Physical Rehabilitation || Peripheral Nerve Injuries

3. Explain the physiological processes after nerve injury and repair.4. Summarize current approaches to surgical and medical

management of peripheral nerve injuries.5. Explain the relevance and general methods of

electromyographic and nerve conduction testing.6. Determine and describe the examination specific to the client

with peripheral nerve pathology.7. Describe rehabilitation interventions for patients with

traumatic peripheral nerve injury, nerve compression andnerve entrapment.

Depending on the nature and extent of peripheralnerve pathology, individuals with peripheral nerve

injury* experience various degrees of recovery and in moreadvanced or severe injury, often do not return to theirprior functional status. Appropriate interventions canreduce the extent of long-term dysfunction. This chapterdescribes the nature of peripheral nerve injury, reviews theexamination shown to aid in determining a diagnosis andprognosis, and describes interventions shown to be effec-tive in the rehabilitation of individuals with peripheralnerve injuries.

OVERVIEW OF THE PERIPHERALNERVOUS SYSTEMThe nervous system is typically divided into central andperipheral components. Central components includenerves that are wholly contained within the brain andspinal cord. Peripheral components include nerves thatoriginate in the brain or spinal cord and end peripherally,as well as cranial and spinal nerves. The peripheral nervoussystem (PNS) includes motor, sensory, sympathetic, andparasympathetic neurons, with most nerves containing amixture of these types of neurons. Efferent pathways (thosethat send messages from the center to the periphery)include somatic motor nerves that innervate skeletalmuscles and the autonomic nervous system (ANS) with sym-pathetic and parasympathetic divisions that regulatesmooth muscle, cardiac muscle, and glandular activity (Fig.18-1). Afferent pathways (those that send messages from theperiphery towards the center) transmit a range of sensorymodalities including touch, position, vibration and pain.1,2

C h a p t e r 18

Peripheral Nerve InjuriesGinny Gibson

CHAPTER OUTLINEObjectivesOverview of the Peripheral Nervous SystemAnatomy of a Peripheral Nerve

Blood Supply of Peripheral NervesPeripheral Nerve End-OrgansPeripheral Nerve Classification

Physiology of the Peripheral Nervous SystemAxonal TransportIon Channels and Nerve ConductionEffects of Movement on Peripheral Nerves

Nerve PathologyMechanisms of Nerve InjuryDouble-Crush SyndromeClassification of Nerve InjurySpecific Nerve LesionsNerve Degeneration and RegenerationFunctional Recovery From Peripheral Nerve Injury

ExaminationPatient HistorySystems ReviewTests and Measures

Evaluation, Diagnosis, and PrognosisIntervention

Patient EducationTherapeutic ExerciseJoint Range of Motion and Muscle StretchingSensory RetrainingManual Therapy TechniquesPrescription, Application, and Fabrication of Devices and

EquipmentElectrotherapeutic ModalitiesPhysical and Mechanical ModalitiesSurgical Intervention

Case StudyChapter SummaryAdditional ResourcesGlossaryReferences

OBJECTIVESAfter reading this chapter, the reader will be able to:1. Describe the mechanisms of and classification systems for

peripheral nerve injuries and their relevance to functionaloutcomes.

2. Describe the etiology and resultant clinical picture ofcommon peripheral nerve injuries.

473

*For clarity, this chapter will use the term injury to refer to allinsults to peripheral nerves.

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Motor nerves originate in the anterior horn of thespinal cord, and sensory nerves originate in the dorsal rootganglia. Sympathetic nerves originate in the lateral hornof the thoracic spinal cord and continue in sympatheticganglia. Parasympathetic nerves originate from the brainand lateral gray matter of the sacral spinal cord and con-tinue in the parasympathetic ganglia. Motor neurons of cranial nerves extend from the brainstem, and sensoryneurons of cranial nerves have their cell bodies in cranialnerve ganglia. Motor and sensory cranial nerves servestructures in the head and neck, with the exception of the vagus nerve, which also continues to the chest and abdomen. Spinal nerves, of which there are 31 pairs, extend from their cell bodies and provide sen-sory and motor functions to all of the body, except thehead.1,2

Spinal nerves, with their contributory dorsal andventral roots, exit the intervertebral foramen and divideinto dorsal and ventral rami (Fig. 18-2). With exception ofthe thoracic region, the ventral rami combine to form thecervical, brachial, and lumbosacral plexuses (Fig. 18-3).1,2

This chapter discusses the examination and managementof clients with nerve damage distal to these plexuses, aswell as injuries to cranial nerves.

ANATOMY OF A PERIPHERAL NERVENeural tissue includes excitable neurons (nerve cells) thatpropagate electrical impulses and glia cells that facili-tate impulse conduction and support and protect theneurons.1 All neurons have a cell body that contains anucleus and organelles (mitochondria, rough endoplasmicreticulum, ribosomes, and Golgi apparatus). Almost all of a neuron’s proteins, enzymes, and organelles are synthesized in the cell body. Most neurons have dendrites,an axon, and terminal branches. Dendrites are branchingand tapering extensions of the axon that receive signalsfrom other neurons, which the axon then carries to the cell body. Signals are then carried away from the cell body toward terminal branches, where electrical

474 PART 2 • Neuromuscular System

CENTRAL NERVOUS SYSTEM

Afferent (sensory) Efferent (motor)

Somatic

Fight or flight

Autonomic

Parasympatheticdivision

Sympatheticdivision

Peripheral nervous system

Rest and digest

Skeletal muscle

Touch,position,vibration,pain

FIG. 18-1 The central nervous system.

Dorsal root

Ventral root

Dorsal root ganglion

Cell body

Sensory neuron

Motor neuron

Dorsal ramus

Ventral ramus

To limbs

To back

FIG. 18-2 Spinal nerves contain motor nerves thatoriginate in the anterior horn of the spinal cord and sensorynerves that originate in the dorsal horn of the spinal cord.

Hypoglossal nerve (XII)

Accessory nerve (XI)

Lesser occipital nerve

Nerve tosternocleidomastoid

muscle

Greater auricularnerve

Ventral rami

A

Nerve tobrachialplexus

Phrenic nerve

Supraclavicularnerves

Nerve totrapezius

muscle

Transversecervical nerve

C1

C2

C3

C4

C5

Cervical plexus

C1

C4

FIG. 18-3 A, Cervical plexus.

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and chemical signals are transmitted to other nerves orend-organs.1,2

In the PNS axons are wrapped in myelin from Schwanncells. A single Schwann cell wraps around an axon in a spiral fashion with small gaps, known as nodes of Ranvier, approximately 1 mm apart. The segments of axonbetween the nodes of Ranvier are called the internodes(Fig. 18-4). The myelin sheath accelerates the propagationof signals along the axon because impulses can jump fromnode to node rather than traversing the entire length of the nerve. This is known as saltatory conduction.Unmyelinated neurons conduct more slowly because they do not have a myelin sheath, although there aresome Schwann cells within bundles of unmyelinatedneurons.1,2

A nerve consists of multiple neurons. Each neuron is surrounded by a semipermeable membrane called the plasmalemma. Groups of neurons are arranged inbundles, called fascicles, and groups of fascicles make up a nerve. Protective coverings of connective tissue, calledendoneurium, perineurium, and epineurium, envelopindividual neurons, fascicles, and groups of fascicles,respectively (Fig. 18-5). The endoneurium, which is com-posed primarily of loose connective tissue, provides elec-trical insulation between neurons and in part, preventselongation of the nerve under tension. The perineurium,which is composed of multiple layers of dense connectivetissue, resists tensile forces from stretching, helps to main-tain intrafascicular pressure, and acts as a chemical barrier.The epineurium is composed of two layers of collagen and

Peripheral Nerve Injuries • CHAPTER 18 475

C4

C5

C6

C7

C8

T1

Cords

B

Ventral rami Anterior divisions

Dorsal scapular nerve

Suprascapular nerve

Subclavian nerve

Axillary nerve

Radial nerveLong thoracicnerve

Median nerveUlnar nerve

Medial brachialcutaneous nerve

Medial and lateralpectoral nerves

Musculocutaneousnerve

Trunks Posterior divisions

Brachial plexus

C5

T1L1

L2

L3

L4

L5

S2

S1

S3

S4

S5

Iliohypogastric nerve

Ilioinguinal nerve

Genitofemoral nerve

Lateral femoralcutaneous nerve

Femoral nerve

Obturator nerve

Lumbosacral trunk nerve

Superior gluteal nerve

Inferior gluteal nerveCommonperoneal

nerveTibial nerve

Posteriorfemoral

cutaneous nerve

Pudendal nerve

Sciaticnerves

Ventral rami

Posterior divisions

Anterior divisions

C

L1

L4

S4

Lumbosacral plexus

FIG. 18-3, cont’d B, Brachial plexus; and C, lumbosacralplexus. From Thibodeau GA, Patton KT: Anatomy andPhysiology, ed 6, St. Louis, 2006, Mosby.

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fibroblasts and accounts for much of a nerve’s cross-sectional area.2 The innermost layer is loose and fills spacearound groups of fascicles, and the outer layer surroundsthe entire nerve. The epineurium provides tensile strengthand cushions fascicles from external trauma. Surroundingthe epineurium is a layer of loose areolar tissue called themesoneurium.3

Along a nerve, the thickness and presence of connec-tive tissue layers vary. Where nerves cross over joints thereis more connective tissue. The epineurium thins distallyand both perineurium and epineurium are absent proxi-

mally at the spinal nerve root. Nerves may be more proneto injury at locations where the layers are thinner orabsent.3

BLOOD SUPPLY OF PERIPHERAL NERVESPeripheral nerves require oxygen to maintain the energylevels needed for axonal transport and cell viability.Nerves receive oxygen via extraneural and intraneuralblood vessels.4 The extraneural vessels lie next to thenerves and the intraneural vessels are within theendoneurium, perineurium, and epineurium (Fig. 18-6).


Myelin sheath

Myelinatednerve fiber

Nucleus of Schwann cell

Saltatoryconduction

Node ofRanvier

A

Axon

B

Neurofibrils

Plasma membraneof axon

Neurilemma

Myelinsheath

FIG. 18-4 A myelinated peripheral nerve. Note that the Schwann cell forms the myelin that wraps around the nerve axon and that the myelin promotes faster nervetransmission by allowing for saltatory conduction. A Courtesy Brenda Russell, PhD,University of Illinois at Chicago; B from Thibodeau GA, Patton KT: Anatomy and Physiology,ed 6, St. Louis, 2006, Mosby.

Epineurium

Endoneurium

Perineurium

Fat

Nervefiber

A

Arteryand vein

Fascicle

Epineurium

Adipose tissue

Perineurium

Fascicle

Nerve fiber withinendoneurium

BFIG. 18-5 Cross-section of a peripheral nerve showing the nerve fibers, fascicles, and groups of fascicles enveloped in endoneurium, perineurium, and epineurium,respectively. From Thibodeau GA, Patton KT: Anatomy and Physiology, ed 6, St. Louis,2006, Mosby.

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The extraneural vessels connect to the intra-neural vesselsthrough the mesoneurium. There are larger vessels in theepineurium and perineurium and only a fine capillarynetwork in the endoneurium. This network of capillariesis susceptible to compression injury.5

Peripheral nerves are immunologically isolated fromthe rest of the body by a blood-nerve barrier, comprisedof tightly packed endothelial cells of the endoneuriumand the internal layers of the perineurium. Injury to anerve and the blood-nerve barrier may result in exposureof the nerve and trigger an immunological response.6

PERIPHERAL NERVE END-ORGANSPeripheral nerves connect distally to end-organs that aresensory receptors, muscles, or glands. Sensory end-organsinclude mechanoreceptors, thermoreceptors, nociceptors,chemoreceptors, photoreceptors, and free nerve endings.Different subtypes of sensory end-organs are listed anddescribed in Table 18-1. Mechanoreceptors, thermorecep-tors, and nociceptors detect sensory stimulation subse-quent to chemical changes or physical deformation of thereceptor.1,2

In the somatic motor system, a single alpha motorneuron and all of the muscle fibers it innervates are knownas a motor unit. A single motor unit, when stimulated suf-ficiently, will cause all of the muscle fibers it innervates tocontract. Within the ANS, efferent pathways signal secre-tions from glands, including sweat glands.1,2

PERIPHERAL NERVE CLASSIFICATIONPeripheral nerves can be classified by axon diameter or byspeed of conduction (Table 18-2). When classified accord-ing to size or diameter of the axon, neurons are referredto as type I, II, III, or IV, with type I the largest and typeIV the smallest. Only sensory neurons are classified bysize. Type I, II, and III axons are myelinated, and type IV axons are unmyelinated. Large diameter axons con-duct rapidly and have lower thresholds for electrical stimulation.1,2

When classified according to nerve conduction velocity(NCV), the speed at which electrical impulses can be prop-agated along the axon, neurons are classified as type A orB, which are myelinated, or type C, which are unmyeli-nated. Both sensory and motor neurons are classifiedaccording to speed of conduction. There are four subtypesof A fibers: A-alpha neurons, A-beta neurons, A-gammaneurons, and A-delta neurons.

PHYSIOLOGY OF THE PERIPHERALNERVOUS SYSTEM

AXONAL TRANSPORTNeurotransmitters, proteins, and organelles are transportedalong axons using a system of microtubules and neu-rofibrils. Anterograde flow provides transport away fromthe cell body and occurs either quickly or slowly. Neuro-transmitters and structures necessary to replenish the plas-malemma are transported quickly, whereas proteins andorganelles needed for new axoplasm or to replenish axo-plasm in regenerating neurons or mature neurons aretransported more slowly. Retrograde flow, toward the cellbody, occurs at a constant slow rate and returns organelles


FIG. 18-6 Vascular supply of the peripheral nerve. Adaptedfrom Lundborg G: Nerve Injury and Repair, Edinburgh, 1988,Churchill Livingstone.

TABLE 18-1 Cutaneous Sensory End-Organ Receptors

Type of Receptor Name of Receptor Encapsulated or Free Stimulation Detected AdaptationMechanoreceptor Ruffini’s corpuscle Encapsulated (thin) Deep pressure, stretch of skin Slow

Pacinian corpuscle Encapsulated Deep moving pressure, stretch, high Rapidfrequency vibration (256 Hz)

Meissner’s corpuscle Encapsulated Light pressure, light moving touch, Rapidlow frequency vibration (30 Hz)

Root hair plexus Free Hair deflection RapidMerkel’s disc Encapsulated Light pressure, constant touch SlowFree nerve ending Free Pressure SlowMuscle spindle Encapsulated (thin) Type Ia: Rate and degree of muscle Slow and rapid

stretch and tensionType II: Degree of stretch and tension

Golgi tendon organ Tendon stretch, muscle tension SlowThermoreceptors Free nerve ending Free TemperatureNociceptors Free nerve ending Free Pain Slow and rapid

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to the cell body for disposal and carries nerve growthfactor toward the cell body. Both anterograde flow and ret-rograde flow require an energy source that is compromisedif circulation is disrupted.8

ION CHANNELS AND NERVE CONDUCTIONTwo ions, potassium (K+) and sodium (Na+), are primarilyresponsible for nerve conduction. At rest, there is moresodium outside and more potassium inside a neuron.These concentrations are maintained by chemical andelectrical gradients together with the sodium-potassiumadenosinetriphosphatase (ATPase) pumps that pump threesodium ions out of the cell for every two potassium ionsthey pump into the cell. At rest, a neuron is more nega-tively charged inside than outside and has a resting mem-brane potential of −60 to −90 mV.

When the nerve is stimulated sufficiently, sodium ionswill enter the neuron, depolarizing it. The depolarizationis quickly followed by repolarization, and this sequence ofdepolarization and repolarization is known as an actionpotential (Fig. 18-7, A). The action potential will then bepropagated along the nerve until it reaches the end of thenerve (Fig. 18-7, B).

A synapse is the meeting point of the axon terminal ofone neuron (the presynaptic neuron) and a dendriticending or cell body of another neuron (the postsynapticneuron). The presynaptic axon terminal has vesicles containing a neurotransmitter that is released into thesynaptic cleft, the space between the presynaptic and postsynaptic nerve, in response to an electrical signal (Fig.18-8). The neurotransmitter then binds to postsynapticreceptors causing the postsynaptic nerve to becomeexcited (i.e., less negative), if more sodium ions enter theneuron, or inhibited (i.e., more negative), if chloride ionsenter the neuron.1,2 Each neuron can receive inputs frommany other neurons and with a sufficient dominance ofdepolarizing inputs, an action potential will start in thepostsynaptic neuron and propagate along the length ofthis nerve.

