15

Brachial Plexus Palsy

ERBS PALSY, KLUMPKES PALSY,
OBSTETRIC PALSY

GENESIS
The frequency of brachial plexus palsy has been
decreasing with improved obstetric management
and is currently 0.37 to 1.89 per 1000 newborns.1,2
Supraclavicular traction or stretching of the brachial plexus during delivery can injure nerve fibers;
hence this injury is sometimes termed obstetric
palsy. The fibers that originate from the fifth and
sixth cervical segments are usually the most commonly and severely affected. Occasionally fibers
from C7, C8, and T1 can also be affected. Lesions
that affect the upper segments (C5C7) result in
Erbs palsy, whereas lesions that affect the lower
spinal segments (C7T1) result in Klumpkes
palsy. There may be associated injuries suggesting
a difficult delivery, such as fracture of the clavicle
or humerus (9%21% of cases), diaphragmatic
paralysis (5%9%), or facial palsy (5%14%).3,4
The position at delivery is related to the risk of
brachial plexus injury, and infants delivered vaginally from an occipitoposterior position have a
higher incidence of Erbs palsy and facial palsy than
those delivered from the occipitoanterior position.5
Traction to the plexus, especially the upper
plexus, occurs during delivery when the angle
between the neck and shoulder is suddenly and forcibly increased, with the arms in an adducted position. This can occur during vertex deliveries when
traction is placed on the head to deliver the aftercoming shoulder, particularly when the shoulders
are caught against the pelvic brim in shoulder dystocia, as forceful contractions push the head and trunk
forward. Brachial plexus palsy can also occur during breech deliveries when the adducted arm is
pulled forcefully downward to free the after-coming
head (accounting for 24% of brachial plexus palsies) or during other malpresentations when the
head is rotated to achieve an occipitoanterior presentation.3 The lower plexus is most susceptible to
injury when traction is exerted on an abducted arm,
such as occurs in vertex deliveries when traction

is applied to an abducted prolapsed arm, or during

breech deliveries when traction is applied to the
trunk or legs while the after-coming arm is fixed
in abduction.3 Spinal nerves are attached to the
vertebral transverse process distal to the intervertebral foramen, encased in funnel-shaped dural
sleeves, and enmeshed in a network of rami,
cords, and trunks to form the brachial plexus;
these factors serve to protect the plexus from traction injury. When traction is excessively rapid and
forceful, then diffuse multifocal injury occurs,
including avulsion of the roots from the cord in
the most severe injuries. Risk factors include technically difficult (57%) or breech (9%) deliveries,
fetal macrosomia (weight >4 kg) (55%), shoulder
dystocia, multiparous mothers, prolonged labor, or
fetal hypotonia leading to loss of the normal cushioning effect of intact muscle tone.3-6 There are
also reports of prenatal-onset brachial plexus injuries in which denervation was demonstrated by
electromyography (EMG) shortly after birth. One
child demonstrated left brachial plexus injury, left
Horners syndrome, left phrenic nerve injury, and
hypoplasia of the left hand in addition to distortion of the first four ribs due to pressure on the
left side of the neck and shoulder from the septum
of a bicornuate uterus.7
The advent of microsurgical techniques and neuroelectrodiagnostic techniques has fostered development of new neurosurgical techniques to repair
brachial plexus injuries, although most infants
recover spontaneously by age 4 months and only
10% to 20% of cases require surgery.8 Severe
lateral flexion of the infants neck at delivery
makes avulsion of the lower brachial plexus nerve
roots four times more common than avulsion of
the upper plexus.8 Among 91 infants observed
through age 2 years who sustained a brachial
plexus birth injury and were treated with only physical and occupational therapy, 63 children with an
upper or middle plexus injury recovered good to
89

90 Neurapraxias (Palsies)
excellent shoulder and hand function.9 Of the
remaining 28 infants, 12 sustained global injury,
resulting in a useless arm, and 16 infants showed
inadequate recovery of deltoid and biceps function
by age 6 months. These authors concluded that
children with global injury would clearly benefit
from early nerve reconstruction. By age 6 months,
careful examination of the infant in the seated
position (in order to evaluate shoulder function)
demonstrated the potential for almost full recovery
in most infants. Recovery of motor and sensory
nerve function is attributed to axonal regeneration
with re-innervations of original target muscle tissue, and functional improvement may continue
for 5 years or longer.10 This longer period of recovery mirrors adaptational mechanisms at the spinal
and supraspinal level, which overcome initial motor
neuron loss.10,11 After perinatal upper brachial

plexus injury to spinal roots C5 and C6, spinal root

C7 contributes to biceps and deltoid innervations,
but this does not occur in the adult.11,12

