CHAPTER 45
Therapist’s Management of Peripheral Nerve Injury

SUSAN V. DUFF, EdD, PT, OTR/L, CHT AND TIMOTHY ESTILOW, OTR/L

Adaptation to Injury

Immediately after PNI the central (CNS) and peripheral nervous systems (PNS) adapt to a reduction in sensory input.1-3 Neural adaptation to changes in input, or plasticity,⁴ ranges from axonal degeneration to topographic reorganization.^1,5 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 Seddon⁶ and Sunderland.^1,7 An appreciation of postinjury adaptations may aid in the design of effective interventions.

Table 45-1 Classification of Injury

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,8 and phagocytic macrophages interact with Schwann cells to remove debris.⁹ 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.⁸ 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.⁹ 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.⁹ 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.¹⁰ The regrowth rate in adults is 1 to 3 mm a day or more for a nerve laceration and repair^11,12 and about 3 to 4 mm a day after a crush.¹² 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.¹³ 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.^10,14-16 These methods are reviewed later in the chapter.

Early Central Changes

1. Removal or unmasking of inhibitory controls in the affected region.17,18 For example, changes in excitatory and inhibitory mechanisms in the spinal cord may alter tonic inhibition, causing tactile hypersensitivity.¹⁹

2. Migration of cells that serve other body parts into deafferented cortical regions3,20

3. Strengthening of existing connections and subthreshold excitatory inputs based on postinjury experience21-23

4. Reorganization of subcortical regions that project to the cortex such as the basal ganglia, brainstem, or thalamus17,24

5. Neurogenesis and sprouting of new pathways25,26

Prehensile Control

Feedback and Anticipatory Control

Somatosensory feedback and anticipatory control are essential components of grasp and manipulation.27-30 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,³⁰ aiding the acquisition of stable grasp points.³¹ 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.^32,33 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.²⁹

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,^27,34 focal hand dystonia,³⁵ and large-fiber neuropathy.³⁶

Previous kinematic and kinetic analyses indicate there is a strong relationship between impaired visual skills or somatosensation and anticipatory control.27-29,31 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.²⁹ To examine the effect of injury on fingertip force scaling, Cole and colleagues³⁴ 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 units³⁷ 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,³⁸ 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.³⁹

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).13 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.

Wrist-Level Injury

Forearm- or Elbow-Level Injury

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.

Functional Implications

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.40 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.13 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 Injury

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.

Functional Implications

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.41-43 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.⁴²

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.²⁹ Premature fatigue from the use of excess grip force may limit endurance during writing and related tasks as shown in other groups.⁴⁴ Reach-to-grasp and pointing movements are less accurate with diminished tactile feedback.²⁷ Furthermore, insufficient tactile feedback makes it difficult to determine the start and end position in tasks such as typing, text messaging, and calculator use.⁴⁵ 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.13,46 Compression may occur at the cubital or Guyon’s canal.⁴⁷ 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.⁴⁸ 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.

Wrist-Level Injury

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.49 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

Functional Implications

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.42 Following an ulnar nerve block, Kozin and colleagues⁴² 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.

Intervention

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.

Evaluation

History

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 Questionnaire50 or the visual analog scale (or pain faces scale for children)⁵¹ 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

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.⁵² (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.⁵³ Some sympathetic changes are seen immediately, but others are not noticeable until 3 to 6 weeks after nerve injury.

Motor Function

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,54 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.⁵⁵

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.⁴³ During muscle testing it is important to be aware of substitution patterns.¹³ Classic substitution patterns for each nerve injury are listed in Table 45-2.

Table 45-2 Potential Substitution Patterns for Each Nerve Injury

APB, abductor pollicis brevis; APL, abductor pollicis longus; EDC, extensor digitorum communis; EDM, extensor digiti minimi; EIP, extensor indicis proprius; FCU, flexor carpi ulnaris; FDP, flexor digitorum profundis; FPB, flexor pollicus brevis; FPL, flexor pollicus longus; IP, interphalangeal; IR, internal rotation; MCP, metacarpophalangeal.

Sensibility

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.13 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).

Dexterity

Patients with PNIs often require alternative strategies and prehension patterns to perform everyday tasks, increasing the effort while decreasing the movement efficiency.39 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.⁵⁶ 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.

Treatment Methods

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.57,58 Once regeneration ensues engagement in meaningful but carefully planned tasks as used with focal hand dystonia⁵⁹ or central lesions⁶⁰ 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.13 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.

Table 45-3 General Goals and Treatment Methods for Each Phase

ADL, activities of daily living; AROM, active range of motion; PROM, passive range of motion.