EFFECTS OF MOVEMENT ON PERIPHERAL NERVESMovement and positioning of the limbs, head, neck, ortrunk can cause nerves to slide, become elongated, orrecoil.9-11 The tissues around peripheral nerves, including


TABLE 18-2 Two Systems for Classifying Peripheral Nerves

By Diameter Function

Fiber Classification Diameter (mm)Ia 12-20 Muscle spindle primary endingsIb 11-19 Golgi tendon organsII 5-12 Touch, kinesthesia, muscle spindle secondary endingsIII 1-5 Pain, crude touch, pressure, temperatureIV 0.1-2 Pain, touch, pressure, temperature

By Conduction Velocity Function

Fiber Classification Conduction Velocity (m/sec)A-alpha 70-120 Alpha-motoneurons, muscle spindle primary endings, Golgi tendon organs, touchA-beta 40-70 Touch, kinesthesia, muscle spindle secondary endingsA-gamma 15-40 Touch, pressure, gamma-motoneuronsA-delta 5-15 Pain, crude touch, pressure, temperatureB 3-14 Preganglionic autonomicC 0.2-2 Pain, touch, pressure, temperature, postganglionic autonomic

Na

K+

out

Nain

0

–70 mV

Electrical

Resting potential

Cell body

“Wave” moves toright away fromcell body

Nerveimpulse

Musclefiber

Axon

Nucleus

Neuron(nerve cell)

Dendrites

Na

+

+

+

+–

–+

+

K = potassiumNa = sodium

A

BFIG. 18-7 An action potential propagating along a nerve.Copyright Royal Society of Chemistry 2006.

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bone, cartilage, muscle, tendon, vessels, and fascia, formtunnels or passageways of various sizes through which thenerves pass. These tunnels may apply pressure to thenerves when the nerves move. Movement at one jointmay require the nerve to lengthen at that joint and canpull on the nerve where it crosses other joints.11 When anerve is elongated it gets narrower,12 intraneural pressureincreases,12-14 blood flow decreases,15,16 and strainincreases.11,17 Strain on the median and ulnar nerves hasalso been shown to increase more with movement (activ-ity) than with maintained postures that impose incre-mental strain.10

NERVE PATHOLOGYNerve pathology can be localized or diffuse and may becaused by acute or cumulative trauma. An isolated nervelesion is termed a mononeuropathy, and a condition withasymmetrical lesions of multiple nerves is termedmononeuropathy multiplex. Symmetrical diffuse nerve dys-function is termed polyneuropathy. Polyneuropathy gener-ally presents initially with symmetric distal symptoms andis most often caused by a disease process rather thantrauma (see Chapter 19).

MECHANISMS OF NERVE INJURYThe mechanism of a nerve injury influences its acute andlong-term consequences and the selection of medical, sur-gical, and rehabilitation interventions. Nerves may beinjured by excessive stretch or compression, inadequateblood supply, or exposure to excessive electric energy, radi-ation, or toxins. Inadequate blood supply is a feature ofmost mechanically-induced nerve injury. Regardless of themechanism of injury, the clinical findings of pain, pares-thesia, and motor impairment are similar for most nerveinjuries.

Nerves may be injured by a single application of highforce traction or by repeated application of lower levels oftraction that would not cause injury if they occurred only

once.18 Acute traction injuries are associated with frac-tures, either directly or secondary to reduction or fixation;joint dislocation; extreme limb or body segment posi-tioning, as might occur during positioning for surgicalaccess; and pulling on a limb segment, as seen in obstet-rical brachial plexus injury. Traction injuries have alsobeen reported during and subsequent to limb-lengtheningprocedures.19 When nerves are stretched by more than 6%to 8% of their original length, intraneural circulation isimpaired15 and compound motor action potentials arereduced.20 Stretching of a nerve by more than 10% to 20%of its original length is associated with structural failure21,22

and changes in compound motor action potentials tocomplete conduction block.20,23 With elongation by 20%to 30% or more, perineural sheaths begin to rupture.24

After intraneural tearing, there is hemorrhage and conse-quently intraneural scarring as a result of proliferation offibroblasts and production of collagen.25

Nerves may be compressed by a variety of mechanisms.Edema from acute and chronic inflammation,26 inflam-matory diseases, increased compartmental pressures,space-occupying lesions, contact against bones, andentrapment within soft tissues, as well as iatrogeniccauses, such as tourniquet27 and blood pressure cuff application, are all associated with compression neu-ropathies.28,29 Koo and Szabo proposed that ischemia mayunderlie the nerve damage associated with compressionneuropathies and that when secondary effects of ischemia,including segmental anoxia, capillary vasodilation, andedema, are managed early, good symptom resolutionfollows. However, with chronic compression, intraneuralfibrosis appears to impede recovery.30

The amount of compression applied to a nerve affectsthe nature and degree of nerve damage. Under normal cir-cumstances the pressure on the median nerve in the carpaltunnel is approximately 2.5 mm Hg.31 Peripheral nerveshave been shown to be damaged, with partial or completeblocking of axonal transport and increased vascular per-meability resulting in edema,32,33 when exposed to pres-sures of more than 30 mm Hg, and complete ischemiaoccurs at pressures over 60-70 mm Hg.34,35 Because thereare no lymphatic vessels in the endoneural space, intra-neural edema can take a long time to resolve.

The nature of a nerve injury also depends on the dura-tion of compression and how much of the nerve is com-pressed.36 Acute and localized compression generally causesless severe injury than chronic and diffuse compression.37

Szabo and Sharkey compared cyclic compression, as onemight see in repetitive motion, with chronic compressionin rats (in this case, chronic compression lasted 6 hours)and found that cyclic and chronic compression causedsimilar changes in nerve conduction velocity.38

Experimental studies of controlled vibration andstudies with workers using vibrating tools have found thatvibration can cause nerve demyelination and fibrosis.39,40

Vibration is thought to cause damage directly and indi-rectly, by causing edema.41 Vibration-induced nerve injuryis common in workers using heavy machinery such asjack-hammers.42

Nerve ischemia may also be caused by vascular occlu-sion43 and other vascular disorders. Chronic ischemia


Receptor

Synaptic vesicles

Postsynaptic membraneSynaptic

cleft

Neurotransmittermolecules

Presynaptic cell Postsynaptic cell

FIG. 18-8 Synaptic transmission. From Thibodeau GA,Patton KT: Anatomy and Physiology, ed 6, St. Louis, 2006,Mosby.

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damages the blood-nerve barrier, causing an influx of pro-teinaceous fluid followed by a proliferation of fibroblastsand intraneural scarring. Since ischemic injury alone doesnot disturb the continuity of the plasmalemma, nervesrecover more readily from this type of injury than fromothers. However, prolonged ischemia may lead to nerveinfarction, which then has a similar prognosis to nerveinjuries with other mechanisms.44,45

When a nerve is subjected to accidental injection, itmay be damaged by the physical trauma of the needle andby exposure to the drug or agent. Accidental injectioninjuries occur most often during medication delivery,46,47

with the sciatic nerve being the nerve most frequentlyinjured by injection.48 Needle-stick injuries to nervesduring acupuncture are rare but have also been reported.49

Injection of a nerve usually causes severe, radiating pain.Nerve lacerations can occur as result of contact with a

sharp object, such as a piece of glass, metal, knife, razorblade, or scalpel, or from contact with a blunt object, suchas components of power tools or other machinery, andgunshot wounds. Sharp injuries may occur intraopera-tively.50 Blunt objects generally produce jagged, shreddedinjuries with ill-defined edges, whereas sharp objectsproduce injuries with a well-defined edge. Gunshotwounds may injure a nerve directly or secondarily as theresult of shock, blast, or cavitation effects.51,52

Nerves may also be damaged by heat, either throughdirect exposure or by exposure to electrical current or radi-ation. Nerve tissue has the lowest electrical impedance ofany body tissue, therefore electrical currents tend to travelalong neurovascular bundles. Most neurovascular bundlesrun deep to the muscles they innervate, thus tissues lyingclose to this pathway may also be damaged. An electricalcurrent can injure nerves directly by heating them andcausing coagulation necrosis or by damaging the nervecell membrane and increasing its permeability.53 Radiationinjury is associated with treatment for cancer, and whenit occurs, the damage to irradiated nerves appears to berelated to an increase in temperature and is generally permanent.54

DOUBLE-CRUSH SYNDROMEDouble-crush syndrome is a phenomenon in which two ormore lesions along the same nerve produce symptomsthat would be less observable or severe if only one lesionexisted.55-57 Double-crush injury is thought to occur whenone lesion disrupts axonal transport and thus impairsdelivery of substances essential to the maintenance ofmembrane integrity and disposal of waste material inother parts of the nerve. Many doubt the existence of thedouble-crush syndrome58,59 or suggest that it is over diag-nosed.60 For example, Chaudhry and Clawson conducteda small study of subjects with amyotrophic lateral sclero-sis (ALS), a disease of motor nerves, to see if the presenceof this nerve disease predisposed nerves to a secondpathology.59 The authors made three predictions thatwould support the concept of double-crush: (1) Therewould be a greater incidence of ulnar neuropathy at theelbow of the motor versus sensory nerve in subjects withALS; (2) in subjects with ALS with an ulnar neuropathy atthe elbow, the sensory fibers should have less involvement

than the motor fibers; and (3) motor nerves from patientswith ALS and ulnar neuropathy at the elbow would havemore axonal loss than motor nerves from patients withALS without ulnar neuropathy. After establishing a defi-nition of ulnar neuropathy at the elbow (a focal reductionin nerve conduction velocity [NCV] of ≥10 m/sec), theinvestigators compared nerves and found that there wasno greater incidence of motor ulnar neuropathy thansensory ulnar neuropathy at the elbow in patients withALS and that in those with ulnar neuropathy at the elbowthere was not a significantly more motor nerve involve-ment than sensory nerve involvement. These findings didnot support the concept of double-crush syndrome. Thethird prediction was supported but only demonstratedthat ulnar neuropathy can affect the motor nerves.59

Despite the paucity of evidence supporting the existenceof double-crush injury, this concept continues to bepopular among clinicians.

CLASSIFICATION OF NERVE INJURYSeveral authors have proposed classifications systems fornerve injury (Table 18-3).61-64 These systems describe theextent of nerve injury. Seddon describes three categoriesof nerve injury: Neurapraxia, axonotmesis, and neu-rotmesis,61,63 whereas Sunderland describes five categories,numbered first through fifth degree, which are similar toSeddon’s, but axonotmesis and neurotmesis are dividedinto two categories each.62 A sixth category, whichincludes concurrent damage at all the levels described bySunderland with some degree of injury to all five tissues,has been proposed by MacKinnon.64

SPECIFIC NERVE LESIONSAlthough nerves may be injured at any location and by avariety of mechanisms, certain lesions are more common.The following section discusses the more common specificperipheral nerve injuries and includes examples of uniquemechanisms of injury. This section is sequenced anatom-ically, starting cranially and proximally and moving cau-dally and distally.

Nerve Lesions Affecting the Head and Neck.Cranial nerves may be injured by external forces such aspenetration from bullets or needles, or by blunt traumacausing fractures.65 Injury may also occur from compres-sion by edema, tumors, and entrapment. For example,pituitary tumors often compress the optic nerves,65 thetrigeminal nerve may be injured in association withmandibular or maxillary fractures,65 mandibular surgery66

or dental work,67,68 and the facial nerve may be injured inassociation with mandibular condyle,69 laterobasal frac-tures,65 and parotidectomy.70 Bell’s palsy, the acute onsetof idiopathic of facial nerve palsy, may occur subsequentto a viral infection71 or may have a vascular cause.65 Glos-sopharyngeal, vagus, and hypoglossal nerve injuries havebeen reported after subluxation of the cervical spine insubjects with rheumatoid arthritis.72,73 Spinal accessorynerve injuries may occur during lymph node biopsy,74-76

and the hypoglossal nerve may be injured by intubation.77,78

Nerve Lesions Affecting the Upper Extremity.Brachial plexus injuries can be caused by blunt trauma


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from falls and lacerations from penetrating injuries, aswell as compression and traction. In a report of 100 con-secutive cases of subjects undergoing surgical repair ofbrachial plexus injuries, most injuries included trauma(motorcycle accidents, gunshot wounds, and penetratingwounds) and nine were iatrogenic.79 Positioning theshoulder in hyperabduction for surgical procedures, suchas mammoplasty, can also be associated with brachialplexus traction injuries.80

Obstetrical brachial plexus palsy (OBPP) is a brachialplexus injury in the newborn. OBPP is associated withincreased birth weight, operative vaginal delivery,81

advanced maternal age, and maternal diabetes.82 Patternsof injury for OBPP are described in Table 18-4. It has beenproposed that this injury occurs when the infant presentsin the vertex position, causing the infant’s shoulder to beimpeded by the mother’s pubic symphysis.83 However, asystematic review of the literature found that OBPP had agreater association with a very short duration of thesecond stage of delivery than with shoulder dystocia orforceps delivery, which are typical with vertex posi-tioning.84 Most infants with OBPP have complete neurological recovery,85 and predictors of optimal recov-ery include intact active elbow flexion by 3 months of age,C7 involvement, and high birth weight.86 Children withOBPP may develop secondary deformities about the shoul-der because of muscle imbalance, which progress with sub-optimal neural recovery.87 In a study of 16 infants (17shoulders) with OBPP without full recovery, nine demon-strated an irregular glenoid, retroversion of the glenoid, orsubluxation of the humerus. The authors of this studysuggest that even with neural recovery, children withOPPB may have functional deficits that are a result ofstructural irregularities.88

Peripheral nerves projecting off the trunks and cords ofthe brachial plexus include the long thoracic and supra-scapular nerves. The long thoracic nerve is susceptible toinjury during first rib resections,89 and a single case reportdescribes an incident of long thoracic nerve palsy after pal-pation along the first rib.90 In studies of the long thoracicnerve in six fresh cadavers, investigators found a tightfascial band arising from the inferior aspect of the brachialplexus and extending to the first rib that caused bow-stringing of the nerve when the shoulder was passivelyabducted and externally rotated and proposed that thisband could damage the nerve because of intermittentdynamic tension.91 The suprascapular nerve may bedamaged where it passes underneath the superior trans-verse scapular ligament at the scapular notch92 or whereit passes under the inferior transverse scapular ligament atthe spinoglenoid notch.93 In a review of 88 cases of iso-lated suprascapular nerve injury, a ganglion or entrapmentby the inferior transverse scapular ligament were the mostfrequent causes.94 Some patients who have a wide trans-verse scapular ligament and a narrow spinoglenoid notchmay be at increased risk for suprascapular nerve inury.95

There are many injuries that may occur more distally in


TABLE 18-4 Patterns of Obstetrical BrachialPlexus Palsy

Type Incidence* Pattern of InvolvementErb-Duchenne 73% Upper plexusTotal plexus injury 25% Total plexusKlumpke’s 2% Lower plexus

*Data from Shenaq SM, Bullocks JM, Dhillon G, et al: Clin Plast Surg32(1):79-98, 2005.

TABLE 18-3 Classification of Peripheral Nerve Injury

Seddon Sunderland Injury Symptoms Mechanism of Injury RecoveryNeurapraxia First degree Structure of nerve Pain Compression, ischemia, Spontaneous and

intact, focal Minimal to no muscle stretch, blunt trauma, complete return withindemyelination, atrophy metabolic derangement, days to monthslocalized area of Numbness toxins, diseasesconduction block Diminished

proprioceptionSecond degree Interruption of Pain Greater nerve compression Spontaneous and

axons, epineurium, Some muscle atrophy or traction complete return withinperineurium, and Complete loss of monthsendoneurium intact motor, sensory and

sympathetic functionAxonotmesis Third degree Disruption of axons, Severe traction, crush with Spontaneous but faulty

injury to funiculi subsequent scarring to no recoverycausing entrapment

Fourth degree Disruption of No pain No conduction because of Incomplete spontaneousperineurium Muscle atrophy scar recovery, surgery likely

Complete loss of required for repair ormotor, sensory, and graftingsympathetic function

Neurotmesis Fifth degree Complete transection Complete laceration No spontaneous of nerve recovery without

surgical intervention

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the upper extremity. Nerve injuries beyond the cords ofthe brachial plexus are summarized in Tables 18-5 and 18-6.

