The brachial plexus consists of nerves from C5-T1 that form roots, trunks, divisions and cords to innervate the muscles of the arm. Brachial plexus injuries are more common in overweight babies and complicated deliveries involving shoulder dystocia. Injury can range from upper root involvement causing inability to abduct the shoulder to complete plexus palsy resulting in a flail arm. The majority of cases involve the C5-C6 roots (Erb's palsy) but spontaneous recovery is possible depending on the severity of the nerve damage.

1. Brachial Plexus
Anatomical considerations:
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.
The axons inside every nerve root are used to innervate many
different muscles. One muscle can be innervated from 1-5 segments
(nerve roots). Simply, the upper roots innervate the upper part of the arm,
while the lower roots innervate the lower parts of the arm and hand. The
brachial plexus involves roots, trunks, divisions and cords.
* Roots:
The anterior rami of the spinal nerves of C5, 6, 7, 8 and T1 form the
roots of the brachial plexus. The roots emerge from the transverse
processes of the cervical vertebrae immediately posterior to the vertebral
artery, which travels in a cephalo-caudal direction through the transverse
foramen. Each transverse process consists of posterior and anterior
tubercles, which meet laterally to form a costo-transverse bar. The
transverse foramen lies medial to the costo-transverse bar and between
the posterior and anterior tubercles.
The spinal nerves which form the brachial plexus run in an inferior
and anterior direction within the sulci formed by these structures. The
dorsal scapular nerve arises from the C5 root and passes through the
middle scalene muscle to supply the rhomboid and levator scapulae
muscles. The long thoracic nerve to the serratus anterior arises from the
C5, 6, 7 roots and also pierces the middle scalene muscle as it passes
posterior to the plexus.
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2. * Trunks and divisions:
Trunks of the brachial plexus pass between the anterior and middle
scalene muscles. The superior trunk lies closest to the surface and is
formed by C5 and C6 roots. The suprascapular nerve and the nerve to
subclavius arise from the superior trunk. The suprascapular nerve
contributes sensory fibers to the shoulder joint and provides motor
innervation to supraspinatus and infraspinatus muscles. The C7 root
continues as the middle trunk, while C8 and T1 roots join to form the
inferior trunk. The trunks divide into anterior and posterior divisions,
separating the innervation of the ventral and dorsal halves of the upper
limb.
The phrenic nerve (C3, 4, 5) passes between the anterior and middle
scalenes and continues over the surface of the anterior scalene muscle.
Diaphragmatic twitch during interscalene brachial plexus, performed with
a nerve stimulator, indicates needle placement anterior to the plexus.
The spinal accessory nerve (cranial nerve XI) runs posterior to the
brachial plexus over the surface of middle and posterior scalenes. Contact
of spinal accessory nerve with a nerve stimulator (stimulating twitch in
trapezius) indicates placement of the needle posterior to the plexus.
* Cords and branches
The cords are named the lateral, posterior and medial cord,
according to their relationship to the axillary artery. The lateral cord
receives fibers from the anterior divisions of the superior and middle
trunks; it is the origin of the lateral pectoral nerve (C5, 6, 7). The posterior
divisions of the superior, middle and inferior trunks combine to form the
posterior cord. The inferior trunk continues as the medial cord and gives
off the median pectoral nerve (C8, T1), the medial brachial cutaneous
nerve (T1) and the medial ante-brachial cutaneous nerve (C8, T1).
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3. The upper and lower subscapular nerves (C7, 8 and C5, 6) leave the
posterior cord and descend behind the axillary artery to supply the
subscapularis and teres major muscles, respectively. The thorcodorsal
nerve to the latissimus dorsi, also known as the middle subscapular nerve
(C6, 7, 8) also arises from the posterior cord.
The lateral cord divides into the lateral root of the median nerve
and the musculocutaneous nerve. The posterior cord gives off the axillary
nerve at the lower border of the subscapularis muscle and continues along
the inferior and posterior surface of the axillary artery as the radial nerve.
The axillary nerve supplies the teres minor muscle before ending as the
superior lateral brachial cutaneous nerve. The medial cord contributes the
medial root of the median nerve and continues as the ulnar nerve along
the medial and anterior surface of the axillary artery. The medial and
lateral roots join to form the median nerve which continues along the
posterior and lateral surface of the axillary artery.
