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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). It is a birth related traction or tearing injury of the brachial plexus root(s) and/ or trunk(s) that results in variable motor, sensory, and functional impairments of the affected upper extremity.1–8


The most commonly cited cause of NBPI is the labor and delivery process, characterized by excessive neck stretching forces during birth, leading to traction injuries including avulsion (preganglionic) or rupture (postganglionic).9–11 Obstetric forces in complicated deliveries can be exaggerated by the maternal, neonatal, and birth risk factors listed below. It is important to note that 46-54% of cases of NBPI occur in the absence of shoulder dystocia.4 There are other uterine forces such as prolonged labor or tachysystole that are risk factors along with cephalopelvic disproportion.4,11 Cases have also been reported in the setting of cesarean delivery.4,9,11 Non-traumatic etiologies may 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.1,10 Extent of injury is variable; it may be global, including all parts of the plexus, or focal.

Epidemiology including risk factors and primary prevention

Globally, NBPI incidence ranges between 0.4 and 4.6 per 1,000 live births.1 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.1–3,5 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. Cesarean delivery 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 1–3,5,9,10

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

According to the abovementioned Kids’ Inpatient Database study, up to 71% of patients had no risk factor. Protective factors included multiple gestation and cesarean section. There appears to be increased risk of NBPI in non-white patients and patients of lower socioeconomic status.1–3,10,12

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.


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; the upper, middle, and lower trunks; the anterior and posterior divisions; the lateral, medial, and posterior cords; and the terminal branches. Prefixed plexuses include roots C4-T1 and postfixed plexuses include roots C5-T2.11

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 classification 1,3,5,13

  • Type I: C5-C6 (Erb’s palsy)
    • Most common; affects about 46% of patients
    • Best outcome; about 80% have full recovery
  • Type II: C5-C7 (Extended Erb’s palsy)
    • 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 surgery
  • 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.

Higher Narakas classification indicates less potential for spontaneous recovery.1,3,6

Seddon classification 1,5,9,10

  • 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 Clinical presentation of children at 2-3 weeks of age according to Narakas classifications is as follows.3

  • Type I: Erb palsy with paralysis of C5-C6 muscles; weakness in shoulder external rotation, abduction, and elbow flexion; “waiter’s tip” posture: shoulder internally rotated with extended and pronated forearm6,14
  • Type II: As above but also with paralysis of C7 muscles; weakness as above but more notable  in wrist and elbow extension6
  • Type III: Global plexus involvement, flaccid paralysis, “flail arm”6
  • Type IV: Global plexus involvement, flaccid paralysis, “flail arm” plus Horner’s syndrome6

The following are pertinent estimates.1,3,5,14

  • 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

Respiratory impairment and potentially diaphragmatic paralysis can be associated manifestations due to the proximity of the phrenic nerve (C3-5).1 Torticollis is very commonly associated.1 Scapular winging is also commonly associated due to the proximity of the long thoracic nerve (C5-7).1 Contractures of the elbow flexors and shoulder internal rotators are common.1,14 Asymmetric growth both in length and circumference of the affected limb is common; typically, dimensions are 95% the size of the unaffected limb.1,5 Osseous deformities most commonly affect the glenohumeral joint. In particular, glenoid dysplasia with posterior glenohumeral subluxation/dislocation is common (discussed further in imaging section).1 Sensation and proprioception can be impaired.

Essentials of Assessment


Review of NBPI risk factors is critical and includes 1,6

  • 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 includes 1

  • 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

Examination of the child with suspected NBPI 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.1,5

  • 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).1,5
  • 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 rapid 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.1,5
  • 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.1,5 Absent sensation may indicate avulsion or rupture. Sensory evaluation may augment motor evaluation if withdrawal to painful stimulus is evoked.1
  • Motor patterns are as follows.1
    • C5-6/upper trunk injuries: absent shoulder abduction, external rotation, elbow flexion, and wrist extension. Hand function is preserved.
    • C5-7/upper and middle trunk injuries: as above but also includes absent elbow extension.
    • C5-T1 injuries: flaccid paralysis of entire affected upper extremity.
    • If Horner’s syndrome (ipsilateral ptosis, miosis, and anhidrosis) is present, suspect injury to C8-T1.