Nerve Lesions Affecting the Lower Extremity.Peripheral nerve injuries of the lower extremities inwomen are often associated with labor and delivery andpelvic surgery. In a study of 6,057 women after childbirth,56 reported a new onset of nerve injury.96 Cardosi, Cox,and Hoffman described a 1.9% incidence of postoperativeneuropathy involving (in order of decreasing frequency)the obturator, ilioinguinal/hypogastric, genitofemoral,femoral, or lumbosacral nerves in a group of women whounderwent pelvic surgery.97 Although rare, compression ofthe femoral nerve was reported in three cases to be asso-ciated with entrapment at the iliopectineal arch.98 Trau-matic femoral nerve injuries may occur as a result ofdisplaced acetabular fractures,99 total hip arthroplasty,100-102

and anterior dislocation of the femur.103 Iatrogenic injuriesare associated with inguinal hernia repair, arterial bypass,appendectomy,104 and hysterectomy.105,106 In a systematicreview of the literature pertaining to gynecological surgi-cal procedures and nerve injuries, Irwin et al found thatimproper placement of retractors was the most commoncause of femoral nerve injury subsequent to gynecologicalsurgical procedures.107 Sciatic nerve compression has beenreported as a consequence of an anomalous course of thesciatic nerve between the two tendinous origins of the pir-iformis muscle.108 Sciatic nerve lesions can occur after ablunt force to buttock region109 or accidental injection48

and as an iatrogenic consequence of hip arthroplasty.101,110

Bradshaw et al described 32 cases of obturator nerveentrapment caused by thick fascia overlying the shortadductor muscle.111 Obturator nerve injuries are oftenassociated with other nerve injuries, although isolatedinjuries have been reported with femur fracture fixation,112

hip replacement,101 and cement extrusion (for hip replace-ment).113 Other nerve injuries that occur more distally inthe lower extremity are summarized in Tables 18-7 and 18-8.

NERVE DEGENERATION AND REGENERATIONNerve recovery after complete nerve transection (neu-rotmesis) occurs if there is no damage to the cell body (Fig.18-9). This process involves changes in the proximal anddistal axon segments, as well as the nerve cell body. Afterneurotmesis, nonviable tissue must be removed and thenthe nerve must regenerate. First, within hours of theinjury, chromatolysis, with breakdown of rough endo-plasmic reticulum, occurs in the injured part of the nerve.The proximal axon degenerates from the site of injury upto at least the closest node of Ranvier. Following thisdegeneration, protein production accelerates to providematerials for nerve regeneration. These new proteins aretransported to the stump of the proximal axon where theyare assembled within approximately 24 hours from theinitial injury. While more proteins are being made fornerve repair, the production of proteins for neurotrans-mission and the proliferation of Schwann cells decrease.114

Axonal sprouting then occurs from the stump, just distalto the last intact node of Ranvier. Each axon forms up to15 sprouts, collectively called a growth cone. Thesesprouts migrate, directed in part by signals received byprojections of the basement membrane of the axon calledfilopodia. The filopodia are sensitive to growth factors,such as nerve growth factor (NGF), that act as targets,attracting regenerating axons.

Because the organelles required for protein synthesisare only located in the cell body, when a nerve is tran-sected the proteins needed for its maintenance and repaircan only reach the proximal nerve segment. Therefore thedistal nerve segment degenerates. This type of degenera-tion is known as Wallerian degeneration and involves dis-integration of the axoplasm and axolemma over thecourse of 1-12 weeks and degradation of the surroundingmyelin. The remnants of these materials are cleared fromthe area by macrophages. Residual Schwann cells in thearea of the distal portion of the injured nerve, respondingto the Wallerian degeneration, stimulate the productionof high levels of NGF for up to 2 weeks after nerveinjury.115 Although NGF promotes nerve regeneration, ithas also been implicated in the development of neuromasand neuropathic pain after nerve injury.

Studies have shown that nerve axons preferentiallygrow toward distal nerve stumps rather than toward othersoft tissues and toward their own distal stump rather thanother distal nerve stumps and that motor neurons growtoward denervated muscle rather than toward innervatedmuscle.116 There are several proposed mechanisms forthese patterns of regeneration. The growth cone andfilopodia are attracted to negatively charged proteinspresent in the basement membrane of the distal nervestump, thus axon sprouts are directed toward the distalnerve segment, specifically the basement membrane.When one axon, from a single growth cone, reaches thebasement membrane of the distal segment of the same


TABLE 18-5 Etiology of Upper Extremity NerveLesions

Nerve Mechanism of InjuryAxillary Anterior shoulder dislocation, trauma during

anterior shoulder stabilization procedures, fracture of the humeral neck*

Musculocutaneous Clavicular fracture†Radial nerve Humeral fractures,‡ compression in the radial

tunnel§¶Median nerve Entrapment in pronator teres,|| compression

in the carpal tunnelUlnar Cross pinning following supracondylar

fractures,¶ entrapment in the cubital tunnel, entrapment in Guyon’s canal

*Kline DG, Kim DH: J Neurosurg 99(4):630-636, 2003.†Bartosh RA, Dugdale TW, Nielsen R: Am J Sports Med 20(3):356-359,1992.‡Ring D, Chin K, Jupiter JB: J Hand Surg 29(1):144-147, 2004.§Portilla Molina AE, Bour C, Oberlin C, et al: Int Orthop 22:102-106,1998.||Johnson RK, Spinner M, Shrewsbury MM: J Hand Surg 4A(1):48-51,1979.¶Skaggs DL, Hale JM, Bassett J, et al: J Bone Joint Surg Am 83(5):735-740, 2003; Taniguchi Y, Matsuzaki K, Tamaki T: J Shoulder Elbow Surg9(2):160-162, 2000.

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TABLE 18-6 Major Nerve Injuries of the Upper Extremity

Nerve Muscles Clinical SignsDorsal scapular Rhomboid major Weakened scapular adduction.

Rhomboid minorSuprascapular Supraspinatus Weakened shoulder abduction and external rotation.

InfraspinatusSubscapular Subscapularis Weakened shoulder medial rotation.

Teres majorLong thoracic Serratus anterior Weakened scapular abduction and upward rotation, incomplete shoulder

elevation through flexion and abduction, scapular winging.Thoracodorsal Latissimus dorsi Diminished ability to depress scapula against resistance.Lateral pectoral Pectoralis major Weakened shoulder flexion, medial rotation, and horizontal adduction.Medial pectoral Pectoralis major (PMa) and minor (PMi) PMa: Weakened shoulder flexion, medial rotation, and horizontal adduction.

PMi: Weakened scapular downward rotation.Axillary Deltoid Weakened shoulder abduction, flexion, and/or extension, shoulder

Teres minor impingement.Musculocutaneous Coracobrachialis Significantly diminished elbow flexion.

Biceps Requires abduction of shoulder to flex the elbow via brachioradialis.Brachialis

Radial Triceps Supination diminished, loss of wrist and MCP extension.AnconeusBrachioradialisExtensor carpi radialis longusExtensor carpi radialis brevis

Posterior interosseus Supinator Full wrist extension but weak, weak ulnar deviation, unable to extend MCP Extensor digitorum communis joints.Extensor digiti minimiExtensor carpi ulnarisAbductor pollicis longusExtensor pollicis brevisExtensor pollicis longusExtensor indicis proprius

Median Pronator teres High (above or near elbow): Weakened pronation; weakened wrist flexion; Flexor carpi radialis loss of digital flexion of IF, MF; weakened flexion of RF and MF; Palmaris longus weakened thumb MCP flexion, loss of thumb opposition, and palmar Flexor digitorum superficialis abduction.Flexor pollicis brevis (superficial head) Benedictine hand: clawing of the index and middle finger.Opponens pollicisLumbricales (1 and 2)

Anterior interosseus Flexor pollicis longus Weakened forearm pronation; weakened flexion of IF, MF; loss of thumb Flexor digitorum profundus (1 and 2) palmar abduction.Pronator quadratus Unable to make the “O” sign with thumb and index finger.Abductor pollicis brevis High (at or above elbow): Weakened wrist flexion and ulnar deviation, loss

Ulnar Flexor carpi ulnaris of DIP flexion RF, SF; loss of MCP flexion SF; weakened MCP flexion RF; Flexor digitorum profundus (3 and 4) loss or significantly diminished IP extension IF, MF, RF, and SF; loss of Palmaris brevis lateral pinch; loss of SF opposition to thumb.

Froment’s paper sign: In presence of ulnar nerve palsy, client will flex thethumb IP joint instead of contracting the adductor pollicis muscle when asked to hold paper between the pads of the thumb and index finger.

Jeanne’s sign: The client may hyperextend the MCP joint in the above task.Egawa’s sign: Client cannot radially and ulnarly abduct the MF.

Deep branch Abductor digiti minimi Weakened MCP flexion SF; loss or significantly diminished IP extension IF,Flexor digiti minimi MF, RF, and SF; loss of lateral pinch; loss of SF opposition to thumb.Opponens digiti minimi Froment’s sign, Jeanne’s sign, Egawa’s sign, clawing of RF and SF.Lumbricales (3 and 4)Palmar interosseusDorsal interosseusAdductor pollicis

MCP, Metacarpophalangeal; IF, index finger; MF, middle finger; RF, ring finger; SF, small finger; DIP, distal interphalangeal; IP, interphalangeal.

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nerve a protein known as actin, found in the growth cone,attaches to the basement membrane of that distal segmentand the other nerve sprouts in that growth cone degener-ate. In addition, a protein called neural cell adhesion mol-ecule (NCAM) that is expressed by muscle attracts motornerves, and for other nerves, axonal regeneration andmyelinization are promoted by the nerve connecting withan end-organ.114

After repair of a transected nerve, the rate of regenera-tion is at the most 10 mm per day. However, regenerationrates differ among fibers, depending on their type and

location (Table 18-9). Small fibers regenerate more quicklythan larger diameter fibers. Therefore C fibers carryinginformation about dull, aching pain and temperature willregenerate more quickly than A-beta and A-delta fibersthat carry information about discriminative touch, pro-prioception, and sharp pain.

Surgical repair of transected nerves does not ensure fullfunctional return. Nerve cell viability, rate of recovery, andaxonal direction all affect the degree of nerve regenerationand the viability of end-organs.117 Additionally, neuromadevelopment and neuropathic pain can contribute to poor


TABLE 18-7 Common Causes of Lower Extremity Nerve Lesions

Nerve CausePeroneal Fractures of the femur, tibia, and fibula;* knee dislocation;† leg crossing; positioning in persons who are

mobility impaired or comatose; and positioning during surgical proceduresDeep peroneal Compression beneath fibular fibrous arch‡ in the anterior tarsal tunnel, from constricting shoe laces and in

the presence of pes cavusSuperficial peroneal nerve Inversion sprain§Tibial Compression because of entrapment in the tarsal tunnel or in the popliteal fossa||Sural Lateral malleolus fracture, calcaneus fracture, small saphenous vein stripping¶

*Data from Mont MA, Dellon AL, Chen F, et al: J Bone Joint Surg Am 78:863, 1996.†Data from Goitz RJ, Tomaino MM: Am J Orthop 32(1):14-16, 2003.‡Data from Fabre T, Piton C, Andre D, et al: J Bone Joint Surg Am 80(1):47-54, 1998.§Data from Johnston EC, Howell SJ: Foot Ankle Int 20(9):576-582, 1999.||Data from Mastaglia FL: Muscle Nerve 23(12):1883-1886, 2000.¶Data from Seror P: Am J Phys Med Rehabil 81(11):876-880, 2002.

TABLE 18-8 Signs and Symptoms of Lower Extremity Nerve Injuries

Nerve Muscle(s) Clinical Signs Sensory LossSuperior gluteal Tensor facia late Trendelenburg gait NoneInferior glutealSciatic Abductor magnus High steppage gait, inability to stand Posterior thigh and calf

Semimembranous on heel or toes Entire foot with exception of medialBiceps femoris malleolus and medial aspect

Common peronealSuperficial Peroneus longus Foot drop, inability to evert the foot Lateral aspect of calf

Peroneus brevis Foot drop Dorsum of footDeep Tibialis anterior First web space of toes

Extensor digitorum longusExtensor hallucis longusPeroneus tertiusExtensor digitorum brevisExtensor hallucis brevis

Tibial Gastrocnemius Inability to plantar flex the ankle and Plantar aspect of foot and toes except Soleus invert the foot medial borderTibialis posterior Toe flexion, abduction, and Flexor digitorum longus adduction lostFlexor hallucis longusIntrinsics on plantar foot

Femoral Pectinius Falling because of an unstable knee Medial distal thighSartorius and difficulty with stair climbing Medial aspect calf and footRectus femorisVastus medialisVastus intermediusVastus lateralis

Obturator Adductor brevis — Medial aspect of thighAdductor magnusAdductor longusGracilis

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functional outcomes despite optimal surgical repair andsubsequent regeneration.

FUNCTIONAL RECOVERY FROMPERIPHERAL NERVE INJURYFor a peripheral nerve to successfully regenerate, four cri-teria must be met: Survival of the cell body; absence ofbarriers, such as scar or bone that would prevent axonalsprouting; accurate growth toward appropriate end-

organs; and accommodation of the central nervous system(CNS) to reorganize mixed afferent signals.118 In addition,functional recovery from peripheral nerve injury may beaffected by the age and cognitive capacity of the patient,the circumstances or nature of the nerve injury, and thesubsequent repair.119

Children tend to have better functional outcomes fromperipheral nerve injury than adults.120-122 Proposed reasonsfor this include that the nerves have less distance to cover


Distal fragmentation of axon and myelin

Phagocytosis of debris

Axonal sprouting

Reconnects

Normal

Transection

Degeneration

Regeneration

Regenerated

FIG. 18-9 Nerve degeneration and regeneration after complete nerve transection. FromLundborg G: Nerve Injury and Repair, Edinburgh, 1988, Churchill Livingstone.

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to reach their end-organ120 and that children have morecerebral plasticity123,124 and better nerve regeneration.125

The latter theory, however, is controversial with studiesshowing both better120 and similar nerve regeneration inadults and children.126,127 Whether age affects recoveryfrom nerve injury beyond childhood is also controversial.One study found no difference in the improvements fromcarpal tunnel surgery between elderly patients (70-89years) and younger adults (30-69 years).128 However,another study with 84 subjects who underwent carpaltunnel release found that patients over the age of 60 faredless well than those between 31 and 59 years of age, withworse symptoms (p = 0.003), poorer functional outcomes(p = 0.046), and less improvement in nerve conductionstudy findings (p = 0.027).129

Patients with traumatic peripheral neuropathies haveworse outcomes than patients with peripheral neu-ropathies from nontraumatic causes.130 Functional out-comes after crush injuries are better than those aftertransection followed by repair or nerve grafting.131 Nervesrepaired sooner fare better, with less cell death, than thoserepaired later.132 Generally, the more proximal a nerveinjury is the poorer the outcome because of the length ofnerve that needs to regrow for reinnervation.

EXAMINATION

PATIENT HISTORYInformation obtained from the medical record and patientinterview includes the patient’s name, gender, race/ethnicity, and primary language. Gender appears to be arisk factor for certain peripheral nerve injuries. Forexample, carpal tunnel syndrome (CTS) seems to be morecommon in women,133 whereas cubital tunnel syndromeaffects more men.134 In the presence of OBPP, a develop-mental and birth history should be obtained.

Specific aspects of the patient history to be emphasizedfor patients with peripheral nerve pathology includeemployment status and sports activities. Since entrapmentmononeuropathy may be caused by specific activities, theclinician should ask the patient about the nature of theiractivities at work, school, and home. Particular attentionshould be paid to repetitive activities and positions oractivities where compression may be placed on a nerve byan external object. For example, suprascapular nerveentrapment has been reported to occur in newsreel cam-eramen as a result of compression of the nerve by the

weight of the camera on the shoulder.135 Although workactivities may affect the risk for nerve injury, there is evi-dence that other factors, such as body mass index, age,and anatomical variation, may play a greater role forindustrial workers with abnormal nerve function.136

Sports-related injuries, whether as employment or leisureactivity, are commonly reported. Examples include supra-scapular and dorsal scapular nerve injury in volleyballplayers137 and cubital tunnel syndrome in throwing athletes.138,139

The medical chart should be reviewed for results ofradiographs, computed tomography (CT), magnetic reso-nance imaging (MRI), nerve conduction studies, and diag-nostic nerve blocks. Radiographic studies, particularly CTand MRI, may reveal presence of a soft tissue mass alongnerves causing compression. Diagnostic nerve blocks andnerve conduction studies aid in localizing sources ofnoxious stimuli and pathways for transmission of noxiousstimuli. Further discussion of nerve conduction studiesfollow later in this chapter.

