eMedicine Specialties > Physical Medicine and Rehabilitation > Plexopathy

Neonatal Brachial Plexus Palsies

Author: Jennifer Semel-Concepcion, MD, Director, Department of Physical Medicine and Rehabilitation, St Charles Hospital and Rehabilitation Center; Chair, Assistant Professor of Physical Medicine and Rehabilitation, State University of New York at Stony Brook School of Medicine
Coauthor(s): Jennifer M Gray, DO, Resident Physician, Department of Physical Medicine and Rehabilitation, State University of New York at Stony Brook; Hany Nasr, MBBCh, Staff Physician, Department of Physical Medicine and Rehabilitation, State University of New York at Stony Brook; Anne Conway, BS, PT, Clinical Coordinator, Department of Physical Therapy, Children's National Medical Center of Washington, DC
Contributor Information and Disclosures

Updated: Jan 14, 2009

Introduction

Background

The first known description of neonatal brachial plexus palsy (BPP) dates from 1779 when Smellie reported the case of an infant with bilateral arm weakness that resolved spontaneously within a few days after birth. In the 1870s, Duchenne and Erb described cases of upper trunk nerve injury, attributing the findings to traction on the upper trunk, now called Erb's palsy (or Duchenne-Erb's palsy).1 In 1885, Klumpke described injury to the C8-T1 nerve roots and the nearby stellate ganglion that now bears her name.

Many cases of BPP are transient, with the child recovering full function in the first week of life. A smaller percentage of children continue to have weakness leading to long-term disability from the injury. The mainstay of treatment for these children is physical and/or occupational therapy in concert with a regular home exercise program. A select few patients may benefit from surgical intervention in the early stages to improve innervation of the affected muscles. Others benefit from tendon transfers performed later to improve shoulder and (sometimes) elbow function.
 
Numerous other nonsurgical treatments, including electrical stimulation and botulinum toxin injections, also may prove effective in the treatment of children with BPP. In view of the variability in presentation, treatment options, and outcome measures, a multidisciplinary approach to the care of the infant with BPP is recommended.

Related eMedicine articles:
 Birth Trauma
Brachial Plexus Injuries, Obstetrical
Brachial Plexus Injuries, Traumatic
Hand, Brachial Plexus Surgery

Pathophysiology

To understand the clinical presentation of brachial plexus palsy (BPP) and provide anticipatory guidance for families affected by the condition, the clinician must first know basic anatomy. As seen in the image below (see also Image 1), the brachial plexus consists of nerves (the ventral rami) from C5-T1. C5 and C6 join to form the upper trunk, C7 travels alone as the middle trunk, and C8-T1 join as the lower trunk. Each trunk divides into anterior and posterior divisions to create the cords, which then subdivide further into branches that supply the muscles of the arm. Injuries of the brachial plexus may be mild, with only temporary sequelae, or devastating, leaving the child with a flaccid, insensate arm.

Brachial Plexus. Image courtesy of Michael Brown,...

Brachial Plexus. Image courtesy of Michael Brown, MD.

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Brachial Plexus. Image courtesy of Michael Brown,...

Brachial Plexus. Image courtesy of Michael Brown, MD.


Severity depends on the number of nerves involved and the degree to which each level is injured. The basic types of BPPs include the following:
  • Erb's palsy affects nerves arising from C5 and C6.
  • Upper-middle trunk BPP involves nerve fibers from C5, C6, and C7 levels.
  • Klumpke palsy results in deficits at levels C8 and T1, although many clinicians agree that pure C8-T1 injuries do not occur in infants and may be indicative of spinal cord injury (SCI).
  • Total BPP affects nerves at all levels (C5-T1).
  • Bilateral BPP demonstrates bilateral involvement.
When defining the severity of a peripheral nerve injury, differentiation between neurapraxic, axonotmetic, and neurotmetic lesions is helpful.
  • Purely neurapraxic lesions do not affect the axon itself. These lesions generally are reversible and do not leave sequelae.
  • Axonotmetic lesions involve disruption of the myelin sheath and the axon, leading to degeneration of the axon distal to the injury. The connective tissue across the lesion remains intact. These injuries improve gradually over 4-6 months, depending on the level of the lesion.
  • Neurotmetic lesions are the most severe, destroying not only the axon and myelin, but also the supporting structures across a nerve. As the proximal end of the nerve attempts to regenerate without this supportive connective tissue, a neuroma may develop. The extent of improvement in the patient's condition depends on the ultimate number of nerve fibers that reconnect distal to the neuroma. Muscle atrophy from a neurotmetic lesion begins 3-6 months after injury and by 1.5-2 years is irreversible.

