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PERIPHERAL NERVE INJURIES

I. General Medical Background
A. Definition A peripheral nerve injury is a condition where the axon of a peripheral nerve (any nerve that has exited from the central nervous system) or its surrounding structures has been subjected to locali ed trauma and!or ischemia and results in a disruption of the conduction of the electrical impulses along its axon" #eripheral nerve injury must be distinguished from neuropathy in that there is a disease process in neuropathy while there is none in peripheral nerve injury" #eripheral nerves may be classified according to their function and site of origin in the $entral %ervous &ystem' $ranial %erves (emerge from the base of the brain" &pinal %erves (emerge from the spinal cord" Autonomic %erves (are intricately associated with the cranial and spinal nerves but differ in function and in the details of the structure and function" B. Classification #eripheral nerve injuries are classified according to the degree of injury" )here are two (*) classification schemes for this+ which are' a" &underland,s $lassification of -egree of %erve .njury

/" /st degree injury (aka %eurapraxia ! %europraxia) .nvolves temporary malfunction in a portion of the axon such as can occur with pressure+ poor circulation or cold" *" *nd degree injury (aka Axonostenosis) &everance of the axon" 0" 0rd degree injury (aka Axonocachexia) 1oss of the endoneurium" 2" 2th degree injury (aka Axonotmesis) 1oss of the endoneurium and the perineurium" 3" 3th degree injury (aka %eurotmesis)

* $omplete nerve section" b" &eddon,s $lassification of -egree of %erve .njury /" %eurapraxia ! %europraxia -escribes nerve injury in which paralysis occurs without structural changes" )his might correspond to &underland4s /st degree injury in a case where the cause of the injury is not withdrawn" 5owever it can be used in cases where the cause is effectively unknown+ and!or might reside in the central nervous system+ and would then not fit into to &underland4s scale" *" Axonotmesis -amage to nerve fibers sufficiently severe to cause complete peripheral degeneration+ but where the internal architecture of the nerve is spared" )his corresponds well to &underland4s *nd degree injury" 0" %eurotmesis %erve injury in which internal structure is severely damaged+ but externally the nerve anatomy appears intact" )his would correspond well to &underland4s 2th (and possibly 0rd) degree injury" &pecial %ote' &ome sources are inconsistent as to their comparisons of the &underland and &eddon classifications and the terminologies used" .t is therefore more practical to use these classifications specifying only the degree of injury and the corresponding structures affected" C. Epidemiolog $an occur in almost all ages" 5igher incidence in violence(prone areas and time periods" )he upper limb is more commonly affected than the lower limb" )he 6acial nerve ($% 7..) is the most fre8uent cranial nerve affected" D. Etiolog )rauma to a peripheral nerve is the common term used in peripheral nerve injuries" )hese can+ however+ be subdivided into various types+ such as' a" 1aceration ( -irect transection (cutting) of the nerve by a sharp object" b" $ompression!.schemia ( -irect compression (crushing) of the nerve by a neighboring object or body+ such as' o Bone o )umor o .nflamed structures c" &tretch ( 9xcessive elongation of the nerve usually by a force exerted distal to the nerve" d" $ontusion ( Bruising of the nerve causing inflammation of the nerve" e" Mixed ( A peripheral nerve may be injured by a mix of the above" ( #eripheral nerves could also be injured at several sites+ such as what happens in a :double crush, injury" 1ocali ed ischemia to the blood vessels supplying the nerve is another identified cause of peripheral nerve injuries" E. Pat!op! siolog " Pat!omec!anics After the initial injury to a peripheral nerve+ the following se8uence of events occur' a" %eural ;esponses to .njury

