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Brachial plexopathy is an injury of the brachial plexus, that is commonly caused by trauma.1

Brachial plexus is a peripheral nervous system structure that extends from the cervicothoracic spinal cord to the axilla and provides motor, sensory, and autonomic innervation to the upper extremities. From proximal to distal, its elements are the following:

  • Roots: ventral rami of cervical roots C5-8 and T1*
  • Trunks: upper (C5-6), middle (C7), and lower (C8-T1)
  • Divisions: 3 anterior divisions and 3 posterior divisions
  • Cords: lateral, posterior, and medial
  • Terminal branches
    • Roots: Long thoracic (C5-7) and dorsal scapular (C5)
    • Trunks: Suprascapular (C5-6)
    • Lateral cord: lateral pectoral (C5-7), musculocutaneous (C5-7), lateral antebrachial cutaneous (C5-6), and lateral branch of the median
    • Posterior cord: upper and lower subscapular (C5-6), thoracodorsal (C6-8), axillary (C5-6), and radial (C5-T1)
    • Medial cord: medial pectoral, medial brachial cutaneous, medial antebrachial cutaneous, ulnar, medial branch of the median (all C8-T1)

* Anomalous innervation is also possible. A “pre-fixed” brachial plexus is formed predominantly from the C4-C7 roots, and a “post-fixed” brachial plexus is formed predominantly from the C6-T2 roots.2

For purpose of treatment and prognosis, the injury on the plexus is divided into

  • Supraclavicular: most common site, involves the root or trunk level3
  • Retroclavicular: least common site, involves the divisions1
  • Infraclavicular: involves the cords or terminal branches1

Based on whether the injury is proximal or distal to the dorsal root ganglion (DRG), they are further characterized as preganglionic and postganglionic, respectively. Clinically, preganglionic injuries (e.g., root avulsions) can be associated with Horner syndrome (disruption of the autonomic trunk), medial scapular winging (injury to long thoracic and dorsal scapular nerve), and denervation of the cervical paraspinal muscles. Root avulsion occurs in up to 75% in supraclavicular lesions.3 Postganglionic injuries typically carry a better prognosis because they often demonstrate greater spontaneous recovery and are more amenable to surgical repair.1


The etiology is variable.1,4


  • Trauma
  • Compression
  • Iatrogenic
  • Radiation
  • Neoplasm
  • Paraneoplastic
  • Infection
  • Autoimmune reaction


  • Congenital malformation
  • Genetic predisposition:
    • hereditary neuropathy to pressure palsy: PMP22 genetic mutation
    • hereditary neuralgic amyotrophy (NA): a point mutation in the SEPT9 gene on 17q25

Epidemiology including risk factors and primary prevention


2 to 3 per 100,000 1


Demographics for brachial plexus injury depend on the etiology of injury. Traumatic injuries are more common in males aged between 15 and 25 years.5 Like traumatic spinal cord injury, these injuries are most often associated with motor vehicle and often motorcycle collisions.6 In adults, the most common cause of brachial plexus injury is trauma, either by compression or traction.3


  • Traumatic: up to 70% from motor vehicle accidents and 22%-49% of athletes in contact sports
  • Compressive: 5.3% in active military (rucksack syndrome), approximately .0001% neurogenic thoracic outlet syndrome
  • Neoplastic: 0.4%
  • Paraneoplastic: 0.5% to 10%
  • Radiation induced: 1% to 14%
  • Obstetrical: 0.4%



Mechanical injury to the myelin sheath or axon itself resulting from traction, compression, or transection.

  • Burner or stinger syndrome: transient and often mild loss of strength or sensation, most often in the C5-6 distribution, secondary to traction, compression injury or direct blow to the brachial plexus without complete avulsion. Common in contact sports and the most common reported peripheral nerve injury in American Football, occurring in 59-70% of all players1,7,10
  • Midshaft clavicular fracture: transection or compression injury to the cords or divisions of the brachial plexus sometimes associated with a subclavian pseudoaneurysm.1,11
  • Shoulder dislocation: compression injury, most commonly affects the axillary nerve, can also affect the posterior cord and musculocutaneous nerve.11,12

Penetrating injuries: by a knife wound, shrapnel, bullet (often a transection), or subsequent hematoma (compression). Commonly affects the infraclavicular plexus.1,11


