Compressive / Entrapment

Author(s): Thiru M. Annaswamy, MD, MA, Jeremy Jones, MD

Originally published:09/20/2014

Last updated:09/20/2014



The brachial plexus is vulnerable to intrinsic and extrinsic compression or entrapment and perioperative damage. Compressive neuropathies are caused by direct pressure on nerves. Entrapment neuropathy describes a compressive neuropathy caused by the patient’s own body.


Intrinsic brachial plexus compression

  1. Primary brachial plexus tumors
    • Schwannomas, neurofibromas, and neurofibrosarcomas occur as solitary tumors.
    • Multiple tumors may occur in patients with neurofibromatosis type 1.
    • Rarely cause symptomatic plexopathies, but they may present with pain or clinical deficits related to the location of the plexus affected.
  2. Metastatic tumors
    • Rarely, metastatic tumors are seen as isolated lesions in the plexus.
    • Lymphoma, bladder cancer, and melanoma occur most frequently.1

Extrinsic brachial plexus compression

  1. Thoracic outlet syndrome (TOS)
    • Causes include congenital fibrous bands, rudimentary cervical ribs, variations in insertion of the anterior scalene muscle, and compression of the subclavian artery or vein.
    • Presents with slowly progressive, unilateral, atrophic weakness of the hand intrinsics and ulnar nerve distribution numbness.
    • Represents a lower trunk plexopathy.2,3
  2. Rucksack palsy
    • Caused by wearing a backpack or carrying a heavy load on the shoulders for a prolonged time period.
    • Presents with painless shoulder/arm weakness and sensory changes, usually unilaterally.
    • It is an upper plexus disorder.4
  3. Neoplasms
    • Direct extension of breast, lung, or thyroid cancer may cause a plexopathy.
    • Shoulder pain is the most common presenting symptom.
    • Masses typically invade the inferior trunk and medial cord.
    • Pancoast syndrome, seen with nonsmall cell lung cancer in the superior sulcus, causes lower plexus weakness and Horner syndrome.1,5
  4. Trauma
    • Fractures, falls, objects falling on the shoulder, and sports injuries are among many causes of traumatic plexus compression.
    • Motor and sensory changes are often seen in the upper trunk pattern.

Perioperative brachial plexus injuries/compression

  1. Classic postoperative paresis
    • Malpositioning causes traction or pressure on the plexus.
    • Patients usually present with weakness and paresthesias in an upper plexus distribution, occasionally bilaterally.6
  2. Postmedian sternotomy plexopathy
    • Sternotomies cause traction injuries to the C8 anterior primary ramus from fracture or upward displacement of the first rib.
    • C8 median, radial, and ulnar-innervated muscles show weakness.6
  3. Axillary node dissections and orthopedic surgeries involving the clavicle/shoulder
    • Plexopathies result from direct injury or edema causing compression/entrapment.
  4. Neonatal brachial plexus palsy (NBPP)
    • Caused by excessive lateral traction applied to the fetal head during delivery.
    • Occurs unilaterally with 3 presenting patterns: upper plexus, upper and middle plexus, and panplexus.6

Epidemiology including risk factors and primary prevention

  1. The prevalence of cancer-associated plexopathies is 0.4%.7 Neurofibromas and schwannomas are the most frequent benign tumors, but direct extension of breast or lung cancer is more common.1
  2. Rucksack palsy has been reported in soldiers (prevalence of 5%), boy scouts, hikers, and manual laborers.4,8
  3. Neurogenic TOS has an estimated incidence of 1 per 1,000,000 and a female to male ratio of 9 to 1.2
  4. Iatrogenic plexopathies related to surgery account for 7% to 10% of brachial plexopathies. The beach chair position has a lower rate of injury during shoulder surgery compared with the lateral decubitus position.9
  5. NBPP has an incidence of 0.04% to 0.3% of all live births.10
  6. Positioning strategies during surgery reduce plexopathies. Arm abduction in supine patients should be limited to 90°.11


The most common pathology is axonal loss causing Wallerian degeneration and loss of the axon distally. Some injuries cause focal demyelination, which has no effect on the distal nerve.6,8