0 ( .f a /st degree injury' o #athological changes are mild or absent" o %o true degeneration or regeneration occurs" .f a *nd to 3th degree injury' o 1ittle histological change at the injury site or proximal to it" o <allerian (Anterograde) -egeneration occurs distally+ which is characteri ed by' ( Axonal -egeneration' &hrinking and fragmentation of the axon distal to the injury" =ccurs within hours after initial injury" Axons can still conduct up to >* hours after injury" 6rom 2? to @A hours post(injury+ axonal continuity is lost+ thus conduction of impulses is no longer possible" Bsually completed at * weeks post(injury but may continue from 3 weeks up to ? weeks post(injury" Because of this+ full assessment of the lesion may start only by the 0rd week post(injury when the nerve may begin exhibiting fibrillation potentials upon 9MG(%$7 testing" ( &egmental (Gombault) -emyelination' -estruction of the myelin sheath through chemical changes wherein lipids break down" =ccurs distally from the site of injury and may reach proximally up to the /st node of ;anvier above the injury" Begins by the ?th day post(injury" -emyelination lags behind axonal degeneration and may continue for ? to *0 days post(injury" o Motor 9nd(plate 6ragmentation takes place 0* hours after injury" ( Motor end(plates retain excitability for up to /C days post(injury" o -uring this whole process+ the following cells play key roles' ( &chwann cells .nitially become active within *2 hours of injury+ exhibiting nuclear and cytoplasmic enlargement+ as well as increased mitotic rate" Act as removers of axonal and myelin debris prior to the arrival of the macrophages" &chwann cells near the injury later degrade" &chwann cells distal to the injury later form cell columns (bands of Bungner) that become important guides for sprouting axons during re(innervation" ( Macrophages Act later to remove debris received from &chwann cells and other debris" ( 9ndoneurial mast cells #roliferate markedly within the first * weeks of injury" ;elease histamine and serotonin to enhance capillary permeability and facilitate macrophage migration" ( 6ibroblasts $reate a dense fibrous scar causing a fusiform (spindle( shaped) swelling of the injured segment which may exist even when healed" Bsually occurs in a 0rd to 3th degree injury and may produce marked scarring in these injuries" &carring may obstruct proper nerve regeneration" ( %euronal cell body

2 %ucleus migrates to the periphery of the cell within A hours of the injury" %issl granules and rough endoplasmic reticula break up and disperse" #rocess is called :chromatolysis", &imultaneously+ there is a brisk proliferative response of perineural glial cells" Most likely signaled by the process of chromatolysis" Glial cell processes extend to the affected neuron and interrupt synaptic connections+ possibly to isolate the neuron for its recovery phase" b" %erve ;egeneration ( .f a /st to *nd degree injury' o ;estoration of function is the rule" o %erve regeneration begins almost immediately after injury" o %o true degeneration or regeneration occurs" ( .f a 0rd to 3th degree injury' o May last for several months" o &e8uence of regeneration may be divided into the events occurring into the following anatomical ones' ( %euronal cell body %ucleus returns to the center of the cell" ;%A synthesis increases and neurotransmitter synthesis decreases" %ucleoproteins reorgani e into compact %issl granules" #roduces vast amount of protein and lipid needed for axonal regrowth" ( &egment between the cell body and the injury site Axoplasm arises from the proximal segment and the cell body" &erves to regenerate the axon tip by enhancing axoplasmic transport of proteins and lipids to the axon tip" ( .njury site Axonal regrowth may be seen as early as *2 hours after injury or may be delayed for weeks in more severe injury" ;ate of axonal regrowth is determined by' ( )he changes within the cell body ( )he activity of the speciali ed growth cone at the tip of the axon sprout ( )he resistance of the injured tissue between the cell body and the end organ ;ate is usually 2 to 3 mm a day in favorable conditions" .f due to a crushing injury+ averages about 0 mm a day" .f suture was performed+ averages about * mm a day" ;ate will eventually gradually decelerate until a rate of C"33 mm a day" ( -istal segment between the injury site and the end organ Axonal regrowth continues into this segment" Multiple axon sprouts may be seen" .f these sprouts encounter debris or empty endoneurial tubes that have decreased in diameter+ sprouts may wander into surrounding tissue and may not reach their intended end organ"