Although the traditional mechanism of injury is lateral neck flexion, the upper rootlets (C5-C7) are 25% as likely to be avulsed as the lower roots (C7-T1). The upper roots (C5-C6), however, are far more likely to be ruptured (88%) because of the anatomy of the transverse processes and the degree of flexibility at that level.

The clinician must also distinguish neonatal BPP from traumatic BPP in older children and adults. The damage in neonates usually results from slow traction injuries, unlike the high-energy shearing type of trauma seen in older individuals. Not only are the latter injuries often more severe, but with similar injuries, infants show a better functional outcome.

This clinical observation is confirmed by Vredeveld and colleagues, who studied 14 infants and 19 adults with surgical evidence of complete avulsion of the C5-C6 roots or upper trunk.2 Electromyography (EMG) showed normal recruitment of biceps and deltoid in the infants and complete denervation in the older individuals. When C7 also was torn, the infants demonstrated complete denervation. Vredeveld and coworkers attributed this observation to neonatal C7 innervation of the biceps and deltoid that subsequently was lost if the C5-C6 roots were functional.

Frequency

United States

An incidence of 0.5-4.4 cases of brachial plexus palsy per 1000 full-term births has been reported; however, a review by Gilbert and colleagues reported an incidence of 0.8-1 case per 1000 births.3

International

Studies in France and Saudi Arabia have suggested an incidence of 1.09-1.19 cases of brachial plexus palsy per 1000 live births.

Mortality/Morbidity

  • The incidence of permanent impairment is 3-25%.
  • The rate of recovery in the first few weeks is a good indicator of final outcome. Complete recovery is unlikely if no improvement is noted in the first 2 weeks of life.

Race

Most studies have not found evidence to support a link between race and the risk of brachial plexus palsy. However, a 2007 study in New York City, by Weizsaeker and colleagues, found that being a member of the black population was independently predictive for Erb’s palsy.4

Sex

Eng and colleagues examined 191 infants with brachial plexus palsy.5 Nearly half of them (49%) were male, and 51% were female.

Age

Neonatal brachial plexus palsy is noted at birth.

Clinical

History

When an infant is born with a brachial plexus palsy, the condition generally is apparent from birth. In a common scenario, the baby weighs over 4 kilograms and is the product of a difficult delivery to a multiparous woman, requiring the use of vacuum extraction or forceps. Upon delivery, which may involve anterior shoulder dystocia, the arm hangs loosely at the child's side. Respiratory depression may indicate an associated phrenic nerve palsy.