Fig. (1): Overview of the brachial plexus
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4. Brachial Plexus Palsy (BPP)
Brachial plexus injuries are more common in over-weight babies,
particularly where delivery is complicated by shoulder dystocia (difficult
labor). A brachial plexus lesion is revealed by lack of movement in the
arm; initially the arm is flaccid. After 48 hours, an upper palsy can be
distinguished from a complete palsy. In upper root palsy (C5,6 and
sometimes C7), the arm is internally rotated and pronated and there is no
active shoulder abduction or elbow flexion (Waiter’s tip position). In a
complete palsy of upper and lower roots, the arm is flail; there may be a
ptosis and a Horner’s syndrome due to damage to the stellate ganglion
(star-shaped collection of nerve cells in the sympathetic chain) adjacent to
C8 and T1. Phrenic nerve palsy should be considered in these cases.
Most infantile injuries to the brachial plexus predominantly involve
the upper trunk (C5,6); the classic Erb's palsy. However, many of these
infants also have impairment of the C7 nerve root, which postpones the
poorer prognosis. Far less frequently, the entire plexus (C5,6,7,8 and T1) or
the lower trunk (C8 and T1; Klumpke's palsy), may be involved.
Incidence:
With improvement in obstetrical care, the incidence of brachial
plexus injuries has decreased significantly. In countries in which
obstetrical care is poor, obstetric brachial plexus palsy (OBPP) is noted
more frequently. The incidence ranges globally from 0.2-4 % of live-
births. According to the World Health Organization (WHO), the
prevalence is generally 1-2 % worldwide, with the higher numbers in the
underdeveloped countries. In the United States, the prevalence is
approximately 0.2 %. Studies in France suggest an incidence of 1.09-1.19
cases per 1000 live-births.
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5. Etiology:
Most neonatal BPP occurs in the birthing process. Risk factors for
this type of injury (OBPP) include:
- Over weight at birth (average vertex BPP is 3.8 - 5.0 kg, average breech
BPP is 1.8 - 3.7 kg, while the average unaffected is 2.8 - 4.5 kg).
- Breech presentation.
- Maternal diabetes.
- Second stage of labor that lasts more than 60 minutes.
- Assisted delivery (e.g. use of forceps or vacuum extraction).
- Previous child with OBPP.
- Intrauterine torticollis.
- Shoulder dystocia (difficult labor).
Other less common causes of neonatal BPP include:
- Neoplasms (e.g. neuromas, rhomboid tumors).
- Intrauterine compression.
- Humeral osteomyelitis.
- Hemangioma.
- Exostosis (overgrowth of bone tissue) of the first rib.
Although the traditional mechanism of injury is lateral neck
flexion, the upper rootlets (C5, 6, 7) are 25 % as likely to be avulsed as the
lower roots (C7, 8 and T1). The upper roots (C5, 6), 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.
Pathophysiology:
Brachial plexus palsy (BPP) results from excessive lateral traction
on the head away from the shoulder. This force on the brachial plexus can
cause varying degrees of injury to the nerves, including rupture of the
nerve roots or trunks, avulsion of the nerve roots from the spinal cord and
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6. traction preserving the continuity of the nerve but causing excessive
scarring. Injury to the brachial plexus may result from demyelination,
axonal degeneration or avulsion. Clinically, this injury results in
disruption of the sensory and / or motor function of the injured nerve.
Spontaneous recovery of function occurs with remyelination, with or
without axonal regeneration and reinnervation of the sensory receptors,
muscle endplates or both. However, in some cases of severe nerve injury
and with avulsion injuries, spontaneous recovery does not occur and
surgical intervention is warranted.
Severity depends upon the number of nerves involved and the
degree to which each level is injured. The basic types of brachial plexus
palsies include:
- Duchenne-Erb palsy; affects nerves arising from C5 and C6.
- Upper-middle trunk BPP; involves nerve fibers from C5, 6, 7 levels.
- Klumpke palsy; results in deficits at levels of 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, 6, 7, 8 - T1).
