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Brachial Plexus Injuries and theElectrodiagnostic Examination

Philip Dean Zaneteas, MD, PhD

AddressRehabilitation Hospital of Indiana, 4141 Shore Drive,Indianapolis, IN 46254-2607, USAE-mail: [email protected] Sports Medicine Reports 20m, 2:7-14Current Science Inc. ISSN 1537-890xCopyright © 2003 by CUITent Science Inc.

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., 'bdineatiOIl ofbrachlalplexus injuriesfboth traumatic and-nontraumatic) remains one of the most challenging diagnos-tic tasks for the sports medicine physician. Evaluation of the'athlete requires not only a detailed history and physical exam-ination, but a comprehensive knowledge of brachial plexusanatomy and the potential mechanisms of injury it maybefall. Having said this, it still remains for the electrodiagnos-Lician10 make the definitive diagnosis as to tile location andseverity of the lesion. This article reviews the current state ofthe literature and field of electrodiagnostics with regard tobrachial plexus injuries. Historically, the literature has pur'sued this problem by means of different conceptual para-digms, including the categorizing of injuries anatomicallyaccording to their location within the brachial plexus, as 'wellas the mechanism of injury, or the injury's anatomic relation-ship to contiguous structures (eg, supraclavicular vs infraclav-icular injuries) 11-,2,3&0,4810,5-7,8-,9,lOj. Vlhatever theetiology, anatomic profile, or mechanism of injury, analysis ofbrachial plexus injuries assumes a detailed knowledge of bra-chial plexus anatomy. ,

Brachial Plexus AnatomyGiven the complexity of the brachial plexus, knowledge ofits contents and anatomic relationships to adjacent struc-

tures is necessary in order to properly plan the electrodiag-nostic study. The ventral or anterior primary rami of C5 toT] represent the initial precursors of the plexus itself Theanterior rami of the C5 and CG roots coalesce to form theupper trunk. The C7 anterior ramus evolves into the mid-dle trunk and the anterior rami from C8 to T] combine toform the lower trunk. At the clavicular level, the respectivetrunks bifurcate into their anterior and posterior divisions.The anterior divisions of the upper and middle trunks coa-lesce to form the lateral cord. The anterior component ordivision of the lower trunk becomes the medial cord. Theposterior cord is formed by all three posterior divisions ofthe respective trunks. The cords, in turn, project from themidpoint of the clavicle to the inferomedial portion of thecoracoid process of the scapula. At this juncture, the cordsgive rise to their respective peripheral nerve branches.

It is within this anatomic context that the electromyo-grapher must analyze the brachial plexus injury and planthe electrodiagnostic study. Injuries can be categorized asoccurring either proximal or distal (superior or inferior) tothe clavicle. Supraclavicular brachial plexus lesions tend toinvolve both flexor and extensor musculature, whereasi'i1II:a-clavicular lesions tend to involve either flexor orextensor musculature, but not both. It is for this reasonthat plexus lesions involving the proximal components ('ie,anterior primary rami and trunks) tend to be dissimilar tolesions involving the more distal elements (ie, cords andterminal peripheral nerve lesions). However, "mixed"nerve lesions may occur, making anatomic localizationmore difficult.

Brachial Plexus LesionsThe classification of brachial plexus injuries into ei thersupraclavicular or infraclavicular injuries is more than justan anatomic ordering, but rather implies certain rnecha-nisms of injury, different degrees of severity, specific.typesof pathology, and varying overall prognosis r 1] ].

Supraclavicular lesions tend to be caused by' closed,downward traction mechanisms or a widening of the shoul-der-cervical spine angle. This mechanism tends to involvethe upper and middle trunks, along v',11t11 transmitted trac-tion to the CS and C6 roots. Infraclavicular plexus injuriescommonly occur with the upper extremity abducted andextended anterior to the frontal plane, 'with stretching of tileinfraclavicular plexus in the region of its distal components.IVieci1anismsof this type have been shown to involve prima-

8 Head and Neurologic Conditions

rily the posterior card,axillaly, and musculocutaneousnerves 112,13··,14).

Although the primary purpose of the e1ectrodiagnosticexamination in a patient with a suspectedbrachial plexuslesion is the anatomic localization of the pathology, it isalso important to determine the type and severity of neuro-pathology present. Nerve injuries essentially fall withintwo categories that are not.mutually exclusive: axonal losslesions and demyelinating nerve lesions.