  • Thoracic outlet syndrome: typically, a compression injury, commonly affecting the lower plexus. It is caused by narrowed thoracic outlet, possibly because of cervical rib (likely a fibrous band running from a rudimentary cervical rib to the first thoracic rib) or hypertrophied anterior scalene or ischemic injury caused by restricted flow through the subclavian artery.2,13
  • Rucksack syndrome: compressive/traction injury, commonly of the upper plexus, with painless weakness and numbness caused by depression of the shoulders while wearing a heavy backpack.1,14


Traction or compression injury most commonly of C5-7 nerve roots associated with shoulder dystocia and excessive lateral flexion of the head and neck, malpositioning, and increased birth weight. Primarily an iatrogenic complication at delivery, although there is some evidence for congenital brachial plexopathy related to in utero fetal position.1, 15, 16

  • Erb palsy: injury to C5-6 (most common)
  • Erb plus palsy: C5-7
  • Flail arm: C5-T1 with Horner syndrome
  • Klumpke palsy: C8-T1 with Horner syndrome


  • Postoperative: compressive injury, often of the upper plexus, caused by patient positioning, less commonly a mechanical or ischemic injury caused by axillary anesthetic block, transaxillary arteriography, or postoperative hematoma.1
  • Poststernotomy: compressive injury, usually affecting C8 and the medial cord, following median sternotomy for cardiothoracic surgery, associated with 1st rib fracture.1


Clinical presentation of plexopathy typically delayed from time of radiation by months to years, depending on type of plexopathy (early transient radiation-induced plexopathy v. delayed radiation-induced plexopathy). Plexopathy results from direct axonal damage, demyelination, and microvascular infarction and more indolently because of compression caused by fibrosis, commonly seen following radiation therapy for breast, lung, lymphoma, and head and neck cancer. Concurrent chemotherapy is associated with increased risk for brachial plexopathy especially with increasing total dose (>50 Gy) and fractional dose (>2 Gy) of radiation. The incidence of radiation-induced plexopathies has decreased with tissue-sparing targeted radiotherapy.

  • Chemotherapy:20-22 Multiple chemotherapeutic agents are known to be neurotoxic including taxanes (e.g. paclitaxel, docetaxel), vinca alkaloids (e.g. vincristine, vinblastine), platins (e.g. cisplatin, oxaliplatin). While these agents are more commonly associated with length-dependent peripheral polyneuropathies, when used in conjunction with radiation therapy or other drug therapy, they may increase the risk of brachial plexus injury.

Primary neoplastic:

Compression injury arising from schwannomas or neurofibromas, usually benign, commonly affect the upper or middle plexus.1

Secondary neoplastic

Compressive or invasive injury usually arising from breast or lung cancer or metastasis to the axillary lymph nodes, usually malignant, commonly affects the medial cord or its terminal branches.1


Primarily demyelinating injury, caused by myelin and neuronal cross-reacting antibodies against tumor antigens, commonly associated with Hodgkin lymphoma.1,8


Known as brachial neuritis, neuralgic amyotrophy (NA), or Parsonage-Turner syndrome, most often affects the upper and middle trunks with involvement of the spinal accessory, long thoracic and suprascapular nerves. Males are approximately two times more commonly affected than females.23 Classically presents with severe upper arm pain, followed by multifocal paresis (usually in a different territory as the pain), possible sensory abnormalities, and gradual atrophy of muscles innervated by the affected plexus. Most affected individuals recover, but some will have persistent pain or weakness, believed to be caused by peripheral myelin cross-reacting antibodies and complement, often, but not always, associated with recent parvovirus or Bartonella henselae infection,1,24 immunization, surgery, and childbirth. Even with severe initial injury, electrodiagnostic evidence of recovery is expected within 6-9 months with many showing full re-innervation by one year.14 Recurrence rates have been reported at 5-26%.