When defining severity of a peripheral nerve injury, differentiation
between neuropraxic, axonotemetic, and neurotemetic lesions is helpful:
* Purely neuropraxic lesions do not affect the axon itself. These lesions
generally are reversible and do not leave sequelae.
* Axonotemetic lesions involve disruption of both 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.
* Neurotemetic lesions are the most severe and destroy 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
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7. connective tissue, a neuroma may develop. The extent of improvement in
the patient's condition depends upon the ultimate number of nerve fibers
that reconnect distal to the neuroma.
Depending on the degree of nerve injury, recovery may be noted
within a few days. In most cases, some degree of spontaneous recovery
occurs within 1 month, although in some injuries evidence of full
recovery may not appear for up to 3 months. Sunderland described a
classification for nerve injuries including 5 degrees of nerve injury:
- 1st
degree injury (neuropraxia): It involves a temporary conduction
block with demyelination of the nerve at the site of injury. Recovery may
take up to 12 weeks.
- 2nd
degree injury (axonotemesis): It results from a more severe trauma
or compression. This causes Wallarian degeneration distal to the level of
injury and proximal axonal degeneration to at least at the next node of
Ranvier. Axonal regeneration occurs at a rate of 1 mm / day or 1 inch /
month and can be followed with an advancing Tinel sign.
- 3rd
degree injury: It is more severe than a second-degree injury, as
regeneration occurs at a rate of 1 mm / day and progress may be followed
with an advancing Tinel sign. However, with the increased severity of the
injury, the endo-neural tubes are not intact. The pattern of recovery is
mixed and incomplete. Reinnervation occurs only if sensory fibers reach
their sensory end organs and motor fibers reach their muscle targets.
- 4th
degree injury: It results in a large area of scar at the site of nerve
injury, precluding any axons from advancing distal to the level of nerve
injury.
- 5th
degree injury: It is a complete transection of the nerve. Similar to a
fourth-degree injury, surgery is required to restore neural continuity.
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8. Examination and diagnosis:
Diagnosis of brachial plexus injuries relies heavily upon the
clinical evaluation; children are first evaluated between birth and 6 weeks
of age with a physical therapist starting at 3 - 4 weeks then at 6 weeks of
age. Follow-up evaluations occur at three-month intervals.
Physical findings:
The newborn infants can have many of the following findings:
- In infants with complete BPP (C5 - T1), the arm is held limply at his side.
Deep tendon reflexes in the affected arm are absent and the Moro
response is asymmetric with no active abduction of the ipsilateral arm. In
children with total arm involvement, careful examination of the child's
eye often demonstrates Horner syndrome. Children with intrinsic hand
weakness, associated with BPP, generally have Horner syndrome and
vice versa. Respiratory status should be evaluated since the phrenic nerve
can be injured simultaneously.
- The infant with upper plexus palsy (C5, 6, 7) keeps the arm adducted and
internally rotated with the elbow extended, forearm pronated, 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 infant with a nerve injury to the lower plexus (C8 - T1) holds the arm
supinated with the elbow bent and wrist extended.
- Sensation should be assessed closely, with the clinician noting any
sensory loss in corresponding dermatomes.
- Reflexes typically absent in the affected limb and should be evaluated.
- In the newborn nursery, it is essential that the physician carefully
inspect the size of the hand and arm and bulk of the pectoralis major.
These children may have a smaller limb with asymmetric palmar creases,
pectoralis atrophy and / or joint contractures at the time of delivery.
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9. The examination consists of a motor evaluation that scores both
individual muscle groups (using the five-point British Research Council
Grading System) and functional muscle group activities, including
abduction, external rotation, hand-to-head, hand-to-back and hand-to-
mouth movements as well as sensory and reflex examinations. Physicians
should compare clinical assessments on subsequent visits every three
months
The back should be inspected carefully, assessing muscle bulk
including the trapezius, rhomboids, supraspinatus, infraspinatus,
latissimus dorsi, teres major, and teres minor. Contracture of the
pectoralis major can be assessed by palpation of the anterior axillary fold
during external rotation.