3 )hus+ timing and the presence of scar tissue at the site of injury affect the course of the regenerating nerve" ( 9nd organ .f a functionally unrelated end organ is reached by axonal regrowth' 6urther development of the axon and remyelination do not occur" .f the intended end organ has undergone degenerative changes due to prolonged denervation that do not allow the establishment of functional connections' Axonal development and maturation are aborted" .f the intended end organ is still viable' 6unctional recovery occurs" $ollateral sprouting (multiple connections to end organs) may also occur" .ncomplete functional recovery more commonly occurs" ( .f end organ is a muscle+ appropriate #) can help maintain the denervated muscles in an optimal condition" ( .f end organ is a sensory organ+ recovery will never be complete" Appropriate compensatory techni8ues are indicated" ( Axonal regeneration is not synonymous with return of function" o Although axonal regeneration may occur over several months+ return of function may take as long as / year" )he process of nerve injury repair may be more appreciated using the following illustration'
%ormal nerve innervating skeletal muscle" )he blue lines indicate the basement membrane"

)he nerve has been transected and <allerian degeneration has begun" )here is corresponding atrophy in the muscle"

#roximal nerve terminals send sprouts toward the &chwann cell tubes" &ome of the sprouts make it into tubes and reinnervate the muscle+ which has undergone neurogenic rearrangement"

=nce a peripheral nerve has been transected+ <allerian degeneration of the distal axons begins and macrophages enter the area to remove the myelin and axonal debris" -uring this process+ the basement membrane which surrounds the axon and &chwann cell remain intact" &chwann cells line up in the basement membrane tube and synthesi e growth factors+ which attract axonal sprouts formed at the terminal of the proximal segment of the severed axon" )he basement membrane tubes provide pathways for the regenerating axons to follow to muscles and skin" )he &chwann cells then remyelinate the newly formed axonsD however+ the newly formed myelin is thinner than normal and the newly formed internodes are shorter than normal"

A #. Clinical $anifestation%s& General presentation of #eripheral %erve .njury' a" 1oss of muscle function or motor paralysis!paresis b" Muscle atrophy c" 6laccidity d" #aresthesia e" 6asciculations f" 9dema g" 6ibrillation in 9MG examination h" Altered reflex activity i" -isturbance in vasomotor activity which eventually leads to trophic skin changes ( .nitially there is vasodilatation for the first * weeks accompanied with increased temperature ( 1ater on+ vasoconstriction and hypothermia ( (() sweating+ pilomotor reaction+ edema (due to interruption of sympathetic fibers) j" )rophic changes follow due to circulatory compromiseD the hand and foot will present with' ( )ransparent shiny skin ( 6ibrosis of the subcutaneous tissue ( $hanges in finger nails ( .ncreased hair (hypertrichosis) ( )rophic ulcers (advance stage) k" Abnormal electrical diagnostic exam l" $ausalgia ( #resents with a triad of hyperpathia+ trophic changes+ and autonomic phenomena over the region of the distribution of the nerve" '. Complication%s& -ue to paralysis+ affected muscle and region may develop' a" $ontracture b" -eformity ( .n the B9 ( deformities or attitudes may develop ( .n the 19 ( gait deviations may be observed -ue to sensory loss+ affected region may develop' a" Blceration b" Gangrene H. Diagnosis 5istory(taking and the patient interview can usually give important clues as to any precipitating factors that caused the injury 9MG(%$7 is the ultimate diagnostic test used to assess the extent of the injury and if any repair had taken place I. Diffe(ential Diagnosis =ther diagnostic tests are usually indicated in peripheral nerve injuries to differentiate from other neuropathies =ther neuropathies rarely have trauma or locali ed ischemia as the causes of the injury J. P(ognosis #rognosis is dependent on' &everity of injury ( .n /st degree injury+ nerve conduction deficit is completely reversible ( .n *nd degree injury+ there is good prognosis for recovery as only the epineurium is affected and other nerve sheaths are still intact ( .n the other degrees of injury+ prognosis becomes poorer if severity is higher due to the affectation of more nerve sheaths )ype of nerve fiber affected

> ( 1arger+ more heavily myelinated fibers have poorer prognosis than smaller unmyelinated fibers

II.

