expanding the differential of shoulder pain

8/4/2019 Expanding the Differential of Shoulder Pain

1/8

JAOA Vol 109 No 8 August 2009 415Schreiber et al Case Report

A 44-year-old man was in his car when it was rear-ended ina minor motor vehicle collision, during which his rightforearm contacted the steering wheel. Shortly thereafter,pain in his right shoulder developed, but initial work-upwas unremarkable. His pain progressed to shoulder girdleweakness over several months and did not improve after2.5 years. At the time of consultation, he complained of right-sided neck pain radiating to the right deltoid muscle andaxilla as well as right shoulder blade pain with shouldergirdle weakness. Repeated electrodiagnostic studies revealed

denervation limited to the serratus anterior and right deltoidmuscles without evidence of cervical radiculopathy. He wasdiagnosed with Parsonage-Turner syndrome, which is aneurologic condition characterized by acute onset of shoulderand arm pain followed by weakness and sensory distur-bance. The authors review patient presentation, physicalexamination, and work-up needed for diagnosis of this syn-drome to help physicians avoid administering unnecessarytests and treatment.

J Am Osteopath Assoc. 2009;109:415-422

In 1943, Spillane1 reported approximately 100 cases oflocalized shoulder girdle neuritis, a condition that typ-

ically included shoulder pain, weakness, asymmetric musclewasting, and sensory symptoms. Five years later, Parsonageand Turner2 described a similar syndrome they termed neu-ralgic amyotrophybut stressed that the pain was of suddenonset and was often severe without any constitutional dis-turbance present from the neck to the hand. Althoughreports have used the terms shoulder syndrome of Parsonage andTurner,2 paralytic brachial neuritis,3 brachial plexus neuropathy,4

and acute brachial neuritis to convey this syndrome,5 we have

elected to use Parsonage-Turner (PT) syndromebecause, in ourexperience, it is the term used most often by clinicians.

In the present report, we first review the literature onPT syndrome, describing its etiologic process as well as toolsfor diagnosis and prognosis. We then present a report of apatient who initially was thought to have radiculopathy. Basedon clinical presentation and evidence of weakness in two mus-cles that are not primarily innervated by the same nerve root,it was clear the patient had PT syndrome. Finally, we includean appendix that outlines the proper physical examination of

muscles affected by PT syndrome. As the present report sug-gests, a thorough medical history, physical examination, andelectrodiagnosis are necessary for proper diagnosis of thiscondition.

Parsonage-Turner SyndromeParsonage-Turner syndrome is well described in the litera-ture. Although its etiologic process is unknown, various stres-sors have been correlated to disease onset. As described ear-lier, acute onset of pain followed by muscle weakness in aseparate peripheral nerve distribution (ie, axillary and tho-racic nerves) rather than a root distribution (ie, two muscles pri-

marily innervated by nerve root C6) is a key element of diag-nosis. Specifically, two weakened muscles sharing primaryroot innervation would suggest a diagnosis of radiculopathyin the proper clinical context. However, in PT syndrome, mus-cles that share root innervation with weakened muscles will beuninvolved. Electrodiagnostic studies should be used to con-firm clinical diagnoses.

Etiologic ProcessThe etiologic process of PT syndrome has not been elucidated.In 1948, Parsonage and Turner2 correlated infection, minorsurgery, minor gunshot wounds, and minor trauma with theprecipitation of the syndrome. Several other stressors, including

unaccustomed strenuous exercise, parturition, and surgery,have also been reported to precede the onset of PT syn-drome.3,4,6 Autoimmune diseases, hereditary factors, and rou-tine vaccinations have also been implicated.4,7 Although therehave been parallels between various stressors and the onset ofPT syndrome, an antecedent stressor is not always found.