Phase One. Following nerve repair, a custom-made immobilization orthosis or cast is used to protect the repair by limiting tension on the repair site for a minimum of 3 weeks. The specific orthosis and position depend on the nerve repaired. Static orthoses provide appropriate biomechanical positioning to prevent overstretching of denervated muscles and deformity of associated structures. Management of pain, edema, and inflammation can be addressed with anti-inflammatory medications and modalities such as ultrasound, phonophoresis, and cryotherapy. Education is often provided to (1) aid in edema reduction via elevation and active movement of noninvolved joints; (2) protect areas of diminished or absent sensation; and (3) review home programs. During this period of immobilization, limitations in performance of ADL are addressed using adapted methods and assistive devices.

Phase Two. After immobilization, place-and-hold techniques and active motion foster muscle activation and movement. Place-and-hold techniques require muscle activation at various lengths and are performed by having the clinician or the individual place the limb in the desired position where it is briefly held. Active motion is initially encouraged through a protected range with gravity eliminated then progressed to full motion against gravity. Aquatic therapy can be beneficial, as the buoyancy of the water can provide assistive AROM. Orthotic positioning is often used to facilitate new movement and function as reinnervation occurs.

To enhance function and neural control in phases two and three, therapeutic activities should focus on motor relearning and adaptive strategies. Traditionally, biofeedback and NMES assist with motor learning and control. Biofeedback provides visual or auditory feedback (or both) when the targeted muscle contracts, aiding relearning of muscle activation or relaxation. NMES augments muscle activation when there is evidence of innervation, but also provides proprioceptive and tactile input to enhance muscle activation and awareness (Fig. 45-10). However, the use of electrical stimulation in full or partially denervated muscle remains controversial.

Multisensory approaches can help maintain cortical representation and allow for faster integration of sensory input on reinnervation. The “sensory glove” introduced by Rosén and Lundborg57 provides auditory feedback to substitute for tactile input during fine-motor tasks after PNI. The type of auditory stimuli varies depending on the texture of the object being grasped. Mirror visual feedback (MVF),^20,58 which uses a mirror image to provide an illusion of movement in the involved hand, may also be another useful strategy. During MVF the individual is instructed to observe a movement being completed by the noninvolved hand in a mirror image located at midline (involved hand is behind the mirror). Theoretically, the visual system interprets the mirror image to be movement of the involved hand, thus stimulating mirror neurons in the brain. The goal is to restore volitional control in the affected hand. During the phase of immobilization, the patient simply observes the reflected image and during the phase of reinnervation, the patient attempts to perform the motion observed in the mirror. Based on the reported success relieving phantom limb pain and complex regional pain syndrome,²⁰ MVF may be successful after PNI⁵⁸ and warrants further investigation.

During the design of therapeutic activities it is important to remember that visual information influences anticipatory control during reach to grasp and object manipulation.³² Engagement with familiar objects and tasks may initially aid motor control. However, as improvement is noted, the introduction of novel objects and tasks may challenge the nervous system to better refine sensorimotor control.⁴¹

Phase Three. Once full available AROM is obtained with gravity eliminated and against gravity, strengthening can begin. Resistance can be in the form of theraputty, theraband, free weights, cuff weights, exercise machines, work simulators, and computer games (e.g., Biometrics Device). Aquatic therapy can also be useful since buoyancy of the water can also provide a form of resistance. As in other phases, correct technique should be emphasized to prevent injury.

Orthotic Positioning

Because of full or partial denervation after injury, individuals are at risk for secondary impairments, such as muscle atrophy, overstretching of the involved muscle–tendon unit, and joint contracture, if care is not properly taken to prevent them.61 Orthoses can immobilize or mobilize involved structures via static or dynamic components. Orthotic design and wear schedule vary depending on the type, extent, and location of the injury along with the phase of neural recovery. Multiple client factors (e.g., cognition, age) and the desired outcome also influence design. Regardless of recovery phase, patient education is vital to maximize compliance with orthosis care and wear.

Orthosis design after PNI requires attention to detail to ensure that there is sufficient support, reasonable fit, allowance for optimum sensation, ease in donning and doffing, a proper line of pull, and appealing aesthetics.⁶¹ In phase one, orthotic positioning (or casting) aims to (1) protect the nerve repair (or rest the involved nerve), (2) maintain anatomic integrity, and (3) prevent deformity. The method and time period of immobilization depend on the severity of the injury and extent of initial medical care. If surgical repair was performed, the individual is immobilized for a minimum of 3 weeks. PNIs not requiring surgical care should be positioned based on the type and level of injury. Positioning goals in phase two are to (1) maintain passive ROM and (2) enhance function during reinnervation.

Radial Nerve Injury

Phase One. After this injury the fingers and wrist need to be supported to prevent shortening of the flexors and overstretching of the extensors. A volar resting orthosis with the wrist in neutral to partial extension and the MCP joints in extension should be worn nightly. During the day a dorsal wrist cock-up supporting the MCP joints in extension with elastic slings allows for digit movement and leaves the volar surface free for sensory input.