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.1,3,5,6

The Modified Mallet Scale

  • Rates the child’s ability to perform 5 active shoulder functions: global abduction, global external rotation, hand to neck, hand to lower spine, and hand to mouth.
  • Scoring ranges from 1 (no function) to 5 (normal function).1,3,5

The Active Movement Scale (AMS)

  • 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.
  • AMS scores at 3 months of age that are <4.5 for thumb, finger, wrist, and elbow flexion and wrist and elbow extension have been noted to be independent risk factors for undergoing microsurgical reconstruction.1,3,5

The Toronto Test

  • Rates the child’s ability to perform 5 movements: elbow flexion, elbow extension, wrist extension, digital extension, thumb extension. Scoring ranges from 0-2 with total possible score of 10.
  • Toronto test scores at 3 months of age that are <3.5 indicate the need for microsurgery 1,3,5,6.

Correlation between the above assessments is poor.3,5

Laboratory studies

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.


Diagnostic imaging can be useful in determining the type of NBPI. Imaging begins with plain radiographs of the glenohumeral joint, clavicle, and chest to assess for humeral and clavicular fractures, osteomyelitis, and tumors.1 Historically, advanced imaging included computed tomography (CT) myelogram, which was utilized in preoperative investigation of nerve root avulsions. Intrathecal nerve roots and pseudomeningoceles, commonly associated with avulsion injury, are well visualized with CT myelography. However, CT myelography is falling out of favor due to its required sedation, contrast, and lumbar puncture.1,5 Magnetic resonance imaging (MRI) will likely replace CT myelography as the study of choice. MRI can visualize intradural nerve roots, ventral and dorsal nerve roots, and nerve root avulsions with associated pseudomeningoceles and peri-scalene soft tissue edema.1,5 A small pilot study suggests that a rapid, non-sedated, volumetric cube proton density MRI protocol, performed at initial clinical presentation, can differentiate between pre and post ganglionic injury, grade the severity of injury, and predict functional performance at 6 months of age.15 Lastly, Ultrasound (US) is more favorable than CT myelography in terms of risk. US provides both static and dynamic value. For example, US allows for visualization of the shoulder joint, neuromas, muscular atrophy, and nerve injury. Phrenic nerve injury may be dynamically deduced in the setting of diaphragmatic paralysis.5

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 US is the preferred initial modality for screening evaluation of glenohumeral dysplasia and malalignment. MRI is the gold standard for grading of glenohumeral deformity and surgical planning.1,5,6

Supplemental assessment tools

Electrodiagnostic (EDX) testing can aid in identifying nerve root lesion location, severity, and presence or absence of reinnervation.1,3,5,16 Still, the use of EDX in NBPI is controversial.1,3,16 Studies may be limited due to challenges in muscle sampling, MUAP interpretation, and MUAP recruitment.16 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.
  • Interrater reliability for nerve root assessment via EDX in NBPI has been reported to be higher for C6-T1 nerve roots than C5.16

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.1,5,17,18 If spontaneous elbow flexion recovery is delayed until 3 months or later, long term functional deficit is expected.5,19 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 microsurgery.5 Indicators of poor motor recovery include the presence of global plexopathy, phrenic nerve involvement, Horner’s syndrome, and nerve root avulsions.1,5

Professional Issues

NBPI is quite distressing to families. Up to 50% of families reportedly pursue litigation against the delivering obstetrician.3 It is incumbent upon the rehabilitation medicine team to provide family education with particular emphasis on rehabilitation goals.

Rehabilitation Management and Treatments

Available or current treatment guidelines

There are presently no accepted, standardized treatment guidelines for NBPI. However, multidisciplinary treatment is standard of care; it optimizes functional recovery and minimizes unnecessary invasive interventions.1,5,17 Collaboration between families and health care professionals is ideal. Two main treatment approaches exist: conservative management and surgical management.1,17 Multidisciplinary management includes physiatry, neurology, electro-diagnosticians, physical and occupational therapy, orthopedic surgery, neurosurgery, and plastic surgery. Conservative and surgical interventions are reviewed below.

