Author(s): Marisa Osorio, DO, Nitin Bajaj, DO
Originally published: November 10, 2011 Last updated: February 5, 2025
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Disease/Disorder

Definition

Neonatal brachial plexus injury (NBPI) is also referred to as neonatal brachial plexus palsy (NBPP), birth brachial plexus palsy (BBPP), obstetrical brachial plexus injury (OBPI), and brachial plexus birth injury (BPBI). NBPI involves either part of or the entire plexus and leads to a varying degree of sensory and motor impairment in the affected upper extremity.1-8

Etiology

Neonatal brachial plexus injuries most commonly occur as a result of the labor and delivery process, where traction forces can cause disruption of the neural structure, including avulsion or rupture.8,9 Non-traumatic etiologies include maternal uterine malformation, placental insufficiency, familial congenital brachial plexus palsy, congenital varicella syndrome, osteomyelitis of the humeral head, presence of a cervical rib, or mass effect from tumor.1

Epidemiology including risk factors and primary prevention

Globally, NBPI incidence ranges between 0.4 and 4.6 per 1,000 live births.1 There appears to be increased risk of NBPI in non-white patients and patients of lower socioeconomic status.1-4,10 In the United States, retrospective analysis of the Kids’ Inpatient Database from 1997 to 2012 revealed a steady, dramatic reduction (47.1%) in NBPI population incidence from 1.7 to 0.9 per 1,000 live births.1-5 This marked reduction has been paralleled by increases in cesarean delivery rates (62.8%). Cesarean delivery may reduce the risk of vaginal delivery related shoulder dystocia and traction injury and may also be associated with earlier gestational age birth and lower birth weights as evidenced by concurrent down trending fetal macrosomia rates during the study period.2 Alterations in obstetric training and management as well as increased rates of multiparous births may also have contributed to the dramatic reduction.1

Risk factors can be divided into the following categories 1-5,9,10

  • Neonatal
    • Shoulder dystocia
    • Fetal macrosomia (birth weight > 4.5 kg)
    • Breech delivery
    • Neonatal diabetes
  • Maternal
    • Gestational diabetes
    • Age > 35 years
    • Obesity or excessive weight gain
    • Abnormal pelvic anatomy
    • Previous infant with NBPI 
  • Birth Related
    • Prolonged labor
    • Instrumented birth (forceps or vacuum extraction)

Up to 71% of patients had no risk factor3 and 46-54% of cases occur in the absence of shoulder dystocia.4 Primary prevention includes early recognition of risk factors. Additionally, training programs emphasizing proper implementation of preventive obstetric maneuvers in response to complicated deliveries are recommended.

Patho-anatomy/physiology

Briefly, the brachial plexus is an intricate network of peripheral nerves supplying the upper extremity with motor and sensory innervation. The brachial plexus includes the ventral rami of nerve roots C5-T1, which become the upper, middle, and lower trunks; followed by the anterior and posterior divisions; the lateral, medial, and posterior cords and terminate as branches that extend to the muscle.

NBPI can be classified anatomically according to nerve root involvement (Narakas Classification) or according to the degree of nerve damage (Seddon Classification).1,9

Narakas classification1,3,5

  • Type I: C5-C6 (Erb’s palsy)
    • Presents with weakness in shoulder external rotation, abduction, and elbow flexion; “waiter’s tip” posture: shoulder adducted and internally rotated with elbow extended and forearmpronated1,3
    • Most common; affects about 46% of patients
    • Best outcome; about 80% have full recovery
  • Type II: C5-C7 (Extended Erb’s palsy)
    • Presents as above with addition of weakness with wrist and elbow extension6
    • Affects about 30% of patients
    • About 60% have full recovery
  • Type III: C5-T1 (global plexus involvement, “flail limb”)
  • Type IV: C5-T1 (global plexus involvement, “flail limb,” plus Horner’s syndrome)
    • Together, types III and IV affect about 20% of patients
    • Worst outcome, limited potential for spontaneous recovery, most do not make complete recovery; may benefit from surgery1,4,7
  • Isolated C8-T1 involvement (Klumpke’s palsy) is very rare in the setting of modern obstetric practice. It has been associated with breech deliveries in the past. It is not typically included in the Narakas classification.
    • If present, clinicians should consider anatomic anomaly (cervical rib), prior complete plexus injury with partial resolution, and central nervous system etiology.

Seddon classification1,6,9

  • Neurapraxia: damage to myelin sheath, intact axon and connective tissue structures. Represents completely reversible loss of nerve conduction.
  • Axonotmesis: damage to myelin sheath and axon, variable connective tissue structure involvement. Represents an intermediate form of injury with recovery difficult to predict.
  • Neurotmesis: damage to myelin sheath, axon, and all connective tissue structures. Represents total and complete disruption of the nerve via avulsion (preganglionic) or rupture (postganglionic).

