Jump to:



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. 1
    • 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
    • Infiltration from lung and breast metastases occur most frequently via lymphatics from the axilla 2,3
  3. Radiation-induced plexopathy
  • Can occur either via direct damage to the nerve or compression due to fibrosis of surrounding tissue 4,5
  • Proposed mechanisms of action include: occlusion of microvasculature, direct injury to myelin sheath/axon, endoneural and perineural fibrosis2,5
  • Delayed onset, progressive weakness and paresthesias. Pain may not be as significant as in neoplastic plexopathy3
  • More commonly affects upper trunk, possibly due to protective effect of clavicle2
  • See Radiation plexopathy topic for further information

Extrinsic brachial plexus compression

  1. Thoracic outlet syndrome (TOS)
  1. True Neurogenic TOS
    • Causes include congenital fibrous bands and rudimentary cervical ribs,
    • Lower plexopathy becomes stretched and angulated superiorly due to fibrous band from first thoracic rib to C7 rib or elongated C7 transverse process6
    • Presents with slowly progressive, unilateral, atrophic weakness of the thenar muscles and ulnar-innervated hand and forearm muscles, and pain in a lower trunk distribution (particularly T1)6
    • Motor weakness may not be apparent initially due to slowly progressive nature of process, allowing for reinnervation by collateral sprouting6
  2. Traumatic Neurovascular TOS
    • Rare, often secondary to mid-shaft clavicular fracture
    • Medial cord most susceptible to injury as it passes behind the middle segment of the clavicle
    • Acutely presets with pain, numbness in medial aspect of arm, forearm, and hand, weakness in ulnar and median-innervated muscles.7
  1. 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.
    • Most common nerves involved include long thoracic, axillary, suprascapular, and musculocutaneous nerves8
  2. 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, due to proximity to axillary lymph nodes and superior sulcus of lung3
    • Pancoast syndrome, seen most commonly with non small cell lung cancer in the superior sulcus, causes lower plexus weakness and Horner syndrome.9
  3. Trauma
    • Fractures, falls, objects falling on the shoulder, shoulder dislocation, and sports injuries are among many causes of traumatic plexus compression.

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 bilaterally10
  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 weakness10
  3. Axillary node dissections and orthopedic surgeries involving the clavicle/shoulder
    • Plexopathies result from direct injury or edema causing compression/entrapment.
    • Abduction greater than 90 degrees of an externally rotated and extended arm, stretches the plexus over the head of the humerus and the coracoid process11
  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 panplexus10

Epidemiology including risk factors and primary prevention

  1. The prevalence of cancer-associated plexopathies is 0.4%.12 Neurofibromas and schwannomas are the most frequent benign tumors, but direct extension of breast or lung cancer is more common1,5
  2. Radiation therapy to chest, neck, or axillary region increases risk for radiation-induced plexopathy, dose of <6000 cGy reduces risk2
  3. Rucksack palsy has been reported in soldiers, boy scouts, hikers, and manual laborers.13
  4. Neurogenic TOS has an estimated incidence of 1 per 1,000,000 and a female to male ratio of 9 to 1.6
  5. Iatrogenic plexopathies related to surgery account for 7% to 10% of brachial plexopathies.14
  6. NBPP has been reported to have an incidence of 0.38 to 5.1 per 1000 live births.15
  7. Positioning strategies during surgery reduce plexopathies. When possible, the head and neck should be kept in a neutral position without allowing lateral flexion, arms should be positioned by the patient’s side, and use of wrist restraints and shoulder plates should be limited. The patient’s position should be monitored throughout the procedure.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 electrodiagnostic or structural effect on the distal nerve1,6