The lesion site determines the following clinical patterns:12

  1. Panplexus
    • Weakness, sensory loss, and absent reflexes in the entire arm.
  2. Upper trunk
    • Weakness primarily in C5-6 innervated muscles, pronator teres (C6-7), and triceps (C6-7-8).
    • Sensory changes in the lateral arm/forearm/hand and thumb.
    • Absent biceps reflex.
  3. Middle trunk
    • Weakness in the triceps, flexor carpi radialis, and pronator teres (C7 muscles).
    • Sensory changes in the middle finger and posterior forearm.
    • Absent triceps reflex.
  4. Lower trunk
    • Weakness in all C8-T1 muscles.
    • Sensory changes in the medial arm/forearm/hand and digits 4 and 5.
    • All reflexes normative.
  5. Lateral cord
    • Weakness in the pronator teres, flexor carpi radialis, and biceps.
    • Sensory changes in the lateral forearm/hand and digits 1 through 3.
    • Absent biceps reflex.
  6. Posterior cord
    • Weakness in the arm extensors, deltoid, and latissimus dorsi.
    • Sensory changes in the lateral arm, posterior arm/forearm, and dorsal hand.
    • Absent triceps and brachioradialis reflexes.
  7. Medial cord
    • Weakness in all ulnar muscles, abductor pollicis brevis, flexor pollicis longus, and flexor digitorum profundus.
    • Sensory changes in the medial arm/forearm/hand and digits 4 and 5.
    • All reflexes normative.

Specific secondary or associated conditions and complications

  1. Erb-Duchenne palsy
    • Characterized by weakness of shoulder abduction, elbow flexion, and arm supination.
    • Limb hangs at the side, medially rotated, forearm extended, and pronated.
    • Seen in upper trunk plexopathies.
  2. Klumpke palsy
    • Characterized by weakness of the hand intrinsic muscles and ulnar-innervated muscles.
    • Results in supination of the forearm and flexion of the wrist and fingers (claw hand).
    • Seen in lower trunk plexopathies.
  3. Radial nerve palsy
    • Characterized by forearm extensor weakness causing wrist drop.
    • Seen in posterior cord plexopathies.



  1. A thorough medical history should be obtained, including medical, surgical, family, and social histories.
  2. Determine the onset of the symptoms and any association (surgery, injury, recreational activity, delivery) or whether the symptoms began insidiously without a known cause. Ask about pain, weakness, and sensory changes.

Physical examination

Thorough musculoskeletal and neurologic examinations should be performed testing manual muscle strength, sensation, and reflexes. The Adson and Roos tests can help rule out TOS.

Functional assessment

Plexus lesions cause varying functional abnormalities and palsies. Evaluate patients’ ability to carry out activities of daily living.


Magnetic resonance imaging (MRI) provides detailed soft tissue visualization. Contrast-enhanced images are obtained for suspected neoplasm, radiation injury, abscesses, and following peripheral nerve surgery. Noncontrast studies are sufficient for acute traumatic injuries and compressive neuropathy. Chest and spine plain radiographs can detect major osseous abnormalities.13Computerized tomography, used in patients who cannot undergo MRI, provides greater detail for bony abnormalities. Ultrasound is subsequently discussed in Cutting Edge Concepts and Practice.

Supplemental assessment tools

Nerve conduction studies (NCS) and electromyography (EMG) help localize and assess lesion age and severity.

Sensory NCS are more important than motor NCS in identifying plexus lesions. Sensory nerve action potentials (SNAPs) may be abnormal in plexus lesions but normative in root lesions. Compound muscle action potentials (CMAPs) may be affected in both.12There are several exceptions including the following:

  1. Distal SNAPs are normative in myelinopathy.
  2. Root lesions from far lateral disks may cause abnormal SNAPs similar to plexopathies.
  3. EMG may be normative in small fiber plexopathies.