Rarely, diabetic patients can experience brachial plexopathy as a result of microvasculitis induced ischemic nerve damage, usually seen in conjunction with lumbosacral plexopathy.25


Hereditary NA presents similarly to idiopathic NA (previously described), but it is frequently recurrent and increased in incidence in certain familial lineages. Of the affected patients, 55% carry a point mutation in the SEPT9 gene on 17q25.24 Neuralgic amyotrophy is a rare disorder that has a reported incidence of 2-3 per 100,000. However, it is thought to be under diagnosed.67

Specific secondary or associated conditions and complications

Paraneoplastic syndrome and NA commonly affect additional peripheral nerves outside the brachial plexus distribution.1,8

Phrenic nerve injury may occur in conjunction with traumatic and non-traumatic plexopathies and may present as hemi-diaphragmatic elevation on chest x-ray.19,23 Approximately 2-6% of babies with neonatal brachial plexopathy will have a concurrent phrenic nerve palsy, which is also a predictor of worse motor recovery23,26.

Traumatic root avulsions may occur in conjunction with brachial plexus injuries in the context of high-energy stretch. Lower roots (C8-T1) are the most susceptible to avulsion. It is important to differentiate root avulsion from brachial plexus injury for treatment and prognostication as complete root avulsions are incapable of regeneration and are not amenable to surgical repair.1

Neonatal brachial plexopathy may be associated with glenohumeral joint dysplasia, joint contractures (shoulder, elbow, supination), posterior shoulder dislocation, or length discrepancies.27,28

Essentials of Assessment


  • Duration of symptoms
  • Characteristics of pain, sensory changes, weakness, and muscle atrophy
  • Infection, activity, or injury associated with onset
  • Change in symptoms with change in head, neck, or arm position
  • Autonomic symptoms
  • Change in function (activities of daily living [ADLs], sports performance, etc.)
  • Personal or familial history of neoplasm, radiation, chemotherapy, demyelinating disorders, diabetes or previous brachial plexopathy
  • Details of pregnancy and delivery in neonatal patients

Physical examination

  • Standardized neurologic examination
    • Tests of manual muscle strength, sensation, and reflexes commensurate with the affected portions of the plexus
    • May include Tinel sign over the brachial plexus
  • Vascular: these exam maneuvers are primarily useful in evaluating for vascular etiologies of brachial plexopathy, including vascular thoracic outlet syndrome (TOS).
    • Radial, ulnar, and carotid pulses
    • Allen test: positive if reperfusion of the hand is delayed greater than 7 seconds
  • Special tests:
    • Adson test:29,30 The Adson test is performed by passively extending, abducting and externally rotating the affected arm while palpating the radial pulse. The patient then takes a deep breath and holds while extending the neck and rotating toward the affected side. The test is positive when there is a decrease or disappearance of the radial pulse. The test is sensitive (up to 94%) but has relatively poor specificity (18-87%) for TOS.
    • Roo test31,32: The Roo test is performed with the patient’s arms in 90 degrees of abduction and external rotation and the shoulder and elbows in the frontal plane of the chest. The patient is asked to open and close their hands repeatedly for 3 minutes. The test is considered positive for TOS if it induces progressive pain in neck to shoulder to arm, paresthesia in the forearm or fingers, arm pallor when elevated and hyperemia when lowered (vascular TOS), or reproduction of the usual symptoms that involve the entire arm. The test has a reported sensitivity of 84% and specificity of only 30% given possible provocation of symptoms of other pathologies including carpal tunnel syndrome, cervical disc disease and shoulder problems.

Functional assessment

Assess for specific deficits in the following:

  • ADLs
  • Fine motor skills
  • Occupational and recreational activities
  • Adaptive equipment/assistive devices

Laboratory studies

There are no required laboratory analyses in the work-up of brachial plexopathy however basic laboratory assessments may be helpful in ruling out alternative causes of weakness or in looking for triggers of NA.