As with other compression injuries, rest is needed to reduce the pain and inflammation that occurs with radial tunnel syndrome. According to Gelberman and colleagues46 the optimal position for radial nerve decompression is 90 degrees of elbow flexion, forearm midposition or supination, and slight wrist extension. This position of rest can be provided in a long-arm orthosis (Fig. 45-11).

Phase Two. At this phase wrist and digit extension often remain absent or weak. A dorsal wrist cock-up orthosis with MCP joint support stabilizes the wrist and MCP joints, allowing for the execution of basic fine-motor skills. Another option is to reestablish a tenodesis pattern to improve hand function during reinnervation (Fig. 45-12A). The tenodesis orthosis uses the intact finger flexors to control wrist extension.⁶² Static nylon cord attached to finger slings suspends the proximal phalanges from an outrigger attached to a dorsal forearm base (Fig. 45-12B). Within the orthosis, active finger flexion passively places the wrist in neutral for a power grip, whereas active wrist flexion passively extends the fingers, allowing for object release. The radial nerve orthosis can be varied to include the thumb, expanding the available prehension (Fig. 45-12C, D). Both orthoses foster a power grip and allow use of the impaired hand in ADL. As strength and control improve, other options such as a dynamic Lycra glove or kinesiotaping can be used.

Phase Three A functional assessment determines if positioning is necessary at this time. If contractures are present, static progressive orthotic positioning may help increase PROM. If an individual has no return, or if recovery of function is insufficient, a referral to a hand surgeon may be warranted to explore surgical options.

Median Nerve Injury

Phase One. To prevent a thumb adduction or webspace contracture, individuals with wrist-level lesions need to wear a night orthosis to maintain passive range in the first webspace. With a high-level lesion, an immobilization orthosis fit in a functional position or a wrist-based thumb spica (Fig. 45-13A) should be worn nightly to maintain length of the intrinsics to the index and middle fingers while supporting the thumb in opposition with the webspace maintained. A short opponens orthosis (Fig. 45-13B) can be worn during the day to provide support to the thumb and allow for use of the digits.

Phase Two. Absent or limited active thumb mobility is the primary impediment to function at this time. A short opponens orthosis that positions the thumb in palmar abduction and opposition (Fig. 45-14) allows thumb-to-fingerpad contact for a radial–digital or pincer grasp. If thenar atrophy is present, the short opponens orthosis may be too uncomfortable. An option is to form a soft orthosis using a “putty-like” material; securing it with an elastic band (Fig. 45-15) or covering it with a thin plastic orthosis. As strength and motor control improve, other options, such as a Benik Hand Splint or neoprene thumb strap, can provide limited support during motion.

Phase Three. Evaluation of function will determine how to proceed at this time and may include the continued use of orthoses. If the individual has no return, or functional recovery is insufficient, surgical options may need to be explored.

Ulnar Nerve Injury

Phase One. Ulnar nerve injuries not requiring surgical repair should be positioned with a dorsal MCP joint blocking orthosis with the MCP joints in flexion to prevent a fixed claw deformity of the ring and small fingers in the intrinsic minus position (Fig. 45-16). An MCP joint blocking orthosis helps redistribute force from the EDC to the IP joints to promote full IP joint extension. If IP joint contracture is present, the immediate goal is to regain motion with serial casting or positioning. Mild contractures are correctable with a static progressive or dynamic PIP joint extension orthosis.

Phase Two. Once strength and motor control improve, less restrictive orthoses can be used. For example, finger loops or cuffs placed over the ring and small fingers can be attached to a palmar bar or wristband with a static line to minimize intrinsic minus posturing, while allowing greater digit flexion and sensibility.

Phase Three. Assessment of function at this time determines how to proceed and may include continued orthosis wear in cases of long-standing injury (Fig. 45-17). If the individual has no return, or recovery is insufficient, surgical options such as tendon transfers may be explored.

Enhancing Neural Recovery and Prehension

Axonal Regeneration After Nerve Repair

Neurotrophic factors are important for regeneration of neurons.63 Unfortunately, after PNI there is a loss in retrograde transport of neurotrophic factors back to the cell body.⁶⁴ This can lead to cell death and halt regeneration. Research suggests that the application of multiple neurotrophic factors (e.g., brain-derived [BDNF] and glial-derived [GDNF]) acting on two different populations of cells may increase survival of damaged neurons and enhance regeneration.⁶⁵ Alternatively, the use of human bone marrow stromal cells (MSCs) may enhance peripheral nerve regeneration.⁶⁶ MSCs are easily harvested through bone marrow aspiration and differentiate into a wide variety of cells, such as stem cells. Early findings suggest that MSCs grow into thick, robust Schwann cells useful in the production of neurotrophic factors. Although neurotrophic factors have been shown to have a positive effect on nerve regeneration, there currently is no clinical application because of the concerns regarding correct dosage and method of application.⁶⁷ Studies explored in animal models may alleviate these issues in the future.