Patient PresentationAlthough the symptoms of PT syndrome vary, patients gen-erally describe a triad of pain, weakness, and sensory symp-toms. The onset is sudden and most often occurs at night,4

Expanding the Differential of Shoulder Pain: Parsonage-Turner Syndrome

Adam L. Schreiber, DO, MA; Ronnen Abramov, DO; Guy W. Fried, MD; and Gerald J. Herbison, MD

From the Department of Rehabilitation Medicine (Drs Schreiber, Abramov,Fried, and Herbison) and the Department of Anesthesiology (Dr Abramov) atJefferson Medical College of Thomas Jefferson University in Philadelphia,Pa, and from Magee Rehabilitation, also in Philadelphia, Pa (Dr Fried).

The results of this report were presented in part during the Associationof Academic Physiatrists Annual Meeting held February 19 through February23, 2008, in Anaheim, Calif.

Address correspondence to Adam L. Schreiber, DO, MA, Thomas Jef-ferson University Hospital, Department of Rehabilitation, 25 S 9th St, Philadel-phia, PA 19107-4408.

E-mail: [email protected]

Submitted July 10, 2008; accepted February 5, 2009.

CASE REPORT


2/8

416 JAOA Vol 109 No 8 August 2009

and symptoms are typically unilateral with a predilection forthe dominant limb.7 The affected muscles can be tender duringthe acute phase, with pain exacerbated by arm or shouldermovement.2-4 The pain is reported as constant in the first sev-eral weeks of onset and then as intermittent from the second

month to 1 year.3,4 Pain in the shoulder or arm is oftendescribed as sharp or throbbing.

Discomfort may last for prolonged periods. One study7

reported that 10% of patients had initial pain that lasted longerthan 60 days. More than 75% of patients had two additionalphases of neuropathic pain that were elicited by movement orprolonged posturing (eg, lying on of the affected limb).7 Thesepain phases lasted up to several months.7 Approximately 65%of patients reported persistent musculoskeletal-type pain at theorigin or muscle insertion of the paretic or compensating mus-cles.7 Patients also had glenohumeral joint pathology, includingsubluxation and frozen shoulder. In addition, 29% of patientshad chronic pain resistant to therapy.7

Generally, weakness manifests days to weeks after theonset of pain and is commonly found in the shoulder girdle andserratus anterior muscle, though other individual musclessupplied by the brachial plexus may be affected.7 However,some reports have described weakness or paralysis occurringconcurrently with the onset of pain.2,4 Sensory loss can occurin up to two-thirds of individuals and is commonly noted inthe lateral distribution of the arm and posterior forearm, withparesthesias in one-third of patients.2,4,8

DiagnosticsElectrodiagnostic evaluation of PT syndrome is most helpful

in confirming diagnosis and localizing the lesion. This evalu-ation consists of two parts: nerve conduction studies (NCS) andneedle electromyography (EMG). This two-part test is some-times referred to as simply EMG, implying both NCS andEMG.

Motor and sensory nerves are measured by NCS, whilemotor response is measured by several parameters. The mostimportant parameter for evaluating PT syndrome is compoundmuscle action potential, which represents the summation of allunderlying individual muscle fiber action potentials. The secondpart of the evaluation is EMG, which involves inserting a needleinto individual muscles to detect nerve injury. The most impor-tant aspect of evaluating PT syndrome is finding nerve injury

in individual muscles. These muscles should not share rootinnervation, which may imply radiculopathy.

Cwik et al9 reported that median and ulnar motor and sen-sory nerve conduction studies are abnormal in only 15% ofpatients with a typical history of PT syndrome. However,Dimitru10 reported that 50% of patients had abnormalitiesthat were found in motor studies of the serratus anterior,

biceps brachii, and deltoid muscles as well as sensory studiesof the median and lateral brachial cutaneous nerves. AlthoughF waves may be abnormal, they have minimal value in local-ization. With abnormal motor studies of the musculocuta-

neous and axillary nerves innervating the biceps and deltoidmuscles, respectively, the compound muscle action potentialcan determine the amount of axonal loss and, therefore, prog-nosis.