At different disease stages

New onset/acute

Ideally, conservative treatment begins immediately. Family education regarding injury etiology and risk factors, expected clinical course, and treatment is essential.1,6,17 Proper positioning of the affected limb is critical.1,5,17 Especially important is increasing the infant’s awareness of the affected limb. This can be achieved via wrist rattle application during waking hours, parental assistance to move the affected limb into the infant’s field of view, and parental mimicry of the infant’s unaffected limb movements by the affected limb. Kinesiology taping may be utilized for positioning and to facilitate or inhibit muscle activity.5,17 Splinting /orthoses may be implemented to optimize shoulder, elbow, forearm, and wrist positioning (resting wrist splint, functional wrist hand orthosis, supinator strap, elbow extension orthosis, supination-external rotation orthosis).1,5,17 Provision of sensory experiences via tactile stimulation with various textures and temperatures, gentle massage, vibration and brushing techniques increases awareness of the limb as well.5,17

Gentle PROM of the affected limb at the shoulder, elbow, wrist, forearm, and fingers may begin at approximately 2 weeks after birth.1,6 PROM should be performed several times per day. PROM earlier than 2 weeks may result in pain.1 Family members should be instructed to avoid holding infants with pressure applied to the axillary region as this can increase stress to the recovering plexus and shoulder joint.

Therapy goals focus on maintaining active and passive range of motion, sensory stimulation, strengthening, and acquisition of developmentally appropriate bimanual gross and fine motor skills. These goals persist throughout recovery. Therapy sessions should occur several times per week in the outpatient clinic and multiple times per day in the home.5,17


The abovementioned conservative techniques continue to be utilized in the subacute period. Additional modalities include the following.

Electrical stimulation promotes functional muscle recovery by inhibiting atrophy and accelerating nerve regeneration improving strength and ROM.1,17 It is typically avoided in the early months due to reduced tolerance. It is better tolerated by older infants and young children. Stimulation settings are such that local muscle twitch is achieved. Treatment duration is typically 20 minutes twice daily.

Constraint induced movement therapy (CIMT) of the non-injured limb for 1 hour per day has been shown to improve mobility, functional capacity, speed, range of motion, and hand manipulation ability.1,17

Muscle imbalance may develop as plexus injury selectively weakens muscle groups. Imbalance results in restricted motion, co-contraction of agonist/ antagonist muscles, and structural joint deformity.14 As such, Botulinum toxin injections may be used off label in NBPI. Injections to healthy antagonistic muscles may alleviate muscle imbalances, co-contractions, and muscle contractures, thus adapting the limb movement pattern to potentiate nerve recovery and motor learning.1,5,14,17

Systematic review by Buchanan et el identified the following 3 indications for botulinum toxin injections; internal rotation/adduction contracture of the shoulder, elbow flexion/ extension lag, and forearm pronation contracture.14 The review demonstrated improvement in all indications following botulinum toxin injections. Of note, injections were often performed in conjunction with therapies, casting, and surgery. Also, treatment effect was less robust in children older than 7.5 years.14

Surgical options include primary and secondary surgeries. Typically, primary surgeries are reserved for infants who demonstrate insufficient or no spontaneous recovery by 3 months of age. Secondary surgeries are reserved for infants or children who require further functional improvement, either post primary surgery or post spontaneous recovery1,17 (see Emerging/ Unique Interventions section below for further detail). It is important to anticipate parental postoperative expectations. Education regarding nerve regeneration is imperative; regeneration occurs at approximately 1 millimeter per day and 1 inch per month. Thus, observational functional gains may not be present for several months postoperatively.5


General therapeutic goals in the chronic period are similar to those of the acute and subacute periods. Emphasis remains on contracture prevention and acquisition of developmentally appropriate gross and fine motor skills.