Axonal LossAxonal loss implies the disruption of axonal continuity tovarying degrees with different prognostic outcomes. AxonalJoss with the preservation of supporting connective tissuestructures (Ie, endoneurium, perineurium, and epineu-rium) is termed (.(xonoLmesis. In this instance, axonalregrowth is possible along the endoneuria] tube with subse-quent reinnervation of its denervated muscle tissues. Incontrast, axonal injury that involves significant disruptionof its supporting Structural clements (endoneurium,perineurium, or epineurium) is termed neuroimesis, Func-tional return in nerve injuries of this type is generally poordue to the breach of endoneurial continuity and the poten-tial for the misalignment of neural tube regeneration.

Brachial plexus injuries characterized by axonal loss arethe most common pathologic category in plexus injuries.Additionally, they generally represent a greater degree ofmorbidity than do demyelinating injuries. From an elec-

. trodiagnostic standpoint, their characterization requiresboth a thorough nerve conduction examination as well asa comprehensive needle examination: accurate identifica-tion of the location of the nerve injury and its severity canonly be accomplished with the aid of needle electrornyo-graphy (EMG). This process.includes the observation ofspontaneous electrical activity and the analysis of volun-tary motor unit action potential recruitment. .

A detailed discussion of the electrodiagnostic needleexamination is beyond the scope of this review, and maybe found elsewhere 11o,3u J; however, the followingpoints should be emphasized:

1. The needle evaluation for spontaneous activityinthe form of positive sharp waves and fibrillationpotentials provides a subjective appraisal of thedegree of spontaneous muscle fiber·denervation.

2. in order to obtain an accurate portrayal of theextent and location of the plexus lesion a pauernofEMG findings must be procured. This can onlyoccur if a sufficient number of muscles are studied.Failure to do so may lead to an inability to makean accurate diagnosis secondary to a paucity ofdata. This remains one of the most common errorsin the elecuodiagnostic examination in a patientwith a suspected brachial plexopathy To reiterate a

well-Imown dictum, "the absence of evidence isnot the evidence of absence."

3. In evaluating motor unit reo-uitment on needleexamination. one is engaged in the analysis ofmotor milt morphology (including amplitude,duration, and phase number) and firing rate (thesequential addition of motor units in response toincreasing resistance, that is, the "size principle").Decreased motor unit recruitment as an indicationof axonal loss requires significant nerve damagebefore becom.ing observable

4. Evaluation of motor unit morphology may be ofsome benefit in that incomplete nerve injuries mayresult in the loss of functioning motor W1jL~givingrise to collateral sprouting. The result is the creationof reinnervated muscle fibers which are added toalready viable motor units. ']11i5 in turn generatespolyphasic motor units with increased amplitudesand durations, as well as increased phases.

Demyelinating Injuries and NerveConduction StudiesDemyelination in brachial plexus injuries most often takesthe form of a focal lesion. The electrodiagnostic investiga-tion of such injuries requires the performance of nerveconduction studies [15]. We discuss both sensory andmotor nerve conduction studies, although there remains arole for other techniques, such as nerve root stimulation, F-waves, and somatosensory evoked potentials .

Depending upon the severity of the demyelinating lesion,the nerve conduction examination may reveal either conduc-tion block or conduction slowing. Conduction block secoild:-ary to demyelination implies destructive alteration Intheneural structure of the myelin but not the axon itself Impulsepropagation across the lesion site is prevented. Incornplete .demyelination may result in only a partial block.in whichimpulses are capable of crossing the lesion site although at aless than normal rate, Vvhat follows is a summation of therespective importance of both sensory and motor nerve con-duction studies [1·,3 ••",4 ••••,5,6,8", 10,13"", 16].

Sensory Nerve Conduction StudiesOnly sensory nerve conduction studies allow for the deter-mination of whether or not the plexus injury is proximalor distal to the dorsal root ganglion. This is espcciallcimportant in detecting nerve root avulsions, because sucl) .injuries GUT)' a poor prognosis for neurologic recovery ..Pregangli onic lesions result in an intact sensory nerveaction potential (SNAP), because the lesion isprox.imaltc .the dorsal root ganglion, which is the origin of tl1(> sensor,nerve cell body. Proximal, postganglionic lesions, howeverresult with either an impaired or absent SNAP responsebecause the lesion is distal to 0.e.~.0~sa1root ganglion

Brachial Plexu~ injuries and the EleclTodiagnCJstic Examination • Luncwas 'J

A limitation inthe evaluation of brachial plexuslesions is the lack of singular sensory responses for delin-eating C5 and Tl roots. For this reason, motor conductionstudies may need to be performed examining the axillaryand musculocutaneous nerves for evaluation of the C5anterior primary ramus. Additionally, the medial antebra-chial cutaneous nerve (with TJ innervation) is studied inorder to evaluate the T] anterior primary ramus.