Unfortunately, the commonly affected long thoracic and

suprascapular nerves are not amenable to reliable surfacerecording. Lo and Mills11 reported conduction block by stim-ulating at the cervical nerve roots, but this is contrary to the con-ventional belief that PT syndrome results from an axonal pro-cess.10 Suarez12 reported that 96.3% of patients with PTsyndrome have abnormal EMG results that are consistentwith the condition.

Needle EMG is useful because it localizes the axonallesion. The most common patterns are single and multiplemononeuropathies. Overlapping myotomic abnormalities,along with concomitant paraspinal muscle denervation, wouldimplicate a more proximal root lesion. With the exception ofthe anterior interosseus nerve to muscles such as the flexor pol-

licis longus, flexor digitorum profundus, and pronatorquadratus, PT syndrome usually affects proximal musculature,most of which are the serratus anterior, biceps brachii, rhom-

boid, supraspinatus, and infraspinatus muscles. However,any part of the plexusand, clinically, any musclecould beinvolved.7

There are several reports of phrenic nerve involvementwith PT syndrome.13,14 Technically, a needle study can revealwallerian degeneration from axonal loss (ie, decreased recruit-ment, fibrillation and positive sharp waves, and polyphasicmotor unit potentials), which can be very specific with patchyinvolvement to specific fascicles of a single nerve.10 With the

suspicion of PT syndrome, evaluations should includescreening nerve roots and paraspinal muscles as well as the ser-ratus anterior, rhomboid, supraspinatus, and infraspinatusmuscles.10 Depending on patient presentation, muscles inner-vated by the anterior interosseus nerve should be screened.With comprehensive screening, PT syndrome with single ormultiple mononeuropathies can be differentiated from radicu-lopathy with myotomic involvement.

In a study by van Alfen and van Engelen,7 MRI scans ofthe cervical spine were not found to correlate anatomicpathology with clinical findings. Furthermore, results of MRIscans of the brachial plexus were abnormal in less than 10% ofpatients.7 These findings support the suggestion that an MRI

scan of the plexus and shoulder girdle or upper arm is seldomrequired to establish a diagnosis.15 However, T2-weightedMRI scans of clinically weak muscles may reveal high signalintensity of the affected muscles. A 2007 report16 revealed thatfindings from magnetic resonance neurography may haveclinically important benefits compared to those from MRIscans and may benefit patients by providing earlier diagnosesof acute or chronic PT syndrome.

In summary, patients with PT syndrome present with asequence of sudden pain, weakness, and sensory loss, whichcan be confirmed by EMG and NCS.

Schreiber et al Case Report

CASE REPORT


3/8

JAOA Vol 109 No 8 August 2009 417

scapular winging in forward flexion. Upper limb deep tendonreflexes, sensation, and motor powerincluding shoulderinternal and external rotatorswere normal with the excep-tion of 2/5 strength in the right shoulder abductors and ser-ratus anterior muscle. Provocative maneuvers were performed

to further assess the patient, but Hawkins, Neers, OBriens,Scarfs, Speeds, and Spurlings maneuvers17 were negative.

Results from a repeated MRI scan of the cervical spine andright shoulder remained unremarkable. Results from nerveconduction studies of the bilateral motor median, ulnar nerveswith F waves, bilateral sensory median, ulnar, and radialnerves were normal. Needle EMG revealed small diffuse fib-rillations and large polyphasic voluntary motor unit potentialswith marked decreased recruitment consistent with denerva-tion of the serratus anterior and right deltoid muscles. Resultsfrom needle EMG of the left supraspinatus, infraspinatus,rhomboid, cervical, biceps, triceps, pronator teres, and firstdorsal interosseous muscles were normal.