The client’s understanding of the current problem andreason for referral to rehabilitation therapy are recorded.Response to other therapies, including past and present,may help in determining prognosis. The mechanism ofinjury and date of injury or onset of symptoms are alsocrucial for diagnostic and prognostic determination. Sincemore proximal injuries have less favorable outcome,recording the level of injury is also essential.

SYSTEMS REVIEWThe systems review is used to target areas requiring furtherexamination and to define areas that may cause compli-cations or indicate a need for precautions during theexamination and intervention processes. See Chapter 1 fordetails of the systems review.

TESTS AND MEASURESThere is no single test shown to accurately assess the pres-ence and status of nerve pathology, thus a battery of testsshould be used to evaluate subjects with suspected nervelesions as in some cases this increases the probability ofmaking a correct diagnosis.140,141

MusculoskeletalPosture. Posture may play a role in the development

or exacerbation of symptoms associated with peripheralnerve entrapment or compression (see Chapter 4).

Anthropometric CharacteristicsEdema. Peripheral nerve injury may be associated with

edema, heat, and redness when there is inflammationpresent and with edema, coolness, and pallor when activemotion is significantly impaired. Limb volume can be esti-mated by water displacement using commercially avail-able hand volumeters (Fig. 18-10) or by circumferentialmeasurements. Hand volumeters have been found to beaccurate within 1%,142 and their standard error can bereduced from 10 ml to 3 ml by placing the device on a height-adjustable table, supporting the patient’s trunk, and measuring the displaced water with a 1-mlmicropipette.143 Circumferential measurements and vol-umetry have both been found to have high interrater and


TABLE 18-9 Rate of Nerve Regeneration byRegion

Location Rate of Regeneration (mm/day)Upper arm 2.5-8.5Proximal forearm 2-6Wrist 1-2Hand 1-1.5Upper leg 2Lower leg 1.5Ankle 1

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test-retest reliability coefficients of 0.99.144 When estimat-ing hand or foot volume with a tape measure, the figure-of-eight method has been found to be most reliable.145-148

There are no standards for these measurements, but com-parison with the uninvolved limb and over time can be usedto evaluate for abnormalities and changes. Note that it isnot uncommon for the dominant hand to be larger thanthe nondominant hand by as much as 10-16.9 ml.149,150

Range of Motion and Muscle Length. Joint contrac-tures and muscle shortening frequently occur after periph-eral nerve injury as a result of unbalanced forces arounda joint. For example, 52% of a sample of patients withcubital tunnel syndrome was found to have elbow flexioncontractures.151 Therefore both active and passive ROM, aswell as muscle length, should be examined in patientswith peripheral nerve injuries. These measurementsshould be performed at least for all areas that the involvednerve crosses.

Muscle Performance. Muscle strength testing is essen-tial for patients with peripheral nerve injuries because aperipheral motor nerve injury will produce specific weak-

ness in the muscles innervated by that nerve. Musclesshould be tested individually rather than with others per-forming similar movements because muscles performingsimilar movements may have different innervations.Muscle weakness that results from peripheral nerve injuryis examined using manual muscle tests. Prolonged weak-ness as a result of motor nerve injury may also bedetectable by observation of muscle atrophy and loss ofmuscle bulk. Although changes in girth measurementsover time have been shown to correlate with other mea-sures of strength, the poor specificity of this method limitsits utility (see Chapter 5).152

The British Medical Research Council (BMRC) devel-oped a scale, later modified by Dellon (Table 18-10), forgrading motor and sensory function after peripheral nerveinjury.153 This scale grades motor function based on thestrength of proximal and peripheral muscles innervatedby the nerve in question to indicate the degree of nervefunction. Since distal weakness indicates less severe ormore distal peripheral nerve involvement than proximalweakness, this scale is helpful for localizing and deter-mining the severity of peripheral nerve injuries and inevaluating recovery.

Assessment of Muscle Function in Children withObstetrical Brachial Plexus Palsy. Several tools are avail-able to examine muscle performance in children withOBPP. The BMRC system as previously described is notsuitable for measuring strength in infants and small chil-dren because it depends on cooperation for tests requiringmanual resistance. A modified BMRC appropriate for chil-dren is described by Gilbert and Tassin.154

Bae et al recently evaluated the reliability of threemovement scales for children with OBPP: The Mallet Classification, the Toronto Test, and the Active MovementScale (AMS).155 Based on examination of 80 children bytwo examiners two different times, each reported fair toexcellent intraobserver and interobserver reliability for all3 of these scales, with higher intraobserver agreementthan interobserver agreement. They did not comment onthe sensitivity or specificity of these tests.

The Mallet Classification is useful for defining recoveryof upper trunk lesions and can be used with toddlers but


FIG. 18-10 Measurement of hand volume (edema) using ahand volumeter.

TABLE 18-10 British Medical Research Council Scale of Nerve Function

Motor Function Sensory FunctionM0 No contraction S0 Absence of sensibility in the autonomous areaM1 Perceptible contraction in proximal muscles S1 Recovery of deep cutaneous pain in the autonomous areaM2 Perceptible contraction in proximal and distal muscles S1+ Recovery of superficial pain in the autonomous areaM3 Contraction of proximal and distal muscles with sufficient S2 Return of some degree of superficial cutaneous pain and

power to allow movement against resistance some tactile sensibility in the autonomous areaS2+ S2 but with an overresponse

M4 Return of function as in stage 3 but synergistic and S3 Return of superficial cutaneous pain and tactile sensitivity independent movements are possible throughout the autonomous area, with disappearance

over response, static 2-point discrimination >15 mmS3+ S3, with localization and recovery of 2-point discrimination

at 7-15 mm in the autonomous areaM5 Complete recovery S4 Complete recovery with static 2-point discrimination at

≤6 mm

Modified by Dellon A, Curtis R, Edgerton M: Plast Reconstr Surg 53:297-305, 1974.

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not infants. To perform this test the child is asked to placethe hands on the back of the neck, on the low back (usingshoulder internal rotation), and to the mouth. The move-ments are evaluated on a scale of I-V, with I being no move-ment and V being normal and symmetrical movement.156

The Toronto Test uses a 0-2 scale to assess elbow flexion,elbow extension, wrist extension, finger extension, andthumb extension with a maximum of 10 points avail-able.157 The AMS is a tool with 8 grades for quantifyingmotor function in infants and older children with OBPP.158

The AMS, which was designed to elicit movements againstgravity or with gravity minimized, examines joint move-ment rather than individual muscle function and does notrequire the child to be able to follow commands. In astudy with 63 infants with OBPP, most components of theAMS were found to have high interrater reliability, withthe exception of forearm rotation.159

NeuromuscularPain. Peripheral nerve injury is often associated with

changes in sensation. Although decreased sensation,causing numbness and tingling, is most common,burning, shooting, and sharp electrical-type pains are alsooften associated with peripheral nerve injuries. In addi-tion, tingling or paresthesias may also be described by thepatient as pain.160 The nature of the pain may help to dis-tinguish nerve-related pain from pain of musculoskeletalorigin. Pain associated with peripheral nerve injury mayindicate normal nerve regeneration but is thought moreoften to be a result of irritation of small diameter noci-ceptive A-delta and C fibers.

Pain may also be caused by neuromas, which arebenign tumors made up largely of nerve cells and nervefibers, that often occur after peripheral nerve injury. Neu-romas are thought to be formed when nerve regenerationis blocked by scar tissue, preventing further regeneration.Movement of adjacent tissues or direct application of pres-sure on neuromas often causes pain by stimulating thenerve enclosed by the neuroma. Standard pain assessmentmeasures (see Chapter 22) may be used to measure painin clients with peripheral nerve injury.

Cranial and Peripheral Nerve IntegrityElectrophysiological Testing. Electrodiagnostic studies

are generally considered the gold standard for evaluatingperipheral nerve integrity. There are electrodiagnosticstudies that examine sensory and motor nerve conduc-tion, known as nerve conduction studies (NCS) or NCVstudies, and studies that examine muscle activity inresponse to stimulation or activation, known as an elec-tromyogram (EMG). Together, these studies can help tolocalize peripheral nerve lesions, determine their severity,and distinguish between neuromuscular dysfunctioncaused by demyelination, axonal damage, motor end-plate dysfunction, and muscle dysfunction. These tests arefrequently used to assist with diagnosis and to evaluaterecovery over time or in response to treatment. Therapistswith specific advanced training and necessary certificationmay perform electrodiagnostic testing in many parts ofthe United States.

NCS can confirm the presence of both symptomaticand asymptomatic nerve pathology.161 A joint literature

review by three medical professional associations pub-lished in 2002 concluded that NCS has high sensitivityand specificity for identifying CTS,162 despite the fact thatthese studies can produce negative results in the presenceof clinical symptoms and positive results in the absenceof symptoms or pathology.163,164 Because of these limita-tions, some still recommend using clinical history andphysical examination rather than NCS to diagnose CTS,and all recommend correlation of study findings withfindings from the clinical examination.140,165,166

It has been suggested that NCS can also be used to iden-tify and predict those at risk for developing CTS. Aprospective study involving 77 subjects without CTSsymptoms but with abnormal NCS at baseline and asimilar number of asymptomatic subjects with normalNCS at baseline found that over a period of 70 months,23% of those with abnormal NCS and only 6% of thosewith normal NCS developed symptomatic CTS (p =0.01).167 However, although Nathan et al’s study of 289workers over 11 years found a strong, direct linear corre-lation between initial severity of median nerve conduc-tion slowing and subsequent development of CTS, theyfound that most workers who developed de novo slowingdid not develop symptoms or CTS. They therefore con-cluded that changes in conduction status of the mediannerve occur naturally with increasing age and do not nec-essarily lead to symptoms and CTS.168 Additionally, in astudy of 700 workers, abnormal median sensory NCS werenot found to be predictive of future hand or finger com-plaints in asymptomatic workers.169 Werner et al recom-mend that if the results of these tests are used forpreplacement screening among active workers, it shouldbe done with caution.169

Provocative Tests to Detect Nerve Injury. Cliniciansoften subject nerves to compression or traction in anattempt to detect nerve injury or dysfunction. Productionof symptoms by these provocative testing maneuvers isthought to indicate nerve injury. Compression can beapplied manually or with a device, and tension is gener-ally applied by placing the client in positions that arethought to put the nerve on stretch and would not elicitsymptoms in normal subjects. This latter type of maneu-ver is referred to as a neural tension test. When neuraltension tests are performed by stretching the nerve alongits course with a series of maneuvers, each subjecting thenerve to greater amounts of tension, the clinician may beable to detect the presence of nerve entrapment or double-crush syndrome. The following are examples of com-monly used provocative tests for peripheral nervepathology; most are tests for specific nerve lesions.

Tinel’s Test. Tinel’s test is used to detect Tinel’s sign,which is a hyperirritability or response to mechanicalinputs such as tapping, and is thought to be indicative ofnerve injury. The presence of this finding may indicate thelocation of nerve injury. Although its presence andadvancing presence (presence along a regenerating nerve)is not always a reliable indicator of nerve injury or ofregeneration following injury,170,171 the lack of an advanc-ing Tinel’s sign is thought to indicate poor nerve regener-ation. Tinel’s test is performed by tapping on the skindirectly over the nerve in question (Fig. 18-11). The speci-


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ficity of this test is limited by the fact that even when anormal amount of force is applied, the Tinel’s sign may bepositive in 20% to 45% of subjects without nerve pathol-ogy172,173 and that when excessive force is applied, thereare even more false-positive outcomes.174 Although manyclinicians find the Tinel’s sign to be a useful indicator ofnerve injury, because of its poor sensitivity (0.63 in sub-jects with electrophysiologically confirmed CTS) andspecificity, it should not be used alone.173

A study by Novack et al suggested that Tinel’s test maybe more reliable for identifying nerve compression inadvanced rather than early stages.175 In addition, Spicheret al proposed a standardizing the technique for elicitingand analyzing Tinel’s sign through use of a vibrostimula-tor to improve standardization and quantification of thestimulation provided and thus possibly improve the utilityof the Tinel’s test.176

Roos Test. Roos test, also known as the elevated armstress test (EAST), is a test of vascular and neurologicalfunction in the upper extremity and is used to screen forthoracic outlet syndrome. To perform this test, the clientis asked to abduct and externally rotate the shoulder to 90degrees, flex the elbow to 90 degrees, and maximally openand close the hand slowly and repetitively for 3 minutes.The test is considered positive if the client reports ordemonstrates an inability to maintain the positionbecause of a sensation of heaviness or weakness of the armor reports tingling or numbness. No studies regarding thevalidity or reliability of the Roos test could be found froma MEDLINE search (1960-2005).

Neural Tension Tests. Neural tension tests can be per-formed on both the upper and lower extremities. Neuraltension tests for the lower extremities include the straightleg raise test (SLR), the slump test, and the prone kneebend test. The SLR and slump test primarily apply tensionto the sciatic nerve, whereas the prone knee bend test primarily applies tension to the femoral nerve (seeChapter 8).

A number of neural tension tests, collectively known asupper limb neural tension tests (ULNTTs), have beendescribed for the upper extremities. The brachial plexustension test, which was first described by Elvey, involvesthe patient being supine and the clinician sequentiallypassively moving the upper extremity into shoulderabduction, lateral rotation and slight extension posterior

to the frontal plane, elbow extension, forearm supination,wrist extension, and digital extension.177 The ULNTTs, asdescribed by Butler, include a series of four basic tests; thefirst and second tests selectively apply more tension to themedian nerve, and the third and fourth selectively applymore tension to the radial and ulnar nerves, respectively(Figs. 18-12 to 18-15).178 Hunter more recently developedtwo tests to evaluate the brachial plexus: The high abduc-tion arm test and the low abduction arm test179 (Table 18-11). For each of these tests, results are documented interms of the ROM at which symptoms are provoked andthe type of symptoms provoked. These tests are generallyperformed bilaterally for comparison.

The median nerve tension test, as described by Butler,has been shown in fresh cadavers to significantly andincrementally change the strain in the mediannerve.10,180,181 The ulnar nerve tension test has also beenfound to strain the ulnar nerve, although less than themedian nerve test strains the median nerve, with thegreatest strain noted at the cubital tunnel. Furthermore,the ulnar nerve test has also been found to increase strainin the median nerve.10 In contrast, the radial nerve testhas been found to produce minimal tension in any spe-cific nerve and is therefore considered neither sensitivenor specific for radial nerve involvement.181

Although ULNTTs have been found to be reliable inboth symptomatic and asymptomatic individuals (ICC 2.1≥0.98; standard error of measurement [SEM] ≤3.4 degreesfor symptomatic and ICC 2.1 ≥0.95; SEM ≤4.9 degrees forasymptomatic),182 the specificity of neural tension testingoverall is called into question by the finding that ULNTTsproduce symptoms or less than full ROM in many asymp-tomatic persons without nerve pathology.183

Elbow Flexion Test. Elbow flexion test is used in theexamination and evaluation of suspected cubital tunnelsyndrome. With the wrists in full extension, the client isasked to actively hold the elbow in maximal flexion for 3-5 minutes.184 Reproduction of the patient’s symptoms isconsidered a positive test. In a prospective, randomizedcontrol study of 44 extremities with cubital tunnel syn-drome, 75% had a positive elbow flexion test. Thisincreased with the addition of pressure on the ulnar nerveto 93%.185 However, since no studies have evaluated thefrequency of a positive elbow flexion test in individualswithout cubital tunnel syndrome, the specificity of thistest is not known.

Phalen’s Test. Phalen’s test is used in the evaluation ofsuspected CTS (Fig. 18-16). The client is asked to flex bothwrists for 1 minute. Any numbness or tingling in themedian nerve distribution during the 1-minute period isconsidered a positive test.186 In a study of 127 patientswith CTS and a control group of 20 without CTS, in whomboth Phalen’s test and NCS were performed, althoughthere was statistically significant relationship between apositive Phalen’s test and slowed NCV, 34% of those withCTS diagnosed by NCS had a negative Phalen’s test and20% of those without CTS by NCS had a positive Phalen’stest, indicating that this test has a sensitivity of 66% anda specificity of 80%.187

Carpal Compression Test. Carpal compression test(CCT), another test for CTS, is performed by the examiner


FIG. 18-11 Tinel’s test of the median nerve at the carpaltunnel. Adapted from Goodman CC, Boissonnault WG, FullerKS: Pathology: Implications for the Physical Therapist, ed 2,Philadelphia, 2002, Saunders.

