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Available online at www.sciencedirect.com

www.elsevier.com/locate/semperi

Neonatal brachial plexus palsyManagement and

prognostic factors
Lynda J.-S. Yang, MD, PhD
Department of Neurosurgery, University of Michigan, 1500 E. Medical Center Dr, Room 3552 TC, Ann Arbor, MI
48109-5338

article info

abstract

Keywords:

Successful treatment of patients with neonatal brachial plexus palsy (NBPP) begins with a

Brachial plexus

thorough understanding of the anatomy of the brachial plexus and of the pathophysiology

Obstetric

of nerve injury via which the brachial plexus nerves stretched in the perinatal period

Neonatal

manifest as a weak or paralyzed upper extremity in the newborn. NBPP can be classied by

Surgery

systems that can guide the prognosis and the management as these systems are based on

Rehabilitation

the extent and severity of nerve injury, anatomy of nerve injury, and clinical presentation.

Outcomes

Serial physical examinations, supplemented by a thorough maternal and perinatal history,

are critical to the formulation of the treatment plan that relies upon occupational/physical
therapy and rehabilitation management but may include nerve reconstruction and
secondary musculoskeletal surgeries. Adjunctive imaging and electrodiagnostic studies
provide additional information to guide prognosis and treatment. As research improves not
only the technical aspects of NBPP treatment but also the ability to assess the activity and
participation as well as body structure and function of NBPP patients, the functional
outcomes for affected infants have an overall optimistic prognosis, with the majority
recovering adequate functional use of the affected arm. Of importance are (i) early referral
to interdisciplinary specialty clinics that can provide up-to-date advances in clinical care
and (ii) increasing research/awareness of the psychosocial and patient-reported quality-oflife issues that surround the chronic disablement of NBPP.
& 2014 Elsevier Inc. All rights reserved.

Introduction
The management of patients with neonatal brachial plexus
palsy (NBPP) begins with the understanding that stretching the
nerves of the brachial plexus in the perinatal period manifests
as a weak or paralyzed upper extremity, with the passive range
of motion greater than the active, in a newborn.

Classication
The most useful classication scheme for the management
and the prognosis of NBPP was proposed by Gilbert and
E-mail address: ljsyang@med.umich.edu
http://dx.doi.org/10.1053/j.semperi.2014.04.009
0146-0005/& 2014 Elsevier Inc. All rights reserved.

Tassin,1 rened by Narakas2,3 (Table 1), and supported by Birch

et al.4 Group I represents the clinical ndings resulting from
injury to the nerve roots C5 and C6characterized by paresis/
paralysis of the deltoid and biceps but active function in the
limb extensors, wrist, and hand. The clinical ndings in Group II
are related to injury of the nerve roots C5, C6, and C7; therefore,
in addition to paresis/paralysis of the deltoid and the biceps,
paresis/paralysis of the triceps and the wrist extensors is also
present, but the long exors and the intrinsic muscles of the
hand are relatively unaffected. Group III represents paresis/
paralysis of the muscles of the entire arm (ail arm), consistent
with injury of all the nerve roots of the brachial plexus (the C5,

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Table 1 The Gilbert and Tassin/Narakas classication

scheme used for grading the severity of NBPP and for
prognosis.

Group

Affected nerve roots

I
II
III
IV

C5 and C6
C5, C6, and C7
C5, C6, C7, C8, and T1
C5, C6, C7, C8, and T1 with
Horner's syndrome

Rate of full
spontaneous recovery
(%)
!90
!65
o50
!0

C6, C7, C8, and T1). Group IV manifests as a ail arm with the
additional presence of Horner's syndrome (ptosis, meiosis, and
anhydrosis) of the ipsilateral eye and face, presuming injury to
all the nerve roots of the brachial plexus with a very proximal
injury to the lower nerve roots. When this classication system
is used between 2 and 4 weeks after birth, it facilitates
determination of the extent of injury to guide prognosis and
subsequent management.
Other classication schemes that guide the prognosis and the
management rely upon the anatomy and physiology of the
nerve injury. Sunderland reported a physiologic scheme comprising ve types of pathology in increasing severity: (1)
neurapraxia (transient nerve injury that may result from a brief
ischemic episode or from any form of compression, demyelination, or axonal constriction or stretch); (2) axonotmesis
(transient or permanent nerve injury in which the majority of
the supporting structures of the nerve, endoneurium, perineurium, and epineurium are preserved, but disruption of the
axonal nerve bers is present); (3) lesion of the axon and the
endoneurium (likely resulting in permanent nerve injury); (4)
lesion of the axon, endoneurium, and perineurium (likely
resulting in permanent nerve injury); and (5) complete transection of the entire nerve (permanent nerve injury).5 For
example, most nerve reconstruction surgeons manage patients

Fig. 1 Waiter's-tip posture of the right arm.

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conservatively before proposing surgical intervention to ensure

that they do not operate on neurapraxic lesions.
There is also an anatomical scheme comprising four categories based on the anatomical location: upper, lower, and total
plexus palsy.6,7 The concept of an upper plexus palsy involving the C5, C6, and sometimes C7 was initially dened anatomically by Erb8 in 1874 after Duchenne9 described four cases
of complete paralysis of shoulder movement and elbow exion
in 1872. The upper palsy, also commonly referred to as Erb's
palsy, is the most common type of NBPP.4,10 Erb's palsy is
visually recognized by the stereotyped waiter's-tip posture
with the arm adducted, shoulder internally rotated, wrist
exed, and ngers extended (Fig. 1). Similarly, Klumpke's palsy
is visually recognized by a accid hand in an otherwise active
arm, characterizing lower plexus palsy,11,12 this type of NBPP
is extremely rare13 (e.g., 1 in 350 patients in the author's
practice). Panplexopathy is characterized by total plexus
palsy, as described by Narakas Groups III and IV, with total loss
of function of the arm (ail arm).

Assessment of the neonate with NBPP

Physical examination
Obstetric providers may suspect NBPP on the basis of initial
observations of the infant in the perinatal period. However,
physical examination and ultimate diagnosis are best
achieved by the combined efforts of neonatologists, neurologists, pediatricians, physiatrists, and occupational/physical
therapists.
The basic premise of the brachial plexus examination relies
on an understanding of the complex anatomy of the nerves of
the brachial plexus (the complete description of the brachial
plexus is outside the scope of this article but can be found in
the published literature14). Many of the maneuvers in the
physical examination are best evaluated by seeking a
patient's voluntary cooperation, which neonates are unable
to provide. Therefore, different strategies must be used to
assess NBPP in neonates compared with older individuals,
although the basic principles remain constant. These strategies will also vary substantially based on the normal development of the infant during the rst 2 years of life as motor
and sensory function mature.
To provide the appropriate context for the physical examination, a thorough family, maternal, and perinatal history
must be obtained. Soon after birth, the treating physician
should assess the infant for skeletal injuries or bony fractures
by clinical and/or radiographic examination because some
musculoskeletal injuries preclude early occupational/physical therapy for NBPP. Note that no substantial evidence exists
to support further injury of the nervous elements with gentle
handling of the neck and the affected limb (during exercises
to ensure passive range of motion), and immobilization is not
recommended except when associated with skeletal injuries.
Surveillance of spontaneous movements and normal reexes
should be performed as part of the observational examination as global neurologic decits may indicate other neurologic disorders that can occur concurrently with NBPP.15
Similarly, keen observation of ptosis and meiosis, consistent

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with Horner's syndrome, indicates lower trunk involvement

