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

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C5, 6, 7 roots and also pierces the middle scalene muscle as it passes

posterior to the plexus.

* 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

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off the median pectoral nerve (C8, T1), the medial brachial cutaneous

nerve (T1) and the medial ante-brachial cutaneous nerve (C8, T1).

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.

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Fig. (1): Overview of the brachial plexus

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

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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.

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.

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- 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

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.

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- 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

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

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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.

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

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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.

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:

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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.

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:

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- 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.

* 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.

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- 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.

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.

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* 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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