EMG of proximal and distal muscles is performed to determine lesion sites, which cause the following abnormal electrophysiologic patterns:12

  1. Upper trunk
    • Lateral antebrachial cutaneous (LAC) SNAP is abnormal.
    • Median and ulnar motor NCS are normative.
    • EMG abnormalities seen in deltoids, biceps, brachioradialis, and supraspinatus and infraspinatus muscles.
  2. Middle trunk
    • Median and radial SNAPs may be abnormal.
    • Median and ulnar motor NCS are normative.
    • EMG abnormalities seen in C7-innervated muscles.
  3. Lower trunk
    • Ulnar, dorsal ulnar, and medial antebrachial cutaneous (MAC) SNAPs are abnormal.
    • Median and ulnar motor NCS may be abnormal.
    • EMG abnormalities seen in ulnar-innervated muscles, flexor pollicis longus, abductor pollicis brevis, and extensor indicis proprius.
  4. Lateral cord
    • LAC and median SNAPs are abnormal.
    • Median and ulnar motor NCS are normative.
    • EMG abnormalities seen in biceps, pronator teres, and flexor carpi radialis.
  5. Posterior cord
    • Radial SNAP is abnormal.
    • Median and ulnar motor NCS are normative.
    • EMG abnormalities seen in radial-innervated muscles.
  6. Medial cord
    • Ulnar, dorsal ulnar, and MAC SNAPs are abnormal.
    • Median and ulnar motor NCS may be abnormal.
    • EMG abnormalities seen in ulnar-innervated muscles and C8-T1 median-innervated muscles.

Early predictions of outcomes

  1. Axonal loss, chronic lesions, and muscle atrophy are associated with worse injury and outcome. Fibrillation potentials and positive sharp waves, graded from 0 to 4, indicate active denervation. However, higher grades do not necessarily correspond to the degree of denervation or worse injuries. Maintaining distal amplitude in evoked responses may be a greater, early predictor for recovery.
  2. Focal demyelinating injuries have a better prognosis and recovery.
  3. NCS/EMG are specific but not sensitive in identifying lesions, limiting its prognostic value.
  4. Two thirds of rucksack palsies recover fully within 2 to 5 months. Classic postoperative paresis and postmedian sternotomy plexopathy generally have rapid, complete recovery.4,6


Available or current treatment guidelines

  1. Pain and paresthesias are treated using oral medications (gabapentin, amitriptyline, opiates).
  2. Occupational therapy assists in strengthening, range of motion, stretching, functional bracing/splinting, and physical modalities. The antigravity environment in aquatic therapy facilitates recovery of movement.14
  3. Specific treatment depends on the etiology.
    • Environmental and activity modifications reduce symptoms in TOS and rucksack palsy.15
    • Surgery to alleviate the compression/entrapment may be required in neoplasms, TOS, and fractures.
    • Reconstruction surgery includes nerve repair, nerve grafts, nerve transfer, functioning free muscle transplantation, and tendon transfers. No specific guidelines describe who should have surgery, but it should be performed earlier rather than in chronic injuries.16
    • Conservative management, including symptom control and functional improvement, is used for those syndromes caused by surgery.

At different disease stages

Indications for surgical nerve reconstruction for NBPP include the following:

  1. Cookie test
    • Inability to bring a cookie to the mouth at 9 months
  2. Towel test
    • Inability to remove a towel covering the face at 6 months
  3. Biceps function not recovered at 3 months

No standard guidelines exist. Practitioners use these tests and ancillary studies to determine when to perform nerve reconstruction.14

Coordination of care

The treating physician should communicate with other physicians, therapists, orthotists, and nurses to assure the patient receives the best care.

Patient & family education

Patients and family should be educated on the cause of impairment and recovery, including any necessary surgery and treatments.

Emerging/unique Interventions

The Disabilities of the Arm, Shoulder, and Hand questionnaire is a reliable instrument to measure upper extremity function and symptoms. The Active Movement Scale assesses motor function in infants with NBPP.

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

  1. NCS/EMG help localize lesions and assess age and severity.
  2. Plexopathies causing axonal injury have a worse prognosis than demyelinating injuries.
  3. Clinical patterns found on examination may localize a plexus lesion.