Laboratory investigations:
Children who recover partial function between examinations
should continue to be followed at three-month intervals. Children, who
fail to improve on subsequent visits or who improve initially but then
plateau at a nonfunctional level, should be evaluated initially via
electromyography (EMG). This will assess the levels of injury and
determine if there is evidence of early reinnervation
Complications:
Children with BPP are at risk for developing complications such as
progressive contractures, bony deformities, scoliosis and posterior
shoulder dislocation. Children with chronic upper trunk plexopathy may
develop external rotation weakness and internal rotation contractures
about the shoulder. This muscle imbalance will progressively alter the
glenohumeral joint.
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10. Prognosis:
Peripheral nerves remyelinate at a rate of 1 mm/day. Thus, if the
nerve is not transected, recovery can be expected by 4-5 months in Erb’s
palsy, 6-7 months for upper-middle trunk palsy and 14 months for a total
BPP. Some authors believe that infants who do not show signs of
spontaneous recovery by 3-5 months are usually left with residual deficits
if managed conservatively. Unfavorable functional outcome is related
more often to faulty reinnervation than to lack of reinnervation. Faulty
reinnervation is especially common in brachial plexus lesions, secondary
to the close proximity of the nerves involved.
Evaluation:
* Electrophysiological evaluation:
- Electromyography: Evidence of denervation is usually not seen before 1
week of age.
- Nerve conduction velocity.
* Physical evaluation:
Assessment is carried out with the infant undressed and in warm
room. Any broken bone, the extent of passive and active range of motion,
sensation, strength and achievement of developmental milestones should
be thoroughly checked. Asymmetrical position of the upper limb is
recorded as the newborn must be held in flexion. If there is scapular
winging, rhomboids are involved. The diaphragm may be also involved.
The following tests are conducted:
* Muscles tone.
* Range of motion (flexibility test) for all the joint include shoulder
internal rotators (subscpularis), pronators and wrist and finger flexors.
* Round measurement.
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11. * Muscles test or functional test according to the infant’s age.
* Reflex testing according the age of the infant (e.g. Moro reflex, placing
reaction, neck righting reaction and grasp reflex).
* Sensory test to detect any sensory disturbance, which interferes with the
treatment progress.
* Activities of daily living (feeding, washing and grooming) with the
affected extremity.
* Mallet System:
Assessment of the function of the shoulder is based on five criteria.
The ability to actively abduct the arm, the ability to externally rotate the
arm, the ability to place the hand behind the neck as well as behind the
back and the ability to place the hand over the mouth.
- Grade I indicates a stiff shoulder or a flail arm.
- Grade II indicates active abduction of 30° or less.
- Grade III indicates active abduction of 30° to 90°, active external
rotation of 20° or less.
- Grade IV indicates active abduction of at least 90°, active external
rotation of more than 20°, and place the hand behind the neck and over
the thoraco-lumbar. The hand can be brought to the mouth without
abduction of the arm.
- Grade V indicates a clinically normal shoulder.
Physical treatment:
Goals:
- To facilitate weak muscles.
- To resume function as soon as neural regeneration has taken place.
- To train motor control.
- To maintain normal range of motion.
- To prevent soft tissue contracture and skeletal deformity.
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12. Methods:
* Facilitatory stimuli such as scratch, painful stimuli, quick stretch,
brushing, brief icing and faradic stimulation.
* Functional strengthening exercises: Active use of involved extremity
using a variety of developmentally appropriate activities to increase
strength and coordination, beginning in gravity eliminated then advance
to against gravity.
* Passive range of motion exercises for all joints of the limb.
* Stretching exercises.
* Scapular mobilization.
* Manipulative exercises.
* Hydrotherapy.
* Sensory stimulation to prevent disuse muscle atrophy by encouraging
muscle growth.
* Motor training:
- It should start within the first month although there may be no activity
in the denervated muscles.
- Early training aims probably to elicit activity in temporarily
denervated muscles, to minimize soft tissue contraction and to set up a
regular pattern of behavior in the parents.
- Training should be direct to age-related actions with particular
emphasis on reaching to touch and eventually to grasping and
manipulate different objects.
- Specific games can be played with the older children, aiming to
improve sensory awareness of the affected limb.
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