Magnetic resonance neurography of peripheral nerve degeneration and regeneration

Abstract

16 ms), coronal and axial T2 fast-spin echo with fat suppression (TR 4600–5000 ms; TE 90–110 ms), and RF spatial saturation pulse outside the volume of imaging for vessel suppression. T2 MRN studies 4 and 6 months after the first operation showed increased signal in the peroneal nerve at and distal to the site of traumatic injury (figure A). A second operation was performed 8 months after the first and no nerve conduction response could be recorded across the scarred anastomosed segment of peroneal nerve. This scarred segment was excised and the resultant gap bridged by two sural nerve grafts. 8 months later, the patient began to show clinical and electromyographic (EMG) evidence of muscle reinnervation. MRN at this time showed partial return to normal of the bright signal in the distal peroneal nerve. By 16 months, strength in peroneal supplied muscles was near normal, the EMG confirmed additional muscle reinnervation, and MRN showed further normalisation of T2 signal in the distal peroneal nerve while signal remained high at the graft repair site (figure B). Our case illustrates the ability of MRN to detect increased signal on T2 sequences in a traumatically injured degenerating human peripheral nerve. We have evidence that chronically degenerated peripheral nerve can show increased signal for at least 3 years following trauma without recovery. Thus the progressive return to normal of signal in the distal peroneal nerve seen after the second operation can be attributed to processes occurring during nerve regeneration. We cannot explain the persistent increase in signal at the graft repair site. In animal models MR imaging has shown increased T2 signal in degenerating segments of injured peripheral nerves. Histological examination showed that greater demyelination resulted in a brighter signal. The basis for the increased MRN nerve signal may be explained by increased water content and/or myelin breakdown products leading to a prolongation of the T2 relaxation time. Soon after trauma, serial clinical and electrodiagnostic examinations cannot reliably distinguish axonotmetic from neurotmetic grades of peripheral nerve injury. Delaying exploratory surgery to determine whether recovery through regeneration is occurring must be balanced against the diminishing chance of obtaining a good functional recovery if muscles remain denervated for longer than 2 years. The clinical decision on whether or not to operate following a peripheral nerve injury should ideally be made as soon as possible. We hope that MRN techniques will eventually distinguish axonotmetic and neurotmetic grades of peripheral nerve injury in a timely manner to minimise the need for exploratory surgery.