(panplexopathy or Klumpke's palsy). A noticeable asymmetric expansion of the chest cavity and difculty with oxygenation or feeding can indicate diaphragmatic palsy resulting
from phrenic nerve injury (the phrenic nerve derives from the
C3, C4, and C5), which can be conrmed with plain radiographs, ultrasonography, or uoroscopy in the intubated
patient. Diaphragmatic palsy can be a dangerous condition
resulting in respiratory embarrassment and early failure to
thrive, and this should be addressed promptly.16 Likewise,
observation of classic postures (e.g., waiter's tip) implies
particular NBPP lesions.
To focus management paradigms, localization of the NBPP
lesion is critical, and neurologic examination is the mainstay
of lesion localization. With regard to specic motor function,
the treating physician should assess the passive and the
active range of motion of the affected arm. Since contractures
and joint subluxations do not develop until several months
after birth, early limitations of passive range of motion imply
other musculoskeletal disorders.17,18 Active range of motion
and muscle power can be difcult to assess because infants
do not follow commands, but engaging the neonate with
simulation or with irritating stimuli can be instructive. Signicant motor and sensory function can be gleaned from
both spontaneous and stimulated responses, so adequate
time should be devoted to sheer observation. Sensory function is similarly difcult to assess in detail, but an overall
impression can be inferred by judging the infant's response to
particular stimuli (e.g., pinprick, pinch, heat, or cold) in the
respective dermatomes. Indications of chewing or biting of
the arm or the hand imply sensory alterations in the affected
area.19 Similarly, presence of skin rashes in dermatomal
distributions can also indicate sensory alterations. As the
infant grows, measurements of the circumference and the
length of the arm can be tracked as indicators of musculoskeletal dysfunction.20

Assessment scales
Assessment of motor function
Assessment scales in NBPP are used to gauge the extent of
injury, prognosticate potential recovery, and determine treatment. Commonly used scales primarily focus on joint angles
or muscle activation. Muscle power is generally expressed via
the U.K. Medical Research Council scale for muscle movement (MRC scale) (Table 2). This scale provides structured
grading of individual muscle groups, but it does not provide
any information about the overall function of the limb or the
child. Because the MRC scale requires voluntary cooperation,
it is difcult to apply in newborns but can be inferred from
Table 2 The UK Medical Research Council scale for
muscle movement (MRC scale) for muscle power.
M0No detectable muscle contraction
M1Palpable muscle contraction without movement
M2Movement in a horizontal plane (gravity eliminated)
M3Movement overcoming the pull of gravity
M4Movement overcoming resistance beyond the pull of gravity
M5Normal strength

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Table 3 The Active Movement scale (AMS) for assessing

motor function in newborns.
Observation

Muscle grade

Gravity eliminated
No contraction
Contraction, no motion
Motion r1/2 range
Motion 41/2 range
Full motion

0
1
2
3
4

Against gravity
Motion r1/2 range
Motion 41/2 range
Full motion

5
6
7

observation of the infant's responses to stimulation or play.

To overcome these difculties in assessing the motor function in newborns, Curtis et al.21 proposed the Active Movement scale (AMS) (Table 3).
As the infant grows, the function of the whole limb
becomes critical, and the Mallet scale provides a quantiable
assessment for shoulder and elbow or upper plexus function
(Table 4).22 To augment the practitioner's assessment of the
limb, the Mallet scale can be used in conjunction with
Gilbert's classication of shoulder paralysis (Table 5), with
some consistency reported between the two systems.4 For
elbow function, an elbow recovery scale has been suggested
by Gilbert and Raimondi23 (Table 6). Similarly, Raimondi24 has

Table 4 The Mallet scale.

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Table 5 The Gilbert scale for assessing shoulder

function.

Table 7 The Raimondi scale for assessing hand function.

Shoulder function

Stage

Flail shoulder
Abduction or exion to 451; no active external
Abduction o901; external rotation to neutral
Abduction 901; weak external rotation
Abduction o1201; incomplete external rotation
Abduction 41201; active external rotation
Normal

0
I
II
III
IV
V
VI

proposed a hand evaluation scale (Table 7) that has been used

to assess hand function after nerve repair/reconstruction and
found to correlate with the preoperative Gilbert and Tassin/
Narakas group.25

Assessment of overall function

Although the above assessment scales have been the mainstay of outcomes reported by surgeons as a measure of
technical success or for preoperative evaluation,2628 they
do little to address the overall function of the child.29 A
scheme based on ve dimensions of disablement was proposed by the National Center for Medical Rehabilitation
Research comprised of pathophysiology, impairment, functional limitation (activity), disability (participation), and societal limitation.30 It well demonstrates the shortcomings of
the assessment scales described above, especially regarding
the functional limitation (activity), disability (participation),
and societal limitation in patients with NBPP. Likewise, the
International Classication of Functioning, Disability, and
Health denes function based on body functions, activities,
and participation.31 Speech dominance32 and limb preference33 have also been studied in the context of NBPP.
Sundholm et al.34 contend that NBPP should be described in
terms of impairment and disability; they reported that many
children had difculty with activities of daily living. With
further regard to self-care and activities of daily living in a
child with NBPP, the Pediatric Evaluation of Disability Inventory (PEDI) is a tool used to determine a child's ability to
perform self-care activities in relation to developmental ageexpected performance.35 The PEDI was unable to discriminate
Table 6 The GilbertRaimondi scale for assessing elbow
function recovery.
Elbow function

Score

Flexion
Nil or some contraction
Incomplete exion
Complete exion

1
2
3

Extension
No extension
Weak extension
Good extension

0
1
2

Extension decit
01301
301501
4501

225

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0
#1
#2

Description

Grade

Complete paralysis or slight nger exion of no use;

useless thumbno pinch; and some or no sensation
Limited active exion of the ngers; no extension of the
wrist or the ngers; and possibility of thumb lateral
pinch
Active exion of the wrist, with passive exion of the
ngers (tenodesis), and passive lateral pinch of the
thumb
Active complete exion of the wrist and the ngers and
mobile thumb with partial abductionopposition.
Intrinsic balance; no active supination; and good
possibilities for palliative surgery
Active complete exion of the wrist and the ngers;
active wrist extension; and weak or absent nger
extension. Good thumb opposition, with active ulnar
intrinsics, and partial pronation/supination
Hand IV, with nger extension and almost complete
pronation/supination

0
I

II

III

IV

between the self-care ability of children with NBPP versus

their peers but was effective in distinguishing between the
different levels of NBPP severity.36 Application of functional
outcomes measures such as PEDI or creation of new patient-/
parent-reported quality-of-life outcomes measures are
important steps toward functional assessments for determining later childhood treatment and for evaluating treatment
efcacy in patients with NBPP.

Supplementary studies
Electrodiagnostic examination
Supplementing the physical examination with electrodiagnostic (EDX) ndings is helpful to determine whether spontaneous recovery is occurring or whether nerve repair/
reconstruction will be benecial, and a thorough discussion
of EDX in NBPP has been published.37 Early referral of neonates with NBPP and extensive nerve injury may improve
outcomes; e.g., the early presence or absence of elbow
extension or elbow exion on clinical examination and of
motor unit potentials on electrodiagnostic examination in the
biceps muscle correctly predicted whether lesions were mild
or severe with respect to long-term involvement in 8594% of
infants.38
EDX ndings can provide information regarding the location, severity, and extent of NBPP. For example, identication
of an avulsed nerve root is critical to NBPP management;
avulsion injuries are considered neurotmetic, spontaneous
recovery does not occur, and surgical nerve reconstruction is
recommended early. Nerve root avulsions are preganglionic
injuries (the motor cell body is detached from its axon, but
the sensory cell body is continuous with its distal axon, Fig. 2)
and generally do not lend themselves to nerve graft repair but
are amenable to nerve transfers if appropriate donors exist.
In contrast, ruptured (Fig. 3) nerve roots/trunks (postganglionic neurotmetic or rarely axonotmetic injuries; EDX studies can identify but cannot distinguish axonotmesis from

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Fig. 2 Avulsion (preganglionic) lesion.

neurotmesis) are more amenable to nerve graft repair or

rarely spontaneous functional recovery, so conservative management is initially recommended. In either circumstance,
preoperative identication of an avulsed nerve root allows
better development of the intraoperative surgical strategy.
EDX studies can also identify neurapraxic lesions, leading
to the sole recommendation of conservative management.
Neurapraxia is characterized by normal motor and sensory
nerve conduction distal to the site of injury without denervation on needle electromyography (EMG) of the relevant
muscles. However, reduced or absent voluntary motor units
may be seen in the muscles. Neurapraxic lesions generally
resolve spontaneously within a period of weeks to a few
months. If neurological recovery does not progress as
expected, further evaluation is warranted.

