Upper extremity proximal mononeuropathies

Author(s): William A. Anderson, MD, Gautam Kothari, DO

Originally published:09/20/2014

Last updated:09/20/2014



Shoulder girdle and upper extremity pain, weakness, and loss of function may result from accessory, long thoracic, axillary, suprascapular, or Musculocutaneous nervemusculocutaneous neuropathies.


  1. All are vulnerable to injury from blunt or penetrating trauma.
  2. Other etiologies include the following:
Accessory nerve Iatrogenic

  • Radical neck dissection
  • Lymph node biopsy
  • Acromioclavicular or sternoclavicular joint dislocation
  • Spontaneous accessory nerve palsy1
Long thoracic nerve Stretch injury

  • Overhead throwing/repetitive activity
  • Tackling
  • Weightlifting

Parsonage-Turner syndrome Iatrogenic

  • Mastectomy
  • Scalenectomy
  • First rib resection
  • Chest tube insertion2
  • Chiropractic manipulation3


  • Thoracic outlet
  • Backpack palsy
Axillary nerve Shoulder fracture/dislocation Compression

  • Aneurysm
  • Tumor
  • Quadrilateral space
  • Backpack palsy

Parsonage-Turner syndrome3,4

Suprascapular nerve Traction

  • Overhead athletes
  • Repetitive overhead activity
  • Retracted rotator cuff tear


  • Stenotic suprascapular or spinoglenoid notch
  • Transverse scapular or spinoglenoid ligament ossification
  • Backpack palsy
  • Spinoglenoid cyst
    • Labrum/capsule injury
    • Sarcoma
    • Metastatic carcinoma



Parsonage-Turner syndrome3,4

Musculocutaneous nerve Intravenous line placement


  • Fracture callus
  • Coracobrachialis muscle5
  • Backpack palsy

Stretch injury

Multifocal motor neuropathy

Upper/lower subscapular nerves Authors are not aware of any reported cases of mononeuropathy Evaluate for spinal nerve/brachial plexus lesion

Epidemiology including risk factors and primary prevention

  1. Overhead athletes and individuals in occupations requiring overhead work are prone to developing suprascapular or long thoracic neuropathy. Emphasis on proper throwing mechanics, ergonomics, and addressing kinetic chain deficits may reduce risk.
  2. Use of proper protective equipment in contact sports to reduce risk of direct trauma or stretch injury to accessory, long thoracic, or axillary nerves.
  3. Assess fall risk and home hazards in older adults to reduce risk of shoulder girdle fracture/dislocation.


  1. Accessory nerve
    • Cranial nerve XI and C1-5 spinal nerves
    • Motor to sternocleidomastoid and trapezius
    • Vulnerable to trauma or iatrogenic injury at posterior triangle of neck6
  2. Long thoracic nerve
    • Arises directly from C5, C6, and C7 ventral rami
    • Motor to serratus anterior
    • Vulnerable to trauma at supraclavicular region
    • Straight course of nerve predisposes to stretch injury2
  3. Axillary nerve
    • C5 and C6 ventral rami
    • Posterior cord of brachial plexus
    • Anterior branch innervates anterior and middle deltoid
    • Posterior branch innervates posterior deltoid and teres minor
    • Sensory to skin over deltoid
    • Vulnerable to entrapment at quadrilateral space bordered by teres minor superiorly, teres major inferiorly, humerus laterally, and long head of triceps medially.
  4. Suprascapular nerve
    • C5 and C6 ventral rami
    • Upper trunk of brachial plexus
    • Motor to supraspinatus and infraspinatus
    • Sensory to shoulder joint
    • Vulnerable to compression at suprascapular or spinoglenoid notch
  5. Musculocutaneous nerve
    • C5 and C6 ventral rami
    • Terminal branch of lateral cord of brachial plexus
    • Motor to coracobrachialis, biceps brachii, and brachialis
    • Terminal extension is lateral antebrachial cutaneous nerve (LACN), which provides sensation to lateral forearm
    • Vulnerable to traction injury at axilla where it pierces coracobrachialis and proximal to elbow where nerve exits brachialis fascia to continue distally as LACN2
  6. Upper and lower subscapular nerves
    • C5, C6, and C7 ventral rami
    • Posterior cord of brachial plexus
    • Motor to subscapularis and teres major