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AB C

D EFIG. 18-13 Upper limb tension test 2a (ULTT2a): Median nerve dominant utilizingshoulder girdle depression and external rotation of the shoulder. A, Position the patientwith the arm at the side, elbow slightly flexed. Then add shoulder girdle depression. B, Extend the elbow. C, Externally rotate the shoulder. D, Extend the wrist, fingers andthumb. E, Abduct the shoulder. Adapted from Butler DS: Mobilisation of the NervousSystem, Edinburgh, 1991, Churchill Livingstone.

A B C

D EFIG. 18-12 Upper limb tension test 1 (ULTT1): Median nerve dominant utilizingshoulder abduction. A, Position the patient with the shoulder abducted to 90 degreesand in neutral rotation, the elbow flexed to 90 degrees, and the wrist in neutral. Thenextend the shoulder to neutral. B, Extend the wrist and fingers. C, Externally rotate theshoulder. D, Extend the elbow. E, Side bend the neck away from the side being tested.Adapted from Butler DS: Mobilisation of the Nervous System, Edinburgh, 1991, ChurchillLivingstone.

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A B

AB

D E

C

FIG. 18-14 Upper limb tensiontest 2b (ULTT2b), radial nervedominant utilizing shouldergirdle depression plus internalrotation of the shoulder. A, Position the patient as inULTT2a and extend the elbow.Then medially rotate theshoulder and pronate theforearm. B, Flex the wrist,fingers, and thumb. Adaptedfrom Butler DS: Mobilisation ofthe Nervous System, Edinburgh,1991, Churchill Livingstone.

FIG. 18-15 Upper limb tension test 3 (ULTT3),ulnar nerve dominant utilizing shoulder abductionand elbow flexion. A, Position the patient as forULTT1. Then extend the wrist and supinate theforearm. B, Fully flex the elbow. C, Depress theshoulder girdle and externally rotate the shoulder.D, Abduct the shoulder. E, Side bend the neckaway from the side being tested. Adapted fromButler DS: Mobilisation of the Nervous System,Edinburgh, 1991, Churchill Livingstone.

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applying direct pressure over the carpal tunnel for 30seconds, with the patient’s forearm held in supination.Reproduction of the patient’s symptoms is indicative ofCTS. Durkan found that this test had a sensitivity of 87%and specificity of 90%.188 Furthermore, Williams et alfound that this test was 100% sensitive in a group of 30subjects with NCS-confirmed CTS and therefore recom-mended that this test be used in lieu of Phalen’s test whenclients are experiencing pain associated with wristflexion.189 Tetro et al found that adding 20 seconds of wristflexion to the CCT flexion improved both the sensitivityand the specificity of this test in patients with and withoutelectrodiagnostically-confirmed CTS.190

Piriformis Tests. Piriformis tests are performed in asubject presenting with sciatic pain and may be used toidentify compression of the nerve by the piriformismuscle. A number of variations of these tests have beendescribed. The flexion, adduction, and internal rotation(FAIR) test, which is intended to compress the sciatic nerveby stretching the piriformis muscle, is performed with theclient sidelying on the uninvolved side with the involvedhip in 60 degrees of flexion and the knee flexed. With the involved hip stabilized, the examiner places a hand onthe lateral aspect of the knee and then applies a down-ward force as if to push the hip into adduction. This test is considered positive if it reproduces the patient’s symptoms.

Beatty described a test that compresses the sciatic nervein the piriformis muscle by contracting rather thanstretching the muscle. For this test the client is positionedas for the FAIR test but is then asked to lift the knee offthe table by abducting the hip. This test is considered positive if it produces pain in the buttock area.191

Fishman et al, in a study with 918 subjects (1,014 lowerextremities) with complaints of low back pain or sciaticaand 88 asymptomatic controls, found that the FAIR testwas more than 96% sensitive and more than 68% specificfor piriformis syndrome and that it was a better predictorof recovery than the current working definition of thissyndrome.192

Comparison of Provocative Tests for Carpal Tunnel Syn-drome. Many studies have compared the sensitivity andspecificity of the various tests recommended for diagnos-ing CTS. Phalen’s test has generally been found to bebetter than Tinel’s test in identifying patients withCTS.193,194 Gellman et al found that Phalen’s test is moresensitive than the Tinel’s test, but Tinel’s test is more spe-cific.195 Priganc and Henry compared five tests used todiagnose CTS, including Tinel’s test, the manual CCT, andPhalen’s test, and found that Phalen’s test is most effec-tive for detecting the severity of CTS.196 Koris et al recom-mended combining a Phalen’s test with a sensory test(using Semmes-Weinstein monofilaments as describedlater) to achieve greater sensitivity and specificity.197

Durkan compared the CCT with Phalen’s test and Tinel’stest. While assuring the amount of pressure being exter-nally applied was maintained at 150 mm Hg for the CCT,he found that of 40 of 46 symptomatic hands had a pos-itive CCT, and of these, 31 had a positive Phalen’s test and25 had a positive Tinel’s test.188 Szabo et al also found thatthe CCT was more sensitive (0.83) for CTS than eitherPhalen’s test or Tinel’s test and that abnormal findings onthe hand diagram (see section on Pain Assessment), nightpain, and abnormal sensibility as determined by theSemmes-Weinstein monofilaments (see section on SensoryTesting) slightly increased the sensitivity of the CCT (to0.86).198 A systematic review of clinical diagnostic tests for CTS found that both Phalen’s test and the CCT werewell supported,199 and a more recent systematic review of clinical tests to diagnose CTS found that the CCT had the highest sensitivity (0.80) and specificity (0.92)overall.200

Autonomic Tests. Most noninvasive tests of peripheralnerve function depend on accurate sensory reporting by


TABLE 18-11 Hunter Tests of the Brachial Plexus

Test Sequential Maneuvers Positive Test FindingsHigh abduction 1. Shoulder abduction, extension and internal rotation Paresthesia: Ulnar nerve distribution, C8-T1 dermatomes

arm test 2. Elbow flexion to 90°3. Elbow extension4. Forearm supination

Low abduction 1. Shoulder adduction and external rotation Paresthesia: Median nerve distribution, C6-C7 dermatomesarm test 2. Forearm supination (wrist neutral)

Data from Hunter JM, Whitenack SH: Entrapment neuropathies of the brachial plexus and its terminal nerves: Hunter traction tests for differentialdiagnosis. In Macklin EJ, Callahan AD, Osterman AL (eds): Rehabilitation of the Hand and Upper Extremity, ed 5, St. Louis, 2002, Mosby; Trotten PA,Hunter JA: Hand Clinics 7(3):505-520, 1991.

FIG. 18-16 Phalen’s test.

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the patient. Two tests that do not rely on the patient’sreport that can objectively examine nerve function are thewrinkle test201 and Moberg’s ninhydrin test.202 Both ofthese tests rely on autonomic nerve functions. Whenusing the wrinkle test for hands, the hands are immersedin warm water at 40-42.2° C, with wrinkling of the skinoccurring in approximately 31/2 minutes if the nerve isintact and taking longer if the nerve is not intact.203-204 Apositive wrinkle test (i.e., wrinkling in more than 31/2

minutes) has been found to be consistent in patients withrecent and complete nerve transection but not in thosewith nerve compressions.204 For the ninhydrin test, theclient’s hand is washed and gently warmed for 10-30minutes. The hand is then pressed for 15-30 seconds ontopreviously untouched white bond paper to absorb anysweat from the hand. The paper is then sprayed with nin-hydrin and dried. If there is sweat present, the ninhydrinwill react with amino acids in the sweat and make thepaper turn blue. If the paper does not change color, nosweat is indicated and there is impaired autonomic func-tion in the hand, indicating probable nerve injury.205

Reflex Integrity. Deep tendon reflex (DTR) testing canhelp establish the presence of nerve pathology even in theabsence of other clinical findings and is performed bytapping on tendons with a reflex hammer. With periph-eral nerves injury, the DTRs will be hyporeactive.Although widely used as part of the clinical examination,some limitations of this test include variability in forceduring the tapping procedure, subjectivity in qualifyingthe response, and the fact that different responses can beproduced by exerting different amounts of force. Marshalland Little examined these limitations by measuring theamount of force needed to produce patellar DTR responsesthat were graded as hyporeflexic, normoreflexic, andhyperreflexic in persons without neural pathology andmeasured the amount of joint angle excursion in the lattertwo using an electrogoniometer.206 The median peak tapforce required to produce hyporeflexia was 12.8 Newtons(N), normoreflexia was 38.0 N, and hyperreflexia was 85.2 N. The authors suggest that the DTR response be

quantified by dividing the quotient of knee excursion bypeak tendon tap force and that this measure be known asbriskness.206

Sensory Integrity. Testing of sensibility is an essentialcomponent of the examination of individuals withperipheral nerve injury and can help localize a nervelesion, and facilitate diagnosis, prognosis, and selection ofinterventions including patients’ educational needs.Sensory test selection should be based on the expectedprogression of sensory return:

Pain and temperature↓

Sharp, pressure↓

Moving 2-point discrimination↓

Static 2-point discrimination

Sensory Testing. Sensory testing is most commonlyperformed with hand-held tools. Consequently, some vari-ables cannot be fully controlled, including the amount offorce used when applying the testing instrument, theamount of vibration because of shaking of the clinician’shand, the amount of time the device touches the client’sskin, and the speed at which the device is applied to theskin.207 Not all of these variables are significant for all typesof sensory testing and thus will be discussed where perti-nent to each tool.

For sensory testing, the examiner should ensure amutually agreeable communication system, establishpatient understanding of the testing procedure, and max-imize patient comfort. Additionally, for all cutaneoussensory testing, vision should be occluded (Fig. 18-17, A),and after orientation to testing procedures, distractingnoise and activities in the testing environment should beminimized. Comfort may improve accuracy as the clientwill be less likely to reposition, thus minimizing extrane-


A BFIG. 18-17 Positioning for sensory testing. A, Vision occluded; B, resting hand in putty.

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ous proprioceptive inputs. The body part to be testedshould rest on a supportive surface to minimize extrane-ous movement and stretching of tissues (Fig. 18-17, B).208

Each nerve root and peripheral nerve receives sensoryinput from a specific area of the body. These areas are dis-tinct but overlap to some degree because adjacent nervescan project into the same region. To localize a nerveinjury, the clinician should examine areas where the prob-ability of overlap is minimized (Table 18-12).

The ability to detect vibration is the first sensory func-tion that is diminished with early peripheral nerve com-pression.209-211 The ability to sense vibration may be testedwith a hand-held tuning fork. This is done by first strik-ing the tuning fork against a surface and then applyingthe single round end of the tuning fork over a bony promi-nence in the area of innervation and asking if the patientperceives the vibration. The sensitivity and specificity ofthis test are not known. Computer-controlled vibrome-ters, either with a fixed or variable frequency, are thoughtto more reliably quantify vibratory sensory loss. Force-defined vibrometers, which first measure skin complianceand then adjust the vibrometer for the force required toovercome skin compliance, have been shown to be reli-able and highly sensitive for early detection of compres-sive neuropathy.212

Sensation of cutaneous pressure is best tested withnylon monofilaments (Fig. 18-18). These have been shownto have high sensitivity, as high as 91%,213 but low speci-ficity for perception of touch.214 Of all hand-held manualdevices, monofilaments appear to have the highest relia-bility.215 Monofilaments are made of a single nylon threadattached to a plastic, hand-held rod. The end of the threadis pressed against the area being tested until it bends, andthe subject is asked to note if they did or did not feel pres-sure from the thread.

Monofilaments of different thickness and stiffness areavailable, corresponding to the amount of force requiredto bend them, ranging from 0.008 gm to 279.4 gm.Semmes-Weinstein monofilament rods (one of the morecommon types of these monofilaments) are marked witha number (ranging from 1.65-6.65) that represents thelog10 of the force in grams required to bend them. Themonofilaments requiring the least force to bend can onlybe felt when sensation is normal, whereas some of the

monofilaments that require more force to bend may befelt even when sensation is impaired. The 1.65 to 2.83monofilament represents the upper end of the normalrange for most people without injury for most parts of thebody and is recommended as the standard for normal sen-sation.216-218 Exceptions are for the face, which is more sen-sitive and can usually feel a finer 2.44 monofilament, andthe plantar surface of the foot, which is less sensitive andcan usually only feel the 3.22 to 3.61 monofilament orthicker.219

When testing with monofilaments (Table 18-13), theclinician should begin with the “normal” monofilamentfor the area of the body being tested and progress to largermonofilaments until one is felt. A form can be used forrecording monofilament testing findings. The monofila-ment is applied perpendicular to the skin and should gen-erally be pressed until it bends. This is required forconsistent application of force. The larger 4.56 and 6.65monofilaments will not bend with manual pressure andshould be pressed until they produce blanching of thepatient’s skin under the tip of the thread. Most monofila-ments should be applied up to 3 times and held in placefor up to approximately 1 second each time and thenremoved. An area may be retested after an approximate 1second wait. To retest an area wait for at least anothersecond before reapplying. The larger 4.56 and 6.65monofilaments should only be applied once. For mostclients, an uninvolved site should be used for comparisonto establish a baseline.

In addition to testing for perception of vibration andlight touch threshold, static 2-point discrimination (s2pd)and moving 2-point discrimination (m2pd) tests, knownas density tests, can be used to quantify sensory percep-tion in a given area. Static 2pd testing examines slow-adapting sensory nerve fibers, and m2pd testing examines fast-adapting sensory nerve fibers.220 Both testsare reported to have high reliability.221

Two-point discrimination, whether static or moving, isalso considered a functional test because s2pd and m2pdhave been found to be predictive of a subject’s ability torecognize objects by feeling them.222 To carry out thesetests in a standardized fashion, the clinician can choosebetween frequently used hand-held instruments, forexample, the Disk-Criminator (Neuroregan, Bel Air, Md),Boley gauge (Research Designs, Inc, Houston, Tex), orother similar aesthesiometers. Use of a paper clip to deter-mine s2pd and m2pd, while handy and economical, is notstandardized. The Disk-Criminator (Fig. 18-19, A) has sta-tionary sets of probes positioned around the perimeter ofthe disks, as well as one single probe. The Boley gauge hasone stationary probe and another moving probe that canbe positioned manually. With either device, the clinicianapplies one or two probes to the skin, without causing thebody part to move (thus causing undesired stimulation ofproprioceptive receptors) for 5 seconds. The patient isasked to identify whether he or she was touched with oneor two of the probes. This is repeated, with 3-4 secondsrest between applications, until the patient can no longerdistinguish between being touched with one or twoprobes. Interpretation for 2pd findings are listed in Table18-14. Moving 2pd is determined as described previously,


TABLE 18-12 Autonomous Sensory Zones forTerminal Nerves

Nerve Surface Body SegmentUlnar Volar Small finger, distal to DIP jointMedian Volar Distal to the DIP joint of index

finger and IP joint of the thumbRadial Dorsal First webspace, anatomical snuffbox

(may be overlap of lateral antebrachial cutaneous nerve)

Superficial peroneal Dorsal Mid-dorsum of the footDeep peroneal Dorsal First dorsal webspaceTibial Plantar Heel

DIP, Distal interphalangeal; IP, interphalangeal.

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A

SEMMES-WEINSTEIN MONOFILAMENTSENSORY TESTING RESULTS

FIG. 18-18 A, Monofilament testing of tactile sensation. B, Sample recording sheet formonofilament testing. B Courtesy North Coast Medical, Morgan Hill, Calif.

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except that the examiner moves the probes in a longitu-dinal, proximodistal manner.223

Variables that significantly affect the reliability of 2pdmeasures with any device include the amount and dura-tion of force application and in the case of m2pd, the rateof motion. Although some authors recommend standard-izing the force by applying sufficient pressure to causeblanching, it has been shown that blanching occurs with

a wide range of forces, ranging from a mean of 19.16 gmto a mean of 36.49 gm with 1 point and from 2.38 gm to14.91 gm when applying 2 points.221

Tactile Gnosis Testing. Patients with peripheral nerveinjuries affecting sensation in the hand may have diffi-culty with tactile gnosis, which is the ability of the handto perform complex functions by feel. A number of testshave been devised and evaluated for assessment and meas-urement of tactile gnosis. These include the Moberg pick-up test (Fig. 18-19, B) and the shape and texture iden-tification (STI) test.