The lesion site determines the following clinical patterns:1

  1. Panplexus
    • Weakness, sensory loss, and decreased or absent reflexes in the entire arm
    • Serratus anterior and rhomboids are usually spared if roots are intact1
  2. Upper trunk
    • Weakness primarily in C5-C6 innervated muscles, such as deltoid, biceps, brachioradialis, supraspinatus, and infraspinatus
    • Pronator teres (C6-C7) and triceps (C6-C8) may be affected due to partial upper trunk innervation
    • Sensory changes in the lateral arm and lateral forearm (axillary and lateral antebrachial cutaneous nerve distribution), as well as lateral hand and thumb (median and radial sensory branches)1
    • Biceps and brachioradialis reflex abnormal
  3. Middle trunk
    • Rare, mimics C7 radiculopathy as middle trunk is formed directly from C7 root.1
    • Weakness in the triceps, flexor carpi radialis, extensor digitorum communis, and pronator teres.
    • Sensory changes in the middle finger and posterior forearm
    • Abnormal triceps reflex.
  4. Lower trunk
    • Weakness in ulnar-innervated muscles, median C8-T1-innervated muscles (ie: abductor pollicis brevus, flexopr pollicis longus, flexor digitorum profundus), and radial C8-innervated (ie: extensor indicis proprius, extensor pollicis brevis) 1
    • Sensory changes in the medial arm, medial forearm, medial hand and digits 4 and 5.
    • Pure lower trunk plexopathy should not have reflex abnormalities
  5. Lateral cord
    • Weakness in pronator teres, flexor carpi radialis, and biceps. 1
    • Sensory changes in the lateral forearm, lateral hand and digits 1 through 3.
    • Abnormal biceps reflex.
  6. Posterior cord
    • Weakness in the arm and wrist extensors, deltoid, and latissimus dorsi.
    • Sensory changes in the lateral arm, posterior arm, posterior forearm, and radial dorsal hand. 1
    • Abnormal triceps and brachioradialis reflexes.
  7. Medial cord
    • Almost identical to lower trunk plexopathy, except for intact radial C8 fibers1
    • Weakness in all ulnar muscles and C8-TI median muscles, ie: abductor pollicis brevis, flexor pollicis longus, and flexor digitorum profundus.
    • Finger extensors are intact
    • Sensory changes in the medial arm, medial forearm, medial hand and digits 4 and 5.

Specific secondary or associated conditions and complications

  1. Erb-Duchenne palsy1
    • Most common type of brachial plexopathy in newborns
    • 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 palsy1
    • Characterized by weakness of the hand intrinsic muscles and ulnar-innervated muscles, with preservation of upper arm 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, radiation, 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.

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. Computerized tomography, used in patients who cannot undergo MRI, provides greater detail for bony abnormalities. Ultrasound is subsequently discussed in Cutting Edge Concepts and Practice.16

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 potential (SNAP) amplitudes may be abnormal in plexus lesions, but normal in root lesions. Compound muscle action potential (CMAP) amplitudes may be affected in both.1 There are several exceptions including the following:

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

F responses may have limited usefulness in the assessment of brachial plexopathies, as the upper extremity muscles tested are often innervated by multiple myotomes. With the presence of motor nerve fibers from unaffected myotomes, a normal F response may be conducted, as an abnormal F response requires all or most of the motor fibers to be affected.1

EMG of proximal and distal muscles is performed to determine lesion sites, which cause the following abnormal electrophysiologic patterns:1

  1. Upper trunk
    • Lateral antebrachial cutaneous (LAC) SNAP is abnormal in amplitude compared to contralateral side.
    • Radial sensory and median sensory studies may be abnormal.
    • Median motor and ulnar motor NCS are normal, and F responses are normal

EMG abnormalities seen in deltoids, biceps, brachioradialis,,supraspinatus and infraspinatus muscles. May additionally see abnormalities in triceps, pronator teres, and flexor carpi radialis1