With time, the risk of glenohumeral dysplasia and bony abnormality increase. For those with motor deficits persisting beyond 3-6 months, 60-80% will develop glenohumeral deformity. Dysplasia and subluxation occur at a mean age of 3 and 6 months of age, respectively. Left untreated, glenohumeral deformity progresses leading to pseudo-glenoid and biconcave glenoid development, further humeral head deformity, and proximal humeral head growth arrest. Progression leads to worsening function and often necessitates surgical intervention. Surgical interventions may include glenohumeral reconstruction with joint reduction and rebalancing, tendon transfers, glenoid and humeral osteotomy.6

Adolescents with persistent deficits may continue to experience muscle imbalance, contracture, limb asymmetries, and atrophy leading to impaired ADLs.8 Variable treatment outcomes and morphological asymmetries associated with functional impairment may result in psychosocial difficulties in children and adolescents with NBPI. Impairments may impact school and activity participation as well as peer socialization.7,8

Coordination of care

Multidisciplinary treatment approach is recommended given the complexity of NBPI and variable extent of injury, prognosis, and recovery pattern. It is unanimous that conservative multidisciplinary treatment be initiated as soon as possible. Early rehabilitation programs can result in improved functional outcomes in infants with spontaneous recovery of elbow function between 3 and 6 months. In cases of insufficient recovery, absent spontaneous recovery, or complete NBPI, surgical intervention is necessary.17

Emerging/unique interventions

Surgical interventions are to be considered in some cases of NBPI. However, there is no formal consensus regarding the indications and timing of surgery in NBPI.1,17 There is a general consensus that Narakas type III and IV will undergo surgery at 3 months. Surgical indications and timing for Narakas type I and II continue to be deliberated.5,6 Classically, per Gilbert et al, primary microsurgery is performed if there is no elbow flexion by 3 months.1,3 Some authors suggest surgery can be delayed until 5-6 months despite the absence of elbow flexion as long as some shoulder function has spontaneously recovered.17 In general, a possible range to expect surgical recommendation is between 3 and 6 months.17 Despite a lack of consensus, the following points are apparent.1,17

  • Patients who undergo microsurgery at 6 months have better outcomes than those who spontaneously recovered elbow flexion at 5 months.
  • Surgery is often recommended for patients with less than antigravity elbow flexion at 6 months of age.
  • Patients with complete NBPI may undergo surgery at 3-4 months of age.

Typical priorities for surgeons, in order, include restoration of hand function, elbow flexion, and shoulder external rotation and abduction.3

Primary surgery (microsurgery) to the brachial plexus is the preferred initial surgical intervention for NBPI. Primary surgery optimizes functional recovery and innervates muscles that may be used in secondary surgeries.1 Microsurgeries include neurolysis (cleaning scar and fibrotic tissue from nerve), nerve transfer, and nerve grafting. In nerve transfer, an expendable fascicle from a functioning nerve is used to innervate a denervated muscle close to the motor endplate. This is advantageous due to short regeneration distance and thus shorter reinnervation time. In fact, nerve transfers may be successful even at 12-15 months of age when grafting would likely not be effective. Nerve transfers may include non-plexus nerves such as the spinal accessory nerve and intercostal nerves. Terminal branches of the plexus such as the ulnar, median, and radial nerves may also be used.6 Nerve grafting utilizes a donor nerve or synthetic conduit that provides a proper recovery pathway for nerve regeneration in the setting of longer regeneration distance.1,17 The repaired nerve must regenerate from the proximal graft site in the neck to the distal target muscle before the muscle becomes permanently atrophied due to denervation.6

Secondary surgeries include muscle, tendon, and nerve branch transfers. They may include arthrodesis and osteotomies as well. Secondary surgeries are for children who have functional motor deficits regardless of undergoing primary surgery. Secondary surgeries have very specific functional goals and more limited potential for recovery compared to primary brachial plexus surgeries. Secondary surgery nerve transfers such as spinal accessory to suprascapular, partial ulnar nerve to musculocutaneous nerve transfer, and partial radial nerve to axillary nerve transfer are examples.1,6

The timing of peripheral nerve surgery is critical. Functional motor recovery is dependent upon successful reinnervation occurring prior to permanent muscle atrophy from denervation. Furthermore, postoperative hand and arm functional recovery is inversely related to age at surgery; thus, early surgery is recommended. Microsurgery has resulted in improved postoperative shoulder function in 60-80% of cases and at least antigravity elbow flexion in 80% of cases.1

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

One study comparing adolescents with NBPI with typically developing age matched peers found that self-determination levels were similar between both groups. Self-determination was described as the process by which one controls one’s own life; namely, decision making, goal setting, and perseverance to achieve goals.8 Self-determination is prerequisite to transitioning into adulthood and linked with successful post school employment, social, and family interactions. As such, rehabilitation medicine physicians must encourage adolescents with NBPI to assume age appropriate, goal driven, self-regulated, autonomous behavior in an effort to pursue their ultimate academic and or career goals.8