The pick-up test, as described by Ng et al, is performedfirst with vision available and then with visionoccluded.224 The client is asked to pick up 12 objects (coins[2 sizes], a key, a paper clip, screw, washer, safety pin, nail,wing nut, and metal nuts [3 sizes]) from a table, one at atime, and place them in a small container as quickly aspossible. The time required is recorded. Then the test isrepeated with the other hand. Finally, the client is askedto identify each object with vision and without vision.Dellon later modified the test to include standard metalobjects.225

The STI test, introduced by Lundborg and Rosen, whichinvolves the patient identifying the shape and texture ofa variety of objects, has been found to have good sensi-tivity (95%), although poor specificity (40%) for identify-ing CTS, but good specificity (90%) and sensitivity (100%)for identifying patients with recent nerve laceration andrepair.226 This test has also been shown to be responsive toearly but not later improvements after partial nerve lacer-ations, in contrast to 2pd testing, which is insensitive toearly changes but responsive to later changes.227 Thesefindings suggest that the STI may be a good test for eval-uating patients with severe sensory involvement, as occurswith total nerve lacerations and early in recovery, but isnot specific enough to accurately differentiate higherlevels of ability or less severe involvement.

Multifunction Computer-Controlled Devices for SensoryTesting. A number of computer-controlled tools are avail-able for sensory testing. One of these, the AutomatedTactile Tester (ATT) (Topical Testing, Inc, Salt Lake City,Utah) measures pressure sensitivity, as well as vibration,temperature, and pain sensation, while controlling foramplitude of application, rate of application, and lengthof time the stimulus is applied.228 The ATT has been foundto be more sensitive and reliable for testing light touchand vibration after surgical decompression for CTS than


TABLE 18-13 Interpretation of MonofilamentTest Findings

Filament Interpretation Color1.65-2.83 Normal Green3.22-3.61 Diminished light touch Blue3.84-4.31 Diminished protective sensation Purple4.56-6.65 Loss of protective sensation Redover 6.65 Untestable Red striped

A

BFIG. 18-19 A, Testing of 2-point discrimination with theDisk-Criminator. B, Items from the Moberg pick-up test fortactile gnosis.

TABLE 18-14 2-Point Discrimination in theHand

Static 2 Point Discrimination InterpretationLess than 6 mm Normal6-10 mm Fair11-15 mm PoorOne point perceived ProtectiveNo points perceived Anesthetic

Data from American Society for Surgery of the Hand: Examination andDiagnosis, ed 2, Rosemont, Ill, 1983, The Society.

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the usual manually applied devices, Semmes-Weinsteinmonofilaments and a tuning fork.229

Cardiovascular/Pulmonary. Peripheral nerve injuryoften occurs in conjunction with damage to other struc-tures and for this reason, assessment of peripheral circu-lation is essential (see Chapter 29).

FunctionWork, Community, and Leisure Integration. Compres-

sion neuropathy may be associated with activities thatinvolve repetitive movements or vibration. However, sincethis is not a universal association and since the majorityof people with CTS or ulnar entrapment do not performjobs that involve repetition230,231 and most people withrepetitive strain injuries do not have compression neu-ropathy,232 it should not be assumed that a patient’s nerveinjury is related to their occupation.

EVALUATION, DIAGNOSIS, AND PROGNOSISMost clients who fall into the Guide for Physical TherapistPractice233 preferred practice pattern 5F: Impaired periph-eral nerve integrity and muscle performance associatedwith peripheral nerve injury will have the following typesof abnormal examination findings: Loss of or diminishedstrength, loss of or diminished ROM, impaired sensation,and hyporeactive stretch reflexes. In addition, integu-mentary integrity may be secondarily compromised. Thefollowing section describes rehabilitation interventionsthat have been shown to optimize outcomes for patientswith peripheral nerve injury.

INTERVENTIONClients with peripheral nerve injuries are referred forrehabilitation before and after surgical interventions andwhen surgery is not anticipated. After peripheral nerveinjury, interventions should progress from those thatfocus on protection and immobilization to those thatfocus on restoring physical and functional abilities as thenerve recovers. These interventions should be modifiedaccording to findings on the examination, the level andmechanism of injury, and any associated injuries.

PATIENT EDUCATIONClients with absent or impaired protective sensationshould be instructed in measures to protect skin integrity.For patients with upper extremity involvement, thisshould include abstaining from holding cigarettes orcooking at a stovetop. For those with lower extremityinvolvement, this should include wearing shoes wheneverwalking. All patients with sensory impairment should beespecially vigilant during activity involving use of sharpobjects such as nail clippers, and patients who requiresplinting should regularly inspect under the splint forareas of pressure, rashes, and signs of maceration.

Personal and ergonomic factors may increase the riskfor nerve compression or entrapment. Since smoking andobesity increase the risk for CTS, wellness programs thatpromote smoking cessation and weight reduction mayreduce the incidence or severity of CTS.234

THERAPEUTIC EXERCISEStrength Training. Although muscle strengthening

exercises will not increase strength in patients with com-plete motor denervation, strengthening exercises can beeffective with partial innervation and during reinnerva-tion. Strengthening exercises may be started as soon as thepatient can perform active muscle contraction (seeChapter 5). The use of electrical stimulation for strength-ening denervated muscles is discussed in detail the sectionon Electrotherapeutic Modalities.

JOINT RANGE OF MOTION AND MUSCLE STRETCHINGOnce immobilization for acute nerve injury is no longernecessary, joint ROM and muscle stretching may beneeded to regain ROM and soft tissue length lost becauseof immobilization. After surgical nerve repair soft tissuelengthening should be performed with caution, particu-larly if the nerve was repaired under tension or with agraft. Muscle stretching is recommended when nervecompression or entrapment is caused by muscle shorten-ing, as with cubital tunnel syndrome due to tightness ofthe flexor carpi ulnaris or piriformis syndrome due totightness of the piriformis muscle compressing the sciaticnerve. Muscle stretching is also recommended whenmotor nerve injury causes weakness of one muscle andresultant shortening of its antagonist.

SENSORY RETRAININGSensory desensitization and reeducation programs aregenerally performed together or in sequence in patientswith sensory nerve injuries that cause reduced sensationor pain. These interventions are intended to reduce hyper-esthesia and promote reorganization of cortical represen-tation of the involved limb.

Desensitization. Desensitization programs are des-cribed by several authors235-237; however, no published controlled studies evaluating the effectiveness of theseinterventions were found. Frykman and Waylett, whodescribed a graded, self-introduced application of less tomore irritating sensory stimuli, recommend 20-30 minutesessions, 2-3 times daily.235 Barber later described a similargraded introduction of stimuli but recommended a spe-cific progression from fixed textures, to loose materials in a container for limb immersion, to vibration, applied3-4 times daily for 10 minutes each time.236 Media com-monly used for desensitization programs are shown in Fig.18-20.

Sensory Reeducation. After nerve injury, even withoptimal surgical repair, cell death and axonal misdirec-tion can result in poor sensory localization and poor functional outcome.131,238 The initial nerve injury, as wellas axonal misdirection during regeneration, can altersensory representation because of cortical reorganiza-tion.239,240 The degree of cortical reorganization variesaccording to the nature of the injury. Crush injuries,where the basement membranes remain relatively intact,cause less axonal misdirection131 and therefore little corti-cal reorganization after recovery.241 In contrast, after com-plete nerve lacerations and repair, there is much distortion


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of somatosensory cortical maps causing previously well-defined areas to become diffuse240 and adjacent areas toexpand.242

Sensory reeducation may improve functional outcomeafter nerve injury by facilitating more appropriate corticalreorganization. Animal studies, with adult monkeys withperipheral nerve injuries, suggest that the following fourcomponents are necessary for sensory reeducation to beeffective. First, stimulation must be spatially discreterather than generalized to avoid “perceptual confusion.”Second, areas of skin with normal sensation should bestimulated less than areas with abnormal sensation toavoid under representation of the areas with abnormalsensation. Third, stimulation must be actively pursued bythe client and correct (versus incorrect) responses heavilyand specifically rewarded, while praise for randomattempts should be avoided. Fourth, training should bedesigned to improve both spatial and temporal discrimi-nation.243 There is some suggestion that training shouldalso occur bilaterally244 because tactile sensory inputs to

one side can activate the ipsilateral, as well as the con-tralateral, cerebral hemisphere.245

Various studies in human patients have found thatsensory education can improve sensory outcome andfunction after peripheral nerve injury. Imai, Tajima, andNatsumai found that 24 patients who performed a 15-20minute sensory reeducation program involving identifica-tion of the roughness of sandpaper and identification ofthe shapes of wooden forms and metal objects, once ortwice a day after median nerve repair at the wrist per-formed better on object identification tests (p < 0.05) andhad lower cutaneous pressure thresholds, although theydid not perform better on tests of s2pd and m2pd than 22patients who did not participate in this activity.246,247 Sim-ilarly, a larger, prospective randomized controlled trial of65 subjects with digital nerve injuries found that patientswho received early tactile stimulation with a rotating orstatic stimulus several times a day had better sensoryrecovery than patients who did not receive sensory reed-ucation (p < 0.02).248


A B

C

FIG. 18-20 Media for graded desensitization. A and B,Containers of loose materials; C, tactile sticks.

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Based on these findings, it is recommended thatsensory reeducation be included in the treatment ofpatients with sensory loss after peripheral nerve injury.Sensory reeducation programs generally include introduc-tion and identification of increasingly complex tactileinputs with and without vision occluded. Stimulationshould be focused on the area with reduced sensation andcorrect performance should be consistently and stronglyreinforced.

MANUAL THERAPY TECHNIQUESNerve Mobilization. Nerve gliding techniques (Figs.

18-21 to 18-24) are commonly employed after nerveinjury or repair with the goal of mobilizing nerves fromsites of compression or entrapment after a period ofimmobilization.249 Studies suggest that nerve gliding,when performed in conjunction with tendon gliding, mayimprove function in patients otherwise immobilized fornerve compression injury.

A prospective randomized trial with 28 subjects (36hands) with CTS found that subjects who performedtendon and nerve gliding exercises for 4 weeks and whowere provided with wrist splints had statistically signifi-cantly (p < 0.03) greater lateral pinch strength than subjects who were only provided with a wrist splint.However, symptom severity and functional status werenot significantly different between the groups.250 Similarly,a larger study involving 240 hands with CTS found thatonly 43% of those who performed tendon and nervegliding exercises required surgical intervention as com-pared to 71.2% of those who did not perform these exercises.251

After surgical nerve repair, some recommend delayingall forms of mobilization to avoid disruption of the repair.Chao et al found in an in vitro study of 100 digital nervetransections in 10 human cadavers with 0-10 mm of nerveresected before suturing that when tendon gliding wasperformed in a splint there were no nerve disruptionswhen up to 5 mm of the nerve was transected, and whengliding was performed without a splint, there were nonerve disruptions when up to 2.5 mm of the nerve wastransected.252 A similar study with fewer subjects foundthat nerve repairs with up to 5 mm of resection were notdisrupted by passive mobilization when limited by anextension blocking splint, and repairs with up to 2.5 mmof resection could withstand mobilization through fullpassive ROM.253

Although these results may lead the clinician to initi-ate early controlled passive mobilization after nerve injuryand repair, it is important to keep in mind that nervemobilization does pose risks to nerve regeneration. Forexample, application of continuous passive motion for 10minutes, twice daily for 6 weeks after nerve repair in acanine model, beginning on postoperative day 1, wasfound to result in more scar formation and nerve hypo-vascularity than did immobilization.254 Furthermore, sur-gical nerve repair techniques that minimize nerve tensionwere found in a study of sciatic nerve surgical repair inrats to optimize recovery as measured by nerve conduc-tion velocity, muscle cross-sectional area, proprioceptive

function, and motor function.255 Given the conflicting evi-dence about the risks and benefits of nerve mobilizationafter nerve injury, further research is needed to clarify theoptimal timing of nerve mobilization after different typesof nerve injury.

PRESCRIPTION, APPLICATION, ANDFABRICATION OF DEVICES AND EQUIPMENT

Splinting and Orthotics. Orthotics may be used toprotect repaired nerves or insensate areas, rest limb seg-ments to assist in resolving inflammation, promote func-tion, or prevent deformity after nerve injury. For at least3-4 weeks after nerve repair, orthotics are generally usedfor immobilization and to minimize tension on thenerve.256 However, as noted previously, it is uncertain ifsuch immobilization improves outcome.257 Soft, nonre-strictive splints made of neoprene can also be used toprotect nerves or areas with sensory loss as a result ofnerve injury from thermal or mechanical trauma.

Body segments are often immobilized to reduce inflam-mation of musculoskeletal structures, and many authorsrecommend using splints to manage compressive neu-ropathies under the premise that this will help resolve anunderlying inflammatory state. Despite the fact that his-tological studies suggest that edema and fibrosis ratherthan inflammation are more commonly associated withnerve compression,258 studies indicate that splinting doeshelp reduce symptoms from nerve compression. A sys-tematic review of nonoperative treatment practices of CTSsuggests that splinting does reduce symptoms but thatsurgery is more effective,259 and elbow splinting alone orin conjunction with steroid injection were both found tobe similarly effective treatments for cubital tunnel syn-drome, with both decreasing symptoms and increasingNCV.260

Evidence indicates that full-time splint wear is moreeffective than just nighttime wear for reducing symptomscaused by nerve compression. Walker et al found thatpatients with CTS who wore a splint full-time had bettersymptom control and nerve conduction than those whoonly wore the splint at night (p < 0.05). A weakness of thisstudy was that some subjects assigned to night-time wearonly wore the splint more than instructed and some full-time wear subjects wore the splint less thaninstructed.261

Although functional splints (Fig. 18-25) can dynami-cally assist or substitute for muscle function after motordenervation, few studies are available to help cliniciansand clients make more informed decisions regarding useof splints for these purposes. Functional orthotics forupper extremity nerve injuries have been found to be mostuseful for subjects with nerve injuries involving the dom-inant hand,262 and ankle-foot orthoses (AFO) have beenfound to increase activity level while not decreasingmuscle strength in patients with unilateral dorsiflexorparalysis.263

A single-subject study comparing three different splintdesigns (a static volar wrist cock-up splint, a dynamic te-nodesis suspension splint, and a dorsal wrist cock-upsplint with dynamic finger extension) and no splint after


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A C DB

FIG. 18-22 Median nerve gliding exercise. A, The forearm is in neutral rotation, the wrist inneutral extension, and the fingers and thumb are flexed. B, The wrist remains in neutral, thefingers extend, and the thumb lies in neutral beside the index finger. C, While the thumbremains in the neutral position, the wrist is extended while finger extension is maintained. D, The wrist is returned to neutral extension, and with the fingers and thumb also in neutralextension, the forearm is supinated. E, With the forearm still in supination, a gentle stretch isapplied to the thumb.

E

A B

FIG. 18-21 Brachial plexus gilding exercise. A, The head is laterally flexed toward theaffected side with the elbow, wrist, and fingers of the affected side in flexion. B, Thehead comes to the neutral position. C, The hand is moved across the chest and down tothe hip level. D, The patient gradually extends the elbow and increasingly abducts theshoulder into the position in E. F, Lateral cervical flexion to the opposite side is the finalcomponent of this maneuver.

C

E

D

F

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E F

C

D

A B

FIG. 18-24 Ulnar nerve gliding exercise. The sequence is performed only to the pointwhere slight tension is produced. When this point is reached, the patient is asked toback off slightly. The first three positions emphasize the distal ulnar nerve and beginwith a position of minimal stress. A, The head is in the midline and the shoulder isforward flexed and adducted. The elbow is extended and the wrist and fingers areflexed. B, The wrist and fingers are extended. C, The elbow is flexed. The final threepositions in the sequence focus on the proximal ulnar nerve with the distal segment in amore neutral position. D, The shoulder is abducted, the elbow is extended and the wristbrought to neutral. E, External rotation of the shoulder is added. F, The neck is laterallyflexed away from the affected side.

A BFIG. 18-23 Radial nerve gliding exercise. The patient stands with the body in a relaxedposture. A, The shoulder is depressed. B, The arm is internally rotated and the wrist isflexed. C, The neck is laterally flexed away from the affected side. D, The shoulder isextended while wrist flexion is maintained.

