Commentary to “Combined Reconstruction of the Ulnar Nerve after its wide Resection by Nerve Grafting at the Site of the Resection and distal Transfer of the Anterior Interosseus Nerve to the deep Branch of the Ulnar Nerve”

The authors present the case of a 46 year old patient who was treated for recurrent neurofibroma of the proximal ulnar nerve by complete resection and primary grafting in combination with transfer of the anterior interosseous nerve (AIN) to the deep motor branch of the ulnar nerve (DMBUN) [1]]. Although motor recovery did not occur, the authors conclude that this approach should always be considered in proximal injuries of the ulnar nerve.

The indication for complete resection of the nerve seems justified after multiple recurrences and subsequent resections of neurofibroma resulting in a non-functioning nerve and chronic pain. However, postoperative pain levels should have been reported.

In contrast, the argument for the AIN transfer is harder to make in the case presented. While I strongly agree that nerve transfers are an intriguing concept, this case report does not provide a very convincing example. In fact, it does not seem very surprising that there was no return of motor function.

The poor recovery of intrinsic hand muscles after high ulnar nerve injuries is a well-known clinical phenomenon and has been extensively documented [2] [3]. One major obstacle is the long distance between the coaptation site and the motor end plates of the intrinsic hand muscles [4]. To shorten the distance to the target muscles and thus improve motor recovery, transfers of the AIN to the DMBUN have been proposed since the 1990s [5] [6] [7]. These procedures should therefore not be considered “experimental”. However, although excellent results were achieved in some of these early reports, the recovery of true intrinsic hand muscle function has been called into question very recently [8]. Possible reasons for persistent clawing deformities after distal AIN transfers are the (still) long distance of about 10 cm from the AIN coaptation site to the intrinsic muscles, the low donor-to-target axon ratio and the different composition of muscle fibers [8] [9] [10] [11].

Apart from these anatomical difficulties specific to the distal ulnar nerve, the main reason for failure in this case is very likely the late timing of reconstruction. The authors state that the patient demonstrated “complete ulnar nerve palsy” for at least 18 months before the first presentation at their institution. Considering that clinical signs of nerve palsy such as clawing only occur if more than about 70% of nerve fibers are already absent, it can be assumed that the nerve had been severely compromised for years and that the motor end plates were completely degenerated at the time of reconstruction [12]. The process of degradation of motor end plates is probably different in humans than in animal models and therefore experimental data are limited [13]. Clinical experience, however, suggests that recovery of motor function significantly diminishes 6 months after nerve injury and reinnervation is, at least in adults, probably impossible after 12 to 18 months [14] [15] [16]. Preoperative nerve conduction studies may hint towards the potential for reinnervation. Absent compound muscle action potentials (CMAP) have been associated with poor recovery [17].

As in many cases, this patient was referred to the reconstructive hand surgeon too late. An earlier nerve transfer might have yielded a better result. In the interest of our patients it is therefore important to reach out to neurologists and other specialists to increase awareness about the possibilities of peripheral nerve surgery.

in The HTMl is an older version published!!

Publication History

Article published online:
16 February 2023

• References

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