Nerve conduction studies (NCS)

The principles of performing NCS in an infant and a young
child are similar to that for an adult patient. However, due to
the infant's age and size, appropriate modications must be
made to accommodate the developing nervous system. It is
commonly accepted that the normal values in NCS vary with
age, and motor conduction velocities in newborns are

Fig. 3 Rupture (postganglionic) lesion.

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approximately half that of adults. NCS in infants is important

but has signicant challenges with quantifying axonal loss
and with correlating the extent of axonal loss with future
recovery.
Using NCS to diagnose avulsion (preganglionic lesions) in
NBPP relies on an understanding of the spinal nerve roots.
The sensory nerve action potential (SNAP) is preserved, but
loss of compound motor action potential (CMAP) coupled
with denervation potentials and loss of voluntary motor unit
action potential (MUAP) recruitment are consistent with the
diagnosis of nerve root avulsion.39 Identication of a preganglionic lesion by EDX studies may be confounded by the
simultaneous presence of both preganglionic and postganglionic lesions. Contrastingly, EDX studies that demonstrate
both motor and sensory axon loss and loss of SNAP and
CMAP are consistent with nerve root/trunk rupture (a postganglionic lesion). Therefore, the presence or the absence of
SNAPs in the context of an absent CMAP from the respective
muscles is the EDX feature that differentiates the avulsion
injury from rupture of the nerve roots.
The axonal viability index has been used to study the
outcomes of infants affected by NBPP,40 and it is dened as
the ratio of the amplitude of the CMAP of the involved side to
that of the unaffected limb. Motor conduction study results
were used to distinguish children with poor outcomes at
1 year of age from those with partial or complete recovery:
those with poor outcomes had an axonal viability index of
o10% for the axillary nerve, o20% for the proximal radial
nerve (triceps), and o50% for the distal radial nerve. Generally, an absent CMAP was associated with a poor outcome.

Electromyography (EMG)
EMG comprises assessment of the muscle at rest and then
during voluntary movement. At rest, the muscle is evaluated
for signs of abnormal spontaneous activity, which is consistent with lack of nervous input. The presence of brillation
potentials and positive sharp waves indicates that nerve
degeneration is occurring. MUAPs are evaluated by assessing
the amplitude, phase, duration, and ring rate-related to
force. Theoretical and animal studies suggest that neonates
likely develop denervation potentials earlier than the adult
time period of 1421 days.41,42 The quality and the quantity of
MUAPs in infants and children are also different from the
standard denition with adult norms. A normal adult MUAP
is triphasic, infant MUAPs are often biphasic, and the amplitude of MUAPs in children aged 03 years ranges between 200
and 700 V.43,44 The recruitment pattern is difcult to elicit as
voluntary activity is not easily controlled or graded since
infants cannot follow commands.
When assessing voluntary muscle activation, EDX focuses
on the presence and the number of voluntary motor units
present and characterizes their morphology recruitment
patterns. Nerve regeneration and reinnervation of muscles
is indicated by collateral sprouting from surviving axons,
appearing as polyphasia, large amplitude units, or increased
duration potentials. Evidence of axonal regeneration is suggested by the presence of nascent units, which are small in
amplitude, highly polyphasic, and have prolonged duration.

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Utility of EDX in NBPP

The practical utility of EDX in NBPP is controversial. Many
contend that needle EMG is overly optimistic when compared
to the patient's clinical presentation and ultimate outcome.4548 The phenomenon of synkinesis (aberrant reinnervation) further confounds EDX ndings and may be the
practical phenomenon underlying the clinical issue of cocontractions45: synkinesis may allow innervation of antagonist muscles that preclude the desired movement. Motor unit
interference pattern was also found to consistently overestimate future clinical recovery, and no correlation was seen
between this particular EMG nding and recovery of clinical
strength.44 Although EDX must be interpreted with caution
and in the context of other clinical information, the sensitivity of EDX for detecting a postganglionic rupture was 92.8%
but only 27.8% for preganglionic avulsion injuries,49 indicating that EDX can be useful in the appropriate situation.

Radiologic examination
In the immediate postnatal period, radiographic imaging may
be indicated urgently to assess for the presence of clavicular
or humeral fractures or diaphragmatic asymmetry, but the
focus of this section will be imaging of the nervous brachial
plexus elements. Keep in mind that neurological decits in
NBPP may mask symptoms due to coincidental, but more
distal, nerve lesions resulting from fractures of the long
bones in the arm,50 and ignoring these coincidental lesions
can lead to decreased outcomes after intervention.
Traditionally, imaging studies of the brachial plexus in NBPP
are performed only when microsurgical nerve repair/reconstruction is indicated due to the potential complications from
the imaging procedure. However, with modern magnetic resonance imaging (MRI) techniques, imaging may be taking its
place in the management arena. Like EDX, radiologic investigations supplement the clinical presentation by attempting to
provide information on the type, location, and extent of nerve
injury. Ideally, radiographic studies of the brachial plexus
should delineate the course of the pathoanatomy of the cervical
spinal roots, from their origin as dorsal and ventral rootlets at
the spinal cord through the vertebral foramina, the extraforaminal spinal nerve roots, the trunks, the divisions, and the
cords of the brachial plexus down to the terminal branches
innervating the muscles of the arm. At present, this remains an
unrealistic ideal as does the functional imaging of central
connections of the brachial plexus in babies. However, the
reported sensitivity of computerized tomography/myelography
(CTM) for detecting a postganglionic rupture was 58.3% and
72.2% for preganglionic nerve root avulsion.49 Consequently,
radiographic imaging is concentrated on these injury types, but
more specically on nerve root avulsions.
Later, a child fails to recover as predicted or new neurological symptoms develop, radiographic examination can
reveal arachnoid cysts compressing the spinal cord or herniation of the spinal cord into a large pseudomeningocele51
and supercial siderosis.52

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for diaphragmatic paralysis consequent to a phrenic nerve

lesion, for which plication may be necessary.16 The integrity
of the diaphragm is essential when the phrenic nerve is being
considered as a possible donor in a nerve transfer in babies
with suspected multiple root avulsions.

Ultrasonography
Few, if any, reports exist regarding the use of ultrasonography (US) in NBPP. We have had some experience applying US
preoperatively and comparing the preoperative CTM or MRI
and intraoperative pathology with the US results. In our
experience, the utility of US is complementary to that of
CTM or MRI as US can give information on the muscles and
the location of the brachial plexus neuroma to facilitate the
formation of strategies for nerve reconstruction. Furthermore, to avoid radiation from x-rays, US can be used to
assess for diaphragmatic movement (phrenic nerve function).

Computed tomography/myelography
CTM has been the long-preferred NBPP diagnostic tool at
most specialty brachial plexus centers. Many investigators
reported high sensitivity in the assessment of intradural root
avulsions,5355 and it permits separate evaluation of the
ventral and the dorsal nerve roots in the intradural space
(Fig. 4). However, the disadvantages of CT-myelography are
the need for general anesthesia and lumbar puncture for
intrathecal contrast introduction, as well as radiation exposure. Other difculties include the inability to determine the
correct spinal level,56 but the absence of hypodense root
shadows with or without a pseudomeningocele is suggestive
for nerve root avulsion/preganglionic injury. Note that the
presence of a pseudomeningocele is not an absolute proof of
root avulsion. CT-myelography cannot assess for ruptures
(postganglionic injury) or other types of lesions of nerve roots
within the foramen or in their extraforaminal course.