Brushart and colleagues^14,15 used a rat model to determine that intraoperative low-frequency electrical stimulation provided to the nerve 1 hour after repair accelerates the axons’ ability to cross the repair site and helps direct them to the appropriate sensory or motor fiber. Electrical stimulation was also found to correlate with an up-regulation of neurotrophic factors in the neurons.¹⁴ In the future it may be feasible and safe to provide electrical stimulation directly to human nerves intraoperatively to enhance success of nerve repair.⁶⁸

Prehension and Sensorimotor Control

Neural regeneration and reorganization are activity-dependent processes21 induced more favorably in enriched environments.⁶⁹ Exercise has proven beneficial for axon regeneration in animals,¹⁶ yet for humans participation in meaningful, and challenging, goal-directed activity that engages attention and motivation may best enhance neural recovery.^21,59 If used prudently, biofeedback and NMES can augment feedback and promote task success.

Even if motor return is good, functional outcome can be poor if hand sensibility is not restored.⁷⁰ Sensory retraining is one method of fostering neural reorganization. According to Lundborg,⁷¹ sensory reeducation aims to (1) aid interpretation and promote normalization of distorted hand maps, (2) refine cortical receptive fields to a higher resolution of sensory information, and (3) improve sensory processing. The two phases of sensory retraining are (1) desensitization to address neuropathic pain and (2) sensory reeducation to enhance functional prehension. Please see Chapter 46 for further details on sensory reeducation.

Case Study

Phase One

Evaluation

At rest MC postured his wrist in flexion, MCP joints in slight flexion, and IP joints in flexion. Because of weakness and joint contracture, MC could only exhibit the following patterns: a raking grasp, weak lateral pinch, and a weak scissors grasp between his fingers. During bimanual tasks, MC could not stabilize objects with his right hand, and he relied on both hands to grasp and lift objects. Findings for the initial and final objective assessments are listed in Tables 45-4 through 45-8 (online).

Table 45-4 Case Study: Sensibility (Median and Ulnar Nerve Distributions)

Functional Limitations

Factors Affecting Neural Recovery

Intervention

For MC it was essential to prioritize goals and treatment and continually reevaluate his progress due to his significant involvement from multiple PNIs. At this phase of treatment MC exhibited significant AROM impairments in his right upper extremity (RUE). The late initiation of his rehabilitation program and his age required modification of the typical treatment goals and strategies listed earlier. His goals for treatment and the strategies used to attain them are shown in Table 45-9 (online). Individual education included a review of therapy goals, precautions, timeline/expectations in recovery, and explanation of functional deficits and the cause.

Table 45-9 Case Study: Therapy Goals

AROM, active range of motion RUE, right upper extremity; PROM, passive range of motion.

Phase Two

Phase Three

Goals for this phase are listed in Table 45-9 (online). MC primarily focused on strengthening his RUE and improving his prehensile control. After 1 year of therapy, MC displayed maximum therapeutic benefit and was referred to a hand surgeon for consultation regarding surgical options. He continued to display intrinsic minus posturing and had evidence of muscle wasting (Fig. 45-18A). He also was unable to oppose his thumb or small finger (Fig. 45-18B).

At discharge his reevaluation showed progress in most areas as shown in Tables 45-4 through 45-8 (online) including dexterity. Based on his current function and surgical consultation it was determined that he would receive tendon transfers. See Chapter 59 for tendon transfer results.

Summary

Because of the tremendous potential for peripheral nerve regeneration, rehabilitation after compression or traction injuries or after lacerations and repair can be quite rewarding. The key to success is to adhere to precautions initially to rest and protect the nerve, then provide an enriched therapeutic environment as the individual progresses through the phases of recovery. This strategy enhances not only peripheral recovery but central reorganization. Furthermore, if greater emphasis is placed on fostering reorganization and recovery of sensorimotor control, the patient may be able to regain flexible and efficient prehensile skill after nerve injury.

Video 45-1 Grip Formation: note wide aperture (width between thumb and fingers) during reach-to-grasp of blocks.

Video 45-2 Demonstration of two of three components of in-hand manipulation; translation (palm to fingers) and shift (movement along fingertips).

Video 45-3 Use of an orthosis with ring and small finger loops attached to a palmar bar to minimize “intrinsic minus” or claw posturing after ulnar nerve injury.

Video 45-4 CASE: subtest form the Jebsen Test of Hand Function, turning cards.

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