Seddon classification differentiation is critically important as it portends different potential for recovery. Neurapraxia and axonotmesis have potential for spontaneous recovery. Neurotmesis cannot recover spontaneously and requires surgical intervention.

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

Clinical presentation and prognosis are variable and dependent upon the anatomical location and severity of NBPI. Serial physical examination remains the gold standard for diagnosis and prognosis.3,5

The following are pertinent estimates.1,4,6

  • Most infants will have full spontaneous recovery (reportedly up to 70%); however, full recovery without sequalae may be lower. Most recovery occurs within the first year of life.
  • At least 10- 30% remain with residual deficits such as weakness, contracture, and impaired function.
  • 20-30% typically require surgical intervention.

Specific secondary or associated conditions and complications

Two of the most common secondary sequelae are torticollis 11 related to shoulder dystocia and scapular winging due to injury to the long thoracic nerve.1 In severe palsies, there can be associated diaphragmatic paralysis.1,11 Infants with persistent weakness are likely to develop glenohumeral subluxation and dysplasia as a result of neuromuscular imbalance at the glenoid.1 Long term sequelae include contractures at the shoulder and elbow, asymmetric limb growth with reported dimensions typically 90-95% the length and circumference of the unaffected limb and more significant differences when the palsy is more severe.12,13

Essentials of Assessment

History

Review of NBPI risk factors is critical and includes1,7

  • Neonatal birth number, birth weight, and shoulder dystocia
  • Maternal diabetes status and history of prior NBPI births
  • Birth related risk factors such as instrumented delivery
  • Prenatal, perinatal, and postnatal clinical course including APGAR scores, motor and sensory findings, presence of torticollis, and any indication of involvement of the contralateral upper extremity

Differential diagnosis includes1

  • Humeral or clavicular fracture
  • Humeral osteomyelitis
  • Tumor with mass effect
  • Hemiplegic cerebral palsy
  • Spinal cord injury
  • Isolated peripheral nerve palsy
  • Congenital varicella infection

Physical examination

Physical examination is the mainstay in diagnosing suspected NBPI and should include observation, inspection, palpation, range of motion, muscle tone, motor and sensation, and primitive and muscle stretch reflexes. The goal of initial assessment is to anatomically localize and grade severity of the injury. Typically, lower motor neuron signs are expected.1,6,10

  • General observation is necessary to assess for achievement of age appropriate gross motor and fine motor developmental milestones.1
  • Inspection may reveal asymmetries in limb length and circumference, atrophy, torticollis, scapular winging, asymmetric chest expansion (may indicate phrenic nerve involvement).1,6
  • Palpation may reveal underlying bony abnormalities, masses, and contractures.1
  • Range of motion of the shoulder, elbow, wrist, and hand should be evaluated.1
  • Glenohumeral dysplasia and shoulder subluxation/dislocation are indicated by loss of passive shoulder external rotation and presence of shoulder internal rotation contracture.
  • Muscle tone is typically normal or hypotonic. If hypertonia is present, central etiologies should be considered.1,6
  • Primitive reflexes, especially asymmetric Moro reflex, may be helpful in localizing a C5-C6 injury. Muscle stretch reflexes are typically absent or diminished in the distribution of the injury. Brisk reflexes suggest central etiologies.
  • Sensation to painful stimuli should be tested in C5-T1 dermatomes. Observation of responsive grimacing can be helpful.1,6 Absent sensation may indicate avulsion or rupture. Sensory evaluation may augment motor evaluation if withdrawal to painful stimulus is evoked.1

Functional assessment

There are three standardized, validated assessments that reliably assess upper extremity recovery and function in NBPI. They are typically performed serially over time. These include the following.

The Modified Mallet Scale14

  • Rates the child’s ability to perform 5 active shoulder functions: global abduction, global external rotation, hand to neck, hand to lower spine, hand to mouth and hand to abdomen.
  • Scoring ranges from 1 (no function) to 5 (normal function).

The Active Movement Scale (AMS)15

  • Rates the child’s ability to move the limb in space in antigravity and gravity eliminated positions. There are 15 test movements used to evaluate the entire brachial plexus. Scoring ranges from 0-7 with scores above 5 indicating antigravity strength.

The Toronto Test16

  • Rates the child’s ability to perform 5 movements against gravity: elbow flexion, elbow extension, wrist extension, digital extension, thumb extension. Scoring ranges from 0-2, reflecting absent movement, partial movement against gravity and full antigravity movement, with total possible score of 10.
  • Toronto test scores at 3 months of age that are <3.5 indicate the need for microsurgery.