Because of the severe sharp acute onset of shoulder painfollowed by profound weakness and evidence of denervationin the serratus anterior and deltoid muscles, in the absence ofany abnormalities in the cervical spine and shoulder on MRI,the patient was diagnosed as having PT syndrome. The diag-nosis was reported to the referring physician with recom-mendation for conservative treatment with pharamacologicpain management and aggressive outpatient physical therapy.

DiscussionShoulder pain, muscle weakness, and sensory abnormalitiesare common complaints in patients with PT syndrome. Var-

ious more common pathologies, such as cervical radiculopathy,shoulder pathology, osteoarthritis of the neck or shoulder,somatic dysfunction, and myofascial pain, must be differenti-ated by medical history, physical examination, and selective useof electromyographic and imaging studies. Concomitant dis-orders may complicate the diagnosis of PT syndrome vs otherconditions. A full neurologic and musculoskeletal examinationof the upper limbsfocusing on the trapezius, serratus ante-rior, deltoid, and rotator cuff muscleswill implicate specificperipheral nerve pathology.

Although electrodiagnostic tests are needed, such toolshave certain pitfalls (eg, patient intolerance, technical error).Another pitfall may occur with EMG. On needle EMG, up to

25% polyphasic motor unit potentials in the deltoid muscle maybe normal.18 On a root screen to evaluate the patient for radicu-lopathy, when polyphasic motor unit potentials are encoun-tered in the deltoid, findings may be considered normal unlessother C5 and C6 innervated muscles have abnormal motorunit potentials or abnormal spontaneous activity. The con-tralateral deltoid muscle may be studied for proportionalpolyphasicity. In PT syndrome, if isolated polyphasic motorunit potentials are disregarded, then axillary nerve involvementmay be overlooked.

A detailed review of physical examination techniques is

PrognosisThe prognosis of PT syndrome is generally favorable. Theduration of pain and severity of muscle weakness and atrophyprognosticates recovery. Severe pain typically resolves, butthe persistence of pain negatively impacts the time for motor

recovery.4,8Motor restoration is unpredictabletwo-thirds of patients

may begin recovery in as early as 1 month, with proximalinvolvement improving better then distal involvement.4,8 Uni-lateral disease has demonstrated quicker recovery after 1 yearand was similar to bilateral disease after 2years. In one study,4

approximately 60% of upper trunk mononeuropathies recov-ered to normal function in 1 year, in comparison to lower trunkmononeuropathies, which resolved in 1.5 to 3years. Althoughpatients with weakened muscles recovered within 4 weeksand demonstrated complete recovery within 6months, gen-eral motor recovery can continue for up to 3 years.4

A less favorable prognosis was found in patients with

early, severe, and rapid weakness and wasting and prolongedor recurrent pain patterns with no motor recovery signs before3 months.2,8 This finding is inconsistent with Tsairis et al,4

who reported that the rate of motor recovery was 36% withinthe first year, approximately 75% the second year, and 89% bythe third year.

Report of CaseA 44-year-old man was in his car when another vehicle hitthe rear end of his car 2.5 years ago. His right forearm madecontact with the steering wheel. He was seen in an emergencydepartment and was discharged the same day.

Shortly after the collision, right shoulder pain developed.The patient followed up with an orthopedist soon after themotor vehicle crash. Electromyography, NCS, and magneticresonance imaging (MRI) were performed 2 months afteronset of symptoms, but results revealed that the cervical spineand right shoulder were normal. During the following severalmonths, his pain did not improve but progressed to shouldergirdle weakness.

The patient returned to the orthopedist 2.5 years after themotor vehicle collision. At his initial presentation, the patientcomplained of right-sided achy, stabbing, and burning neckpain that radiated into the deltoid muscle, axilla, and rightshoulder. He quantified the severity of pain as seven out of 10

on a visual analog scale. He also complained of shoulder girdleweakness that not only limited his ability to lift his arm but alsolimited his ability to perform activities of daily living, includingsleep. His medical history was not clinically significant forneurologic or musculoskeletal disease.