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

New onset/acute

  1. Negative prognostic factors include more proximal lesions and severe axonopathy.
  2. Accessory, long thoracic, and suprascapular neuropathies with a history of blunt or no trauma and no compressive pathology generally respond well to conservative treatment.2,7
  3. Axillary nerve
    • Traumatic or partial lesions respond well to conservative measures.2,8
    • Complete deltoid paralysis or history of stretch injury are negative prognostic factors.2
  4. Compressive lesions may progress without surgery.
  5. Parsonage-Turner syndrome
    • Pain followed by weakness and sensory deficit.
    • Recovery is usually gradual over a period of months to years.
    • Functional recovery may be complete; however, neurologic deficits often persist.9
  6. Early surgical exploration is indicated in cases of severe deficit caused by sharp or penetrating trauma.8


  1. Those who are likely to respond well to conservative treatment will show improvement on physical exam or electrodiagnostic (EDX) studies within 3 to 6 months.
  2. If no improvement, consider evaluation for possible nerve graft because prognosis for improvement is best if done within 6 months.


  1. Neurologic improvement is unlikely.

Specific secondary or associated conditions and complications

  1. Neuropathic pain
  2. Musculoskeletal pain secondary to shoulder girdle instability and/or dysfunction
  3. Functional impairment secondary to muscle weakness, pain, or contracture



  1. Mechanism of injury and associated factors
  2. Symptoms
    • Location
    • Onset
    • Frequency
    • Duration
    • Intensity
    • Exacerbating/relieving positions and movements
  3. Predisposing athletic activities or vocational risk factors
  4. Medical history
    • Shoulder injury
    • Tumor/malignancy
    • Chemotherapy/radiation10
    • Iatrogenic causes (eg, surgery, chiropractic manipulation, intravenous line placement)
    • Infection/Lyme disease
    • Systemic inflammatory disease/vasculitis
    • Brachial plexopathy
    • Parsonage-Turner syndrome
    • Hereditary neuralgic amyotrophy

Physical examination

Physical exam must start with differential diagnosis of cervical radiculopathy and/or brachial plexopathy in mind. Consider primary or secondary musculoskeletal conditions, which may complicate the diagnosis. Weakness in multiple muscles with different peripheral nerve innervation (eg, biceps and deltoid weakness) may point to a more proximal etiology (eg, radiculopathy, plexopathy).

  1. Accessory nerve
    • Shoulder drooping with asymmetric neckline
    • Scapula moves lower and further from midline
    • Abnormal shrug test may be present
    • Scapular winging may be present
  2. Long thoracic nerve
    • Decreased active shoulder forward flexion
    • Winging of inferior border of scapula with shoulder forward flexion or shoulder flexion with internal rotation
  3. Axillary nerve
    • Failure to maintain arm in fully extended position
    • Shoulder girdle weakness
    • Deltoid and/or teres minor atrophy may be present
    • Neurovascular assessment of affected arm to rule out lesion of posterior circumflex humeral artery11
  4. Suprascapular nerve
    • Atrophy of either infraspinatus or both supraspinatus and infraspinatus
    • Pain reproduced with extreme shoulder extension or internal rotation
    • Weakness of external rotation is greater than abduction12
  5. Musculocutaneous nerve
    • Biceps and brachialis wasting
    • Elbow flexion weakness
    • Tenderness to palpation of lateral biceps tendon
  6. Upper and lower subscapular nerves
    • Belly press; rotation without elbow dropping posterior to midsagittal plane of trunk indicates impaired upper subscapularis function
    • Lift off; rotation with the hand off the lumbar spine without extending the elbow evaluates lower subscapular function

Functional assessment

Functional assessment based on nerve injury occurring in isolation or with other associated musculoskeletal or vascular deficits or systemic illness impact recovery and rehabilitation potential. Dominant versus nondominant involvement can affect the need for support aids and assistance with activities of daily living (eg, feeding, grooming, bathing).