  • LFTs may be elevated in cases of NA associated with Hepatitis E virus infection
  • Serology for Borrelia bugdorferi, Bartonella henslae or HIV as precipitants of NA in the correct clinical context.23 Genotyping for suspected hereditary NA.24
  • Anti-Hu, Yo, CV2/CRMP-5, Ma2, Tr, Ri, or amphiphysin antibody enzyme-linked immunosorbent assay in suspected paraneoplastic syndrome.8


  • Radiograph: cervical spine fracture, clavicle fracture, first rib fracture, scapular fracture, presence of cervical rib, shoulder dislocation, elongated C7 transverse process, superior sulcus lung mass.1,3,23
  • Magnetic resonance imaging: 93% sensitive for avulsion injuries, 60% sensitive for all causes of brachial plexopathy, evaluates for tumor, hematoma, metastatic disease, mechanical disruption of the brachial plexus.33,34
  • Magnetic resonance neurography: evaluation of intrafascicular or extrafascicular pathology of the brachial plexus and terminal branches.35
  • Computed tomography with contrast: bony injury, metastatic disease, root avulsion.1 It is the gold standard for evaluation for root avulsions.3
  • Ultrasound: 76% sensitive and 96% specific for detection of brachial plexopathy, evaluates for vascular insufficiency, hematoma, pseudoaneurysm, anterior scalene hypertrophy.36 A recent case report demonstrates use of ultrasound in treatment planning for neonatal brachial plexus injury.37
  • Positron emission tomography evaluates for body-wide malignancy.1,8

Supplemental assessment tools


Sensory nerve action potentials: help anatomic localization

  • C5 DRG: lateral antebrachial cutaneous (LAC)
  • C6 DRG: superficial radial
  • C7 DRG: median (third digit)
  • C8 DRG: ulnar (fifth digit)
  • T1 DRG: medial antebrachial cutaneous (MAC)
  • Upper trunk: LAC, median (thumb)
  • Middle trunk: superficial radial
  • Lower trunk: ulnar (fifth digit), MAC
  • Lateral cord: LAC, median (thumb), median (second digit)
  • Posterior cord: superficial radial
  • Medial cord: ulnar (fifth digit), MAC

Compound motor action potentials:

  • Upper trunk: musculocutaneous (biceps), axillary (deltoid)
  • Middle trunk: radial (anconeus)
  • Lower trunk: ulnar (abductor digiti minimi [ADM] and first dorsal interosseous [FDI]), median (abductor pollicis brevis [APB]), radial (extensor indicis [EI])
  • Lateral cord: musculocutaneous (biceps)
  • Posterior cord: axillary (deltoid), radial (extensor digitorum [ED], EI, and anconeus)
  • Medial cord: ulnar (ADM, FDI), median (APB)

Evoked potentials: Evoked potentials are not necessary in the diagnosis of brachial plexopathy however they may be helpful in ruling out a more central process. Intraoperative neurophysiology may help in diagnosing root avulsions and determining viable donor nerve for surgery in the event of equivocal pre-operative studies.38


  • Upper trunk: supraspinatus, infraspinatus, biceps, deltoid, triceps, pronator teres, flexor carpi radialis (FCR), brachioradialis, extensor carpi radialis (ECR)
  • Middle trunk: pronator teres, FCR, triceps, ECR, ED
  • Lower trunk: APB, flexor pollicis longus, pronator quadratus, FDI, ADM, flexor digitorum profundus, flexor carpi ulnaris (FCU)
  • Lateral cord: biceps, pronator teres, FCR
  • Posterior cord: latissimus dorsi, deltoid, triceps, brachioradialis, ECR, ED, EI
  • Medial cord: APB, flexor pollicis longus, FDI, ADM, FCU, flexor digitorum profundus

Single fiber EMG: generally, not required in a brachial plexopathy work-up unless there is strong concern for a neuromuscular junction disorder.2

Early predictions of outcomes

In general, infraclavicular lesions have better prognosis than supraclavicular lesions and nerve root avulsions have little chance of spontaneous recovery.39 The presence of atrophy and weakness on clinical exam and axon loss on nerve conduction studies suggest severe injury and consequently a worse prognosis. Axon loss is best determined during nerve conduction studies by decreased amplitude in comparison with the contralateral side (if unaffected). The axonal viability index, the ratio of amplitude of the involved side to the unaffected limb, has been used for electrodiagnostic prognostication in newborns.40 An axonal viability index <10% for the axillary nerve, <20% for the proximal radial nerve and <50% for the distal radial nerve were shown to have poorer outcomes. Multiple authors have also used a modified Dumitru and Wilbourn scale to classify the severity of brachial plexus injury as mild, moderate, and severe based on SNAP and CMAP amplitudes.41

Spontaneous recovery is rare with complete axonal discontinuity, manifested by complete absence of CMAPs, absence of motor unit action potentials (MUAPs) despite good effort, and abnormal spontaneous activity.2 With complete conduction block, MUAPs may be absent but distal CMAPs should still be present without significant abnormal spontaneous activity.38 It is important to note that many of the proximal nerves cannot be directly assessed, and root stimulation studies are necessary to detect proximal conduction block.