On initial presentation, the patient was in discomfort. Hewas afebrile with stable vital signs. The patients trapezius, ser-ratus anterior, deltoid, supraspinatus, infraspinatus, and teresminor muscles were thoroughly examined using the techniquesdescribed in theAppendix. Physical examination revealed70 degrees of active shoulder abduction with right medial


CASE REPORT


4/8


provided in theAppendix. If the trapezius or serratus anteriormuscle is weak, scapular stabilization will be affected, andshoulder muscles will demonstrate pseudo-weakness if notpositioned in the proper plane. The scapula is stabilized by thetrapezius muscles in the frontal planealso commonly referred

to as the coronal planeand the serratus anterior muscle in thesagittal plane. The instability typically affects the rotator cuffmuscles of external rotation and the deltoid muscles.

If a patients serratus anterior muscle is weak, the physi-cian should test the patients external rotators with the patientsarms at his or her sides. If the trapezius muscle is weak, theexternal rotators should be tested with the patients armsabducted 90 degrees. If the external rotators are tested in posi-tions of scapular instability, pseudo-weakness can implicaterotator cuff pathology or suprascapular neuropathy. Middledeltoid strength will seem compromised if the trapezius muscleis weak. The axillary innervated anterior deltoid muscle can betested in the sagittal plane, where the scapula is stabilized by

the serratus anterior muscle.Current treatment options for patients with PT syndrome

include physical therapy, osteopathic manipulative treatment,and medication. Physical therapy should focus on active andpassive range-of-motion exercises to prevent disuse atrophyand shoulder contracture. Mobilization of the region shouldinclude the treatment of the glenohumeral and scapulotho-racic joints as well as the cervical spine. Use of osteopathicmanipulative treatment to mobilize the shoulder, neck, and sur-rounding thoracic and scapulothoracic joints with myriadtechniques, including the seven stages of Spencer, may helprelieve restriction and pain.19,20 Ultrasound, electrical stimu-

lation, and heat may be beneficial for the patient. Adequateanalgesia is necessary for patient comfort, but there is no lit-erature supporting a specific class of medication. Likewise,there is limited literature supporting the use of oral steroids forpatients with PT syndrome.6

In the present report, we discuss physical examinationin depth because findings of weakness are easily missed or mis-interpreted. Examination of less commonly examined musclesmust be considered when shoulder range of motion is limitedwith scapular winging. Proper positioning during physicalexamination prevents detection of pseudo-weakness in therotator cuff, deltoid muscle, or both, which can implicate incor-rect peripheral nerve injury and possible misdiagnosis.

Generally, imaging provides no correlative data towardPT syndrome diagnosis, and a routine needle EMG root screenmay miss the muscles affected. Therefore, examination of thecommonly affected serratus anterior, rhomboid, supraspinatus,and infraspinatus muscles are necessary.6 Medical history,physical examination, and results from EMG will preventmisdiagnosis as well as unnecessary tests and procedures.

ConclusionParsonage-Turner syndrome must be included in the differ-ential diagnosis of patients with shoulder pain, weakness, and

sensory abnormalities. With a high index of suspicion, med-ical history, muscle weakness, and electrodiagnostic abnor-malities will elucidate the diagnosis.

Acknowledgments

We thank Jeremy Simon, MD, and Theera Vachranukunkiet, MD,for allowing us to use their photographs in the present report.

References1.Spillane JD. Localised neuritis of the shoulder girdle: a report of 46 patientsin the MEF. Lancet. 1943;2:532-535.

2. Parsonage MJ, Turner JWA. Neuralgic amyotrophy: the shoulder-girdlesyndrome. Lancet. 1948;1:973-978.

3. Turner JWA, Parsonage MJ. Neuralgic amyotrophy (paralytic brachial neu-ritis); with special reference to prognosis. Lancet. 1957;2:209-212.