Another limitation of sensory studies in the evalua-tion of brachial plexus lesions is their intrinsic quality ofphase cancellation with temporal dispersion. This resultsin deterioration and drops in SNAP amplitudes onsequential proximal studies across the presumed plexuslesion site. This is not a problem with compound motorunit action potential (ClvlAP) amplitudes onmotor nerveconduction studies.

Motor Nerve Conduction StudiesMotor nerve conduction studies and CMAP evaluationhave limited usefulness in the evaluation of brachialplexus injuries. This is due 10 the fact that most upperextremity motor conduction study techniques are per-formed distal to the location of most brachial plexusinjuries. However, by stimulating proximally (ie, in thesupraclavicular region at Erb's point) and distally (infra-clavicular) to the presumed site of the brachial plexuslesion, one can attempt to determine whether or not con-duction block or slowing exists. Motor conduction veloc-ities and latencies are of limited value, even in theinstance of studies in the opposite extremity for purposesof comparison. Fromthe standpoint of the CMAP, this

'-'[n-~);'re~ult in a~l' a-bl;'orn~al wa~~ef;rm on the affectedside, characterized by a reduced amplitude, temporal dis-persion, and possible "multiphasicity" in appearance,especially when compared with the comparable CMAP inthe opposite extremity.

It has been shown that the most salient measurement tobe obtained in the assessment of the ClvlAP is its amplitude[3 e e [. "111eCMAP amplitude is an indication of the numberof viable motor nerve axons that can be elicited by proximalstimulation across the presumed brachial plexus lesion site.If on comparison with the comparable opposite extremityCl\1AP response there is a relative decrease in amplitudeand morph 01 ogic asymmetry, one may infer a certaindegree of conduction block (clearly implied in the absenteof a res pons e) or axonal loss

We may conclude that in evaluating bracbialplexuslesions. the needle examination provides the opportunity'to localize the lesion, especially in the more proximal seg-ments of the brachial plexus. Witlj this in mind, recentauthors have sought to provide further specific guidelinesin planning the electrodiagnostic examination in order tomaximize the acquisition of potential obtainable informa-tion from the patient [3°c,4eo,8o [.

Brachial Plexus AnalysisIn planning the electrodiagnostic examination. it is importantto view the [MC examination as an extension of the physicalexamination, along with the patient's clinical historvanc] theradiographic work-up (eg, radiographs, computed W11l0SW-

phy scan, 'magnetic resonance imaging). To reiterate, the com-ponents of the brachial plexus can be divided anatomicallybased on its relative positiontothe clavicle. In this way, a gen-eral preliminary classification of brachial plexus pathologymay be constructed in the form of supraclavicular and infra-clavicular brachial plexopathies. "111isin no way, however,implies pathologic regional exclusivity. VViththis in mind,numerous authors have provided overview tables to helporganize and compartmentalize the various roottrunk, cord,and peripheral nerve components. as well as their respectiveinnervated musculature (Table 1) [1- ,3uA..o,S-7,9, 10,] 6).

Supraclavicular PlexopathiesRoot lesionsRoot lesions (ie, cervical anteriorprimary rami) may occurin combination with trunk and peripheral nerve injuries.The most commonly found lesions involve CS to C6 or CSto C7 130"). Moreover, because the dorsal scapular and longthoracic nerves originate at the root level, needle evaluationof their respective innervated musculature (ie, the rhom-boids and serratus anterior) can assist in the overall evalua-tion of potential root pathology. The cervical paraspinalmuscles should always be studied as well, to rule out a con-comitant radiculopathy [17].