FEATURES
Lesions that affect the upper segments (C5, C6,
and sometimes C7) result in Erbs palsy, paralyzing the abductors, external rotators, and extensors
of the shoulder as well as injuring the flexors and
supinators of the forearm (Fig. 15-1). The infants
arm tends to hang limply adducted and internally
rotated at the shoulder, with pronation and extension at the elbow, absent biceps and brachioradialis tendon jerks, and absent Moro response on the
side of the lesion.3,4 If C7 is also involved, then a
wrist drop will be noted, with the hand flexed in a

FIGURE 15-1. This large-for-gestational-age infant experienced shoulder dystocia,

resulting in a traumatic delivery that damaged his left brachial plexus, affecting C5,
C6, and C7 and resulting in Erbs palsy. This injury paralyzed the abductors, external
rotators, and extensors of his left shoulder and injured the flexors and supinators of
his forearm. His arm hangs limply adducted and internally rotated at the shoulder,
with pronation and extension at the elbow, absent biceps and brachioradialis tendon
jerks, and absent Moro response on the side of the lesion. Due to involvement of C7,
he manifests wrist drop, with the hand flexed in a waiters tip position and with an
absent triceps jerk.

Brachial Plexus Palsy 91

waiters tip position and with an absent triceps
jerk. Upper plexus injuries (Erbs palsy) may be
present without lower plexus injuries; however,
lower plexus injury is usually accompanied by
some degree of upper plexus damage. Lesions that
affect only lower spinal segments (C7, C8, and
T2) are much less common, and loss of C7 results
in paralysis of the elbow, wrist, and finger extensors, causing wrist drop. Loss of C8 and T1 causes
loss of wrist and finger flexors as well as intrinsic
hand muscles causing extension of the metacarpal-phalangeal joints and flexion at the proximal
and distal interphalangeal joints (Klumpkes
palsy).3,4 The infant manifests a flexed arm with
the shoulder in a normal position with flexed wrist
and fingers, absent grasp reflex, sensory loss, and
loss of sweating on the arm and hand. Injury to T1
at the root level can affect sympathetic fibers to
the face, resulting in ipsilateral Horners syndrome
(ptosis, miosis, anhydrosis, facial flushing, and failure of iris pigmentation). Lesions that affect C5 and
C6 are most common and account for 58% to 72%
of brachial plexus palsies, followed by those affecting C5, C6, and C7 (18%) and those affecting the
entire brachial plexus (C5T1) (10%). Most cases
are unilateral (56% right-sided, 41% left-sided),
with only 3% affecting both arms.3,6

MANAGEMENT AND
PROGNOSIS
Diagnosis is based on clinical features of lower
motor neuron weakness. Additional studies may
help determine prognosis, such as motor conduction velocities in the median and ulnar nerves;
assessment of sensory action potentials in the
median, ulnar, and radial nerves; EMG of affected
muscles; radiographs; and magnetic resonance
imaging (MRI) or myelography with contrast
when avulsion of roots is suspected. Although
the mainstay of treatment is physical therapy with
range-of-motion exercises, no treatment is advised
during the first 7 to 10 days after birth because
traumatic neuritis makes arm movement painful.3
Physical therapy should then be promptly initiated
because contractures can develop quickly in this
condition. For upper plexus injuries, range-ofmotion exercises should be initiated for the
shoulder and elbow, along with abduction of the
arm with the scapula fixed by one hand in order
to prevent the development of scapulohumeral
adhesions.3 For middle and lower plexus injuries,
the paralyzed hand and wrist require range-ofmotion exercises as well as a long opponens
splint to maintain the hand and wrist in a position

of function, with the wrist slightly extended and

the phalanges slightly flexed.3
Complete recovery occurs in 70% to 92% of
cases; in most of the remaining cases, recovery
is partial. Recovery usually begins distally, with
all cases of complete recovery evident by age 5
months. Although some improvement may continue through age 18 months, no improvement
has been noted after age 24 months. Children with
residual deficits usually manifest shoulder muscle
weakness (especially in the external rotators),
with associated muscular atrophy and contractures. Infants with lower plexus injuries are less
likely to make a complete recovery than those with
upper plexus injuries. Associated elevation of the
hemidiaphragm on chest radiograph, Horners syndrome, inability to retract or shrug the shoulders, or
scapular winging may indicate damage to nerve
fibers that originate from spinal roots close to the
cord, thereby signifying avulsion, which is an irreversible injury. The most useful prognostic indicator is recovery that begins within 2 weeks after
delivery.3 The towel test has been advocated
as a clinical tool to assess shoulder and elbow
flexion/extension, biceps contraction, and finger
flexion/extension because absence of biceps recovery by age 3 months is an indication to consider surgical reconstruction.13 The infants face is covered
with a towel, and the infant is then observed to see
if he or she can remove the towel with either arm.
Among 21 infants with brachial plexus palsy, none
of the infants could remove the towel with either
arm at 2 to 3 months; at 6 and 9 months, all infants
could remove the towel with the normal arm, but 11
of 21 could not remove it with the affected arm.13
Surgery may be indicated if there is little
improvement by 4 to 6 months, with early neural
repair resulting in improvement in 90% of cases,
and repair after 6 months resulting in improvement in only 50% to 70% of cases.8 Older children with brachial plexus injuries (>3 years after
injury) require tendon and muscle transfers to
achieve functional improvement. Neuromas involving ruptured nerve roots of C5 and C6 are the most
common lesions (found in 95% of plexi explored).
If EMG conduction post-neuroma decreases by
more than 50% compared with pre-neuroma, the
lesion is excised with grafting of the proximal and
distal nerve roots, which usually involves interpositional sural nerve grafts to guide the proximal
sprouting neural bulb to the severed ends.8 Pseudomeningoceles due to nerve root avulsions are
thought to be predictive of significant injury to
the brachial plexus and can be visualized by MRI.14
Some children in whom complete neurologic
recovery is apparent may develop a shoulder