4. Tsairis P, Dyck PJ, Mulder DW. Natural history of brachial plexus neu-ropathy: report on 99 patients.Arch Neurol. 1972;27:109-117.

5.Misamore GW, Lehman DE. Parsonage-Turner syndrome (acute brachial neu-ritis).J Bone Joint Surg. 1996;78:1405-1408. http://www.ejbjs.org/cgi/content

/full/78/9/1405. Accessed July 2, 2009.6. Simon JP, Fabry G. Parsonage-Turner syndrome after total-hip arthroplasty.

J Arthroplasty. 2001;16:518-520.

7. van Alfen N, van Engelen, BG. The clinical spectrum of neuralgic amy-otrophy in 246 cases [published online ahead of print December 21, 2005].Brain. 2006;129:438-450. http://brain.oxfordjournals.org/cgi/content/full

/129/2/438. Accessed July 2, 2009.

8.Dillin L, Hoaglund FT, Scheck M. Brachial neuritis. J Bone Joint Surg Am.1985;67:878-880.

9. Cwik VA, Wilbourn AJ, Rorick M. Acute brachial neuropathy: detailedEMG findings in a large series [abstract]. Muscle Nerve. 1990;13:859.

10.Dumitru D. Brachial plexopathies and proximal mononeuropathies. In:Dumitru D, Amato AA, Zwarts MJ. Electrodiagnostic Medicine. 2nd ed.Philadelphia, Pa: Hanley & Belfus; 2002:815-817.

11. Lo YL, Mills KR. Motor root conduction in neuralgic amyotrophy: evi-

dence of proximal conduction block. J Neurol Neurosurg Psychiatry.1999;66:586-590. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=10209168. Accessed July 2, 2009.

12. Suarez GA. Immune brachial plexus neuropathy. In: Dyck PJ, Thomas PK.Peripheral Neuropathy. 4th ed. Philadelphia, Pa: Elsevier Saunders; 2005:2299-2308.

13.Beydoun SR, Rodriguez R. Neuralgic amyotrophy misdiagnosed as diaphrag-matic rupture. Muscle Nerve. 1996;19:1181-1182.

14. Cape CA, Fincham RW: Paralytic brachial neuritis with diaphragmaticparalysis. Contralateral recurrence. Neurology. 1965;15:191-193.

15.Helms CA, Martinez S, Speer KP. Acute brachial neuritis (Parsonage-Turnersyndrome): MR imaging appearancereport of three cases. Radiology.1998;207:255-259. http://radiology.rsnajnls.org/cgi/reprint/207/1/255. AccessedJuly 10, 2009.

16.Duman I, Guvenc I, Kalyon TA. Neuralgic amyotrophy, diagnosed with mag-

netic resonance neurography in acute stage: a case report and review of theliterature. Neurologist. 2007;13:219-221.

17.Malanga GA, Nadler SF. Musculoskeletal Physical Examination: An Evidence-Based Approach. Philadelphia, Pa: Elsevier; 2006.

18.Preston DC, Shapiro BE. Analysis of motor unit potentials. In: Preston DC,Shapiro BE, eds. Electromyography and Neuromuscular Disorder: Clinical-Electrophysiologic Correlations. Newton, Mass: Butterworth-Heinemann;1998:195.

19.Patriquin DA, Jones JM III. Articulatory techniques. In: Ward RC, ed. Foun-dations for Osteopathic Medicine. Baltimore, Md: Williams & Wilkins; 1997:777-780.

20.Patriquin DA. The evolution of osteopathic manipulative technique: theSpencer technique.J Am Osteopath Assoc. 1992;92:1134.


CASE REPORT


5/8


scapula to retract the scapula. The lower fibers of thetrapezius muscle originate from the T6 through T12 spinous

processes and insert on the medial spine (medial to theaxis of rotation) of the scapula. These fibers depress andretract the scapulaperforming the opposite function of theupper fibers. All three regions of the trapezius muscle rotatethe glenoid fossa of the scapula toward the frontal plane(Supplemental Figure 1).