Physical

  • Newborn findings
    • The infant with complete brachial plexus palsy (BPP; C5-T1) typically lies in the nursery with the arm held limply at his/her side. Deep tendon reflexes (DTRs) in the affected arm are absent, and the Moro response is asymmetrical, with no active abduction of the ipsilateral arm.
    • In children with total arm involvement, careful examination of the child's eye often demonstrates Horner's syndrome (ie, miosis, ptosis, anhidrosis), suggesting injury to the stellate ganglion.6
    • Children with intrinsic hand weakness associated with BPP generally have Horner's syndrome, and vice versa.
    • Respiratory status should be evaluated, since the phrenic nerve can be injured simultaneously.
    • The infant with an upper plexus palsy (C5-C7) keeps the arm adducted and internally rotated, with the elbow extended, the forearm pronated, the wrist flexed, and the hand in a fist. In the first hours of life, the hand also may appear flaccid, but strength soon returns.
    • The right side is injured in 51% of cases. Left BPP occurs in 45% of patients and bilateral injuries, in 4%.
    • The infant with a nerve injury to the lower plexus (C8-T1) holds the arm supinated, with the elbow bent and the wrist extended.
    • Sensation should be assessed closely, with the clinician noting any sensory loss in corresponding dermatomes.
    • Reflexes, typically absent in the affected limb, should be evaluated. This examination is particularly important in distinguishing BPP from hemiparesis. Reflexes do not typically return except in the mildest injuries.
    • In the newborn nursery, it is essential that the physician carefully inspect the size of the hand and arm and the bulk of the pectoralis major muscle, along with palmar dermatoglyphics and limb range of motion (ROM), looking for clues indicating when the injury occurred. On occasion, injuries occur prior to onset of labor. In these cases, a child may, at the time of delivery, already have a smaller limb with asymmetrical palmar creases, pectoralis muscle atrophy, and/or joint contractures.
  • Associated injuries
    • The pediatrician must perform a careful examination of the infant with a BPP to look for associated injuries.
    • The most common associated (not causative) injuries include the following:
      • Clavicular and humeral fractures
      • Torticollis
      • Cephalohematoma
      • Facial nerve palsy
      • Diaphragmatic paralysis
  • Findings in older children
    • The root level(s) and severity of injury ultimately determine the clinical picture and, in part, the outcome as a child ages.
    • The older child with BPP involving the upper trunk typically has difficulty with active shoulder abduction, forward flexion, symmetrical elbow flexion, and forearm supination.
    • With shoulder abduction, the medial edge of the scapula often can be seen protruding above the shoulder line, a manifestation referred to as Putti sign.
    • The reduction in shoulder abduction is due in part to weakness of the deltoid and in part to the lack of external rotation, which is needed for the greater trochanter to slide past the coracoacromial arch.
    • The term "trumpet sign" describes the child's typical pattern of bringing objects to the mouth (ie, shoulder abduction accompanied by elbow flexion).
    • Posterior subluxation of the humeral head can develop as the internal rotators of the shoulder overpower the weaker external rotators and become contracted.
    • Mild shortening and atrophy of the limb are observed.
    • Biting of the fingernails and hands to the point of tissue damage is not infrequent (4.7%) in children with BPP and is more prevalent in children with total BPP.
    • The child should be reevaluated on a regular basis to ensure that scoliosis does not develop from muscle imbalance and asymmetrical motor patterns.

Related eMedicine topics:
Horner Syndrome [Oncology]
Horner Syndrome [Ophthalmology]

Causes

For many years, blame has been placed on the obstetrician when a neonate has been diagnosed with brachial plexus palsy (BPP). The assumption has been that the method of delivery and the traction applied to the head and neck during the birthing process cause the injury as the shoulder crosses the pubic arch. This theory has been supported by the fact that less than 1% of all BPP cases have been found in cesarean section deliveries.

A retrospective study by Jennett and colleagues7  (reiterated by Allen and coworkers8 ) questioned this assumption and noted that there are 2 separate populations of children with BPP: those with shoulder dystocia and those without it. Jennett found that 22 of the 39 children with BPP who were studied did not have documented shoulder dystocia. Rather than having the traditional risk factors listed above, these infants had an average birth weight of 2.5-3.5 kg, and most were born to young, nulliparous women.

Gherman and colleagues proposed that the brachial plexus in many cases has been stretched in utero or in the descent of the fetus and may not represent a traction injury associated with the final stages of delivery.9 They reviewed birth records of 9071 children delivered vaginally to determine the extent of association between shoulder dystocia and BPP. A total of 40 cases of BPP were noted (17 cases without shoulder dystocia and 23 cases with associated shoulder dystocia).

When shoulder dystocia occurred, the risk of BPP was 18.3-32%. According to Gherman, the characteristics of the injury in children with BPP were different in the presence and absence of shoulder dystocia. When dystocia was present, the affected shoulder usually was anterior (81%), but in children with BPP and no shoulder dystocia, the injured shoulder often was posterior (68%). Children who did not have shoulder dystocia but who sustained BPP tended to be slightly smaller than were unaffected children, exhibited an associated clavicular fracture, and were subject to a less favorable outcome.

In 2002, the AmericanCollege of Obstetricians and Gynecologists recommended cesarean delivery for fetuses with an estimated weight of 5 kg or more, to reduce the prevalence of shoulder dystocia. If practitioners were to follow the recommendation, the affect on the cesarean delivery rate would be negligible, but the shoulder dystocia rate, which in this category of births is 20%, would be reduced.