C5 rootEvaluation of the C5 root remains somewhat problematicfrom a nerve conduction standpoint, because it lacks an exclu-sive sensory nerve conduction technique specific to CS. More-over, it remains difficult 'to differentiate between a C5 injuryand an upper trunk lesion. 111e musculocutaneous CMAP,however, can be studied with recording at the biceps, in addi- .tion to UJeaxillary CMAP with recording at the deltoid. Theneedle examination should include C5 innervated muscula-ture and the cervical paraspinal musculature. It is within thiscontext that root avulsions should be considered; it representsa potentially catastrophic injury and may occur with othercoincident brachial plexus trauma. Cervical myelography canassist in making this diagnosis 118}.If the root avulsion occursdistal to the dorsal TOotganglion, one would expect to findintact SNAP responses wheretechnically feasible (sensorystudies to the thumb, induding the median and radial d l sen-sory studies, as well as the lateralantebrachial cutaneous nerve,call be utilized for evaluation of the C5 and C6 roots). Addi-tionally one may find significant abnormalities on the CMAPstudies listed above, including decreased amplitudes with tem-poral dispersion and multiphasicity The needle examinationcan show ongoing denervation (ie, fibrillation potentials, posi-tive sharp waves) in the C5 musculature.

10 Head and Neurologic Conditions

Table I. Upper extremity motor innervation at the root, trunk, and cord levels

Upper trunk (CS-C6)SupraspinatusInfraspinatusDeltoidBicepsSupinatorPronator teresFlexor carpi radialisErachioradialisExtensor carpi radialisTriceps

Middle trunk (el)TricepsPronator teresFlexor carpi radialisHexer carpi ulnarisExtensor carpi radialisExtensor digitorumExtensor carpi ulnaris

Lateral cordBicepsPronator teresFlexor carpi radialis

Lower trunk (C8-T I).TricepsExtensor digitol-urnFlexor carpi ulnarisFlexor digitorum profundusFlexor pollicis longusAbductor pollicis brevisFirst dorsal interosseousAbductor digiti quinti

Medial cordFlexor carpi ulnarisFlexor digitorum profundusAbductor digiti quintiFirst dorsal interosseousFlexor pollicis longusAbductor pollicis brevis

C6 rootSensory evaluation of the C6 root can be accomplished byperforming sensory nerve conduction studies of the radialdt (thumb), median di. and lateral antebrachial nerves.Additionally, the superficial radial nerve may also be stud,ied; however, its C6 innervation is less than the otherslisted. The needle examination should include all C6-innervated muscles.

C7motIsolated C7 root lesions are very rare. C7 root injury gener-ally occurs in conjunction 'with trauma to other portions ofthe brachial plexus. lts sensory evaluation can be per-formed via the median d2 or d3 sensory studies. The motorstudy to the triceps may be of some benefit with proximalstimulation at Erb's point. This may reveal findingssugges-tive of conduction block or slowing when compared withthe contralateral side. The needle examination shouldincorporate the investigation of C7 musculature.

C8 tootThe ulnar d5 sensory studyis used to evaluate the C8 root.The 111010rstudy generally utilized for the C8 root alsoincludes the ulnar motor study to the abductordigitiquinti.Other potential studies that may be utilized include themedian motor study to the abductor polJicis brevis and theradial motor study to the extensor indicis proprius.The nee-dle examination should include C8-innervated muscles.

Tl rootThe medial antebrachial cutaneous sensory study may beutilized forT1 root evaluation. 111emotor study most oftenutilized is the median motor study to the abductor pollicisbrevis (generally more T1 innervation than the ulnar inner-

Posterior cordDeltoidTricepsBrachioradiallsExtensor carpi radialisExtensor carpi ulnaris

vated abductor digiti qui nti ). The needle examinationshould include all T1-innervated musculature.

"\lith regard to the evaluation of the brachial plexus at theroot level (ie, the anterior primary rami component), C5 andC6 root involvement tends to be more common in acute bra-chial plexitis/Parsonage Turner syndrome [19,20,21-,22],whereas C8 to T1 involvement tends to be more common inneurogenic thoracic outlet syndrome [23J, metastatic plexop-athies, Pancoast tumor syndrome, and complications frommedian sternotomy.

Brachial plexus: proximal peripheral neuropathiesLong thoracic neuropath)'The long thoracic nerve is innervated via the C5, C6, andC7 anterior primary rami as a purely motor nerve. It sup·plies motor innervation to the serratus anterior. The C5 tcC7 anterior primary rami join to form the long thoracicnerve before progressing to create the upper and middletrunks of the brachial plexus [24-26J.