Laboratory studies are not typically of significant clinical utility in NBPI. They may be more useful in the clinical work up of other elements of the differential diagnosis.

Imaging

Imaging begins with plain radiographs to assess for concomitant humeral and clavicular fractures.1 Historically, preoperative computed tomography (CT) myelogram was used to evaluate the brachial plexus for nerve root avulsions, but magnetic resonance imaging (MRI) is more commonly used as it can visualize intradural nerve roots, ventral and dorsal nerve roots, and pseudomeningoceles from nerve root avulsions without the radiation and sedation that is necessary with CT.1,6,13

Surveillance imaging is critically important in monitoring glenohumeral joint integrity, growth, and development in children with NBPI. Glenoid dysplasia characterized by retroverted glenoid, flattened humeral head, and posterior subluxation/dislocation is frequent. Dynamic ultrasound is the preferred initial modality for screening evaluation of glenohumeral dysplasia and malalignment.13,17 MRI is the gold standard for grading of glenohumeral deformity and surgical planning.1,6,7

Supplemental assessment tools

Electrodiagnostic (EDX) testing can aid in identifying nerve root lesion location, severity, and presence or absence of reinnervation.1,3,5,18 Still, the use of EDX in NBPI is controversial.1,3,18 Studies may be limited due to challenges in muscle sampling, MUAP interpretation, and MUAP recruitment.18 EDX may be valuable in detecting subclinical nerve and muscle responses, prognostication, and surgical planning. Some important electrodiagnostic considerations include the following.1

  • Preserved SNAP response in an insensate region indicates a preganglionic injury (avulsion).
  • Given the incidence of C5-C6 involvement, Erb’s point stimulation is performed to assess axillary, radial, and musculocutaneous motor nerves.
  • Muscles with absent or minimal clinical volitional movement are sampled to detect electrical activity.
  • In the setting of NBPI, EMG should be performed no sooner than 14-21 days after injury to reliably demonstrate active denervation. If intrauterine etiology of NBPI is suspected, it may be reasonable to perform the study earlier.
  • EMG can be used to evaluate viability of donor nerves to improve outcomes19

Early predictions of outcomes

The most widely accepted early predictor of outcome is spontaneous recovery of elbow flexion. Patients with return of elbow flexion by 2-3 months will likely have normal function.1,6,20,21 If spontaneous elbow flexion recovery is delayed until 3 months or later, long term functional deficit is expected.5,21 Patients with return of elbow flexion after 6 months of age have poorer function than those who regain elbow flexion between 3 and 6 months.1 Horner’s syndrome as well as lack of antigravity elbow flexion, wrist flexion/extension, and finger flexion during the first 3 months of life have been reported as independent risk factors predicting need for early microsurgery.6 Indicators of poor motor recovery include the presence of global plexopathy, phrenic nerve involvement, Horner’s syndrome, and nerve root avulsions.1,6

Professional issues

NBPI is quite distressing to families. One study showed 48% of families in the United States reportedly pursue litigation against the delivering obstetrician.22 It is incumbent upon the rehabilitation medicine team to provide family education with particular emphasis on rehabilitation goals.