Laboratory studies

Consider if infectious (eg, Lyme) or vasculitic etiology is suspected: complete blood count, erythrocyte sedimentation rate, C-reactive protein, antinuclear antibody, and Lyme studies. Creatine kinase may be considered if myopathy/myositis is suspected.


Static imaging

  1. Plain radiographs to evaluate for fracture/dislocation
  2. Computed tomography to evaluate for deeper osseous abnormalities
  3. Magnetic resonance imaging/magnetic resonance neurography
    • Space-occupying lesion
    • Direct nerve compression
    • Nerve lesion

Dynamic imaging

  • Ultrasound
    • Evaluate for dynamic impingement
    • Needle localization for injection

Supplemental assessment tools

EDX studies

  1. Test for differential diagnoses.
  2. Localize and evaluate degree of nerve injury. Of note, proximal stimulation for motor nerve conduction studies (NCS) is controversial and not reliable.
  3. Accessory nerve
    • NCS
      • Motor NCS should be carried out bilaterally to compare compound muscle action potential (CMAP) amplitudes and assess axon loss.
    • Electromyography (EMG)
      • Upper, middle, or lower segments of trapezius can be studied. Needle EMG of multiple trapezius segments and other shoulder muscles should be sampled.
  4. Long thoracic nerve
    • NCS
      • CMAP is not reliable.
      • If sensory abnormalities are present, perform LACN, radial, and median sensory NCS.
    • EMG
      • Needle examination of serratus anterior.
      • If other muscles are weak or sensory abnormalities are present, a complete plexus screen should be carried out.
  5. Axillary nerve
    • NCS
      • Axillary nerve injury and upper trunk plexopathy may present similarly.
      • Bilateral LACN studies should be performed.13
      • Radial sensory nerve should be studied if posterior cord lesion suspected.
    • EMG
      • If deltoid is abnormal, other upper trunk and posterior cord innervated muscles and cervical paraspinals should be sampled.
      • Teres minor can be studied if quadrilateral space lesions suspected.
  6. Suprascapular nerve
    • NCS
      • Motor NCS may detect CMAP amplitude loss in side-to-side comparison.
      • Focal slowing at spinoglenoid notch may be detected at the infraspinatus.
      • LACN study with side-to-side comparison should be done if plexopathy is suspected.
    • EMG
      • bBth supraspinatus and infraspinatus should be sampled.
      • Important to screen other muscles of the C5/6 roots and upper trunk of brachial plexus.
  7. Musculocutaneous nerve
    • NCS
      • Focal motor lesion evaluated by motor NCS recording from the biceps and stimulating at Erb point.
      • If lesion is more distal, sensory abnormalities of lateral antebrachial cutaneous nerve may be present with sparing of motor branch.
    • EMG
      • More reliable.
      • Evaluate biceps brachii and coracobrachialis.
      • Brachialis is less preferable because of dual innervation from musculocutaneous and radial nerves.

Early predictions of outcomes

Prognostic value of EDX studies is limited in cases of severe early involvement. For example, atraumatic accessory and long thoracic neuropathies tend to have good outcomes even in the presence of severe EDX abnormalities.7

  1. Reduced/absent CMAP amplitude and/or motor unit recruitment on needle EMG are seen in both neurapraxic and axonal lesions.
  2. Degree of abnormal spontaneous activity does not correlate with severity.
  3. Combined axonal and neurapraxic involvement may be present.


Available or current treatment guidelines

Treatment is guided by the mechanism and extent of nerve injury addressing any associated muscular, osseous, or vascular pathology and the extent of functional impairment.