Cutting edge concepts and practice

Neuromuscular ultrasound (NMUS) is of interest for diagnosis and image-guided therapy in plexopathies. NMUS can visualize the movement of structures and identify lesions and masses. It relies on operator skills, which could be a limitation.13Magnetic resonance neurography, available in some large academic institutions, increases visualization of individual plexus segments and peripheral nerves.


Gaps in the evidence-based knowledge

Several studies found high satisfaction with surgical treatment, whereas others demonstrate comprehensive rehabilitation improves outcomes. However, these studies tend to be small, leaving a lack of adequately powered, good outcome data on long-term functional outcomes after surgery and rehabilitation.17,18


1. Das S, Ganju A, Tiel RL, Kline DG. Tumors of the brachial plexus.Neurosurg Focus. 2007;22:E26.

2. Wilbourn AJ. Thoracic outlet syndrome surgery causing severe brachial plexopathy.Muscle Nerve. 1988;11:66-74.

3. Klaassen Z, Sorenson E, Tubbs RS, et al. Thoracic outlet syndrome: a neurological and vascular disorder.Clin Anat. 2013 May 29. doi: 10.1002/ca.22271. [Epub ahead of print]

4. Nylund T, Mattila VM, Salmi T, Pihlajamaki HK, Makela JP. Recover of brachial plexus lesions resulting from heavy backpack use: a follow-up case series.BMC Musculoskelet Disord. 2011;12:62.

5. Patel A, Carter J, Friedlander P, Kandil E. Brachial plexus compression: a rare sequella of malignant papillary thyroid carcinoma.Int J Clin Exp Med. 2013;6:606-608.

6. Wilbourn AJ. Plexopathies.Neurol Clin. 2007;25:139-171.

7. Jaeckle KA. Neurological manifestations of neoplastic and radiation-induced plexopathies.Semin Neurol. 2010;30:254-262.

8. Ferrante MA. Brachial plexopathies: classification, causes, and consequences.Muscle Nerve. 2004;30:547-568.

9. Scully WF, Wilson DJ, Parada SA, Arrington ED. Iatrogenic nerve injuries in shoulder surgery.J Am Acad Orthop Surg. 2013;21:717-726.

10. Foad SL, Mehlman CT, Ying J. The epidemiology of neonatal brachial plexus palsy in the United States.J Bone Joint Surg Am. 2008;90:1258-1264.

11. American Society of Anesthesiologists Task Force on Prevention of Perioperative Peripheral Neuropathies. Practice advisory for the prevention of perioperative peripheral neuropathies: an updated report by the American Society of Anesthesiologists Task Force on prevention of perioperative peripheral neuropathies.Anesthesiology. 2011;114:741-754.

12. Preston DC, Shapiro B. Electromyography and Neuromuscular Disorders: Clinical Electrophysiologic Correlations. Philadelphia, PA: Elsevier; 2005.

13. Wippold FJ, Miller-Thomas MM, Cornelius RS, et al. ACR appropriateness criteria® plexopathy. Reston, VA: American College of Radiology; 2009.; accessed 2/14/14.

14. ACOG Task Force on Neonatal Brachial Plexus Palsy. Neonatal brachial plexus palsy. American Congress of Obstetricians and Gynecologists; Washington DC; 2013.

15. Washington State Department of Labor Industries. Work-Related Neurogenic Thoracic Outlet Syndrome: Diagnosis and Treatment. Olympia, WA: Washington State Department of Labor and Industries; 2010.

16. Chuang DC. Brachial plexus injury: nerve reconstruction and functioning muscle transplantation.Semin Plast Surg. 2010;24:57-66.

17. Choi PD, Novak CB, Mackinnon SE, Kline DG. Quality of life and functional outcome following brachial plexus injury.J Hand Surg.1997;22:605-612.

18. Zhou JM, Gu YD, Xu XJ, Zhang SY, Zhao X. Clinical research of comprehensive rehabilitation in treating brachial plexus injury patients.Chin Med J.2012;125:2516-2520.

Author Disclosure

Thiru M. Annaswamy, MD, MA
Nothing to Disclose

Jeremy Jones, MD
Nothing to Disclose

Related Articles