Magnetic resonance imaging

MRI is becoming the preferred modality for imaging the brachial
plexus in infants and yields similar information to CTM with
regard to the proximal nerve roots (Fig. 5). MRI avoids the use of
ionizing radiation, does not require lumbar puncture, can be
performed with mild sedation in babies, and may be more costeffective despite the different MRI techniques applied at different institutions.57 Intact, avulsed, compressed, or scarred intradural spinal nerves are all possible to detect by MRI, as the
methodology continues to improve. Furthermore, using differential techniques, imaging of extraforaminal roots, trunks,
divisions, cords, and terminal branches is possible.56 In contrast, although magnetic resonance neurography (MRN) is an
imaging technique that is highly sensitive in detecting lesions
of the peripheral nerves in adults, it has not been applied
successfully in NBPP due to the small size of the nerves.

Treatment
Conservative management/rehabilitation and therapy

Plain radiographs
X-ray examinations can show fractures of the cervical spine,
humerus, or clavicle in the newborn. A chest x-ray can assess

The severity of neonatal brachial plexus palsy (NBPP) ranges

from mild nerve stretch injuries with rapid recovery to nerve

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Fig. 4 A CTM image of an avulsion lesion (A) coronal (B) axial.

root avulsions with no spontaneous recovery. Correspondingly, a signicant percentage of NBPP patients do not regain
full arm function, so the principles of rehabilitation remain
constant: maintain range of motion (ROM) at all relevant
joints to avoid contracture formation, encourage muscle
strengthening, prevent compensatory movement patterns,
and, most importantly, promote normal childhood
development.

Overall rehabilitation management

Rehabilitation management includes the development of
treatment plans that address both short- and long-term
goals. Regardless of whether nerve repair/reconstruction
occurs, occupational and/or physical therapy should be initiated to optimize outcomes; e.g., the infant who develops
early contractures as well as the child who has no contractures will not recover function. The therapist must formulate

Fig. 5 A MR image of an avulsion lesion (A) coronal (B) axial.

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treatment strategies by considering the upper extremity in

the context of the motor power of each muscle, potential
safety precautions, functional recovery, and the long-term
psychosocial effects of NBPP; this can only be accomplished if
the therapist understands the anatomy of the brachial plexus
intimately. Proximal stability and core strength are critical
and underlie the distal mobility and ne/gross motor coordination. Therapy evaluation and treatment can and should
begin as early as day 1 of life, particularly in cases where the
infant is otherwise medically stable.
The most important goal of early therapy for NBPP patients
is maintenance of soft tissue and joint exibility. Passive
range-of-motion exercises are critical and must be taught to
the parents/caregivers to be performed routinely at home.58
These exercises can be performed safely and effectively to
gently stretch the relevant muscles and joint structures to
avoid development of contractures (resulting from excessive
contraction of the functioning muscles that are not counterbalanced by the paretic muscles). As formal therapy appointments wane, the need for parent-initiated home exercises
arises, and multimedia formats have been reported
effective.59
Children with NBPP risk developing skeletal deformities of
the trunk and the affected extremity due to poor bone growth
associated with weakness of certain muscles, unopposed
activities of other muscles, or muscle imbalance.60

Infants
Motor training should begin as early as possible to stimulate
activity in denervated muscles, to enable muscles to be
activated as soon as nerve regeneration has taken place, to
prevent or minimize soft tissue contractures, and to minimize ineffective substitution movements. Motor training
should continue for as long as nerve recovery is still occurring
(potentially for years).
In addition to range-of-motion home exercises, parents
should be educated regarding the need for tummy time at
each diaper change to promote symmetrical head rotation
and positioning. Torticollis is an abnormal head posture,
including ipsilateral tilt, contralateral rotation, and translation, and has been associated with NBPP.61 Persistent
torticollis can lead to plagiocephaly and facial asymmetry;
deformational plagiocephaly can be appreciated as early as 6
weeks of age with a preexisting diagnosis of torticollis.62 For
infants with torticollis, parents should be encouraged to vary
the position of the infant's head during play, feeding, and
sleeping. Use of positioning wedges may be helpful. Home
programs using neck stretches to address tightness of the
sternocleidomastoid muscle may be required for some
infants and should be taught to families by appropriately
trained therapists, and aggressive intervention is rarely
required.
In some instances, a newborn will require a hand/elbow
splint prior to discharge from the hospital (e.g., tightness of
the nger joints and/or signicant atrophy of the thenar
eminence, especially when associated with Horner's syndrome). An elbow exion splint may be indicated if subluxation is present. Extreme hyperextension of the elbow reects
absent biceps muscle activity in the context of intact triceps
muscle activity, causing severe muscle imbalance. Passive

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range-of-motion exercises for elbow exion should be performed with careful attention to position of the forearm in
supination or pronation (whichever position prevents subluxation from occurring).
Pain should be absent during newborn range-of-motion
exercises. If pain is present, re-evaluate for skeletal injury.
Sensory alterations can be present and manifest as the absence
of or impaired sensation in all or part of the extremity, based
upon the pathoanatomy of the nerve injury. With altered
sensation, hyperesthesia and allodynia are expressed in the
newborn with fussiness or chewing of the affected part of the
arm. Desensitization can relieve the symptoms and can be
achieved by the use of a rm touch versus a light touch, the use
of infant massage, a variety of texture inputs from fabrics, or
vibratory input from infant toys.
If a skeletal fracture is present, the arm should be immobilized using a sling, with the shoulder adducted and internally rotated and the elbow exed at 901 so that the arm rests
upon the infant's chest for the rst few weeks. The newborn
should be lifted by scooping the newborn under the buttocks
with one hand and under the head with the other versus
lifting the infant under the axillae. Teaching families to dress
the involved extremity rst and undress it last can reduce
unnecessary movement of the involved extremity during the
healing phase of the fractured area(s).
Once the infant's muscles are stretched and prepared for
activity, elicitation of active (versus passive) range-of-motion
exercises can be encouraged by stroking, tapping, or vibrating
the muscle belly. Elicitation can occur in gravity-eliminated
positions, progressing to antigravity positions, and ultimately
in weight-bearing positions that are developmentally appropriate for the patient. Vibration/stroking can be used to elicit
biceps contraction or elbow exion to achieve movement
patterns of the hand to the face or the mouth, elbow
extension such as batting at toys overhead, and wrist extension patterns to facilitate reaching for toys. The therapy
sessions should include interventions that facilitate the
patient's current level of generalized development. The
impact of the weak arm upon developmental milestones
should be a major focus of every therapy session.
Infants with NBPP learn quickly to adapt to their development with a unilateral bias since there is generally no
accompanying cognitive decit. For example, to preclude
the bias, progression toward symmetrical development
begins with learning to roll to both the right and the left
sides. Some infants master the commando crawl, while
others will not learn to crawl and will progress directly from
sitting to walking. Protective reactions in the affected extremity are often delayed or weak, yet they must be a focus of
therapy. A small therapy ball can be used to develop forward
protective reactions in the prone and the sitting positions.
Similarly, with the increasing popularity of the back-tosleep campaign, prone activities and bilateral neck rotation
must be encouraged to promote maximal function of the
recovering muscles and to prevent plagiocephaly. Use of
inhibitory or facilitative Kinesio-taping (KMS, LLC, Albuquerque, NM) and dynamic weight-shifting activities can maximize the development of proximal stability within the trunk
and the shoulder area. Flexibility throughout the neck and
the trunk is imperative for optimal shoulder range of motion.

