DESCRIPTION

• The brachial plexus contains sensory and motor nerves to the upper extremities, stemming from the cervical and thoracic spine (commonly C5–T1 roots).
• The brachial plexus contains a consistent pattern of nerves that innervate predictable muscles and skin regions.
• Brachial birth palsy is a flaccid upper extremity paralysis caused by traction injury of the brachial plexus during birth.
• It can produce a proximal stretch, avulsion, or rupture type injury. Classifications are as follows:

EPIDEMIOLOGY

• There is no predominance of gender, but variations in clinical care, preventive measures, and birth weight may explain estimates of incidence to range from 0.4 to 4 per 1,000 live births.
• Incidence drops from 0.2% with vaginal delivery to 0.02% after cesarean section as there is a probable mechanical basis for the plexopathy.
• Erb palsy is the most commonly encountered plexus injury.

ETIOLOGY

• Downward mechanical force on the shoulder during delivery can lead to stepwise stretch injury, resulting in either transient or permanent damage or total avulsion of nerve roots.
• Upward mechanical force (i.e., after face delivery) is less frequent and leads to isolated lower plexus palsy (C8–T1 injury = Klumpke).
• Avulsion injury carries the worst prognosis, particularly if proximal to the cell body of the motor nerve (preganglionic), as these injuries cannot spontaneously recover.

RISK FACTORS

• Large size for gestational age, multiparity, prolonged labor, breech position, difficult delivery—especially when forceps- or vacuum-assisted
• Diabetic mothers and/or neonatal birth weight >4.5 kg
• Although there is no genetic basis per se, previous delivery leading to obstetric palsy is a risk factor.

GENERAL PREVENTION

• Careful positioning of the upper extremity during childbirth and conversion to cesarean section when necessary
• Prevention of long-term disability and contracture can be minimized with exercise of the child’s joints and functioning muscles every day beginning at 3 weeks of age.

PATHOPHYSIOLOGY

• Seddon and Sunderland have described classification systems to describe degree of injury.
  • Neuropraxia (grade I)
    • Mildest form, interruption of conductions
    • The myelin sheath is disrupted, whereas the axons remain uninjured.
    • Complete spontaneous recovery over weeks
  • Axonotmesis (grade II to IV)
    • The myelin sheath and the axon are both disrupted with varying degrees of endoneurial or perineurial damage.
    • Recovery varies from full or incomplete over months to years.
  • Neurotmesis (grade V)
    • Most severe
    • There is a complete disruption of the myelin sheath, axon, and surrounding connective tissue (endoneurium, perineurium, and epineurium).
    • Recovery is incomplete to absent.
• Lesions also can be classified according to their relation to the dorsal root ganglion (preganglionic or postganglionic).
  • Preganglionic lesions occur proximal to the dorsal root ganglion and involve avulsion from the spinal cord. Implementation of nerve transfer is usually a better strategy for these lesions.

COMMONLY ASSOCIATED CONDITIONS

Horner syndrome, phrenic nerve injury, and long thoracic nerve injury (winged scapula) may be observed and are associated with preganglionic injury and a poor prognosis.