C D

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A B

C

FIG. 18-25 Functional splints. A, A median nerve palsy splintdesigned to position the thumb to allow opposition. B, Aradial nerve palsy splint designed to assist wrist and fingerextension. C, An ulnar nerve palsy splint designed to preventhyperextension of the MCP joints and allow the long fingerextensors to extend the fingers when the intrinsic musclesare not able to contract. All of these splints are intended tobe used during functional activities.

radial nerve injury found that the patient had significantlybetter function with the two dynamic splints but not withthe static splint.264 Despite this, the subject preferredwearing the static splint because it was supportive, easy todon, and had better cosmesis.

In general, the functional impact of a splint shouldalways be carefully evaluated since this may differ amongindividuals. A small study with five subjects investigatingthe functional impact of knee immobilizers (made-to-fitBecker knee extension splint) for femoral nerve palsyfound that two subjects reported falling less in the fol-lowing year and that overall, after 5-7 days of using theorthosis, walking distance increased from a mean of 66feet to a mean of 269 feet.265

Nerve injury often results in muscle weakness or imbal-ance. In this circumstance antideformity splints can beused to promote a more normal balance of forces or redi-rect forces. Table 18-15 describes some of the orthoticscommonly used for upper and lower extremity nervepalsies (see also Chapter 34).

Assistive Devices. Patients with peripheral nerveinjuries may need assistive devices for a short period oftime while waiting for reinnervation or reconstructive

surgery, such as a nerve or tendon transfer, or for the long-term, if motor reinnervation does not occur (seeChapter 33).

ELECTROTHERAPEUTIC MODALITIESIn patients with peripheral nerve injuries, electrical stim-ulation (ES) can be used to stimulate denervated muscleand facilitate muscle contraction in weakened reinner-vated muscle and for pain management. The applicationof ES to promote peripheral nerve regeneration is alsobeing investigated.

Electrical Stimulation. Some clinicians use ES to tryto preserve muscle function and reduce the rate of atrophyand fibrosis in denervated muscle. Such stimulation is gen-erally provided via surface electrodes using direct currentstimulation. The research regarding the application of ESto denervated muscle has had mixed outcomes. This ismost likely because of variations in treatment parameters,types of electrodes (transdermal versus implanted), timingof treatment, and the muscle being stimulated. Moststudies examining the effects of ES on denervated musclehave used animal models and have explored two ques-tions. First, does electrical stimulation retard or prevent

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muscle atrophy? Second, does electrical stimulation inter-fere with or promote reinnervation? Factors that shouldbe considered when evaluating the research on the use ofES include that rates of atrophy in denervated muscle varybetween muscle fiber type, within species and betweenspecies, and that rates of atrophy may vary, depending onthe amount of passive stretch imposed on the denervatedmuscle.

Many authors suggest that electrical stimulation of de-nervated muscle in animals minimizes muscle atrophyand fibrosis while nerve regeneration takes place.266-268

Others report that ES of denervated muscle does notproduce this desired effect.269-271 Overall, most studies thathave found ES to be effective for this application haveused implanted electrodes in animals, producing a highlevel of compliance and a regular schedule of interventionless likely to be found in a clinical situation. It is suggestedthat poorer outcomes in human studies may be a result ofpoor compliance, low frequency of treatments, the use ofexternal electrodes, and inadequate stimulation levels forthe depth of muscles requiring stimulation.272 Further-more, muscle fatigue and the potential for skin damagemay have limited the effectiveness of ES for treatment ofdenervated muscle in humans.273

Overall, well-controlled animal studies using implantedelectrodes have shown that ES with 0.4-7 ms pulse width,with 200 to 800 contractions per day, can reduce muscleatrophy in denervated muscle, when compared withunstimulated denervated controls, and can maintainmuscle mass and maximum force generation capacity atthe same level as in innervated controls.274

In humans, similar benefits have been found whenimplantable electrodes were used. Nicolaidis and Williamsimplanted electrodes in 15 human subjects with periph-eral nerve transections and applied stimulation for 127-346 days. Other treatment parameters included a voltagebetween the minimum required to generate muscle twitchto a maximum of 10.5 V, a frequency of 130 Hz, a pulsewidth of 1.007 ms, and an on : off time ratio of 1.5/24seconds. The outcomes of this treatment were comparedto outcomes of others studies where ES was not provided,and the authors reported improved grip strength, pinchstrength, and MMT outcomes for patients with ulnar andmedian nerve injuries and improved MMT outcomes forelbow, wrist, and digital extension for patients with radialnerve injuries.275 These assessments were based on com-parison with patients from other studies and were notevaluated statistically.

TABLE 18-15 Splints for Upper and Lower Extremity Peripheral Nerve Injuries

Nerve Lesion Type of Splint* Indication RationaleHigh median nerve Elbow, wrist, and IF/MF extension restriction Postsurgical Decrease tension on repaired nerve.

splintLow median nerve Wrist/hand flexion immobilization or Postsurgical Decrease tension on repaired nerve

restriction splint (dorsal blocking splint) when tendons also injured.Thumb/opposition/abduction immobilization Functional and Position the thumb in opposition to the

splint (opponens splint) (web spacer) antideformity index finger to promote pinching activities. Maintain web space.

High radial nerve Elbow flexion/wrist extension immobilization Postsurgical Minimize tension on radial nerve.splint

Wrist/MP/thumb extension mobilization splint Functional Utilizes tenodesis.Wrist/MP/thumb extension immobilization Antideformity Maintain length of extrinsic flexors and

splint prevent overstretching of extensors.Wrist extension splint (cock-up splint) Functional, antideformity Prevent wrist drop.Wrist extension immobilization splint Postsurgical Decrease tension on repaired nerve.

Posterior interosseous MP extension mobilization splint Functional Maintain extension of MP joints, nerve promote active flexion.

High ulnar nerve Wrist flexion immobilization splint (dorsal Postsurgical Decrease tension on repaired nerve.blocking splint)

Metacarpophalangeal extension restriction Functional, antideformity Transmit EDC force distal to assist insplint (figure-of-eight splint) interphalangeal extension, fourth

and fifth digits if FDP innervated.Cubital tunnel Elbow flexion restriction splint Symptom reduction Limit stretch of the ulnar nerve. May

syndrome or postsurgical restrict flexion of the elbow.Low ulnar nerve Metacarpophalangeal extension restriction Functional, antideformity Transmit EDC force distal to assist in

splint interphalangeal extension (fourth and fifth digits).

Digital nerve MP flexion, IP extension immobilization splint Postsurgical Protect repair.Hand-based or digital-based, volar or

dorsal, depending on site of injury.Femoral nerve Long leg brace with spring-loaded knee Functional Assist in ambulation.

AFO Functional antideformity Assist in ambulation.

*Common names of splints are provided in parentheses, splints are described using the American Society of Hand Therapists Splint ClassificationSystem.IF, Index finger; MF, middle finger; MP, metaphalangeal; IP, interphalangeal; AFO, ankle-foot orthoses; EDC, extensor digitorum communis; FDP, flexordigitorum profundus; AFO, ankle foot orthosis.

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Although the evidence from animal studies seem toindicate that ES may help patients with denervated musclemaintain muscle strength and prevent atrophy until themuscle is reinnervated, there is evidence to suggest thatthis intervention may not accelerate nerve regeneration ormay even retard nerve regneration.276-278 Herbison et al’sstudy comparing electrically stimulated soleus muscles(stimulated daily for 8 hours, with 4 mA, 4 ms pulse at 10 Hz) with nonstimulated soleus muscles in rats withbilaterally crushed sciatic nerves found that although thestimulation reduced atrophy, it did not improve nerveregeneration.279 Furthermore, Love et al found that ESapplied for 7 days with either trains of 0.2 ms pulses, at20 pps for 10 seconds every 30 seconds or with 0.2 mspulses, at 100 Hz for 600 ms every 60 seconds diminishedaxonal sprouting in partially denervated rat soleus musclescompared with unstimulated controls (p < 0.02).280

Electrical Stimulation for Neural Regeneration.Various investigators have studied whether ES can accel-erate nerve recovery or improve the specificity of nerveregeneration. Although ES is not yet generally used clini-cally for these purposes, it may be adopted in the futureif results continue to be positive. Some studies have shownpositive results with the application of ES to injurednerves. For example, continuous ES with pulsed electricalcurrent with a 0.2 ms pulse duration and frequency of 4 pps applied after nerve crush injuries in rabbits for 24hours daily for 4 weeks was found to result in faster recov-ery of twitch force and tetanic tension than a control con-dition without stimulation.281 Similarly, after transectionand sutured repair of femoral nerves in rats, ES applied for 1 day to 2 weeks with 0.1-ms duration pulses of 3-voltamplitude delivered in a continuous 20 pps train, wasfound in one study to accelerate nerve recovery, with stim-ulated nerves taking 3 weeks to regenerate as compared to8-10 weeks for unstimulated controls, and with stimulatednerves having more specific motor reinervation.282

Electrical Stimulation for Transdermal Drug Delivery(Iontophoresis). Iontophoresis with a corticosteroid mayhelp reduce symptoms in patients with nerve injuries withinflammation. Banta evaluated the effect of iontophoresison CTS by initially treating a group of 23 patients withCTS with wrist splinting and nonsteroidal antiinflamma-tory drugs (NSAIDS) for 6 months. Four of these patients(17%) had symptomatic improvement. For the remaining19 who failed this initial 6 months of wrist splinting andNSAIDs alone, iontophoresis with dexamethasone sodiumphosphate was added. In this latter group, 58% of hands(11 of 19) showed improvement.283 This suggests that ion-tophoresis with a corticosteroid may be effective for somepatients with inflammatory nerve injuries. Since ion-tophoresis can cause skin burns where the electrodes areplaced, these electrodes should not be placed on skin withreduced sensation.

PHYSICAL AND MECHANICAL MODALITIESHeat. Heat is not commonly used for treatment of

patients with nerve injury because it can increase inflam-mation during the acute recovery phase. However, heatmay be used in the later rehabilitation of patients withperipheral nerve injury to facilitate stretching of musclesthat have shortened as a result of weakness or denervation

of the antagonist and for pain management. A prospec-tive, randomized controlled study investigating the effectsof a low-level heat wrap (104° F) on wrist pain of variousetiologies, including CTS, found that patients with CTSshowed statistically significant improvement in pain (p =0.001), joint stiffness (p = 0.004), grip strength (p = 0.003),and patient-rated wrist evaluation (PRWE) scores (p =0.0015) compared to subjects taking oral placebos.284

Cold. Cryotherapy may occasionally be used tocontrol inflammation and edema after trauma thatincludes damage to peripheral nerves, surgical nerverepair, or decompression,285 or when soft tissue inflam-mation causes nerve compression. However, there hasbeen little experimental investigation of the effectivenessof cryotherapy in these circumstances. In general, the roleof cryotherapy in managing nerve lesions is limitedbecause cold can delay nerve regeneration and nerves maybe damaged if cooled excessively. There are reports ofsuperficial nerve damage as a consequence of cryotherapybeing applied for other reasons in an area over a superfi-cial nerve286,287 and of phrenic nerve injury as a conse-quence of cooling of the heart before cardiac surgery.288,289

Ultrasound. Pulsed ultrasound may promote recoveryfrom nerve injury by nonthermal mechanisms. Further-more, unlike continuous ultrasound, which increasestissue temperature and may adversely affect nerve laten-cies, pulsed ultrasound at intensities up to 1.0 W/cm2 hasbeen found to have little or no effect on nerve latencies.290

A randomized, double-blind controlled study of 34patients with electrodiagnostically confirmed bilateralCTS, where pulsed ultrasound (20%) at 1 MHz, 1.0 W/cm2

was applied for 15 minutes for 20 treatments 2-5 times perweek over the carpal tunnel of one wrist, while sham ultra-sound was applied to the other wrist, found that thosetreated with ultrasound had less pain and better motordistal latency and sensory NCV than those who receivedthe sham treatment (p < 0.0001).291 This was true directlyafter completion of the intervention, 8 weeks after start-ing, and a 6-month follow-up.

Despite conflicting evidence, treatment with continu-ous ultrasound, which can heat tissues, is generally notrecommended after nerve injuries because this interven-tion may exacerbate inflammation in an injured nerve orsurrounding tissues. For example, in one study, continu-ous ultrasound at 3 MHz frequency, at either 1.5 or 0.8 W/cm2 intensity was found to reduce NCV in patientswith chronic CTS when sham ultrasound did not.292 Incontrast, a study of the effects of continuous ultrasoundon acute experimentally-induced CTS in rabbits found thatcontinuous ultrasound at 3 MHz frequency, 1.5 W/cm2

intensity applied for 5 minutes resulted in greater recoveryof compound muscle action potential (CMAP) amplitudethan ultrasound at 0.2 W/cm2 or sham ultrasound.293

Hydrotherapy. Despite a dearth of evidence, contrastbaths, which involve immersing a limb segment in alter-nating cold and hot water, are often used clinically inpatients with edema from any cause, including peripheralnerve injury.294,295 It is proposed that the alternatingcooling and heating will cause alternating vasoconstric-tion and vasodilation, respectively, to pump fluid out ofan edematous area. However, there is very little publishedresearch on the effectiveness of this intervention for any

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application and none showing that this is an effectivetreatment for reducing edema.296 Furthermore, it has beenshown that contrast baths at temperatures commonlyused clinically (15° C for the cold and 40° C for the hot)do not cause sufficient changes in soft tissue temperatureto cause alternating vasoconstriction and vasodilation.297

Laser Light Therapy. Laser light therapy, also knownas low level laser therapy (LLLT), is thought to reduceinflammation298,299 and promote formation of new bloodvessels300 and proliferation of fibroblasts.301 For nervesspecifically, studies have produced conflicting results,showing that LLLT may result in decreased302,303 orincreased304,305 distal latencies, reduced NCV,306 andincreased action potential amplitude. Furthermore, somehave not found LLLT to have any significant effects onnerve conduction.307-309 Some studies in animal modelshave also suggested that LLLT may promote nerve regen-eration310 or reduce nerve degeneration after injury.311

Although the evidence is conflicting, LLLT is commonlyused around the world to treat patients with peripheralnerve injuries, and since its initial Food and Drug Admin-istration (FDA) clearance for treatment of pain associatedwith CTS in 2002, its use has rapidly increased for this andmany other applications in the United States.

The clinically based evidence for the use of LLLT forpatients with nerve injuries is also conflicting. Evidence insupport of this intervention includes a small study ofpatients with CTS, with 10 treated subjects and 30 controlsubjects, that found that LLLT using a 830-nm wavelengthGaAs laser, with a treatment dose of 1080 mJ applied 6times, resulted in reduced symptom severity (pain, numb-ness, and tingling) and improvements in sensory nerveconduction 15 days after treatment only in the experi-mental group.312 However, on reevaluation at 10 weeksand 54 weeks after treatment, both the experimental andthe untreated controls had returned to their pretreatmentstates. Other uncontrolled302 or poorly controlled studies313

on the use of LLLT for CTS also suggest that this may bean effective intervention. Additionally, a small double-blind, placebo-controlled study with 16 experimental sub-jects and 14 controls on the effects of LLLT in patients withtrigeminal neuralgia found that in the treatment group, 10had complete resolution of symptoms, 2 had a reductionof pain and the remaining had little to no resolution ofpain, whereas in the control group, 1 person had completeresolution of symptoms, 4 had some reduction of pain, and9 had little or no effect.314 In contrast to these findings,another small double-blind, randomized controlled trialwith 15 subjects with electrodiagnostically-verified CTSfound that the treated group, who received treatment 3 times per week for 5 weeks using a GaAlAs laser with a860-nm wavelength with a 60-mW beam applied for 15seconds to deliver at treatment dose of 6 J/cm2, had similarfindings on the Levine CTS Questionnaire, the Purdue Pegboard Test, and NCS, as the control group.315

SURGICAL INTERVENTIONAlthough rehabilitation clinicians do not perform surgery,they are often involved in the care of patients with nerveinjuries that are surgically treated. Several factors deter-mine the need for surgical interventions, including natureof the injury, whether the injury produces a closed or

open wound, and the amount of time between injury and presentation. For severe nerve transections thatpresent early, surgical nerve repair is generally indicated.If a nerve injury is associated with an open wound, the wound is generally surgically explored, whereas closedwounds are often observed for up to 3 months and only surgically explored if evidence of nerve regenerationis lacking. Surgery is also often indicated when pressureon a chronically compressed nerve produces symptoms.

