Restoration of sensory function and lack of long-term chronic pain syndromes after brachial plexus injury in human neonates.

Obstetric complications are a common cause of brachial plexus injuries in neonates. Failure to restore sensation leads to trophic injuries and poor limb function. It is not known whether the infant suffers chronic neuropathic or spinal cord root avulsion pain; in adults, chronic pain is usual after spinal root avulsion injuries, and this is often intractable. The plexus is repaired surgically in severe neonatal injures; if no spontaneous recovery has occurred by 3 months, and if neurophysiological investigations point to poor prognosis, then nerve trunk injures are grafted, while spinal cord root avulsion injuries are treated by transferring an intact neighbouring nerve (e.g. intercostal) to the distal stump of the damaged nerve, in an attempt to restore sensorimotor function. Using a range of non-invasive quantitative measures validated in adults, including mechanical, thermal and vibration perception thresholds, we have assessed for the first time sensory and cholinergic sympathetic function in 24 patients aged between 3 and 23 years, who had suffered severe brachial plexus injury at birth. While recovery of function after spinal root avulsion was related demonstrably to surgery, there were remarkable differences from adults, including excellent restoration of sensory function (to normal limits in all dermatomes for at least one modality in 16 out of 20 operated cases), and evidence of exquisite CNS plasticity, i.e. perfect localization of restored sensation in avulsed spinal root dermatomes, now presumably routed via nerves that had been transferred from a distant spinal region. Sensory recovery exceeded motor or cholinergic sympathetic recovery. There was no evidence of chronic pain behaviour or neuropathic syndromes, although pain was reported normally to external stimuli in unaffected regions. We propose that differences in neonates are related to later maturation of injured fibres, and that CNS plasticity may account for their lack of long-term chronic pain after spinal root avulsion injury.