On one level, because of i lS long anatomic course, injuries to the long thoracic nerve are more likely than if its terminal muscle innervation were more proximally locatedWe see this in the relatively common stretch or uactio:injuries tbat occur with athletic endeavors. Additionall,because the long thoracic nerve possesses multi-leve

. innervation (ie, C5-C7), it has a greater statisticaUikelihood for involvement in a wide variety of pathologic an,biomechanic mechanisms involving the proximal regieof the brachial plexus.

The clinical presentation of a long thoracic neuropathis well known (ie, scapular "winging"), with altered glenchumeral biomechanics. Additionally, a (:7 radiculopathmay also present in this manner. It should be rememberethat scapular winging as a clinical entity may be caused t

.Brachial Plexus Injuries and the Electrodiagnostic Examination • Zaneteas 11

any combination of long thoracic, dorsal scapular, or spi-nal accessory nerve injury 127] A spinal accessory nerve·conduction study tothe trapezius has been described,which may assist in the evaluation of scapular winging[28J. The electrodiagnostic evaluation of the long thoracicnerve does notindude a sensory nerve conduction study,because it is a pure motor nerve. A motor nerve conductionstudy has been described, however, but there is somedebate as to its actual clinical usefulness 13"]. In contrast,the needle examination remains the most important com-ponent of the EMG study. '111epresence of axonal loss find-ings and decreased motor unit recruitment allow one tomake the diagnosis.

Dorsal scapular nellJeThe dorsal scapular nerve originates within the body of thescalenus medius muscle and supplies the levator scapulaeand the rhomboids during its course. Trauma to the dorsalscapular nerve may result in lateral winging of the scapula,but unlike long thoracic neuropathies, significant dysfunc-tion with regard to shoulder girdle mechanics is rare. As apure motor nerve, sensory studies are not applicable;motor studies to the rhomboids are not felt to be clinicallyhelpful. The diagnosis of dorsal scapular pathology istherefore dependant on the needle examination.

Suprascapular ne7lleThe suprascapular nerve is the only peripheral nerve thatoriginates from the upper trunk with primarily C5 innerva-tion, and some CG contribution. It is susceptible to injuryduring its course as it passes through the posterior triangle .of the neck to the superior border of the scapula, where itpasses through the suprascapular notch and supplies thesupraspinatus. It then passes around thespinoglenoidnotch and terminates.in the infraspinatus. There are nocutaneous nerve branches that can be studied electrodiag-nostically [29-36J.

The clinical presentation of suprascapular neuropathiesincludes poorly localized shoulder girdle pain, weakness inshoulder abduction, and external rotation along with intactsensation. The presence of deltoid pathology and/or scapularwinging should alert the physician to a more generalizedprocess such as acute brachial plexitis (Parsonage Turner syn-drome). In this instance, .however, the involvement of thesuprascapular nerve merely represents a component of amore generalized neuropathic condition with an autoim-mune etiology, which may simultaneously involve multiple'brachial plexuscornponentsat the root and trunk levels.

. It remains the task of the electrodiagnostic examina-tion La determine the anatomic level (posterior triangle,suprascapular notch and spinoglenoid notch as potentialentrapment sites), and degree and type of suprascapularnerve injury (axonal loss and/or demyelinating pathol-ogy). As with other peripheral nerve injury evaluations (ie,long thoracic and dorsal scapular nerves), motor nerve

conduction studies have limited diagnostic efficacy. Theneedle examination remains the most important d iagnos-tic tool for delineating the extent of nerve trauma. Finally,other C5 and C6 musculature, along with the cervical

. paraspinal musculature, should also be examined to ruleout a more diffuse process.

Axilla/I' l1e7lJCAxillary nerve innervation is supplied by the C5 10 C6 roots(anterior primary rami) via the posterior cord. As a termi-nal branch of the posterior cord, it supplies the deltoid andteres minor muscles. The greatest frequency of axillarynerve trauma occurs with blunt trauma, {or example,shoulder dislocation. Contact sports such as football alsopossess a high incidence of injury 137,38).

The electrodiagnostic examination of the axillary nerveshould include a needle examination in all three compo-nents of the deltoid, because the nerve injury may not beuniform in all three branches. The teres minor should beexamined along with the triceps to help rule out a poste-rior cord lesion. The differential diagnosis should includeC5 and/or CG radiculopathies, as well as an upper trunkbrachial plexopathy. The axillary motor study can be per-fonned with side-to-side comparison of the CMAPs, whichassists in evaluating axonal loss severity 13••••r 15). 'There areno sensory studies available to assess the sensory branch ofthe axillary nerve.