The primary options for surgical nerve repair are end-to-end coaptation and nerve graft (autograft, allograft).End-to-end coaptation, after partial or complete nervetransection, involves suturing the epineurium of the sep-arated nerve endings together (known as epineural repair)or suturing individual fascicles or groups of fascicleendings together (known as fascicular repair). Individualfascicle repair is uncommon because the many suturesrequired can cause excessive scaring.

If there is a gap between the nerve endings because theproximal and distal nerve segments have retracted or aportion of the nerve was so damaged it needed to excised,then a repair by end-to-end coaptation, which wouldrequire bringing the proximal and distal nerve stumpstogether, would place excessive tension on the nerve. Inthis circumstance, a nerve graft may be used. A conduitmay also be placed around a nerve lesion or an area ofnerve repair to reduce adhesion of the nerve to surround-ing tissues and to direct nerve growth.

CASE STUDY 18-1

TRANSECTION OF THE ULNAR NERVE

ExaminationPatient HistoryTR is a 31-year-old, left-handed construction worker whofell through glass and sustained a puncture wound to theleft cubital tunnel, resulting in transection of the ulnarnerve. He underwent an ulnar nerve repair without ante-rior transposition on the day of injury and was placed ina long-arm, above-elbow cast postoperatively. He pre-sented to physical therapy 2 weeks after surgery. TR hasno other medical issues. Since his injury, the patient hasbeen on medical leave from work. Functional limitationsinclude that the patient is completing 100% of bilateraltasks with his nondominant right hand. To manage meal-time activities, he purchases fast food or prepares ready-to-eat meals. Before his injury, the patient prepared hisown meals four to five times per week. He has managedindependent dressing by selecting clothing with few or nofasteners. The patient stated that he planned to return towork on modified duty in 1 week (3 weeks from date-of-injury) and full duty in 2 weeks.

Tests and MeasuresMusculoskeletalPosture TR’s sitting and standing postures are within

normal limits (WNL). His left shoulder is held in a posi-tion of slight elevation, perhaps to accommodate theweight of the cast.

Anthropometric Characteristics A hand volumeterwas used to avoid submersing to the level of the surgical

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incision. Volumetric testing revealed moderate edema inthe left hand with displacement of 37 cc more water thanthe right. The hands were warm to touch and of normalcolor. The 11-cm surgical incision was dry, red within 0.2 cm beyond the wound margins, and without odor, andthe area surrounding the wound (along the medial andposterior elbow) was pink, tender, and edematous. Cir-cumferential measures of the elbow taken in line with theelbow crease were 26 cm on the right and 32 cm on theleft. Sutures were still in place.

Range of Motion and Muscle Length Initial measure-ments of passive and active motion were taken with carein order to not cause pain. Passive ROM (PROM) about theleft shoulder and elbow were deferred in order to not placetension on the ulnar nerve. Active ROM (AROM) of theshoulder, elbow, and wrist joint were taken with the prox-imal and distal joint to each tested joint placed in such aposition to not place tension on the ulnar nerve. Rightupper extremity ROM was full but is provided as referencefor those measures that are not full on the left. Resultswere as follows:Joint motion Right Left Left

AROM AROM PROMShoulder flexion 0-180° 0-120° NTShoulder hyperextension 0-60° 0-40° NTShoulder abduction 0-180° 0-150° NTElbow flexion 0-140° 15-60° NTWrist extension 0-80° 0-20° 0-60°Wrist flexion 0-75° 0-40° 0-75°Wrist ulnar deviation 0-40° 0-25° 0-40°Thumb CMC adduction Full Full† NTThumb MCP flexion 0-50° 0-40° NTMCP abductionIndex 0-25° 0-10° 0-25°Middle (radial/ulnar) 0-15°, 0-15° 0-5°, 0° 0-15°,

0-15°Ring 0-20° 0° 0-20°Small 0-35° 20°‡ 0-35°MCP flexion*Index 0-90° 0-90° 0-90°Middle | 0-90° |Ring −15°Small � −20° �

PIP flexion*Index 0-100° 0-100° 0-100°Middle 0-105° 0-105° 0-105°Ring 0-110° 15-90° 0-110°Small 0-110° 20-90° 0-110°DIP flexion*Index 0-70° 0-70° 0-75°Middle 0-70° 0-70° 0-75°Ring 0-70° 0° 0-70°Small 0-70° 0° 0-70°

*Composite metacarpophalangeal (MCP), proximalinterphalangeal (PIP), and distal interphalangeal (DIP) passiveflexion is full, indicating adequate length of the extensordigitorum communis.†Thumb carpometacarpal (CMC) adduction carried out by theabductor pollicis brevis.‡Small finger abduction because of contraction of the extensordigiti minimi.

Muscle Performance Manual muscle testing revealedweakness of the muscles innervated by the ulnar nerve, with flattening of the hypothenar eminence, asfollows:Muscle Right LeftFlexor carpi ulnaris 5/5 0/5Flexor digitorum profundus (III and IV) 5/5 0/5Abductor digiti minimi 5/5 0/5Opponens digiti minimi 5/5 0/5Flexor digiti minimi 5/5 0/5Lumbricales (III and IV) 5/5 0/5Dorsal interosseus 5/5 0/5Palmar interosseous 5/5 0/5Adductor pollicis 5/5 0/5

Pinch and grip strength was measured at the sixth post-operative week using a dynamometer and pinch meter.The dynamometer handle was set on the second level.Average measures (3 trials) were as follows:Test Right LeftGrip 110 lb 48 pounds2-point pinch 22 lb 19 pounds3-point pinch 27 lb 18 poundsLateral pinch 30 lb 8 pounds

Left-hand grip strength measures were approximately44% of the right (nondominant hand). Left 2-point pinchstrength average was 86% of the right, left three-pointpinch strength average 66% of the right, and left lateralpinch strength average was 27% of the right. On testinglateral pinch strength, Froment’s sign was noted.

NeuromuscularPain TR reported pain about the elbow at a level of 5/10

with activity and 2/10 at rest.Peripheral Nerve Integrity There was a positive Tinel’s

sign at the left inferior cubital tunnel with pain radiatingproximally and distally.

Sensory Integrity With vision occluded, sensorytesting using Semmes-Weinstein monofilaments showedabsent sensation (using the 6.65+ monofilament) alongthe ulnar border of the volar and dorsal hand, along thevolar small finger and ulnar half of the ring finger, alongthe dorsal surface of the small and ring finger metacarpals,and along the dorsal small finger and ulnar half of the ringfinger. Given this finding, 2-point discrimination was notpursued initially.

Cardiovascular/Pulmonary: The Allen’s test, per-formed over the radial and ulnar arteries at the wrist, wasfollowed by timely flushing of the skin.

Evaluation, Diagnosis and PrognosisFindings included presence of edema, timely woundhealing, muscle paralysis in muscles innervated by theulnar nerve, and absent sensation along the ulnar nervedistribution. These findings are consistent with ulnarnerve injury at the cubital tunnel. Consequently, TR is atrisk for developing joint contractures and muscle short-ening, as well as being susceptible to injury to the skin.Functionally, the patient’s participation in activities ofdaily living (ADLs), work, and leisure activity is reduced.The patient is relatively young, which should facilitate afavorable outcome, but he has risk factors that couldimpede progress, including insufficient nutrient intake

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associated with dietary changes because of decreased inde-pendence in meal preparation and employment thatincludes forceful and repetitive activity. Full motor recov-ery may be expected in 1 year and good sensory recoveryin 1-2 years.

InterventionSkin ProtectionTR was instructed in measures to protect skin integritywhile participating in meal preparation and to visuallymonitor all activities involving sharp instruments. He wasencouraged to use a protective glove when cooking. Tominimize tissue damage because of skin dryness, thepatient was instructed to use a moisturizing lotion severaltimes per day. On his return to work, the patient was pro-vided with recommendations to wear a protective glovewith a rubberized fabric in the palm to both protect theskin and increase his ability to maintain objects in thehand by increasing friction (between the glove and anobject) and to use cylindrical foam tubing around handlesof tools.

Edema ManagementThe patient was provided with written materials instruct-ing him to elevate the left arm while sleeping to minimizeaccumulation of fluids in the distal extremity. A light com-pressive garment was provided to minimize edema but tonot be so restrictive as to compress the nerve.

Muscle Stretching and Range of MotionMuscle stretching and passive joint ROM exercises wereincorporated due to lack of expected progress to increasethe length of the triceps and maintain length of the exten-sor digitorum communis muscle/tendons, the extrinsicdigital flexors, and the volar PIP joint capsule of the ringand small finger. The triceps muscle may have becomeshortened because of postoperative immobilization andmovement restriction to minimize tension on the ulnarnerve. The extensor digitorum communis muscle oftenbecomes shortened as a result of the loss of the opposingflexor digitorum profundus. The digital flexors sometimesare shortened because of postoperative positioning. Thevolar PIP joint capsule often becomes short as a result ofthe inefficiency of the extensor digitorum communis toalone effectively extend the PIP joint. The patient wasinstructed how to avoid overstretching the ulnar nerve.

Strength TrainingActive contraction of uninvolved muscles of the left upperextremity was initiated at the onset of rehabilitation tomaintain ROM throughout the limb. A resistive exerciseprogram was initiated at 6 weeks after surgery when in-nervation to the flexor carpi ulnaris was evident. Thisprogram of resistive exercise was progressively modifiedwith sequential return of the ulnar nerve innervatedmuscles as expected in the following order: Flexor carpiulnaris, flexor digitorum profundus (III and IV), abductordigiti minimi, opponens digiti minimi, flexor digitiminimi, lumbricales (III and IV), dorsal and palmarinterossei, and adductor pollicis. Resisted exercise pro-gressed in three phases as follows: Moving the limb

segment through full AROM, place and hold exercises,moving the limb segment through full ROM and againstgravity (for the flexor carpi ulnaris), and moving the limbsegment against increasing resistance. The latter phase wasimplemented once each muscle reached a grade 3+/5. Theamount of resistance required to engage the patient in thislevel of exercise was at 70% of his 1 repetition maximum.TR was instructed to complete 10 repetitions and engagein exercises 3 times per day each day.

Sensory RetrainingWhen TR began to perceive moving touch along the volarsurface of the small and ring fingers, a sensory reeduca-tion program was initiated. The program included object,shape, and material identification through tactile explo-ration for at least 15-20 minutes, once or twice a day. Onattempting to identify the above inputs, the patient wasto visually confirm whether his response was correct.

Toward the end of his rehabilitation, a desensitizationprogram was initiated as part of a home program as aresult of complaints of hypersensitivity along the ulnardigits. TR was informed of possible but unconfirmed ben-efits of desensitization protocols. He was instructed toobtain materials from his home that were nonirritating,potentially irritating, and definitely irritating and to applythese textures for 20-30 minute sessions, 2-3 times daily.

Nerve MobilizationTR was provided with written instruction and demonstra-tion in ulnar nerve gliding techniques by the fifth post-operative week with full flexion of the elbow avoided untilthe sixth postoperative week.

Splinting and OrthoticsAt the time of the initial evaluation, a thermoplastic ante-rior elbow splint was fabricated to maintain the elbow inalmost full extension. By the fourth week, wear of thissplint decreased to night only and was discontinued by 5weeks. At this time, a neoprene sleeve was applied at nightto gently restrict flexion of the elbow while sleeping,without being compressive to the nerve. On reinnervationof the flexor digitorum profundus, a splint was fabricatedto block the MCP joint of the ring and small finger inflexion, for the purposes of transmitting extensor digito-rum communis force distally to the PIP joint.

Electrical StimulationOn reinnervation of muscles supplied by the ulnar nerve,ES was used to enhance muscle contraction during exer-cises to increase strength and muscle hypertrophy. Ini-tially, parameters were set to not cause excessive fatigue ofnewly innervated muscle.

UltrasoundPulsed ultrasound was used initially to reduce possiblechronic inflammation, resulting in edema and pain aboutthe elbow.

OutcomeEighteen months after his initial injury, TR had full AROMand PROM in the left upper extremity. He had mild inter-

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mittent “burning” sensations in the fifth digit. Grip mea-sures increased on the left by 50%. Lateral pinch, 2-pointpinch, and 3-point pinch increased by 30%, 32%, and55%, respectively. The patient returned to work, withmodifications, 2 months after his injury. During thecourse of treatment, he sustained one partial thicknessburn injury to the tip of the ring finger from placing hishand on a hot stove.

Please see the CD that accompanies this book for a casestudy describing the examination, evaluation, and inter-ventions for a patient with carpal tunnel syndrome.

CHAPTER SUMMARYThis chapter describes the examination, evaluation, andintervention for patients with peripheral nerve injury.Motor function, sensation, and sympathetic function islikely to be compromised, thus requiring examination ofmuscle strength, length, and balance and examination ofquantitative and qualitative sensory functions, as well asexamination of skin integrity. Intervention for patientswith nerve injury may be brief, and the goals of treatmentaimed toward relieving the causative factors, or long-term,while waiting for reinnervation of motor and sensory end-organs. In the latter case, treatment emphasis may shift toprevention of associated deformities and injury to skin, aswell as facilitation of functional independence. Treatmentmay include patient education, edema management,muscle strengthening and lengthening, desensitization,sensory reeducation, electrical stimulation, ultrasound,splinting, and training with assistive devices.

ADDITIONAL RESOURCES

Useful FormsRecording sheet for monofilament testingBritish Medical Research Council (BMRC) Scale of Nerve Function

BooksDyck PJ, Thomas PK: Peripheral Neuropathy, ed 4, Philadelphia,

2005, WB Saunders.Senneff JA: Numb Toes and Aching Soles: Coping with Peripheral

Neuropathy, San Antonio, 1999, Medpress.Senneff JA: Numb Toes and Other Woes: More on Peripheral

Neuropathy, San Antonio, 2001, Medpress.

Web SitesThe Neuropathy Association: www.neuropathy.orgPeripheral neuropathy: http://www.ninds.nih.gov/disorders/

peripheralneuropathy/peripheralneuropathy.htm

GLOSSARY

Action potential: The change in electrical potential of a nervewhen it is stimulated.

Afferent: Carrying impulses toward a center, as in nerves trans-mitting impulses toward the central nervous system.

Autonomic nervous system (ANS): Efferent pathways thatinclude the sympathetic and parasympathetic divisions, whichregulate smooth muscle, cardiac muscle, and glandular activity.

Axon: A projection or outgrowth of a nerve cell that conductsimpulses away from the cell body.

Central nervous system (CNS): Nerves that are wholly con-tained within the brain and spinal cord.

Cranial nerves: Twelve pairs of nerves that have their origin inthe brain.

Dendrite: Branching and tapering extensions of the axon thatreceive signals from other neurons.

Denervation: Loss of nerve supply.Double-crush syndrome: Two or more lesions along the same

nerve that produce a set of symptoms and that would be lessobservable if only one lesion existed.

Efferent pathways: Nerve cells carrying impulses away fromthe central nervous system.

Electromyogram (EMG): A graphic record of the electricalactivity associated with contraction of a muscle.

Fascicle: A bundle of fibers, as in a nerve fiber tract.Glia: Cells and fibers that form the supporting elements of the

nervous system.Infarction: Insufficiency or cessation of blood supply resulting

in tissue necrosis.Ischemia: Local deficiency of blood supply can be caused by

mechanical obstruction of the circulation.Mononeuropathy: An isolated nerve lesion.Mononeuropathy multiplex: Asymmetrical lesions of multi-

ple nerves.Motor unit: A single alpha motor neuron and all the muscle

fibers it innervates.Myelin: Lipids and proteins that form a sheath around certain

nerves.Nerve conduction velocity (NCV): The speed at which elec-

trical impulses can be propagated along the axon.Neuroma: Abnormal growth of nerve cells.Neurons: Nerve cells.Neurotransmitter: A chemical agent released by a presynaptic

cell that stimulates or inhibits the postsynaptic cell.Nodes of Ranvier: A short interval in the myelin sheath of a

nerve.Peripheral nervous system (PNS): Nerves that may originate

in the brain or spinal cord but end peripherally and includecranial and spinal nerves.

Plasmalemma: Plasma membrane.Plexus: A network of nerves, or blood or lymphatic vessels.Polyneuropathy: Symmetrical diffuse nerve dysfunction.Schwann cells: Any of the cells that cover the nerve fibers in

the peripheral nervous system and form the myelin sheath.Synapse: The meeting point of the axon terminal of one neuron

and a dendritic ending or cell body of another neuron or cell.Wallerian degeneration: The degenerative changes of an axon

and its myelin sheath distal to a focal lesion.

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