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Page 2 of 12 Bryan et al. Plast Aesthet Res 2022;9:53 https://dx.doi.org/10.20517/2347-9264.2022.39

[2]
branch reinnervation have been described . This review discusses common and emerging hand and wrist
reanimation themes, specifically looking at more recent techniques for the neurotization of muscles
innervated by the anterior interosseous nerve (AIN) and distal radial nerve branches.

OVERVIEW OF NERVE INJURIES AND REPAIR
A basic understanding of the physiology of nerve repair is required to understand the factors that contribute
to the success of nerve transfers. After traumatic transection, the nerve fibers distal to the injury lose contact
with the neuronal cell body. Axonal regeneration is the primary means of recovery for these injuries and
involves Wallerian degeneration, axonal regeneration, and end-organ reinnervation. Any disruption of
these 3 processes can affect functional outcomes . Wallerian degeneration, or the clearing process of the
[3]
distal stump, serves to create a microenvironment in which axonal regrowth and reinnervation can occur.
This process generally occurs within the first week after the injury, after which a peripheral nerve will start
to regenerate at a rate of approximately 1 to 3 millimeters (mm) per day toward a distal target. However,
muscle fibrosis and atrophy begin as early as 3 weeks following denervation . Given the distance needed to
[3]
travel in a distal nerve injury, irreversible functional damage can occur within a few months . Although the
[3]
window for repair and functional recovery is generally accepted as within 12 to 15 months, it is ideal for
motor nerve regeneration and target reinnervation to actively occur within 3 to 4 months. Some evidence
[4]
suggests this is a critical time point, after which regeneration outcomes start to become poor . Of note,
timing is different with sensory nerves. Target muscles with pure sensory receptors are less time-sensitive to
regeneration, but mixed motor nerves degrade even more rapidly, with repairs delayed more than one
month demonstrating significant functional decline .
[5]

Not all nerve injuries require repair, as management depends on injury severity and resulting functional
deficits. Nerve transfers and other surgical options such as nerve grafting and tendon transfers are generally
reserved for Sunderland grades IV and V injuries, which involve complete loss of axonal, endoneurial, and
[6,7]
perineural continuity; and spontaneous recovery is not expected . This contrasts with Sunderland grades
I-III, which involves damage of local myelin to axons and endoneurium with intact perineurium. Full
recovery is expected in these cases and management is generally conservative . Although nerve grafting was
[8]
predominantly favored in the past for severe injuries, recent advances in nerve transfer techniques have led
to faster, superior outcomes and created a paradigm shift in the treatment strategy for all peripheral nerve
injuries . This is especially true for nerve injuries in the upper extremity, with the most common
[2]
indications for nerve transfers including restoration of shoulder abduction, elbow flexion, radial nerve
[6]
function, and hand function .
ANATOMY, NERVE FUNCTION, AND INJURY CONSEQUENCE
To discuss the outcomes of high AIN and radial nerve transfer techniques, this review provides a general
overview of the anatomy and function of particular nerves of interest: the AIN and radial nerve branches in
the forearm, including the posterior interosseous nerve (PIN) and the nerve to the extensor carpi radialis
brevis (ECRB).

Anterior interosseous nerve
The AIN is a motor branch of the median nerve (C8-T1) with some joint branches that provide
proprioceptive and deep pain feedback. It innervates the deep muscles in the forearm that control finger
flexion, specifically the flexor pollicis longus (FPL), the lateral portion of the flexor digitorum profundus
(FDP), and the pronator quadratus (PQ) [9,10] . It can be found branching from the median nerve at the cubital
fossa, usually on the distal border of the pronator teres muscle. However, the origin of the AIN and its
relation to the pronator teres muscle can be variable .
[11]