In 2003, Raio and coworkers identified an increased incidence of brachial plexus injury among fetuses weighting more than 5 kg (2.86% vs 0.85% in fetuses weighing 4.5-4.599 kg), especially fetuses that developed shoulder dystocia.10 The authors suggested that when the estimated birth weight exceeded 4.5 kg, women should be informed of the increased risk of perinatal morbidity (including brachial plexus palsy) prior to making a decision on the mode of delivery.

  • Most neonatal BPP occurs in the birthing process. Risk factors for this type of injury, also referred to as obstetrical BPP (OBPP), include the following:
    • Large birth weight (average vertex BPP, 3.8-5.0 kg; average breech BPP, 1.8-3.7 kg; average unaffected, 2.8-4.5 kg)
    • Breech presentation
    • Maternal diabetes
    • Multiparity
    • Second stage of labor that lasts more than 60 minutes
    • Assisted delivery (eg, use of mid/low forceps, vacuum extraction)
    • Forceful downward traction on the head during delivery11
    • Previous child with OBPP
    • Intrauterine torticollis
    • Shoulder dystocia
The aforementioned study by Weizsaeker and colleagues compared pregnancies and deliveries involving 45 infants with Erb's Palsy with 90 controls.4  The risk for the condition was higher for children whose mother had gestational diabetes. Mothers who did not have gestational diabetes but who nonetheless gave birth to children with Erb's palsy were found to have higher blood glucose values after a 50 g glucose challenge. Other variables found to be independently predictive of Erb's palsy were a long deceleration phase of labor, a long second stage, high birth weight, and high neonatal or maternal body mass. Being a member of the black population also was found to be independently predictive.
  • Other, less common causes of neonatal BPP include the following:
    • Neoplasm (eg, neuromas, rhabdoid tumors)
    • Intrauterine compression
    • Humeral osteomyelitis
    • Hemangioma
    • Exostosis of the first rib

More on Neonatal Brachial Plexus Palsies

Overview: Neonatal Brachial Plexus Palsies
Differential Diagnoses & Workup: Neonatal Brachial Plexus Palsies
Treatment & Medication: Neonatal Brachial Plexus Palsies
Follow-up: Neonatal Brachial Plexus Palsies
Multimedia: Neonatal Brachial Plexus Palsies
References
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Further Reading

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Keywords

neonatal brachial plexus palsies, palsy, plexus, brachial plexus, brachial plexus injury, brachial plexus palsy, brachial plexus injuries, Erb palsy, obstetric brachial plexus palsy, obstetrical brachial plexus palsy, brachial plexus birth palsy, birth brachial plexus palsy, traumatic peripheral nervous system injury, congenital brachial plexus palsy, Erb's palsy, Klumpke's palsy, Duchenne-Erb's palsy, Erb palsy, Klumpke palsy, Duchenne-Erb palsy

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Contributor Information and Disclosures

Author

Jennifer Semel-Concepcion, MD, Director, Department of Physical Medicine and Rehabilitation, St Charles Hospital and Rehabilitation Center; Chair, Assistant Professor of Physical Medicine and Rehabilitation, State University of New York at Stony Brook School of Medicine
Jennifer Semel-Concepcion, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Jennifer M Gray, DO, Resident Physician, Department of Physical Medicine and Rehabilitation, State University of New York at Stony Brook
Jennifer M Gray, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Association, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Hany Nasr, MBBCh, Staff Physician, Department of Physical Medicine and Rehabilitation, State University of New York at Stony Brook
Disclosure: Nothing to disclose.

Anne Conway, BS, PT, Clinical Coordinator, Department of Physical Therapy, Children's National Medical Center of Washington, DC
Anne Conway, BS, PT is a member of the following medical societies: American Physical Therapy Association
Disclosure: Nothing to disclose.

Medical Editor

Teresa L Massagli, MD, Residency Director, Professor, Department of Rehabilitation Medicine and Pediatrics, University of Washington School of Medicine
Teresa L Massagli, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD, Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital
Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

 
 
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