Thoracic outlet syndromeThe term thoracic outlet syndrome (TOS) refers to a syrnp-10m complex that actually represents more than one clin-ical entity [21.,22,23]. It continues to remain a point ofcontroversy in the medical literature. As a syndrome, itincorporates a constellation of clinical findings and com-plaints that can challenge even the most astutediagnosti-ci an. From the standpoint of etiology, it has beensubdivided into vascular and neurogenic subcategories.Whereas the former is characterized by compression ofthe subclavian blood vessels, the later is characterized bycompression to the brachial plexus itself The clinicalconundrum occurs because of the relative similarity oftheir clinical presentations.

The neurogenic form of TOS is a rare entity as Con-firmed on dectrodiagnostic testing. It generally involves-the lower trunk and/or the C810 T1 anterior primary rami.Upper trunk involvement is less frequent (unlike acute bra-chial plexitis; Parsonage Turner syndrome).

The el ectr od iagrrost ic evaluation Dfthe·neuiogenicform ofTOS remains the lynch-pin in the diagnosis-of thisentity [210]. Electrodiagnostic findings may include 1)decreased median motor CJviAP(the EMC parameter mostaffected); 2) ulnar SNAP less than 10 uV in 50% ofpatients; and 3) axonal Joss findings in the lower trunkmusculature (especially abductor pollicis brevis and firstdorsal interosseus).

12 Head and Neurologic Conditions

Trunk lesionsThe electrodiagnostic evaluation of trunk lesions requiresthe differentiation between the more proximal brachialplexus elements listed above (eg; the respective anteriorprimary rami and the more proximal individual peripheralnerves) and the trunks themselves (including their termi-nal branches).

Upper trunk lesionsBlectrodiagnostic evaluation of the upper trunk incorporalessensory and motor conduction studies as well as the needleexamination. There is general agreement that me most opti-mal sensory studies include the lateral antebrachial cutane-ous and the median d] studies !4u ,8-]. Potential motorstudies include both the axillary (to the deltoid) and themusculocutaneous (to the biceps) nerves. One must beaware, however, that peripheral nerve entrapments or injuriesto these nerves may provide misleading information, givingthe impression of an upper trunk lesion instead of a periph-eral nerve injury. The needle examination includes all of theupper trunk innervated muscles listed above, as well as thecervical paraspinal musculature.

Potential etiologies causing neurologic lesions involv-ing the upper trunk include acute brachial plexitis (Parsbn-age Turner syndrome), obstetric palsies, postoperativeparalytic syndromes, and the burner/stinger syndrome.

j'

Burner or stinger syndromeFrom the standpoint of the sports medicine physician, theburner or stinger represents a ubiquitous neurologic injuryto the brachial plexus that is very common in football play-ers. There has been considerable debate regarding the exactnature of the burner syndrome from the standpoints of itsinjury mechanism, pathophysiology, and anatomic loca-:tiOI1. This is partly due to the current limitations in thefield of electrodiagnostics to examine the proximal regionsof the brachial plexus. Essentially, the burner represents atraumatic proximal injury to the plexus primarily involvingthe cervical roots and the trunks. It still remains within thecapability of the EMC examination to obtain asignificantamount of inforinauon that will further define the injL11Yto a relatively high degree of sensitivity and specificity. Inconsidering the evaluation of a patient who may be suffer-ing a burner, It may be helpful to view the clinical presenta-tion as a symptom complex characterized by a sharp;burning pain radiating from the supraclavicular region,extending distally down the arm !39",40~43].

The localization of the site of injury may be related 10'

the injury mechanism itself. Supraclavicular injuries tendto be secondary to traction mechanisms, with multipleinvolvement at botb the root and trunk levels. Theupperand middle trunks tend to have a higher incidence. Infra-clavicular injuries tend to be secondary to shoulder abduc-tion/exiension mechanics, which tend to involve cords andterminal nerves generally, and the posterior cord and axil-lary nerve more specifically. In both types of biornecha-

, nisrn, the suprascapular nerve is commonly involved.. Distal peripheral nerves may also be involved at their sites· of origin, induding the musculocutaneous, radial, median,

and ulnar nerves.