Medical Management
A. P!a(macologic .f pain related to the nerve injury is experienced+ traditional narcotic pain medications+ or non(narcotic neuropathic pain medications may be administered" B. $edical " S)(gical .n /st to *nd degree injuries+ the nerve is expected to recover to almost normal function within 0 to A weeks .n higher degrees of injury+ due to the possibility of scar formation that will affect nerve regeneration+ recovery may take longer and there will be a greater possibility of complete loss of function .n any case+ while waiting for the recovery of function+ the following major goals are to be observed' a" 6or sensory loss' protection of the affected region from any injury b" 6or motor loss' splinting to preserve joint and muscle function At present+ there is no medical treatment to help a nerve recover from injury+ or to help it regenerate sooner+ more completely+ or faster &urgery is only indicated when nerve regeneration is clearly not occurring sufficiently well to restore the desired function" 9MG(%$7 usually is the diagnostic test to check for this" &urgical interventions for nerve injury are decided depending on the length of the injured nerve' ( .f less than 0 cm' o Microscopic reconstructive nerve surgery or using an absorbable conduit like %eurotube is used ( .f greater than 0 cm' o %erve grafting using a nerve from some other part of the body may be performed o .f the nerve to be replaced is very long+ nerve transplantation from another donor may be possible+ but re8uires prolonged immunosuppression after transplantation )endon transfers may be indicated in case the nerve injury had not responded to other surgical intervention" ( ;arely done presently due to the availability of newer nerve repair surgical interventions"

III.

#hysical )herapy 9xamination+ 9valuation E -iagnosis

A. Points of Emp!asis in E*amination Basing on the clinical manifestations of peripheral nerve injuries+ #) examination on the following areas has to be included' a" &ubjective information ( $hief complaint( look for' o &ensory loss or changes o 1oss of motor function o #ain (if any+ this will most probably be due to the injury itself and not the nerve affected+ except in the case of causalgia where there is pa) o Any aggravating or alleviating circumstances that affect the injury ( 5istory of present injury( completed including any precipitating factors ( 5eredito(familial diseases( like diabetes mellitus (to rule out any other non(traumatic causes of the nerve injury) ( #atient,s lifestyle( particularly the effect the injury has on recreational and work activities b" =bjective information

? ( .nspection( look for signs of' o )rophic skin changes (particularly hand and foot) ( )ransparent shiny skin ( $hanges in finger nails ( .ncreased hair (hypertrichosis) ( )rophic ulcers (advanced stages) o &cars (particularly for lacerations) o 7isible atrophy o -eformity (contractures) o #resence of attachments (orthosis) o General abnormal posture or gait pattern o =ther signs (particularly 599%) findings and speech difficulty if cranial nerve injury is suspected) $ardiovascular ! #ulmonary systems assessment (i) 7ital signs( if there is suspected vagus nerve injury or injury to nerves that innervate the muscles of respiration (ii) $hest expansion measurements( for suspected injury to nerves that innervate the muscles of respiration (iii) Auscultation of breath sounds( if there is suspected complication of poor pulmonary function #alpation( note down' (i) Muscle tone( if muscles innervated by the nerve are flaccid (ii) &kin temperature( skin over affected region innervated by affected nerve' ( Bsually hyperthermic for first * weeks post(injury due to vasodilatation ( 5ypothermic afterward due to vasoconstriction (iii) )rophic skin changes (particularly hand and foot) ( 6ibrosis of the subcutaneous tissue (iv) &kin mobility+ texture+ and consistency( particularly over region innervated by affected nerve (v) &kin turgor( if peripheral vasculature is affected %eurologic system assessment (i) &ensation( assessed if there is sensory loss or changes (hypesthesia+ paresthesia) ( Assess the following' &uperficial sensations .mportant to examine because of their protective functions May be assessed by dermatomal distribution or peripheral nerve distribution ( A review the patient,s chief complaint will give :clues, on whether to do a dermatomal or peripheral nerve distribution sensory assessment A patient who will complain of sensory loss that is :strip(like, will most probably have a dermatomal distribution sensory loss (e"g" nerve root level injury) A patient who will complain of sensory loss that is specific to one part of the body only will most probably have a peripheral nerve distribution sensory loss (e"g" peripheral nerve level) $omponents' ( #ain ( )emperature (both hot and cold) ( 1ight touch