The number of fibrillation potentials and positive sharp waves on electromyography testing does not predict the severity of injury. Such abnormal spontaneous activity represents spontaneous depolarization of a muscle fiber in the setting of any kind of denervation. It may be seen in a primary demyelinating disorder with secondary axonal loss or a primary axonal injury.2


Identification and avoidance of repetitive activities, extreme range of motions and excessive load carriage via shoulder straps that induce pain or weakness is critical. No equipment or strengthening has been proven to decrease the risk of brachial plexus injury.10

Workplace modifications and assistance with transportation may need to be addressed.

Social role and social support system

A recent publication about patient reported outcomes of health-related quality of life after neonatal brachial plexus suggests that physical limitations, followed by social health, and to a lesser degree, emotional health remain significant long-term issues in these patients.42

Depression: Rates of depression are higher among those with traumatic brachial plexus injury, commonly reported around 30%, which may also reflect a high rate of concurrent TBI.43 Indeed, traumatic brachial plexopathy has been associated with anger, frustration, pain, unemployment, social isolation, and change in body image.44 Importantly, like back pain literature, patients with comorbid depression and brachial plexus injury have poorer outcomes in rehabilitation.43

Marriage status: In one study of 34 patients who had undergone surgical treatment for brachial plexus injury a mean of 7 years prior, 47% were married at the time of the survey and 65% of participants had been married at least once. Most stated that their brachial plexus injury had little or no role in their relationships.45

Professional issues

Return to work (RTW): needs careful evaluation of time since injury, nature and extent of recovery, current deficits and functional status, and work environment. RTW status should be determined only after maximum medical improvement. Functional capacity evaluation can be a useful tool to determine accurate restrictions and RTW.

Rates of employment do seem to be affected by injury. In Choi et al’s functional outcome study, 18/34 patients were working at the time of the survey (mean 7 years after injury). Of the 24 who were employed prior to injury, 13 returned to work and 8 within the first year of injury. Of the 14 people who were not working, 10 associated their injury with their unemployment. Of note, these authors found that motor function and functional status did not correlate with employment.45

The presence of brachial plexus injury in polytrauma is of poor prognostic significance. Analysis of outcomes 10 years after trauma reveals that those with brachial plexus injury have lower rates of employment and worse outcome scores.46

Return to play: in athletes, careful evaluation and counseling are required prior to clearing the athlete to return to play.7

Rehabilitation Management and Treatments

Available or current treatment guidelines


Approximately 25% of adults who have a brachial plexus injury will suffer from severe neuropathic pain that can last for years.3 Neuropathic pain secondary to brachial plexopathy may respond to the following medications:

  • Gabapentin
  • Pregabalin
  • Amitriptyline
  • Duloxetine
  • Opioids


Non-pharmacologic pain management alternatives include the following:

  • Topical agents e.g., Lidocaine patch or ointment
  • Transcutaneous electrical nerve stimulation, H-wave therapy
  • Desensitization therapy
  • Pulsed radiofrequency ablation/dorsal root entry zone thermocoagulation47
  • Sympathetic blockade
  • Spinal cord stimulator or peripheral nerve stimulator