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Symmetrical movement patterns facilitate motor planning

and proper development. A motor pattern program should be
initiated to avoid the inadvertent establishment of compensatory motor patterns. Neglect of the affected extremity can
occur, so the affected arm should be brought into the child's
visual eld as much as possible. Encourage the child to
explore the involved hand at midline with the other hand
and, if appropriate, encourage mouthing of the involved
hand. Toys such as play mats, overhead play gyms, wrist
rattles, toys that make noise or vibrate, and lightweight
rattles with small-diameter handles may be used at home
to encourage bilateral integration. Additionally, rehabilitation
management of the toddler, older children, and teenagers has
been discussed in detail elsewhere.63

Botulinum toxin injections

In children with NBPP, botulinum toxin has been used in the
treatment of contractures.64 In a study of 22 children who still
had contractures after serial casting, application of botulinum
toxin type-A (Dysports) to the biceps brachii, brachialis, pronator teres, and pectoralis major muscles combined with serial
casting of the elbow for 30 days resulted in signicantly
increased elbow extension and nine-hole peg test scores but
no change in the Mallet scale or the muscle power after 12
months. Botulinum toxin injections to the triceps muscles have
been utilized to promote elbow exion by temporarily relaxing
the antagonist muscle, but no formal studies support this use.

Pain management
Pain in NBPP, if it occurs, usually does so as the infant
matures, but its presence is difcult to detect in infants and
in young children. In those with chronic disablement, discomfort results from overuse movements, such as keyboarding or performing a task at home or at school. Treatment
goals for the child with pain include the following: (1)
reducing the pain with oral or cutaneous medications, (2)
determining the substituted movement patterns that are
causing the pain, and then (3) teaching the patient to move
more effectively (e.g., use of adaptive equipment)in such a
way that minimizes pain as well as overuse of the adjacent
joints during that particular task.

Education and communication

Education of the families regarding the anatomy, clinical
presentation, and treatment options for brachial plexus palsy
is critical for optimal outcomes for the patient and the
practitioner. NBPP is a complex disorder with acute and
chronic ramications; therefore, it can be overwhelming
and difcult to comprehend. The emotional response may
be similar to those of families who are grieving a loss and
may have signicant effects upon the mother's postpartum
recovery. Fathers tend to react differently than mothers, and
their feelings cannot be discounted. Appropriate communication with pediatricians and other medical care providers of
the patient (such as social workers and neuropsychologists)
can facilitate comprehensive care for the patient and the
family and can reduce the approximately 50% incidence of
pursuit of malpractice by affected families presenting to a
specialty clinic (unpublished data). Therefore, early referral to
an interdisciplinary brachial plexus clinic is often benecial.

38 (2014) 222234

A systematic approach aids in the education of parents/

caregivers. One paradigm consists of identifying the patient
with a chronic disablement, introducing the patient to an
appropriate clinic, assessing the physical/developmental
progress, assessing for biological risks, establishing the cost
and the ability of the parents to cover the cost, and, most
importantly, setting and managing expectations.65

Nerve reconstruction
The appropriate selection of NBPP patients who may benet
from surgical intervention remains controversial, and several
different paradigms have been reported.6668 Most NBPP
surgeons agree that all patients with neurotmetic lesions or
nerve root avulsions are reasonable surgical candidates.
Some consider absent or signicantly impaired hand function, in the context of a ail arm at birth, to be an absolute
indication for nerve surgery as soon as the infant reaches the
age of 3 months69 and/or by 34 months of age for those
patients who demonstrate no spontaneous recovery of
shoulder external rotation and elbow exion/forearm supination at that time. Some surgeons proceed with surgical
exploration if the true shoulder and elbow movement is
absent by 6 months of age, since they feel that the potential
benets from repairing neurotmetic lesions generally outweigh the risks of negative exploration.70 Surgery for NBPP is
rarely performed before 3 months of age and is almost always
performed before 9 months of age.
Early assessment by a specialty center allows institution of
conservative management options, determination of the
severity of the brachial plexus lesion(s), addressing of social
and psychosocial issues, and appropriate time needed to
consider the recommended treatment options for the
parents/caretakers.

Nerve reconstruction strategies

The goal of nerve reconstruction in patients with NBPP is the
restoration of hand grasp function, elbow exion, shoulder
movements, and the extension of the elbow, wrist, and
ngers, in order of priority. The surgical repair/reconstruction
strategy depends upon the number of available viable proximal spinal nerve stumps for grafting (i.e., for ruptures/
postganglionic lesions), the cross-sectional area of the
stumps, and the availability of donor nerves for neurotization
or nerve transfer operations (i.e., for avulsion/preganglionic
lesions). The resultant functional outcome is determined by
integrity of the specic surgical connections made between
proximal and distal stumps and/or between donors and
recipients. A thorough discussion of surgical strategies is
outside the scope of this review.70

Post-operative care
After nerve repair/reconstruction, some surgeons place the
infant's upper body in a prefabricated cast to limit movement
of the head and the affected arm for 2 weeks, whereas other
surgeons do not immobilize. Patients undergo clinical examinations at our outpatient clinic initially at frequent intervals
and then at 6-month intervals. Recovery of function can
occur up to 45 years after nerve reconstruction.

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Outcomes
Natural history
The natural history of NBPP, around which the management
and the prognosis revolve, remains the subject of speculation
and controversy in the literature. The complete potential
scope of NBPP is difcult to dene because of the variety of
theoretical combinations of lesions within the elements of
the brachial plexus; e.g., because the brachial plexus is
comprised of ve roots, three trunks, six divisions, three
cords, and ve terminal branches, thousands of theoretically
different brachial plexus lesions are possible for the nerves
alone, even without regard to additional musculoskeletal
issues, although the most common form of NBPP is the
supraclavicular upper trunk lesion.
Further difculties with the sheer determination of the
natural history include the denition of recovery and the
potential bias introduced by the referral patterns of reporting
physicians71,72 since many patients with Erb's palsy recover
spontaneously and are not referred to the specialists who
publish most reports. With these caveats in mind, some
authors provide an encouraging view of the natural history
of NBPP with over 80% occurrence of a favorable functional
outcome or complete recovery,7378 whereas other authors
provide a opposing view, with less than 50% with good
recovery or freedom from persisting disabilities.72,7983
As the absence of spontaneous clinical improvement persists over increasing time, the potential for recovery diminishes,74,84,85 and early recovery (clinical improvement within
weeks with functional recovery by 34 months) is generally
associated with favorable outcomes.74,86 The predictors of
recovery described above use simple clinical muscle assessments (e.g., Narakas Classication). Other authors have constructed paradigms based on more complicated statistical
analyses of multiple independent clinical variables.38,75,87
Regardless, a number of children appear normal and seem
to have recovered function, but the affected extremity is not
equally functional, when measured by more appropriate
sensitive tests.

38 (2014) 222234

231

strategies, and varied assessment techniques) preclude direct

comparison of surgical results among studies. Therefore, the
following describes the results from representative studies
and reviews.92 Clarke et al. reported that early improvements
in neurologic function were produced by neurolysis but were
unsustained over time, whereas nerve grafting after resection
of the neuroma-in-continuity produced signicant improvements in function with a mean follow-up of 4 years.93 Shenaq
et al.94 reported that in 282 NBPP infants with a mean followup of 5 years, 75% had good to excellent results after primary
and secondary reconstructive surgery. Gilbert et al.91,95
reported the results of 436 patients who underwent nerve
reconstruction and secondary reconstructive procedures for
NBPP: 80% with Group I palsy and 61% with Group II palsy had
good or excellent shoulder function after 4 years. For
elbow function, the study reported good results in all of the
Group I and II patients and good results in 81% of Group III
and IV patients. In general, hand function after C8-T1 injury
is difcult to recover, and secondary shoulder reconstructive
procedures improve the overall outcome. These results reect
the complex nature of the surgical strategy and the need to
evaluate the treatment course longitudinally, even after a
primary surgery is completed.
Additionally, neurotizations or nerve transfers are often
undertaken as part of the nerve reconstruction or alone as an
isolated procedure. The spinal accessory nerve has been used
widely to neurotize the suprascapular nerve to improve
shoulder function by reinnervating the supraspinatus and
infraspinatus muscles (part of the rotator cuff). The results of
this transfer are difcult to assess because it is often done in
conjunction with other nerve transfers to restore deltoid
muscle function and conicting reports exist.96,97 In contrast,
nerve transfers to restore elbow exion generally yield good
to excellent results.98102
Regardless of the neurologic recovery, functional recovery
also can be compromised by musculoskeletal defects (e.g.,
contractures and joint subluxation), even with appropriate
therapy. When spontaneous recovery and/or primary nerve
reconstruction does not yield adequate functional recovery,
addressing the consequent shoulder difculties103 and the
lack of hand function104 can signicantly improve the outcomes of patients with NBPP.

