulnar nerve injuries may have difficulty controlling ball release during throws. Lost or weakened FDP function prevents DIP joint flexion used to secure items against the palm during the translation component (palm-to-fingers or fingers-to-palm movement) of in-hand manipulation.
Clinicians have an opportunity to influence prehensile recovery following PNI by conducting sensitive evaluations and implementing creative treatment strategies. Individual participation in carefully designed, therapeutic activity after injury may contribute to neural regeneration and reorganization following injury and repair.
As with other hand injuries it is important to consult with the referring physician to discuss how much tension was placed on the nerve repair, the ideal orthotic position and the duration of limb immobilization. Nerve injuries are typically immobilized for a minimum of 3 weeks.
After obtaining relevant information from the physician, pertinent medical history and demographics can be obtained from a questionnaire or interview, including the cause and timing of the injury, date of injury, age, type of treatment to date, social/work information, and hand dominance. The nature of current problems, comorbidities, and an assessment of psychosocial factors, ADL status, and vocational or school requirements should also be acquired. A pain assessment using an instrument such as the McGill Pain Questionnaire or the visual analog scale (or pain faces scale for children) should be conducted. The presence of an advancing Tinel’s sign , induced by tapping on the nerve (to elicit a distal tingling sensation), may be used to gauge current and ongoing progression in regeneration. The physical assessment needs to be customized to the phase of recovery and compared with the noninvolved limb.
Sympathetic function is assessed via observation and palpation and includes an assessment of (1) vasomotor function (e.g., skin color, skin temperature, edema); (2) sudomotor function (sweat); (3) pilomotor function (gooseflesh); and (4) trophic changes (nutrition to skin and nails). Figure 45-9 shows the effect of loss of function in the sebaceous glands of the palm innervated by sympathetic nerve fibers. A quick test of sympathetic function is the wrinkle test, found to have 97% sensitivity and 95% specificity. (See Chapter 11 for more detail.) Absence of sympathetic function is highly suggestive of absent sensibility because of the high resilience those fibers have to mechanical trauma. Some sympathetic changes are seen immediately, but others are not noticeable until 3 to 6 weeks after nerve injury.
During phase one (immobilization) the motor assessment includes an examination of active (AROM) and passive range of motion (PROM) of noninvolved joints. After immobilization (phase two), AROM and PROM of the involved joints can be tested as well as prehension patterns through general observation or with tests of hand function such as the Sollerman’s Test of Hand Grip, which is a standardized hand function test based on common hand grips and consisting of 20 ADL items (see Chapter 12 ). To guide testing of muscle function the therapist can follow the predictable sequential pattern of muscle reinnervation and the ability to (1) produce an observable and palpable contraction without joint motion; (2) hold a position, yet not produce the same position; (3) move the involved joint actively; and (4) tolerate resistance.
After the patient has been cleared by the surgeon for strength testing and resistive exercise, there are a few ways to measure strength. The manual muscle test (MMT) is the most widely used and involves a standard 0 to 5 grading scale (absent to normal grades). The action of the muscle being tested is resisted at the distal end of the moving bone while the proximal joint is stabilized. Resistance can be provided isometrically by asking the individual to hold the position or isotonically by resisting throughout the range. Another frequently used tool is the hand-held dynamometer. This device measures the magnitude of force generated versus the amount of resistance tolerated. Although calibrated grip-and-pinch dynamometers measure gross hand strength, hand-held dynamometry tests the strength of individual muscles. During muscle testing it is important to be aware of substitution patterns. Classic substitution patterns for each nerve injury are listed in Table 45-2 .
|Radial Nerve||Median Nerve||Ulnar Nerve|
|Elbow extension assisted via gravity via supination and shoulder external rotation.||Pronation via brachioradialis from supination with gravity assist. Shoulder IR can substitute.||Thumb adduction via medial APB with slight palmar abduciton. Thumb adduction held by APB with slight flexion via FPL (look for APB, EPL, FPL contraction).|
|Supination via biceps.||Wrist flexion via FCU and APB into ulnar deviation.||Finger abduction via EDC if MCP joint extends. If MCP joint flexion blocked at index and small fingers abduct via EIP and EDM. Test abduction of long finger in MCP neutral.|
|Wrist extension via tenodesis action of finger flexors. If fingers held extended, then wrist cannot extend.||Finger flexion compromised except action of ulnar FDPs. Finger flexion achieved passively via tenodesis of wrist extensors.||Finger adduction via finger flexors if MCP joint flexion allowed. Prevention: block MCP joint flexion by testing on a flat surface. Watch for index substitution by EIP.|
|Finger extension via tenodesis action of wrist flexors.||Thumb IP joint flexion achieved via pull of APL from thumb abduction and wrist extension. Test with wrist in neutral and thumb adducted.||MCP joint flexion via lumbricals at index and long. Ring and small MCP joint flexion achieved only with addition of IP joint flexion.|
|Thumb extension via assist from APB (slip to EPL tendon).||Palmar thumb abduction via APB. Test: thumb moves perpendicular to index to avoid substitution by APL.||IP joint extension weak in index and long fingers. Substitution at ring and small fingers achieved via EDC if MCP joint hyperextension blocked.|
|Partial thumb opposition achieved via FPB (deep) and adductor pollicis. Substitution: flexed thumb pulp contacts lateral small finger.|
|MCP joint flexion at index and long fingers via intrinsics.|
|IP joint extension at index and long fingers weak, yet present because interossei are intact.|
The sequence of return in sensibility is from (1) deep pressure and pinprick, to (2) moving touch, to (3) static light touch, and then to (4) discriminative touch. Initially, localization is poor, and the sensation elicited radiates proximally or distally. Accurate touch localization is one of the last functions to return. Passive sensibility can be tested using the Semmes–Weinstein monofilaments or the Weinstein Enhanced Sensory Test (WEST) for touch–pressure; and the Discriminator for static and moving two-point discrimination. Active sensibility can be tested using Moberg’s Picking-Up Test or general tests of tactile gnosis or stereognosis (see Chapter 11 for more details).
Patients with PNIs often require alternative strategies and prehension patterns to perform everyday tasks, increasing the effort while decreasing the movement efficiency. Timed dexterity tests can be used to document baseline performance and improvements in fine-motor efficiency. Common dexterity tests (see Chapter 12 for details) include the Nine Hole Peg Test, the Purdue Pegboard Test, and the Jebsen Taylor Hand Function Test. These and other tests can be used to test components of in-hand manipulation. Although normative data are available on most tests, it is worthwhile to also compare performance against the noninvolved hand.
Impairments and function are important issues to address following PNI. Yet, methods aimed at motor learning and control can facilitate the transition from poor to smooth coordination, enhancing function. Initially, therapeutic strategies that encourage the use of noninvolved structures or provide supplemental feedback may aid this process. Substituting one form of feedback for another while awaiting peripheral nerve regeneration may preserve central neural function. , Once regeneration ensues engagement in meaningful but carefully planned tasks as used with focal hand dystonia or central lesions may aid reorganization and lead to better functional recovery.
Management by Phase
Postinjury management can be organized into three phases of recovery: phase one refers to early healing when immobilization is required; phase two is the period of reinnervation when remobilization, sensory reeducation, and active motor control is emphasized; and phase three stresses strengthening and functional performance. Rehabilitation methods often include orthotic positioning, AROM, biofeedback, neuromuscular electrical stimulation (NMES), and functional tasks. Adjunctive methods include massage, edema management, and sensory reeducation. The goals and common treatment methods for each phase are listed in Table 45-3 . Orthotic positioning is reviewed in greater detail in the next section.