  • Surgical management:1,48,49 Options include direct end to end repair, neurolysis, nerve grafting and nerve transfer (neurotization). Surgical management should generally be done within 6 months of injury.5 A systemic review done in 2017 looking at 43 studies found that in stretch and blunt injuries to the brachial plexus, found that the optimal time for surgical correction is between 3 and 6 months.50
    • Timing is a crucial factor in determining the outcome after surgery as the distal nerve and the neuromuscular junction become increasingly incapable of accepting reinnervation by 20–24 months.
    • In post-ganglionic injury, it is prudent to wait for 3–4 months for spontaneous improvement to occur. The best chance of improvement is in the first 3 months after injury and the next best time window is within the next 3 months.
    • The indications for immediate/early repair (within 3–4 weeks postinjury) are (i) sharp, open injury, (ii) associated vascular injuries, (iii) flail limb with severe deafferentation pain, and (iv) preganglionic injury with pseudomeningoceles on magnetic resonance myelography.51
    • A provisional plan for reconstruction, usually aimed at providing elbow flexion and shoulder abduction and external rotation, is made. Potential donors for nerve transfers are considered and availability of these checked.
    • Pre-operative electromyography (EMG) of muscles innervated by potential donor nerves may be helpful in identifying subclinical injury to these nerves.52
    • Early traumatic brachial plexopathy
      • Neurolysis/Nerve graft
        • Transection/severe axonal injury: with no return of motor function (nerve grafts shown to be most effective within the first 8 weeks)
        • Traction/mild to moderate axonal injuries: early nerve graft is controversial.
        • Most utilized is the sural nerve. Graft length of graft of 6–8 cm is acceptable for obtaining satisfactory results, as results are poorer for more extensive lesions requiring longer graft lengths.53
    • Late traumatic brachial plexopathy
      • Tendon transfer
      • Free muscle transfer
  • Surgical complications:54 Nerve transfers for brachial plexus injury are not without complication risk. Nerve transfers may borrow from other important nerve such as the phrenic nerve, intercostal nerves, and spinal accessory nerve. In one functional outcomes study, the rate of hemidiaphragm paralysis or elevation (1-1.5 intercostal spaces) was 84% on the surgically treated side however no pulmonary problems were reported in the postoperative period. Other complications included transient finger and thumb paresthesia (57%) and wound infection (3%).
  • Outcomes and rehabilitation after surgery:
    • To date, outcome reporting for brachial plexus surgery has largely centered on motor recovery and typically has not included measures of function or non-musculoskeletal recovery.55 The available literature is significantly limited by small sample sizes and retrospective studies. For preganglionic injuries, Kline et al found that 40% of C5-6 injuries spontaneously recovered in 3 to 4 months, whereas 15% of C5-7 injuries recovered in 3 to 4 months, and only 5% of flail arms (C5-T1) had functional recovery. Thus, preganglionic total arm brachial plexus injury seems to be the type of injury that may benefit most from earlier nerve reconstruction procedures, especially for hand function reconstruction, which can be obstinate to treatment.56
      In general, partial injuries have a better outcome in a majority of cases, while the results in global avulsions are not very satisfactory.51 In one retrospective review, patients who underwent nerve transfers after traumatic global brachial plexus avulsion scored consistently better on the DASH score and NRS score than those before surgery. There was also a significant correlation between the change in NRS scores and patient satisfaction.54 In another large retrospective review of over 300 patients that underwent brachial plexus surgery, eighty-seven percent of patients were satisfied with the results and 83% would undergo the procedure again.57 In upper brachial plexus injury in adults, specifically, per a systematic review by Ali et al, the Oberlin procedure and nerve transfers are the more successful approaches to restore elbow flexion and shoulder abduction, respectively, compared with nerve grafting or combined techniques.58 In a study done by Rasulic et al., sixty-nine patients who underwent surgical correction for brachial plexus injury participated in a quality of life study looking at functionality, pain, quality of life, patient satisfaction, and psychosocial health.59 Of the patients who underwent only exploration and neurolysis, 35.3% showed a good quality of recovery; whereas patients who underwent nerve reconstruction using nerve grafting had a better rate of good quality recovery at 56.7%.59 Sixty-nine percent of patients continued working after surgery. About 76% reported having pain regularly and 18.8% reported depression or anxiety.59
    • Clear rehabilitation protocols have not been defined in the literature for post-brachial plexus repair rehabilitation and close communication between the surgical and rehabilitation teams is essential to optimize outcomes.
  • Nonsurgical management:1,60
    • Occupational therapy
    • Functional bracing/orthotics


  • Prevention: relies on physical and occupational therapy with patient/family adherence to range of motion programs.
  • Management:
    • Non-operative:28,61 Splinting and serial casting have been employed following brachial plexus birth palsy in elbow flexion contracture prevention and management. Serial casting may initially improve more severe contractures and nighttime splinting may be effective in preventing contracture progression.
    • Operative:62 Children with brachial plexus birth palsy demonstrate improved short- and long-term functional outcomes if they undergo internal contracture release and/or muscle tendon transfer procedures.


