The majority of serious peripheral nerve injuries do not lead to actual transection of the nerve, but rather leave the nerve in continuity. As described earlier, initially it may be difficult to distinguish closed nerve injuries that recover on their own (neurapraxic and axonotmetic grades) from those that do not (neurotmetic grade) and therefore require a surgical repair. Serial clinical and electrodiagnostic evaluations, often over a period of months, have traditionally been the mainstay of decision making in the management of closed traumatic peripheral nerve injuries.
MRI has been used to evaluate muscle signal changes in the clinical setting of a variety of peripheral nerve disorders (Fig. 32.11) [20-22]. MRI was shown to detect increased signal in denervated muscle groups that is most prominently seen using short tau inversion recovery (STIR) or T2-weighted pulse sequences . The increased signal intensity correlates with
the degree of muscle denervation seen on EMG and weakness found on clinical examination. In general, the threshold for producing an increased STIR signal is weakness graded at 3 or less out of 5 (i.e. at or below antigravity on the Medical Research Council grading scheme) and conspicuous muscle denervation changes of 3+ or more seen on the EMG [20,23]. The MRI muscle signal changes occur as early as 4 days following a traumatic nerve injury, in contrast to the 2-3 weeks required for EMG evidence of denervation to develop in muscle. These signal changes normalize with muscle reinnervation, as assessed both clinically and by electrodiag-nostic studies.
In the setting of pure neurapraxic injuries (i.e. demyelination without axonal loss) or disuse muscle atrophy, the involved muscles exhibit normal signal characteristics on STIR and T2 pulse sequences. In contrast, in severe axonotmetic and neurotmetic injuries, both of which involve loss of axons, increased STIR and T2 signal appears in the affected muscles as a result of muscle denervation. MRI of muscle, therefore, can be useful in distinguishing neu-rapraxic from the more severe axonotmetic and neurotmetic grades of injury soon after trauma. In chronically denervated muscles, atrophic changes eventually occur, with the development of fatty infiltration after several months, which is best visualized on Tl-weighted images, along with the eventual normalization of signal on T2 and STIR pulse sequences.
We have been attempting to determine whether MRI can be used to localize and determine the grade of a traumatic peripheral nerve injury, and thereby help to determine whether surgery would be of benefit in a more expeditious manner. Soon after traumatic nerve injuries, electrodiagnostic testing can reliably identify neurapraxic injuries by virtue of the ability of such injured nerves to conduct nerve action potentials distal to the site of partial or complete conduction block. Neurapraxic injuries also exhibit no electromyographic or MRI evidence of muscle denervation . In contrast, electrodiagnostic studies cannot distinguish between complete axonotmetic and neurotmetic grades of nerve injury soon after acute trauma.
Using high-resolution MRI techniques, we have found that traumatic injuries produce increased signal in nerves on T2 and STIR pulse
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