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cells after nerve injury ( Arthur-Farraj et al., 2012 ). In addition, the expres-
sion of trophic factors and adhesion molecules is determined by c-Jun. Thus,
the regeneration tracks, and thereby the regenerative potential of the out-
growing axons, is influenced by c-Jun. The sprouts that are formed from
the tip of the axon, with their filopodia, are orchestrated by extracellular
guidance cues for their advancement, the retraction, as well as the turning,
that is, direction of growth, which is mediated by the actin filaments within
the growth cone ( Bloom & Morgan, 2011 )( Fig. 7.1 ).
The permissive cues that guide the advancement of the growth cones are
critically restored as soon as possible by the surgeon. The previously
described basic concepts of nerve repair include preparation of the nerve
ends to create a fresh nerve end without necrotic cells and a careful approx-
imation of the nerve ends without tension ( Yi & Dahlin, 2010 ). Compen-
sation for the mushrooming of the fascicles by a meticulous co-aptation,
even leaving a minor gap, that allows formation of a fibrin matrix with mac-
rophages and migration of Schwann cells is one of the steps in the surgical
procedure. Finally, the nerve repair is completed by application of sutures or
glue. These steps are essentially the same when a nerve reconstruction pro-
cedure is done, but it is important that the nerve grafts as well as the proximal
and distal nerve ends are handled accurately avoiding drying of the tissues.
Hereby, the Schwann cells can be kept viable and the signal transduction
mechanisms necessary for proliferation and production of growth factors
can be preserved.
Different experimental procedures, including pharmacological treat-
ment ( Kvist, Danielsen, & Dahlin, 2003 ), have been described to improve
motor reinnervation after a delayed nerve repair ( Sulaiman & Gordon,
2009 ). There is also a possibility to reactivate the chronically denervated
Schwann cells by treatment with the transforming growth factor b
(TGF- b )( Sulaiman & Gordon, 2009 ). Recent clinical experiences also
indicate that it is a possibility to overcome the problem with chronically
denervated Schwann cells by transferring regenerating axons from another
source, by a nerve transfer procedure, closer to the target. A variety of nerve
transfers have been described for the upper extremity ( Lee & Wolfe, 2012 ).
One of these nerve transfer procedures can be done when an axillary nerve
injury is overlooked in young adults after shoulder trauma ( Dahlin, Coster,
Bjorkman, & Backman, 2012 ). In nerve transfers, a freshly transected nerve
fascicle from an uninjured nerve is transferred, without residual problems
from the donor nerve, to the distal nerve segment of a previously injured
nerve. It is an advantage if the transfer can be made very close to the target.
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