Middle trunl: lesionsAs an isolated brachial plexus lesion, middle trunklesions are considered extremely rare. Generally, the middIe trunk represents an unlikely site for a traction. injuryalthough it can be affected by penetrating injuries. Th:middle trunk represents the continuation of the C7 anterior primary ramus. Care must be taken to distinguislmiddle trunk lesions from C7 radiculopathies and pesterior cord lesions.

The evaluation of the middle trunk may incorporatthe median sensory study to d3 (middle finger) with

· radial motor study to the extensor digiiorum communimuscle. The needle examination includes C7 innervate,musculature (eg, triceps, anconeus, pronator teres, flexccarpi radialis, extensor carpi radialis, extensor digitorumwith the exception of the serratus anterior.

Lower 'lnmh lesionsThe lower trunk is formed via the fusion of the C8 and 'Janterior primary rami. Trauma to the lower trunk ofterepresents a problematic situation; reinnervation is modifficult given the relative distance of the innervation to irespectively assigned musculature in the brachial plexianatomic paradigm [44]. The differential diagnosisextensive and should include C8 and 1'1 radiculopathieas well as median and ulnar peripheral neuropathies, arfocal lesions at the root level From a technical standpoiiit can be very difficult to distinguish alowertrunk lesi:from a medial cord lesion.

The lower trunk can be evaluated electrodiagnosticawith me use of an ulnar sensory nerve conduction study

· d5 (little finger), the dorsal cutaneous ulnar nerve, and tmedial antebrachial cutaneous nerve. r111emotor nerve ccduciion studies may include the ulnar motor study to tfirst dorsal interosseous and the abductor digiti mini]Othermotor options include the median motor study to 1

abductor poJlicis brevis or the radial motor study to 1

exiensorindids proprius The needle examination indu.the C8 and '1'1 innervated musculature (eg, flexor caulnaris, flexor digitorurn profundus 4/5, extensor digitoncommunis, extensor carpi ulnaris, abductor digiti minifirst dorsal interosseous, and abductor pollicids brevis).

Brachial Plexus Cord LesionsBecause of the relative proximity of the respective cordtheir ter nrinal peripheral nerves, cord injuries tencpresent.with more exclusive axonal loss findings on rdle examination with regard to individual periph(nerves This represents a significant difference from I

and trunk lesions.

Brachial Plexus Injuries and the £lectrodiagnostic Examination· Zaneieas J3

Medial Cord LesionsThe medial cord is the continuation of the anterior divi-sion of the lower trunk. Its electrodiagnostic evaluationincludes the medial antebrachial cutaneous sensory study

. (to evaluate C8 and T1 roots), along with the ulnar sensorystudy to dS. Motor studi es ind ude UK: thenar and hypothe-nar musculature. It should be noted that lesions involvingthe lower Hunk as well as the medial cord may present inthe same manner with regard to either absent or decreasedSNAPs or CMAPs. The needle examination is important indifferentiating lower trunk from medial cord lesions. Spe-cifically, medial cord lesions will present with axonal lossfindings in C8- to Tl-innervated thenar and hypothenarmusculature, whereas C8-innervated radial musculaturewill be spared. If both groups of muscles are found to har-bor axonal loss pathology, then a lower trunk lesiorishould be suspected.

Lateral Cord LesionsThe lateral cord represents the continuation ofthe anteriorprimary rami of the upper and ~iddle trunks. It is impor-tant in lateral cord lesions to distinguish between proximaland distal lesions. This is accomplished by evaluating thepectoralis major muscle (superior and middle compo-nents) because its innervation (lateral pectoral nerve) issupplied from U1eproximal part of the cord 13·.]. The ter-minal portion of the cord supplies the lateral half of themedian nerve (eg, pronator teres innervation). The remain-der of the median innervated musculature is supplied bythe medial cord.

Theelectrodiaguqstic evaluation of the lateral cordincludes sensory and motor conduction studies as well as adetailed needle examination: The sensory exam mayinclude the lateral antebrachialcutaneousnerve and themedian d l to d3 sensory studies. The motor studies includethe musculocutaneous study to the biceps. The needleeXamination should focus on the biceps, brachialis, prona-tor teres, and flexor carpi radialis. Upper trunk lesions canbe ruled out by the absence of-axonal Joss findings in thedel toid, brachioradialis, supraspinatus, and infraspinatus.