Surgical outcomes
Primary nerve reconstruction
The indications for surgical nerve reconstruction in NBPP
vary among different practitioners, with the exception of
Narakas Group III and IV lesions, for which nerve reconstruction is generally recommended. For example, some feel that
the inability to pass the cookie test at 9 months is a
reasonable indication for surgery,88,89 whereas others rely
upon the towel test (inability to remove a towel covering
the faces at 6 months with the affected arm)90 or the lack of
biceps function at 3 months of age.91 Many practitioners use a
combination of these clinical observations supplemented by
ancillary studies to guide their practice, standard guidelines
or critical pathways have been developed.
Similarly, many challenges (including the variability of
anatomical lesions in the complex brachial plexus structure
and adjacent musculoskeletal elements, differing surgical

Conclusion
In the 21st century, infants who sustain NBPP have an overall
optimistic prognosis, with the majority recovering adequate
functional use of the affected arm. However, of utmost
importance are (i) early referral to interdisciplinary specialty
clinics that can provide up-to-date advances in clinical care
and (ii) increasing research/awareness of the psychosocial
and patient-reported quality-of-life issues that surround the
chronic disablement of NBPP.

refere nces

1. Gilbert A, Tassin JL. Surgical repair of the brachial plexus in

obstetric paralysis. Chirurgie. 1984;110(1):7075.

232

SE

M I N A R S I N

E R I N A T O L O G Y

2. Narakas AO. Obstetrical brachial plexus injuries. In: Lamb

DW, ed, The Paralysed Hand. The Hand and Upper Limb.
Edinburgh [Lothian]; New York, NY: Churchill Livingstone;
1987. 116135.
3. Narakas AO. Injuries to the brachial plexus. In: Bora FWJ, ed,
The Pediatric Upper Extremity: Diagnosis and Management. Philadelphia, PA: Saunders; 1986. 247258.
4. Birch R, Bonney G, Wynn Parry CB. Birth Lesions of the
Brachial Plexus. Surgical Disorders of the Peripheral Nerves.
London: Churchill Livingstone; 1998;209233.
5. Sunderland S. Nerves and nerve injuries. In: Green DP,
Hotchkiss RN, Pederson WC, et al., eds. Green's Operative
Hand Surgery, 4th ed. New York, NY: Churchill Livingstone;
1999. 750779.
6. Sunderland S. A classication of peripheral nerve injuries
producing loss of function. Brain. 1951;74(4):491516.
7. Dodds SD, Wolfe SW. Perinatal brachial plexus palsy. Curr
Opin Pediatr. 2000;12(1):4047.
8. Erb W. Uber eine eigentumliche Lokalisation von Lahmungen im Plexusbrachialis. Verh Naturhistorisch Med Ver Heidelberg. 1874;2:130136.
9. Duchenne GBA. De l'electrisation localisee et de son application a
la pathologie et a la therapeutique, 2nd ed. Paris: J. B. Balliere;
1872.
10. Gilbert A. Long-term evaluation of brachial plexus surgery in
obstetrical palsy. Hand Clin. 1995;11(4):583594 [discussion
94-5].
11. Dejerine-Klumpke A. Contribution a l'etude des paralysies
radiculaires du plexus brachial. Paralysies radiculaires
totales. Paralysies radiculaires inferieures. De la participation de lets sumpathiques oculo-pupillaires dans ces paralysies. Rev Med Paris. 1885;5:591616.
12. Ulgen BO, Brumblay H, Yang LJ, Doyle SM, Chung KC.
Augusta Dejerine-Klumpke, M.D. (1859-1927): a historical
perspective on Klumpke's palsy. Neurosurgery. 2008;63
(2):359366 [discussion 66-7].
13. al-Qattan MM, Clarke HM, Curtis CG. Klumpke's birth palsy.
Does it really exist? J Hand Surg Br. 1995;20(1):1923.
14. Medical Research Council of UK. AIDS to Examination of the
Peripheral Nervous System, 4th ed. London: Saunders (Guarantors of Brain); 2000.
15. Alfonso I, Alfonso DT, Price AE, Grossman JA. Cortical
dysplasia and obstetrical brachial plexus palsy. J Child Neurol.
2008;23(12):14771480.
16. Bowerson M, Nelson VS, Yang LJ. Diaphragmatic paralysis
associated with neonatal brachial plexus palsy. Pediatr Neurol. 2010;42(3):234236.
17. Hoeksma AF, Wolf H, Oei SL. Obstetrical brachial plexus
injuries: incidence, natural course and shoulder contracture.
Clin Rehabil. 2000;14(5):523526.
18. Steeg AM, Hoeksma AF, Dijkstra PF, Nelissen RG, De Jong BA.
Orthopaedic sequelae in neurologically recovered obstetrical
brachial plexus injury. Case study and literature review.
Disabil Rehabil. 2003;25(1):18.
19. McCann ME, Waters P, Goumnerova LC, Berde C. Selfmutilation in young children following brachial plexus birth
injury. Pain. 2004;110(1-2):123129.
20. Uysal H, Demir SO, Oktay F, Selcuk B, Akyuz M. Extremity
shortness in obstetric brachial plexus lesion and its relationship to root avulsion. J Child Neurol. 2007;22(12):13771383.
21. Curtis C, Stephens D, Clarke HM, Andrews D. The active
movement scale: an evaluative tool for infants with obstetrical brachial plexus palsy. J Hand Surg Am. 2002;27
(3):470478.
22. Mallet J. Obstetrical paralysis of the brachial plexus. II. Therapeutics. Treatment of sequelae. Priority for the treatment of
the shoulder. Method for the expression of results. Rev Chir
Orthop Reparatrice Appar Mot. 1972;58(suppl 1):166168.