To assess the upper fibers, have the patient in a seatedposition and ask him or her to shrug and retract his or hershoulders. Observe for any side-to-side differences in ele-vation. Then, forcefully depress the shoulders, noting anymuscle weakness (Supplemental Figure 2).

To examine the middle trapezius, have the patient flexforward 90degrees at the waist and horizontally abduct thearms to 120 degrees. Monitor for any lateral winging andinability to fully abduct the arms. Then, depress the patientsarms at the elbow (ie, toward the ground), observing fordecreased horizontal abduction and lateral sliding of the

A thorough physical examination is essential for physi-cians to determine the presence and extent of muscle weak-

ness in patients suspected of having Parsonage-Turner syn-drome. The following paragraphs describe muscle-testingtechniques for examining various muscles of the shoulder.More information and videos on muscle-testing techniquesare available through the Thomas Jefferson University JEF-FLINE Web site.1

TrapeziusThe trapezius muscle is divided into the upper, middle,and lower regions and is innervated by the spinal accessorynerve from the C3 and C4 nerve roots. The upper fibers ofthe trapezius muscle originate at the occipital protuber-ance and the upper ligamentum nuchae and insert on thelateral third of the clavicle and acromion. These fibers ele-vate and retract the scapula. The middle fibers of thetrapezius muscle originate at the C7 through T5 spinous pro-cesses and insert on the acromion and lateral spine of the


CASE REPORT

Appendix

Supplemental Figure 1.Action of the trapezius muscle. The upperfibers cause scapular Elevation and Retraction (A), the middle

fibers cause scapular Retraction (B), and the lower fibers causescapular Depression and Retraction (C). Each of the three regionsof the trapezius muscle contribute to the Upward Rotation ofthe glenoid fossa of scapula in the frontal plane.Abbreviations:A, anterior; L, lateral border of scapula; M, medial border ofscapula; P, posterior; S, superior border of scapula.

A B

C

R

S

LM

A

E

PUR

R

S

LM

A

PUR

R

S

LM

A

D

PUR


6/8


scapula (Supplemental Figure 3).To examine the lower fibers, the patient remains at

90 degrees of flexion at the waist and places their shoulders

in the diving position of 180 degrees flexion. Look for thearms to be at the same level. The examiner pushes down atthe elbow and looks for decreased flexion and sliding of thescapula cephalad over the upper ribs (Supplemental Figure4).Alternatively, the patient may be tested in the prone posi-tion.

Another method of detecting trapezius weakness isto have the patient place their back to the wall and abducttheir shoulder in the frontal plane. If the trapezius is weak,

the patient will compensate by trying to bring his or hershoulder into the sagittal plane, using the serratus ante-

rior muscle as the primary abductor (Supplemental Figure 5).

Serratus AnteriorThe serratus anterior muscle is innervated by the long tho-racic nerve arising from the C5, C6, and C7 nerve roots.The muscle originates on the upper eight ribs and inserts onthe costal aspect of the medial border of the scapula. It pro-tracts the scapula and rotates the glenoid up in the sagittalplane (Supplemental Figure 6).

To examine the strength of the serratus anterior muscle,place the patients arm to 90 degrees of flexion with theelbow fully flexed, and position the elbow in slight hori-zontal adduction across the body. From behind the patient,place one hand on the opposite scapula to stabilize thepatient while the other hand is on the patients elbow,pulling the shoulder posterior and inferior, noting any

weakness or scapular winging (SupplementalFigure 7).2

DeltoidThe deltoid muscle is innervated by the axillarynerve from the C5 and C6 nerve roots. The del-toid originates at the acromion and inserts onthe deltoid tubercle. It primarily abducts thehumerus.