Cutting Edge/ Emerging and Unique Concepts and Practice

Comprehensive rehabilitative care, regardless of indication, implores the concept of optimization of function and quality of life. In treating children with NBPI, it is critical to consider patient expectations and concerns in assessing quality of life. One qualitative study found that physical health, social health, and emotional health are common general domains impacting health related quality of life in children with NBPI. NBPI specific health related quality of life content includes: medical care, recreation, arm hand/appearance, independence, having to explain the arm/ hand to others, and self-esteem/ body image.7

Gaps in the Evidence-Based Knowledge

Debate surrounding the indications and timing of NBPI surgical intervention persists. As such, the clinical utility of imaging studies such as the rapid, non-sedated, non-contrast, volumetric PD Cube MRI increases. Pilot study demonstrates that this MRI protocol can differentiate pre and postganglionic injury as well as predict functional outcome. More extensive research is needed to determine the validity of this biomarker.15

Despite the unanimous consensus that treatment of NBPI begin with conservative management, certain rehabilitation techniques are lacking in evidence such as bracing, positional techniques, and taping to reduce glenohumeral dysplasia and shoulder and elbow contractures, weight shifts using the affected limb, and aqua therapy.17

Inclusion of NBPI specific content in assessing health related quality of life via patient reported outcomes is necessary to better capture specific challenges endured by this patient population.7


  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. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. Chang KW-C, Austin A, Yeaman J, et al. Health-Related Quality of Life Components in Children With Neonatal Brachial Plexus Palsy: A Qualitative Study. PM R. 2017;9(4):383-391. doi:10.1016/j.pmrj.2016.08.002
  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. Vakhshori V, Bouz GJ, Alluri RK, Stevanovic M, Ghiassi A, Lightdale N. Risk factors associated with neonatal brachial plexus palsy in the United States. J Pediatr Orthop B. 2020;29(4):392-398. doi:10.1097/BPB.0000000000000706
  11. Dunbar DC, Vilensky JA, Suárez-Quian CA, Shen PY, Metaizeau J-P, Supakul N. Risk factors for neonatal brachial plexus palsy attributed to anatomy, physiology, and evolution. Clin Anat. 2021;34(6):884-898. doi:10.1002/ca.23739
  12. Merrison H, Mangtani A, Quick T. The shifting demographics of birth-related brachial plexus injury: The impact of socio-economic status and ethnic groups. J Plast Reconstr Aesthet Surg. 2021;74(3):560-568. doi:10.1016/j.bjps.2020.08.091
  13. El-Sayed AAF. Intermediate type of obstetric brachial plexus palsy. J Child Neurol. 2016;31(14):1628-1630. doi:10.1177/0883073816669462
  14. Buchanan PJ, Grossman JAI, Price AE, Reddy C, Chopan M, Chim H. The use of botulinum toxin injection for brachial plexus birth injuries: A systematic review of the literature. Hand (N Y). 2019;14(2):150-154. doi:10.1177/1558944718760038
  15. Shen PY, Nidecker AE, Neufeld EA, Lee PS, James MA, Bauer AS. Non-Sedated Rapid Volumetric Proton Density MRI Predicts Neonatal Brachial Plexus Birth Palsy Functional Outcome. J Neuroimaging. 2017;27(2):248-254. doi:10.1111/jon.12389
  16. 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
  17. 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
  18. Hems T. Questions regarding natural history and management of obstetric brachial plexus injury. J Hand Surg Eur Vol. July 2021:17531934211027116. doi:10.1177/17531934211027117
  19. Hems TEJ, Savaridas T, Sherlock DA. The natural history of recovery of elbow flexion after obstetric brachial plexus injury managed without nerve repair. J Hand Surg Eur Vol. 2017;42(7):706-709. doi:10.1177/1753193417712924

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

Author Disclosure

Deborah Cassidy, DO
Nothing to Disclose

Amy Tenaglia, MD
Nothing to Disclose

Hana Azizi, MD
Nothing to Disclose