Slings and cautious positioning may be helpful in cases of flail arm to prevent secondary nerve and limb injury.

Etiology-specific treatment

  • Neuralgic amyotrophy:23
    • Conservative/symptomatic
      • Analgesia (usually multiple agents are required, often including an opioid)
      • Immunomodulation (limited evidence suggests that early treatment with high dose prednisone may shorten pain duration and improve functional recovery)
    • Surgical
      • Neurolysis
        • Especially for patients with hourglass nerve constriction
      • Resection and grafting
  • Radiation-induced brachial plexopathy:17,49,60
    • Early
      • Heparin or warfarin may prevent microvascular infarction
      • Neurolysis may relieve compression caused by fibrosis
      • Hyperbaric oxygen does not appear to be an effective treatment
    • Late
      • Nerve graft
      • Tendon transfer
      • Free muscle transfer
  • Paraneoplastic brachial plexopathy:8
    • Oncologic management, as indicated
    • Intravenous immunoglobulin
    • Plasmapheresis
    • Immunomodulators: prednisone and azathioprine (unclear but may increase risk of tumor progression)
  • Obstetrical brachial plexopathy:1,63
    • Rates of spontaneous recover range from 66-92%9
    • Up to 35% of children will have residual shoulder weakness, contracture, or joint deformity9
    • Primarily conservative management: passive range of motion and activity requiring bilateral extremity involvement, this consists of occupational therapy, splinting, and kinesiotaping9
    • Chemodenervation with botulinum toxin type A can be effective in modulating the muscle imbalance that occurs in the affected arm9
    • Nerve graft (commonly performed if no improvement in 3-9mo, evidence is unclear if early nerve grafts results in improved outcome)
    • Nerve transfer/Neurotization (infants who underwent nerve transfer with Narakas grade 1 brachial plexopathy had similar long-term gross motor outcomes in shoulder abduction and elbow flexion compared to those who improved without requiring surgery).26,64

Coordination of care

An integrated care team should include a physiatrist, neurologist, neurosurgeon, hand surgeon, occupational therapist, physical therapist, electro-diagnostician, pain specialist, and possibly an oncologist or pediatric neurologist. Resources, including psychology, vocational rehabilitation, ergonomics, and driver training, can be included as necessary.

Patient & family education

Counseling regarding etiology, treatment options, prognosis for recovery, and prevention of secondary complications is a critical component for the overall plan of care.

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

  • Sensory nerve action potentials are more sensitive than compound motor unit action potentials to determine axonal loss in brachial plexopathy.1
  • Electromyography is critical for localizing the injured portion(s) of the brachial plexus.1
  • Myokymic discharge helps to differentiate radiation induced from neoplastic brachial plexopathy.2,65
  • The efficacy of nerve grafts after traumatic brachial plexopathy diminishes with time after 8 weeks.48

Cutting Edge/ Emerging and Unique Concepts and Practice

Recent evidence indicates that successful surgical management can cause dynamic changes within the brain resting state networks, which includes not only the sensorimotor network but also the higher cognitive networks such as the salience network and default mode network, which indicates brain plasticity and compensatory mechanisms at work66

Gaps in the Evidence-Based Knowledge

Although the standard of care in managing traumatic brachial plexopathies is to delay nerve grafts for 3 to 6 months while monitoring for recovery, there is emerging evidence to suggest that delaying beyond 2 months might result in poor outcomes. However, nerve grafts performed at earlier time points may result in unnecessary surgery in individuals who would otherwise demonstrate some degree of spontaneous recovery. Further research is needed to assist in determining prognosis before 2 months and establishing the most effective timing for surgical intervention.


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Original Version of the Topic

Ninad S. Karandikar, MBBS, Michael J. Burns, MD. Brachial Plexopathy: Differential Diagnosis and Treatment. 9/20/2013

Previous Revision(s) of the Topic

Ninad S. Karandikar, MBBS, Elissa Zakrasek, MD. Brachial Plexopathy: Differential Diagnosis and Treatment. 8/16/2017

Author Disclosure

Clarice Sinn, DO, MHA
Nothing to Disclose