1. Peripheral nerve lesion
pathophysiology

2. Peripheral Nerve Injuries

3. PATHOLOGY
Nerves can be injured by ischaemia ,compression,
traction, laceration or burning. Damage varies in
severity from transient and quickly recoverable loss of
function to complete interruption and degeneration.
There may be a mixture of types of damage in the
various fascicles of a single nerve trunk.

5. Nerve injury and repair
(a) Normal axon and target organ (striated muscle). (b)
Following nerve injury the distal part of the axon
disintegrates and the myelin sheath breaks up. The
nerve cell nucleus becomes eccentric and Nissl bodies
are sparse. (c) New axonal tendrills grow into the mass
of proliferating Schwann cells. One of the tendrill will
find its way into the old endoneurial tube and (d) the
axon will slowly regenerate.

6. Nerve injury and repair

7. Introduction
• Anatomy
Peripheral nerves are made up of
axon endoneurium
Connective tissue perineurium
epineurium
Nerve trunks myelinated fibre
unmyelinated fibre
Myelin, protein-lipid complex
function, insulating layer
increase conduction rate

8. • Myelinated nerve are separated by nodes of Ranvier, at
these points , the axons are bare.
• Impulses jump from one node to the next ---
Saltatory Conduction
• Conduction in unmyelinated nerve is slower and
dependent on the diameter of axon.
axon
Ranvier node

9. Cause: damage of cell body,axon, myelin sheath,
connective tissue, blood supply
Three basic processes
1. Wallerian degeneration
2. Axon degeneration
3. Demyelination

10. Neurapraxia
Axonotmesis
Neurotmesis

11. Neurapraxia
Seddon(1942) coined the term 'neurapraxia' to describe
a reversible physiological nerve conduction block in
which there is loss of some types of sensation
and'muscle power followed by spontaneous recovery
after a few days or weeks. It is due to mechanical
pressure causing segmental demyelination and is seen
typically in 'crutch palsy', pres- sure paralysis in states
of drunkenness ('Saturday night palsy') and the milder
types of tourniquet palsy.

12. In Seddon's original classification, neurotmesis meant
division of the nerve trunk, such as may occur in an
open wound. It is now recognized that severe
degrees of damage may be inflicted without actually
dividing the nerve. If the injury is more severe,
whether the nerve is in continuity or not, recovery
will not occur. As in axonotmesis, there is rapid
wallerian degeneration, but here the endoneurial
tubes are destroyed over a variable segment and
scarring thwarts

14. CLASSIFICATION OF NERVE
INJURIES
Seddon's description of the three different types of
nerve injury (neurapraxia, axonotmesis and
neurotmesis) served as a useful classification for many
years. Increasingly, however, it has been recognized
that many cases fall into an area somewhere between
axonotmesis and neurotmesis. Therefore, following
Sunderland, a more practical classification is offered
here.
First degree injury This embraces transient ischaemia
and neurapraxia, the effects of which are reversible.

15. Second degree injury This corresponds to Seddon's
axonotmesis. Axonal degeneration takes place but,
because the endoneurium is preserved, regeneration
can, lead to complete, or near complete, recovery
without the need for intervention.
Third degree injury This is worse than axonotmesis. The
endoneurium is disrupted but the perineurial
sheaths are intact and internal damage is limited.
The chances of the axons reaching their targets are
good, but fibro- sis and crossed connections will limit
recovery.

16. • Distal axon degeneration, following section or
severe injury, with degeneration of the myelin.
The process occurs within 7-10 days of injury
and this portion of the nerve is inexcitable
electrically.