Conservative care

  1. Appropriate in the absence of sharp/penetrating trauma or compressive lesion
  2. Relative rest
    • Avoid heavy lifting and activities that worsen symptoms
  3. Controlled mobilization to prevent contracture
  4. Pain control
    • Ice/heat
    • Transcutaneous electrical nerve stimulation
    • Neuropathic medicines and anti-inflammatories
    • Nerve blocks
    • Acupuncture
  5. Therapeutic exercise
    • Range of motion
    • Postural modification and proprioceptive exercises for stabilization
    • Controlled strengthening exercises of the shoulder girdle musculature to enhance compensatory muscle strength and regain muscular balance

Surgical treatment

  1. Early exploration is indicated in cases of penetrating or sharp trauma with severe deficit
  2. Appropriate in setting of space-occupying lesion
  3. Appropriate if no improvement with conservative management and/or absence of reinnervation on EDX testing at 3 to 6 months
  4. Options for surgery may include the following:
    • Nerve graft/transfer; prognosis is best when done within 6 months of injury14
    • Arthroscopy with decompression and excision15
    • Tendon/muscle transfers or fusion procedures may be considered in chronic cases

Coordination of care

Multimodal team approach with physical and occupational therapy to maximize function, reduce pain, and address social and vocational needs. Nurses and caregivers can work together to aid in positioning and ergonomic modifications.

Patient & family education

Counsel patient/family regarding expected course of improvement depending on type of lesion (eg neurapraxic vs axonal) and importance of physical therapy to prevent contracture and improve function.

Emerging/unique Interventions

Serial neuromusculoskeletal examination and EDX studies to assess for recovery over the first 3 to 6 months.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  1. Suspect Parsonage-Turner syndrome if history of severe pain followed by weakness and sensory loss, with antecedent illness, viral infection, vaccination, child birth, and surgery, without trauma.
  2. EDX studies are often useful to establish baseline findings, confirm location and severity of lesion, and assign prognosis.
  3. Surgical consultation if sharp or penetrating trauma or if compressive lesion is identified.
  4. Consider surgical consultation if no clinical or EDX improvement at 3 months. Prognosis for surgical treatment is most favorable when done within 6 months of injury.


Cutting edge concepts and practice

See the Imaging section for details on the use of MRI and ultrasound in the evaluation UNE.


Gaps in the evidence-based knowledge

Limitations of EDXstudiesinprognostication of earlyproximal neuropathies.


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2. Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity.Neurol Clin. 1999;17:525-548.

3. Dumitru D, Zwarts MJ. Brachial plexopathies and proximal mononeuropathies. In: Dumitru D, Amato AA, Zwarts MJ, eds.Electrodiagnostic Medicine. 2nd ed. Philadelphia, PA: Hanley & Belfus; 2002:800-813.

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7. Friedenberg SM, Zimprick T, Harper CM. The natural history of long thoracic and spinal accessory neuropathies.Muscle Nerve.2002;25:535-539.

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

10. Johansson S, Svensson H, Larson LG, et al. Brachial plexopathy after postoperative radiotherapy of breast cancer patients.Acta Oncol. 2000;39:373-382.

11. McInnis KC, Krivickas LC. Peripheral nerve injuries of the shoulder and upper arm. In: Akuthota V, Herring SA, eds.Nerve and Vascular Injuries in Sports Medicine. New York, NY: Springer; 2009:87-112.

12. Mendoza F, Main K. Peripheral nerve injuries of the shoulder in the athlete.Clin Sports Med.1990;9:331-342.

13. Williams FH, Kumiga B. Less common upper limb mononeuropathies.PM R.2013;5(5 Suppl):S22-S30.

14. Terzis JK, Kostas I. Suprascapular nerve reconstruction in 118 cases of adult posttraumatic brachial plexus.Plast Reconstr Surg.2006;117:613-629.

15. Iannotti J, Ramsey M. Arthroscopic decompression of a ganglion cyst causing suprascapular nerve compression.Arthroscopy. 1996;12:739-745.

Author Disclosure

William A. Anderson, MD
Nothing to Disclose

Gautam Kothari, DO
Nothing to Disclose

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