Biology Reference
In-Depth Information
1. INTRODUCTION
Peripheral nerve injuries belong to the most challenging and difficult
surgical reconstructive problems, and often cause partial or total loss of
motor, sensory, and autonomic functions. The consequences of nerves inju-
ries, which occur in approximately 2.8% of trauma patients (
Huelsenbeck
et al., 2012
), may be disastrous and can result in substantial functional loss,
thus interfering with many aspects of a person's life because of permanently
impaired sensory and motor functions. Moreover, development of second-
ary problems, such as neuropathic pain, dysesthesia, and cold intolerance is
frequently observed following nerve injuries. In addition, nerve injuries
have also a substantial economic impact on the society in terms of health care
and long periods of sick leave (
de Putter et al., 2012
).
Despite the ability of the peripheral nerve to regenerate and reinnervate
denervated target organs has been recognized for more than a century, clin-
ical and experimental evidences show that the regeneration is usually far
from satisfactory, especially after severe injuries (
Navarro, Vivo, &
Valero-Cabre, 2007; Pfister et al., 2011; Sun et al., 2009
). So far, there is
no technique to guarantee total recovery and normalization of functional
sensibility following repair of an injured nerve. The poor outcome reflects
the complexity of peripheral nerve injuries and the diversity of cellular and
biochemical events, which are required to regain function. Indeed, a nerve
injury differs from most other types of tissue injuries in the body, since it is
not only a local repair process that is required. The processes of nerve regen-
eration and target reinnervation are complex, involving many factors which
lead to immediate as well as long-term physiological, biochemical, and cel-
lular changes (
Fig. 8.1
)(
Lundborg, 2005
).
First of all, dramatic changes occur at the level of the damaged nerve
(
Geuna et al., 2009
). After a peripheral nerve traumatic lesion, at the level
of the nerve injury, changes begin almost immediately, both proximally and
distally to the lesion. In the proximal segment, axons degenerate for some
distance back from the site of injury. Within hours after injury, the axon pro-
duces a great number of collateral sprouts that advance distally. After nerve
transection, the distal segment undergoes a slow process of degeneration
known as Wallerian degeneration, which starts immediately after injury
and involves myelin breakdown and proliferation of Schwann cells.
Schwann cells and macrophages are recruited to the injury site and phago-
cytize all the myelin and cellular debris. As the axon sprouts from the