38 (2014) 222234

23. Gilbert A, Raimondi P. Evaluation of results in obstetric

brachial plexus palsy. The elbow. International meeting on
obstetric brachial plexus palsy. Heerlen, NL; 1996.
24. Raimondi P. Evaluation of results in obstetric brachial plexus
palsy. The hand. International meeting on obstetric brachial
plexus palsy. Heerlen, NL; 1993.
25. Kirjavainen M, Remes V, Peltonen J, Rautakorpi S, Helenius I,
Nietosvaara Y. The function of the hand after operations for
obstetric injuries to the brachial plexus. J Bone Joint Surg Br.
2008;90(3):349355.
26. Gilbert A, Tassin J-L. Obstetrical palsy: a clinical, pathologic,
and surgical review. In: Terzis JK, ed, Microreconstruction of
Nerve Injuries. Philadelphia, PA: WB Saunders; 1987. 529553.
27. Waters PM. Comparison of the natural history, the outcome
of microsurgical repair, and the outcome of operative reconstruction in brachial plexus birth palsy. J Bone Joint Surg Am.
1999;81(5):649659.
28. Gilbert A, Khouri N, Carlioz H. Birth palsy of the brachial
plexussurgical exploration and attempted repair in twenty
one cases. Rev Chir Orthop Reparatrice Appar Mot. 1980;66
(1):3342 [author's transl].
29. Piatt JH Jr. Birth injuries of the brachial plexus. Pediatr Clin
North Am. 2004;51(2):421440.
30. Butler C, Chambers H, Goldstein M, et al. Evaluating research
in developmental disabilities: a conceptual framework for
reviewing treatment outcomes. Dev Med Child Neurol. 1999;41
(1):5559.
31. World Health Organization. International classication of
functioning, disability, and health. Geneva: World Health
Organization; 2001;125 (11).
32. Auer T, Pinter S, Kovacs N, et al. Does obstetric brachial
plexus injury inuence speech dominance? Ann Neurol.
2009;65(1):5766.
33. Yang LJ, Anand P, Birch R. Limb preference in children with
obstetric brachial plexus palsy. Pediatr Neurol. 2005;33
(1):4649.
34. Sundholm LK, Eliasson AC, Forssberg H. Obstetric brachial
plexus injuries: assessment protocol and functional outcome at age 5 years. Dev Med Child Neurol. 1998;40(1):411.
35. Dumas HM, Fragala-Pinkham MA, Haley SM, et al. Computer
adaptive test performance in children with and without
disabilities: prospective eld study of the PEDI-CAT. Disabil
Rehabil. 2012;34(5):393401.
36. Ho ES, Curtis CG, Clarke HM. Pediatric Evaluation of Disability Inventory: its application to children with obstetric
brachial plexus palsy. J Hand Surg Am. 2006 Feb;31(2):197202.
37. Spires MC, Leonard JA, Wolfe J. The role of electrodiagnosis
in infants with brachial plexus palsies. In: Chung KC,
McGillicuddy JE, Yang L J-S, et al., eds. Practical Management
of Adult and Pediatric Brachial Plexus Palsy. London: Elsevier;
2011.
38. Malessy MJA, Pondaag W, Yang LJS, Hofstede-Buitenhuis SM,
le Cessie S, van Dijk JG. Severe obstetric brachial plexus
palsies can be identied at one month of age. PLoS One.
2011;6(10):e26193.
39. Smith SJ. The role of neurophysiological investigation in
traumatic brachial plexus lesions in adults and children.
J Hand Surg Br. 1996;21:145147.
40. Heise CO, Siqueira MG, Martins RS, et al. Motor nerve
conduction studies in obstetric brachial plexopathy for a
selection of patients with a poor outcome. J Bone Joint Surg
Am. 2009;91:17291737.
41. Van Dijk JG, Pondaag W, Malessy MJ. Obstetric lesions of the
brachial plexus. Muscle Nerve. 2001;24:14511461.
42. Gonik B, McCormick EM, Verweji BH, et al. The timing of
congenital brachial plexus injury: a study of electromyographic ndings in the newborn piglet. Am J Obstet Gynecol.
1998;178:688695.

E M I N A R S I N

E R I N A T O L O G Y

43. Carmo RJ. Motor unit action potential parameters in human

newborn infants. Arch Neurol. 1960;3:136140.
44. Sacco G, Buchthal F, Rosenfalck P. Motor unit patterns at
different ages. Arch Neurol. 1962;6:366373.
45. Heise CO, Siqueira MG, Martins RS, et al. Clinicalelectromyography correlation in infants with obstetric brachial plexopathy. J Hand Surg Am. 2007;32:9991004.
46. Sherburn EW, Kaplan SS, Kaufman BA, et al. Outcome of
surgically treated birth-related brachial plexus injuries in
twenty cases. Pediatr Neurosurg. 1997;27:1927.
47. Clarke HM, Curtis CG. An approach to obstetrical brachial
plexus injuries. Hand Clin. 1995;4:563581.
48. Gilbert A, Razaboni R, Amar-Khodja S. Indications and
results of brachial plexus surgery in obstetrical palsy. Orthop
Clin North Am. 1998;19:91105.
49. VanderHave KL, Bovid K, Alpert H, et al. Utility of electrodiagnostic testing and CT myelography in the preoperative
evaluation of neonatal brachial plexus birth palsy. J Neurosurg Pediatr. 2012;9(3):283289.
50. Bodner G, Buchberger W, Schocke M, et al. Radial nerve palsy
associated with humeral shaft fracture: evaluation with US
initial experience. Radiology. 2001;219:811816.
51. Miravet E, Sinisterra S, Birchansky S, et al. Cervicothoracic
extradural arachnoid cyst: possible association with obstetric brachial plexus palsy. J Child Neurol. 2002;17:770772.
52. Aquilina K, Kumar R, Lu J, et al. Supercial siderosis of the
central nervous system following cervical nerve root avulsion: the importance of early diagnosis and surgery. Acta
Neurochir (Wien). 2005;147:291297.
53. Slooff ACJ, Versteege CWM, Blaauw G, et al. Radiological and
related investigations. In: Gilbert A, ed, Brachial Plexus Injuries. London: Martin Dunitz Ltd.; 2001. 3137.
54. Hashimoto T, Mitomo M, Hirbuki N. Nerve root avulsion of
birth palsy: comparison of myelography with CT myelography and somatosensory evoked potentials. Radiology.
1991;178:841845.
55. Walker AT, Chaloupka JC, de Lotbiniere AC, et al. Detection
of nerve rootlet avulsion on CT myelography in patients
with birth palsy and brachial plexus injury after trauma. Am
J Roentgenol. 1996;167:12831287.
56. Birchansky S, Altman N. Imaging the brachial plexus and
peripheral nerves in infants and children. Semin Pediatr
Neurol. 2000;7:1525.
57. van Ouwerkerk WJR, van der Sluijs JA. Radiographic assessment in pediatric brachial plexus palsies. In: Chung KC,
McGillicuddy JE, Yang L J-S, et al., eds. Practical Management of
Adult and Pediatric Brachial Plexus Palsy. London: Elsevier;
2011.
58. University of Michigan Brachial Plexus Program. Home
Exercise Therapy Program for Brachial Plexus Palsy. Ann
Arbor, MI: Evolution Media; 2007.
59. Murphy KM, Rasmussen L, Hervey-Jumper SL, et al. Assessment of a home exercise DVD for children with brachial
plexus palsy. PM R. 2011;4(3):190197.
60. Shepherd RB. Brachial plexus injury. In: Campbell SK, ed,
Decision Making in Pediatric Neurologic Physical Therapy. Philadelphia, PA: Churchill Livingstone; 1999. 235259.
61. Hervey-Jumper SL, Justice D, Vanaman M, Nelson VS, Yang L
J-S. Torticollis associated with neonatal brachial plexus
palsy. Pediatr Neurol. 2011;45(5):305310.
62. Oh AK, Hoy EA, Rogers GF. Predictors of severity in deformational plagiocephaly. J Craniofac Surg. 2009;20:16291630.
63. Nelson VS, Justice D, Rasmussen L, Popadich MG. Rehabilitation concepts for pediatric brachial plexus palsies. In:
Chung KC, McGillicuddy JE, Yang L J-S, et al., eds. Practical
Management of Adult and Pediatric Brachial Plexus Palsy.
London: Elsevier; 2011.

