Brachial Plexus and/or Cervical Nerve Root Injuries at Birth

Neonatal brachial plexopathy is believed to be secondary to stretching of the plexus by traction, the nerve roots being anchored by the spinal column and cord. Lesion severity depends on the degree of stretch, but axonal injury is the usual result. If the epineurial nerve sheath remains intact, nerve regeneration down to the denervated muscles occurs at a rate of about 1 mm per day. Complete rupture of the nerve sheath as well as the axons leads to poor reinnervation. With severe traction injuries, there may be additional damage to spinal nerve roots, including root avulsion. Diagnosis requires imaging, and computed tomography (CT) myelography remains more reliable than magnetic resonance imaging (MRI). Upper brachial plexus injuries involve the junction of C5 and C6 roots (Erb’s point), and lower injuries involve the junction of C8 and T1 roots.

Upper Brachial Plexus Injury (Erb Palsy). This is the most common of the brachial plexus injuries, affecting muscles supplied by C5 and C6 and accounting for 90% of the total incidence. An asymmetric Moro response is usually the first indication of the injury. The upper extremity assumes the “waiter’s tip” position: the shoulder is adducted and internally rotated, the elbow is extended, and the forearm is pronated, with the hand in flexion. A mild sensory loss may develop over the lateral aspect of the shoulder and arm, but is difficult to elicit. Associated fractures of the clavicle or humerus must be ruled out, and fluoroscopic examination should be carried out to exclude the rare diaphragmatic paralysis caused mainly by a C4 lesion.

Lower Brachial Plexus Injury (Klumpke Palsy). A pure lower brachial plexus injury is uncommon, and most cases of Klumpke palsy involve the more proximal muscles supplied by C7 or C6. An absent grasp reflex is the most prominent clinical feature. There may be involvement of sympathetic fibers from T1, causing Horner syndrome (ptosis, miosis, anhidrosis). A significant sensory deficit is usually present, occasionally resulting in unwitting trauma to fingers. Prognosis for full recovery in these infants is poor. The upper extremity often remains small and distally foreshortened.

Management. Immediate management should include evaluation for underlying structural lesions of the neck and shoulder. Over the initial 3 to 6 months, there may be significant spontaneous improvement, aided by functional positioning, passive range-of-motion exercises, and splinting. Electrodiagnostic testing can aid in assessing the extent of motor and sensory axon injury and presence of reinnervation. Treatment of neonatal brachial plexus injury is conservative. No surgical procedure is likely to improve the immediate situation or the prognosis. The limb should be placed in its best functional position, that is, across the chest, not abducted and flexed. Gentle, passive, range-of-motion exercise should be initiated within 7 to 10 days of birth. Hand and wrist splints can be constructed later as necessary. Failure to show any clinical improvement over 3 to 6 months is an indication at some centers for surgical exploration, neurolysis, and cable nerve grafting. Electrodiagnostic studies are of diagnostic value in determining the extent of the injury but have not been proven useful, to date, in identifying patients best suited for surgical intervention. After the child is 5 to 6 years of age, muscle transfers may be helpful.

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