92 Neurapraxias (Palsies)
contracture or subluxation during growth; therefore, ongoing monitoring and intervention is
recommended to minimize functional problems.9
Glenoid dysplasia and posterior shoulder subluxation with resultant shoulder stiffness is a wellrecognized complication in infants with neonatal
brachial plexus palsy. It is attributed to slowly progressive glenohumeral deformation due to muscle
imbalance and/or physeal trauma. Clinical signs
include asymmetric axillary skin folds, asymmetric
humeral shortening, asymmetric fullness in the
posterior shoulder region, and/or a palpable click
during shoulder manipulation (thereby resembling the clinical signs of congenital hip dislocation).15 Among 134 infants with neonatal brachial
plexus palsy who were followed monthly, 11
(8%) had posterior shoulder dislocation diagnosed
at a mean age of 6 months, as evidenced by a rapid
loss of passive external rotation between monthly
examinations and confirmed by ultrasound.15

DIFFERENTIAL DIAGNOSIS
Arthrogryposis and neonatal muscular dystrophy
should be easily distinguished by the presence of
joint stiffness or ankylosis and the absence of
associated features suggesting birth trauma. Sometimes pseudoparalysis may occur after a humeral
fracture.
References
1. Leffert RD: Brachial plexus injuries, New York, 1985,
Churchill Livingstone, pp 91120.

2. Towner D, Castro MA, Eby-Wilkens E, et al: Effect of

mode of delivery in nulliparous women on neonatal intracranial injury, N Engl J Med 341:17091714, 1999.
3. Painter MJ, Bergman I: Obstetrical trauma to the neonatal
central and peripheral nervous system, Semin Perinatol
6:89104, 1982.
4. Al-Rajeh S, Corea JR, Al-Sibai MH, et al: Congenital brachial palsy in the eastern province of Saudi Arabia, J Child
Neurol 5:3537, 1990.
5. Pearl ML, Roberts JM, Laros RK, et al: Vaginal delivery
from the persistent occiput posterior position: influence
on maternal and neonatal morbidity, J Reprod Med
38:955961, 1993.
6. Boo NY, Lye MS, Kanchanamala M, et al: Brachial plexus
injuries in Malaysian neonates: incidence and associated
risk factors, J Trop Pediatr 37:327330, 1991.
7. Dunn DW, Engle WA: Brachial plexus palsy: intrauterine
onset, Pediatr Neurol 1:367369, 1985.
8. Laurent JP: Neurosurgical intervention for birth-related
brachial plexus injuries, Neurosurg Quart 7:6975, 1997.
9. DiTaranto P, Campagna L, Price AE, et al: Outcome following nonoperative treatment of brachial plexus injuries,
J Child Neurol 19:8790, 2004.
10. Birch R: Obstetrical brachial plexus palsy, J Hand Surg Br
27:38, 2002.
11. Vredeveld JW, Blaauw G, Slooff BA, et al: The findings in
paediatric obstetric brachial palsy differ from those in
older patients: a suggested explanation, Dev Med Child
Neurol 42:158161, 2000.
12. Korak KJ, Tam SL, Gordon T, et al: Changes in spinal
cord architecture after brachial plexus injury in the newborn, Brain 127:14881495, 2004.
13. 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
29:155158, 2004.
14. Abbott R, Abbott M, Alzate J, et al: Magnetic resonance
imaging of obstetrical brachial plexus injuries, Childs Nerv
Syst 20:720725, 2004.
15. Moukoko D, Ezaki M, Wilkes D, et al: Posterior shoulder
dislocation in infants with neonatal brachial plexus palsy,
J Bone Joint Surg Am 86:787793, 2004.