38 (2014) 222234

233

64. Basciani M, Intiso D. Botulinum toxin type-A and plaster cast

treatment in children with upper brachial plexus palsy.
Pediatr Rehabil. 2006;9:165170.
65. Godfrey MM, Nelson EC, Wasson JH, et al. Microsystems in
health care: planning patient-centered services. Jt Comm J
Qual Saf. 2003;29:159170.
66. Borschel GH, Clarke HM. Obstetrical brachial plexus palsy.
Plast Reconstr Surg. 2009;124:144e155e.
67. Bertelli JA, Ghizoni MF. The towel test: a useful technique for
the clinical and electromyographic evaluation of obstetric
brachial plexus palsy. J Hand Surg Br. 2004;29:155158.
68. Haerle M, Gilbert A. Management of complete obstetric
brachial plexus lesions. J Pediatr Orthop. 2004;24:194200.
69. Pondaag W, Malessy MJ. Recovery of hand function following
nerve grafting and transfer in obstetric brachial plexus
lesions. J Neurosurg. 2006;105:3340.
70. Malessy MJA, Pondaag W. Nerve repair/reconstruction strategies for neonatal brachial plexus palsies. In: Chung KC,
McGillicuddy JE, Yang L J-S, et al., eds. Practical Management of
Adult and Pediatric Brachial Plexus Palsy. London: Elsevier;
2011.
71. Jahnke AH Jr, Bovill DF, McCarroll HR Jr, James P, Ashley RK.
Persistent brachial plexus birth palsies. J Pediatr Orthop.
1991;11(4):533537.
72. Wickstrom J. Birth injuries of the brachial plexus. Treatment
of defects in the shoulder. Clin Orthop. 1962;23:187196.
73. Bennet GC, Harrold AJ. Prognosis and early management of
birth injuries to the brachial plexus. Br Med J. 1976;1
(6024):15201521.
74. Gordon M, Rich H, Deutschberger J, Green M. The immediate
and long-term outcome of obstetric birth trauma. I. Brachial
plexus paralysis. Am J Obstet Gynecol. 1973;117(1):5156.
75. Michelow BJ, Clarke HM, Curtis CG, Zuker RM, Seifu Y,
Andrews DF. The natural history of obstetrical brachial
plexus palsy. Plast Reconstr Surg. 1994;93(4):675680 [discussion 81].
76. Donn SM, Faix RG. Long-term prognosis for the infant with
severe birth trauma. Clin Perinatol. 1983;10(2):507520.
77. Brown KL. Review of obstetrical palsies. Nonoperative treatment. Clin Plast Surg. 1984;11(1):181187.
78. Bisinella GL, Birch R. Obstetric brachial plexus lesions: a
study of 74 children registered with the British Paediatric
Surveillance Unit (March 1998-March 1999). J Hand Surg Br.
2003;28(1):4045.
79. Adler JB, Patterson RL Jr. Erb's palsy. Long-term results of
treatment in eighty-eight cases. J Bone Joint Surg Am. 1967;49
(6):10521064.
80. Gjorup L. Obstetrical lesion of the brachial plexus. Acta
Neurol Scand. 1966;42(suppl 18):180.
81. Rossi LN, Vassella F, Mumenthaler M. Obstetrical lesions of
the brachial plexus. Natural history in 34 personal cases. Eur
Neurol. 1982;21(1):17.
82. Eng GD. Brachial plexus palsy in newborn infants. Pediatrics.
1971;48(1):1828.
83. Eng GD, Koch B, Smokvina MD. Brachial plexus palsy in
neonates and children. Arch Phys Med Rehabil. 1978;59
(10):458464.
84. Sever JW. Obstetric paralysis: its etiology, pathology, clinical
aspects and treatment, with report of four hundred and
seventy cases. Am J Dis Child. 1916;12:541578.
85. Gilbert A, Brockman R, Carlioz H. Surgical treatment of
brachial plexus birth palsy. Clin Orthop Relat Res. 1991;264:
3947.
86. Pondaag W, Malessy MJ, van Dijk JG, Thomeer RT. Natural
history of obstetric brachial plexus palsy: a systematic
review. Dev Med Child Neurol. 2004;46(2):138144.
87. Nehme A, Kany J, Sales-De-Gauzy J, Charlet JP, Dautel G,
Cahuzac JP. Obstetrical brachial plexus palsy. Prediction of

234

88.

89.

90.

91.

92.

93.

94.

95.

96.

97.

SE

M I N A R S I N

E R I N A T O L O G Y

outcome in upper root injuries. J Hand Surg Br. 2002;27

(1):912.
Marcus JR, Clarke HM. Management of obstetrical brachial
plexus palsy: evaluation, prognosis, and primary surgical
treatment. Clin Plast Surg. 2003;30(2):289306.
Curtis C, Stephens D, Clarke HM, Andrews D. The active
movement scale: an evaluative tool for infants with obstetrical
brachial plexus palsy. J Hand Surg Am. 2002;27(3):470478.
Bertelli JA, Ghizoni MF. The towel test: a useful technique for
the clinical and electromyographic evaluation of obstetric
brachial plexus palsy. J Hand Surg Br. 2004;29(2):155158.
Gilbert A. Long-term evaluation of brachial plexus surgery in
obstetrical palsy. Hand Clin. 1995;11(4):583594 [discussion
594-585].
Alhodaib NI, Clarke HM. Outcomes of treatment for neonatal
brachial plexus palsy. In: Chung KC, McGillicuddy JE, Yang L
J-S, et al., eds. Practical Management of Adult and Pediatric
Brachial Plexus Palsy. London: Elsevier; 2011.
Lin JC, Schwentker-Colizza A, Curtis CG, Clarke HM. Final
results of grafting versus neurolysis in obstetrical brachial
plexus palsy. Plast Reconstr Surg. 2009;123(3):939948.
Shenaq SM, Bullocks JM, Dhillon G, Lee RT, Laurent JP.
Management of infant brachial plexus injuries. Clin Plast
Surg. 2005;32(1):7998 (ix).
Gilbert A, Pivato G, Kheiralla T. Long-term results of primary
repair of brachial plexus lesions in children. Microsurgery.
2006;26(4):334342.
Terzis JK, Kostas I. Outcomes with suprascapular nerve
reconstruction in obstetrical brachial plexus patients. Plast
Reconstr Surg. 2008;121(4):12671278.
Pondaag W, de Boer R, van Wijlen-Hempel MS, HofstedeBuitenhuis SM, Malessy MJ. External rotation as a result of

38 (2014) 222234

98.

99.

100.

101.

102.

103.

104.

suprascapular nerve neurotization in obstetric brachial

plexus lesions. Neurosurgery. 2005;57(3):530537 [discussion
530-537].
Chuang DC-C, Mardini S, Ma H-S. Surgical strategy for infant
obstetrical brachial plexus palsy: experiences at Chang Gung
Memorial Hospital. Plast Reconstr Surg. 2005;116(1):132142.
Kawabata H, Shibata T, Matsui Y, Yasui N. Use of intercostal
nerves for neurotization of the musculocutaneous nerve in
infants with birth-related brachial plexus palsy. J Neurosurg.
2001;94(3):386391.
El-Gammal TA, Abdel-Latif MM, Kotb MM, et al. Intercostal
nerve transfer in infants with obstetric brachial plexus
palsy. Microsurgery. 2008;28(7):499504.
Noaman HH, Shiha AE, Bahm J. Oberlin's ulnar nerve transfer to the biceps motor nerve in obstetric brachial plexus
palsy: indications, and good and bad results. Microsurgery.
2004;24(3):182187.
Wellons JC, Tubbs RS, Pugh JA, et al. Medial pectoral nerve to
musculocutaneous nerve neurotization for the treatment of
persistent birth-related brachial plexus palsy: an 11-year
institutional experience. J Neurosurg Pediatr. 2009;3(5):
348353.
VanderHave KL, Kozin SH. Shoulder sequelae in children
with brachial plexus palsy. In: Chung KC, McGillicuddy JE,
Yang L J-S, et al., eds. Practical Management of Adult and
Pediatric Brachial Plexus Palsy. London: Elsevier; 2011.
Sebastin SJ, Chung KC. Reconstructive strategies for recovery
of hand function. In: Chung KC, McGillicuddy JE, Yang LJ-S,
et al., eds. Practical Management of Adult and Pediatric Brachial
Plexus Palsy. London: Elsevier; 2011.