To examine the deltoid muscle, have thepatient abduct the arm to 90 degrees with theelbow flexed, and push the arm just proximal to the elbowtoward the floor. This technique primarily isolates themiddle deltoid. If there is suspicion of trapezius weakness,


CASE REPORT

Supplemental Figure 2. Examination of the upper fibers of thetrapezius muscle. Patient is seated and asked to shrug and retracthis or her shoulders. To identify muscle weakness, the examinerforcefully depresses both shoulders.

Supplemental Figure 3. Examination of the middle fibers of thetrapezius muscle. The examiner should evaluate the patient for lat-eral winging and inability to fully abduct the arms beforedepressing the arms at the elbow to observe for decreased hori-zontal abduction and lateral sliding of the scapula.

Supplemental Figure 4. Examination of the lower fibers of thetrapezius muscle. The patients arms should be at the same level.The examiner should look for decreased flexion and sliding of thescapula cephalad over the upper ribs.

Appendix (continued)


7/8


have the patient place his or her elbow in flexion, and thenflex and internally rotate the shoulder to 90 degrees to testthe anterior deltoid.

Supraspinatus, Infraspinatus, and Teres MinorThe rotator cuff is made up of four muscles, three of

whichthe supraspinatus, infraspinatus, and teres minormusclescontribute to external rotation of the humerus.They originate at the supraspinatus fossa, infraspinatusfossa, and lateral border of the scapula, respectively, andinsert on to the greater tubercle of the humerus. Thesupraspinatus and infraspinatus are innervated by thesuprascapular nerve and the teres minor by the axillarynerve, both from the C5 and C6 nerve roots.


CASE REPORT

Supplemental Figure 5. Method for detecting weakness in thetrapezius muscle. Patient is instructed to abduct the humerus inthe frontal plane. As shown, the patient attempts to compensatefor weakness of the right trapezius by rotating his scapula intothe sagittal plane to use the serratus anterior muscle for further

abduction.

Supplemental Figure 6.Action of the serratus anterior muscle,causing scapular Protraction and Upward Rotation of the glenoidfossa of scapula in the sagittal plan.Abbreviations:A, anterior;L, lateral border of scapula; M, medial border of scapula; P, pos-terior; S, superior border of scapula.

A

B

Supplemental Figure 7.Examination of the serratus anterior

muscle for weakness or scapular winging. The examiner places onehand on the opposite scapula to stabilize the patient (A) while theother hand pulls the patients shoulder posterior and inferior (B).


(continued on the next page)

P

S

LM

A

PUR


8/8


Examination of the external rotators may be done withthe patients arms at his or her side with the elbows at 90degrees flexion if there is suspicion of weakness in the ser-ratus anterior muscle. Force the arm into internal rotation

by holding the elbow at the side with the one hand and

push the arm just proximal to the wrist with the other hand(Supplemental Figure 8). If there is suspicion of trapeziusweakness, the patients arms must be in abduction to testexternal rotation (Supplemental Figure 9).

References1. MMT video gallery. JEFFLINE Web site. http://jeffline.jefferson.edu

/Publishing/Press/mmt/gallery.html. Accessed July 29, 2009.

2.Herbison GJ. Upper extremity examination [handout]. Philadelphia,Pa: Thomas Jefferson University Department of Rehabilitation; 2006:10-11. Resident lecture series.


CASE REPORT

A

B

A

B

Supplemental Figure 8. Examination of the external rotators ofthe humerus with serratus weakness. The examiner holds thepatients elbow at the side with one hand (A) and forces thepatients arm into internal rotation by pushing with the otherhand, which is positioned proximal to the patients wrist (B).

Supplemental Figure 9. Examination of the external rotatorsof the humerus with trapezius weakness. Patients arm isabducted. The examiner holds the patients elbow with onehand (A) and forces the patients arm down with the otherhand, which is positioned proximal to the patients wrist (B).


expanding the differential of shoulder pain

Documents