It is important to note that the musculocutaneous nerve,because it arises from thelateral cord, should be carefullyevaluated for the presence of an isolated peripheral neuropa-thy 145,46J. AIUlOUgbmusculocutaneous nerve injuries areUnC0l111110n,they may occur secondary to acute shoulder dis-locations and present with biceps and brarhialis weakness,along with sensory dysesthesias in the lateral forearm. TheE.MGevaluation, while including all of the guidelines abovein the assessment of the lateral cord, may also utilize bilateralmusculocutaneous motor studies for comparison purposes.C5-6-innervated muscles should also be studied on the nee-dle examination to assess for the possibility of a cervicalradiculopathy at these levels.

Posterior Cord LesionsThe posterior cord is formed by the joining the posteriorsegments of all three trunks.lt terminates as the radialnerve. As with the lateral cord, it may be possible to differ-entiate between proximal and distal lesions. This requires'needle examination of the latissimus dorsimuscle (proxi-mal innervation by the thoracodorsal nerve) and the teresmajor musde (proximal innervation by the 10\Nersubscap-ular nerve). The deltoid may be examined as a more distal

. muscle (ax.illary nerve innervation), along with the radialinnervated musculature.

The nerve conduction examination in the evaluation ofpotential posterior cord lesions includes the radial dl sen-sory study, as well as motor studies La the deltoid (axillarynerve) and the extensor indicis proprius (radial nerve).

ConclusionsThe evaluation of a brachial plexus lesion requires the inte-gration of a detailed history and physical examination,along with a comprehensive electrodiagnostic examination.lvledlanislTls of injury and anatomic relationships must beintegrated into the planning of the EMG study. A "cookbookapproach" will not suffice given the potential complexityand singularity of each individual case. Moreover, as oneproceeds through the electrodiagnostic study, the acquisi-tion of information may require an alteration in its originaldesign. The EMG diagnostic process remains, therefore, anactive, dynamic endeavor, with exceptional potential forunraveling the mysteries of the brachial plexus.

References and Recommended ReadingPapers of particular interest, published recently have been

highlighted as:Of importance

•• Of major importance

1.' Brown W, Bolton C: Clillical ElectwlI1),ograpll); cdn 2. Burling- .ton, MA: Huucrworth-Heincrnann: 1993.

This is an excellent EMe text thai imcgrarcs elecuodiaguosiic findings.and techniques within the overall anatomic and clinical background.

2. Clancy W, Branci R, Bergfield J: Upper trunk brachial plexus .injuries in contact sports. 11m J Sports Meel 1977,5:209-216.

3." Dumitru 0, Maio AA, Zwarts IVI}:EleClrodiagllo51icMedicillc, edn2. Philadelphia: Hanley & Belfus: 2002 -.

The most outstanding recent text with very detailed analyses ofthe indi-vidual brachial plexus dements and. (heir potential respective injuries. .

4.'· Ferrante MA, Wilbourn AJ. Electrodiagnostic approach to.patient with suspected brachial plcxopathy, NCII101 Clin 2002:20:424-450. .

A very detailed and well-organized article oil OJ(' elecuodiagnosticapproach to brachial plexus injuries. It may be 100 esotericfor thenonspecialist in [MG medicine, however.

5. Ciulian: M: Elecirodiagnostic approach to brachial plexustrauma. American Association of Electrodiagnostic MedicineCourse C: Eiectrodiagnosis in Traumatic Conditions.Oct1998:0rlando, FL; 13-20.. ,

6. Goldstein B:Applied anatomy and electro diagnosis of brachialplexopathies. PI1)'5 Mca Rehabil CliJ1 N Am 1994,5:477-493.

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] 4 Head and Neurologic Conditions

8.. Herrmann ON, Logigian IL: Electrodiagnostic approach tothe patient with suspected morioneuropathy of the upperextremity. Neuio! Clin 2002, 20:452-478.

Another very good article on specific options and approaches in theevaluation of brachial plexus lesions. Makes a very good companionarticle to Ferrante and Wilbourn 14··).

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The best case-based text on electrodiagnostic medicine. It can be uti-lized for the specialist and the nonspecialist alike.14. Mendoza I~ Main K: Peripheral nerve injuries of the shoulder

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One of the recognized leaders in e!ectrodiagnostic medicine, this andother references by Wilbourn 110, 16,22J further clarify a number ofthe points made in this discussion, especially neurogenic thoracicoutlet syndrome.22.. Wilbourn A: Thoracic outlet syndromes. Neural Clin 1999,

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