@ ( #ressure -eep sensations .n upper extremity will be important to assess due to their function in hand placement during basic A-1 .n lower extremity will be important to assess due to their function in transfers and ambulation $omponents' ( Finesthesia ( #roprioception ( 7ibration $ombined cortical sensations .mportant only when achievement of instrumental A-1+ work+ and recreational functions are to be the main focus of intervention (more appropriate for =) intervention+ thus rarely assessed by #)s) (ii) ;eflexes ( M&; ! -);( assessed due to their protective function during muscle ! tendon stretch ( &uperficial reflexes( assessed due to the interplay of these reflexes between sensory and motor innervation (iii) $ranial nerve assessment( assessed when specific cranial nerve injury is suspected and also to rule out $%& involvement (evidenced by multiple cranial nerve affectation) Musculoskeletal system assessment (i) Goint play( assessed if decreased intraarticular movement is evident due to the presence of deformity ! contracture (ii) ;ange of motion ( #;=M( assessed if decreased extraarticular movement is evident due to the presence of deformity ! contracture ( A;=M( will be the most affected if affected nerve innervates muscles responsible for motion at the joint (iii) Muscle strength( when muscle weakness is evident ( 9xtent of muscle weakness will depend on the location of the injury .n more distal injuries (branches or specific nerve affected)( innervated muscles will tend to have absent (C!3) muscle contraction+ except for muscles which have dual innervation .n more proximal injuries (plexopathies+ nerve root injuries+ or anywhere before having branches ! specific peripheral nerves)( innervated muscles will tend to have only partial weakness ( <ill increase once there is recovery of nerve function (iv) 1imb girth measurements( if gravitational edema is evident due to non(functioning of muscle pumps (v) Muscle bulk measurements( when atrophy is evident (vi) 1eg length measurements( if any leg length discrepancy is evident ( &ome lower extremity peripheral nerve injuries may present with functional+ but not actual limb length discrepancy ( 9xamples of instances where functional leg length discrepancy may occur in peripheral nerve injury' &hortening Fnee(locking with subse8uent genu recurvatum (like in poliomyelitis) may occur if the 8uadriceps femoris undergoes prolonged denervation in femoral nerve injury 1engthening

/C 6oot(drop is usually present in common peroneal nerve injury which may lead to plantarflexion contracture if no intervention is applied ( #ostural assessment( note particular attitude (position) of affected and related ! nearby regions ( Gait assessment( note particular deficiencies during the gait cycle that are due to muscle weakness and if any gait deviation is occurring to compensate for muscle weakness ( 6unctional assessment( particularly the effect of any motor or sensory loss on functional activities o Motor loss will lead to inability to do functional activities due to muscle weakness o &ensory loss may cause the functional but unsafe performance of activities o )hus+ important to assess not only the ability to be independent in a functional activity+ but also the safe performance of the activity ( &pecial tests( particularly special tests that provide stress on specific nerves o #erformed to elicit specific nerve affectation o May not be used alone to diagnose peripheral nerve injury o #erformed only as adjuncts to the other components of the patient examination above B. P(o+lem List )he following problems are addressable by #)' a" 1oss of muscle function or motor paralysis!paresis b" Muscle atrophy c" $ausalgia d" #ain e" 9dema f" ;isk of impaired nerve regeneration due to the presence of fibrosis or scar formation g" ;isk of complications due to loss of muscle function or motor paralysis!paresis ( $ontracture ( -eformity ( Gait deviation h" ;isk of complications due to sensory loss or change ( &usceptibility to integumentary injury (ulceration+ gangrene) ( &usceptibility to loss of balance or falling C. P! sical ,!e(ap Diagnosis #) diagnosis falls mainly into the following diagnostic label' a" .mpaired peripheral nerve integrity and muscle performance associated with peripheral nerve injury -ue to the possibility of complications+ additional diagnostic labels may be necessary depending on the degree of nerve injury or specific nerve affected+ such as' a" #rimary prevention!risk reduction for skeletal deminerali ation b" #rimary prevention!risk reduction for loss of balance and falling c" #rimary prevention!risk reduction for cardiovascular!pulmonary disorders d" #rimary prevention!risk reduction for integumentary disorders .f surgical intervention was necessary+ may fall into' a" .mpaired joint mobility+ motor function+ muscle performance+ and range of motion associated with bony or soft tissue surgery

IV.