  1. Middle trunk
    • Radial SNAP may be abnormal, median SNAP when recording middle finger may also be abnormal1
    • Median and ulnar motor NCS are normal.
    • EMG abnormalities seen in pronator teres, trieeps, flexor carpi radialis
  2. 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, as well as median and radial-innervated muscles containing C8/T1 fibers ie: flexor pollicis longus, abductor pollicis brevis, and extensor indicis proprius. 1
  3. Lateral cord
    • LAC and median SNAPs are abnormal.
    • Ulnar and median motor NCS are normal
    • EMG abnormalities seen in biceps, pronator teres, and flexor carpi radialis. 1
  4. Posterior cord
    • Radial SNAP is abnormal.
    • Median and ulnar motor NCS are normal.
    • EMG abnormalities seen in distal and proximal radial-innervated, ie: brachioradialis, triceps, extensor indicis proprious, extensor carpi radialis1
  5. 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 distal median-innervated muscles containing C8-T1 fibers, ie: APB, flexor pollicis longus1

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. After surgery for True Neurogenic TOS, motor recovery is limited as collateral sprouting is already maximal and the distance between lesion and denervated muscles is long(Ferrante 2016)
  5. Two thirds of rucksack palsies recover fully within 2 to 5 months.8 Classic postoperative paresis and postmedian sternotomy plexopathy generally have rapid, complete recovery.14


Available or current treatment guidelines

  1. Pain is treated using oral medications, including anti-epileptic drugs (such as gabapentin and pregabalin), tricyclic antidepressants (such as amitriptyline, nortriptyline, desipramine) and selective norepinephrine and serotonin reuptake inhibitors (duloxetine and venlafaxine). Other options include mixed opioid agonists with norepinephrine reuptake inhibition properties (tramadol and tapentadol), and pure opioid agonists.17
  2. Occupational and physical therapies assist in strengthening, range of motion, stretching, functional bracing/splinting, and physical modalities. The antigravity environment in aquatic therapy may facilitate recovery of movement.
  3. Specific treatment depends on the etiology.
    • Environmental and activity modifications reduce symptoms in rucksack palsy8
    • Surgery to alleviate the compression/entrapment may be required in neoplasms, TOS, and fractures.
    • True Neurogenic TOS is always treated surgically with band sectioning,6
    • Reconstruction surgery includes nerve repair, nerve grafts, nerve transfer, functioning free muscle transplantation, and tendon transfers. No specific guidelines exist regarding who should be referred for surgery. Timing of surgery is particularly important, as early reconstruction will impede ability for spontaneous recovery, but delay may elicit denervation atrophy making reinnervation unlikely.18
    • Conservative management, including symptom control and functional improvement, is used for those syndromes caused by surgery.

At different disease stages

Open nerve injuries

  • transected nerve should be repaired soon after injury (days) in order to reduce fibrosis, reduce tension, and maximize regrowth
  • If nerve transection exists secondary to fracture, fracture should be reduced

Direct nerve repair should be performed if sharp nerve division with minimal gap. 19

Closed nerve injuries

  • If by 6 weeks there is no spontaneous recovery – further evaluation should be obtained with imaging and EMG
  • If no evidence of reinnervation 3-6 months from injury, consider surgical exploration of the nerve.20

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.
  4. Sensory studies play a particularly important role, and there must be a 50% amplitude drop compared to the contralateral side to confirm plexopathy. Maintained evoked amplitude responses may predict earlier recovery.


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.16 Magnetic resonance neurography (MRN), available in some large academic institutions, increases visualization of individual plexus segments and peripheral nerves. In one study, MRN was found to change preclinical impression in 75.2% of patients, and substantially impacted care in 28% of patients.21

The most important factor in technical repair of peripheral nerves is thought to be repair without tension on the nerve.22 The development of nerve conduits using allograft and autograft strategies has been studied to minimize nerve tension. Due to the high donor site morbidity in autograft techniques, alternative methods are being studied which include stem cell implantation and use of growth factors to promote axonal regeneration.23


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. 19,20, 22,23 Guidelines for optimal candidates for surgery and timing for surgical intervention do not yet exist.