Rehabilitation Management and Treatments

See Neonatal Brachial Plexus Injury Part 2

Cutting Edge/ Emerging and Unique Concepts and Practice

See Neonatal Brachial Plexus Injury Part 2

Gaps in the Evidence-Based Knowledge

See Neonatal Brachial Plexus Injury Part 2

References

  1. Nelson MR. Birth brachial plexus palsy. In: Murphy KP, McMahon MA, Houtrow AJ, eds. Pediatric Rehabilitation: Principles and Practice. New York, NY: Springer Publishing Company; 2020. doi:10.1891/9780826147073.0024
  2. Deardorff, M. A. (2025). Nelson textbook of pediatrics (R. Kliegman, J. W. St. Geme, N. J. Blum, A. M. Schuh, R. C. (Robert C. Tasker, C. L. Mack, & K. M. Wilson, Eds.; Edition 22). Elsevier. 
  3. DeFrancesco CJ, Shah DK, Rogers BH, Shah AS. The epidemiology of brachial plexus birth palsy in the united states: declining incidence and evolving risk factors. J Pediatr Orthop. 2019;39(2):e134-e140. doi:10.1097/BPO.0000000000001089
  4. Pulos N, Shaughnessy WJ, Spinner RJ, Shin AY. Brachial plexus birth injuries: A critical analysis review. JBJS Reviews. 2021;9(6). doi:10.2106/JBJS.RVW.20.00004
  5. Johnson GJ, Denning S, Clark SL, Davidson C. Pathophysiologic origins of brachial plexus injury. Obstet Gynecol. 2020;136(4):725-730. doi:10.1097/AOG.0000000000004013
  6. Schmieg S, Nguyen JC, Pehnke M, Yum SW, Shah AS. Team approach: management of brachial plexus birth injury. JBJS Reviews. 2020;8(7):e1900200. doi:10.2106/JBJS.RVW.19.00200
  7. Vuillermin C, Bauer AS. Boston Children’s Hospital approach to brachial plexus birth palsy. J Pediatr Orthop B. 2016;25(4):296-304. doi:10.1097/BPB.0000000000000330
  8. Bergman D, Rasmussen L, Chang KW-C, Yang LJ-S, Nelson VS. Assessment of Self-Determination in Adolescents with Neonatal Brachial Plexus Palsy. PM R. 2018;10(1):64-71. doi:10.1016/j.pmrj.2017.06.013
  9. Orozco V, Magee R, Balasubramanian S, Singh A. A systematic review of the tensile biomechanical properties of the neonatal brachial plexus. J Biomech Eng. 2021;143(11). doi:10.1115/1.4051399
  10. Smith B, Daunter A, Yang L. An update on the management of neonatal brachial plexus palsy—replacing old paradigms. JAMA Pediatr. 2018;172(6):585-591. doi:10.1001/jamapediatrics.2018.0124
  11. Lewis S, Sweeney J. Comorbidities in infants and children with neonatal brachial plexus palsy: a scoping review wto inform multisystem screening. Phys Occup Ther Pediatr. 2023;43(5):503-527. doi: 10.1080/01942638.2023.2169091
  12. Danisman M, Emet A, Kocyigit IA, Hassa E, Uzumcugil A. Examination of upper extremity length discrepancy in patients with obstetric brachial plexus paralysis. Children (Basel). 2023 May 13;10(5):876. doi: 10.3390/children10050876
  13. Osorio M, Lewis S, Tse RW. Promoting recovery following brith brachial plexus palsy. Pediatr Clin North Am. 2023 Jun;70(3):517-529. doi: 10.1016/j.pcl.2023.01.016
  14. Mallet J. Obstetrical paralysis of the brachial plexus. II. Therapeutics. Treatment of sequelae. Rev Chir Orthop Reparatrice Appar Mot. 1972;58(suppl):166-168
  15. Clarke HM, Curtis CG. An Approach to obstetrical brachial plexus injuries. J Hand Aurg Am. 2002;27:470-478.
  16. Michelow BJ, Clarke HM, Curtis CG, et al. The natural history of obstetrical brachial plexus palsy. Plast Reconstr Surg. 1994;93:675-680. Doi:10.1097/00006534-199404000-00001
  17. Menashe S, Ngo A, Osorio M, et al.  Ultrasound assessment of glenohumeral dysplasia in infants.  Pediatr Radiol 2022;52(9):1648-57. doi: 10.1007/s00247-021-05180-y
  18. Spires MC, Brown SM, Chang KW-C, Leonard JA, Yang LJ-S. Interrater reliability of electrodiagnosis in neonatal brachial plexopathy. Muscle Nerve. 2017;55(1):69-73. doi:10.1002/mus.25193
  19. Schreiber JJ, Feinberg JH, Byun DJ, Lee SK, Wolfe SW. Preoperative donor nerve electromyography as a predictor of nerve transfer outcomes. J Hand Surg Am. 2014 Jan;39(1):42-9. doi: 10.1016/j.jhsa.2013.09.042
  20. Frade F, Gómez-Salgado J, Jacobsohn L, Florindo-Silva F. Rehabilitation of neonatal brachial plexus palsy: integrative literature review. J Clin Med. 2019;8(7). doi:10.3390/jcm8070980
  21. Hems T. Questions regarding natural history and management of obstetric brachial plexus injury. J Hand Surg Eur Vol. 2021 Sep;46(7):796-799. doi: 10.1177/17531934211027117
  22. Chauhan S, Chang K, Ankumah N, Yand L. Neonatal brachial plexus palsy: obstetric factors associated with litigation. J Matern Fetal Neonatal Med. 2017 Oct;30(20):2428-2432. doi: 10.1080/14767058.2016.1252745

    Original Version of the Topic

    Robert Rinaldi, MD. Neonatal Brachial Plexus Injury. 11/10/2011

    Previous Revision(s) of the Topic

    Charles Taylor, II, MD, Sheena Pillai, BS, Robert Rinaldi, MD. Neonatal Brachial Plexus Injury. 7/5/2018

    Deborah Cassidy, DO, Amy Tenaglia, MD, Hana Azizi, MD. Neonatal Brachial Plexus Injury. 1/13/2022

    Author Disclosure

    Marisa Osorio, DO
    Nothing to Disclose

    Nitin Bajaj, DO
    Nothing to Disclose