#hysical )herapy #rognosis (including #lan of $are) E .ntervention

// A. Plan of Ca(e #) goals for peripheral nerve injury may best be delineated depending on the stage or phase of the injury )he total number of patient sessions under a single episode of care for peripheral nerve injury may usually last for at least /* to a maximum of 3A visits depending on the rate of return of function 9xamples of #) goals that may be included under each phase' a" Acute stage (immediate post(injury or post(operative care) ( #revent further injury to affected nerve or prevent stretch to sutured nerve or nerve graft ( #revent edema ( ;etard muscle atrophy ( Maintain range of motion on both affected and unaffected areas ( &upport joints distal to the injury ( ;educe fibrosis ( #revent secondary complications due to loss of motor function and!or sensory loss b" #aralysis stage (neural response to injury phase) ( ;educe edema ( &often scar tissue ( ;educe pain ( #revent joint stiffness in related areas ( #rovide sensory input to affected part ( Maintain joint range of motion to affected muscles (including web spaces for hands and feet) ( Maintain muscle function in conjunction with the use of assistive+ adaptive+ orthotic+ protective+ supportive+ or prosthetic devices ( #revent or correct deformities c" $hronic stage (nerve regeneration phase) ( ;eeducate and maximi e excitation of reinnervated muscles ( .mprove muscle strength and power ( .mprove muscle function directed toward performance of skills ( 9ducate patient on possible complications due to sensory loss and compensatory ! protective techni8ues for sensory loss B. Inte(-entions %on(modality (examples) a" )emporary immobili ation( to rest the affected part and promote healing+ preferably in ideal resting position b" Bse of an assistive adaptive+ orthotic+ protective+ supportive+ or prosthetic device( to decrease load on the affected part and maintain muscle function c" Alteration of body mechanics and modification of daily habits( to prevent contributing factors to further or repeated injury if the nerve injury is secondary to repetitive stresses d" 1imb elevation( to reduce edema e" 9xercises( to prevent contractures or limitation of motion and promote return to functional activities ( ;=M exercises o .n acute stage( should be limited only to within pain(free range which will not further injure nerve or provide stretch on an operated nerve ( May be used in affected regions to promote sensory feedback o .n chronic stage( may be applied only until within normal limits if return of function has occurred

/* .f no return of function has occurred and surgery is not considered( functional muscle shortening+ coupled with selective stretching+ is allowable for functional improvement o #roximal joints may be moved throughout the full range of motion in any stage but care must be observed that proximal joint motions that can possibly stretch the affected nerve be avoided during the acute stage ( Muscle strengthening exercises o )o the affected muscles( usually during the chronic stage only to prevent distal stretching of the affected nerves ( .f there is partial innervation (as in plexopathies)+ muscle strengthening may be applied to distal muscles o )o proximal muscles( limited only to isometric contractions in positions that will not stretch the affected nerve during the acute stage ( 6unctional skills training ! work hardening techni8ues o &pecific to muscles that will be utili ed for a specific activity o Bseful only during chronic stage ( $ompensatory techni8ues training o =nly if return of function has not occurred f" Manual therapy techni8ues ( &oft tissue mobili ation to injury site( chronic stage only ( $entripetal massage( to reduce edema with precaution over the injured nerve to avoid further injury ( #assive stretching( may be allowed only during chronic stage g" #atient education( mainly on risk reduction or prevention of complications such as' ( &keletal deminerali ation ( 1oss of balance and falling ( $ardiovascular!pulmonary disorders ( .ntegumentary disorders Modality (examples) a" )hermal agents( to relieve pain ( #recautions must be observed if sensory loss is also present b" 9lectrical stimulation( to relieve pain in chronic cases only ()9%&+ etc") ( )o retard atrophy if used during immobili ation ( <hen coupled with pressure bandages (faradism under pressure)+ may be effective in reducing edema c" #ressure bandaging ! intermittent compression( to reduce edema but with precautions when used over bony prominences to prevent skin irritation or cause other nerve injury d" Bltrasound diathermy( useful over injury site to soften scar tissue (