  1. Preston DC, Shapiro B. Electromyography and Neuromuscular Disorders: Clinical Electrophysiologic Correlations. Philadelphia, PA: Elsevier; 2005.
  2. Khadilkar SV and Khade SS. Brachial plexopathy. Ann Indian Acad Neurol. 2013 Jan-Mar; 16(1):12-18
  3. Custodio C. Electrodiagnostics in cancer rehabilitation. Phys Med Rehabil Clin N Am. 2017:28:193-203
  4. Iyer VR, Sanghavi DA, Merchant N. Malignant brachial plexopathy: A pictorial essay of MRI findings. J Radiol Imaging. 2010 Nov; 20(4):274-278
  5. Stubblefield MD. Neuromuscular complications of radiation therapy. Muscle & Nerve. 2017: 1031-1040
  6. Ferrante MA and Ferrante ND. The thoracic outlet syndromes: Part 1. Overview of the thoracic outlet syndromes and review of true neurogenic thoracic outlet syndrome. Muscle & Nerve. 2017:6
  7. Ferrante MA and Ferrante ND. The thoracic outlet syndromes: Part 2. The arterial, venous, neurovascular and disputed thoracic outlet syndromes. Muscle & Nerve. 2017:10
  8. Makela JP, Ramstad R, Mattila V, Pihlajamaki H. Brachial plexus lesions after backpack carriage in young adults. Clinical Orthopaedics and Related Research. 2006:452:205-209
  9. Das S, Ganju A, Tiel RL, Kline DG. Tumors of the brachial plexus.Neurosurg Focus. 2007;22:E26.
  10. Wilbourn AJ. Plexopathies.Neurol Clin. 2007;25:139-171.
  11. Thomas J. Post-operative brachial plexus neuropraxia: A less recognized complication of combined plastic and laparoscopic surgeries. Indian J Plast Surg. 2014 Sep-Dec; 47(3):460-464
  12. Jaeckle KA. Neurological manifestations of neoplastic and radiation-induced plexopathies.Semin Neurol. 2010;30:254-262.
  13. Nylund T, Mattila VM, Salmi T, Pihlajamaki HK, Makela JP. Recovery of brachial plexus lesions resulting from heavy backpack use: a follow-up case series.BMC Musculoskelet Disord. 2011;12:62.
  14. Desai KR, Nemcek AA. Iatrogenic brachial plexopathy due to improper positioning during radiofrequency ablation. Semin Intervent Radiol. 2011;28(2):167-170
  15. 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.
  16. Bykowski J, Aulino JM, Berger KL et al. ACR appropriateness criteria® plexopathy. J Am Coll Radiol. 2017;14(5S):S225-S233
  17. Gilron I, Baron R, Jensen T. Neuropathic pain: Principles of diagnosis and treatment. Mayo Clinic Proc. 2015;90(4):532-545
  18. Limthongthang R. Bachoura A, Songcharoen P, Osterman AL. Adult brachial plexus injury. Orthopedic Clinics of North America. 2013;44:591-603
  19. Griffin JW, Hogan MV, Chhabra AB, Deal DN. Peripheral nerve repair and reconstruction. The Journal of Bone and Joint Surgery, 2013: 2144-2151
  20. Houdek MT, Shin AY. Management and complications of traumatic peripheral nerve injuries. Hand Clin 31:2015:151-163
  21. Fisher S, Wadhwa V, Manthuruthil C. Clinical impact of magnetic resonance neurography in patients with brachial plexus neuropathies. Br J Radiol. 2016;89(1067)
  22. Palispis WA and Gupta R. Surgical repair in humans after traumatic nerve injury provides limited functional neural regeneration in adults. Experimental Neurology.2017:106-114
  23. Fowler JR, Lavasani M, Huard J, Goitz RJ. Biologic strategies to improve nerve regeneration after peripheral nerve repair. Journal of Reconstructive Microsurgery. 2014

Original Version of the Topic

Thiru M. Annaswamy, MD, MA, Jeremy Jones, MD. Brachial Plexus Compressive / Entrapment. Original publication date: 9/20/14

Author Disclosure

Julia Reilly, MD
Nothing to Disclose

Jennifer A. Baima, MD
Nothing to Disclose