NERVE INJURY

By:
Dr. Mohammed Elsayed Madbouly
Introduction
 Within a nerve, each axon is surrounded by a layer
of connective tissue called the endoneurium. The
axons are bundled together into groups
called fascicles, and each fascicle is wrapped in a
layer of connective tissue called the perineurium.
Finally, the entire nerve is wrapped in a layer of
connective tissue called the epineurium.[
Structure of nerve cell
What is nerve injury ..?
 Nerve injury is an injury to nervous tissue.
 There is no single classification system that can
describe all the many variations of nerve injuries.
 Seddon classification introduced a classification of
nerve injuries based on three main types of nerve
fiber injury and whether there is continuity of
the nerve.
Seddon calssification
 1- Neurapraxia
 is the least severe form of nerve injury, with
complete recovery. In this case, the axon remains
intact, but there is myelin damage causing an
interruption in conduction of the impulse down the
nerve fiber.
 his involves compression of the nerve or disruption
to the blood supply (ischemia).
 There is a temporary loss of function which is reversible
within hours to months of the injury (the average is 6–8
weeks).
 Wallerian degeneration does not occur, so recovery
does not involve actual regeneration.
 There is frequently greater involvement of motor than
sensory function with autonomic function being retained.
 In electrodiagnostic testing with nerve conduction
studies, there is a normal compound motor action
potential amplitude distal to the lesion at day 10,
and this indicates a diagnosis of mild neurapraxia
instead of axonotmesis or neurotmesis.[6]
2-Axonotmesis

 This is a more severe nerve injury with disruption of

the neuronal axon, but with maintenance of the
epineurium .
 because axonal continuity is lost, Wallerian
degeneration occurs.
 This type of nerve damage may cause paralysis of
the motor, sensory, and autonomic, and is mainly
seen in crush injury.[2]
 Loss in both motor and sensory spines is more
complete with axonotmesis than with neurapraxia
 Recovery occurs only through regenerations of the
axons, a process requiring time.
 Proximal lesion may grow distally as fast as 2 to
3 mm per day and distal lesion as slowly as 1.5 mm
per day. Regeneration occurs over weeks to years
 Electromyography (EMG) performed 2 to 4 weeks
later shows fibrillations and denervation potentials in
musculature distal to the injury site
3-Neurotmesis

 is the most severe lesion with no potential of full

recovery
 It occurs on severe contusion, stretch, or laceration
 The axon and encapsulating connective tissue lose
their continuity.
 Disruption of nerve structures sufficient to
involve perineurium and endoneurium as well as
axons and their covering.
 There is a complete loss of motor, sensory
and autonomic function
 EMG are the same as those seen with axonotmetic
injury.
Wallerian degeneration
 is an active process of retrograde degeneration of
the distal end of an axon that is a result of a nerve
lesion.
 It occurs between 7 to 21 days after the lesion
occurs. After the 21st day, acute nerve
degeneration will show on the electromyograph.
Mechanism of Injury

 The pathological process of Wallerian

degeneration is in 3 stages
Axon Degeneration

 Within approximately 30 minutes of injury, there is

a separation of the proximal and distal ends of the
nerve. After a short latency period, the transected
membranes are sealed until degeneration which is
marked by the formation of axonal sprouts. This
occurs in less than a day and allows for nerve
renervation and regeneration
Myelin Clearance

 This occurs by the 7th day when macrophages are

signaled by the Schwann cells to clean up axonal and
myelin debris.
 Usually, the rate of clearance is slower in the Central
Nervous System(CNS) than in the Peripheral Nervous
System (PNS) due to the clearance rate of myelin.
 Another reason for the different rates is the change in
permeability of the blood-tissue barrier in the two
systems. In PNS, the permeability increases throughout the
distal stump, but the barrier disruption in CNS is limited to
just the site of injury. Also in the
CNS, oligodendrocytes inhibit regeneration.
Regeneration

 If soma/ cell body is damaged, a neuron cannot

regenerate. However, if the injury is at the end of
the axon, at a growth of 1mm per day, the distal
segment undergoes granular disintegration over
several days to weeks and cytoplasmic elements
begin to accumulate.
Clinical Presentation

 Reduced or loss of function in associated structures to

damaged nerves
 Gradual onset of numbness, prickling or tingling in feet
or hands, which can spread upward into legs and arms
 Sharp, jabbing, throbbing, freezing, or burning pain
 Extreme sensitivity to touch
 Lack of coordination and falling
 Muscle weakness or paralysis if motor nerves are
affected
 Neuromatous or causalgia pain
Diagnostic Procedures

 Electromyography
 Nerve conduction studies
 Pain assessment
 Sensation deficit and skin condition tests
 Muscle strength/loss
 Functional deficits
Outcome Measures

 Depends on various criteria including pain and

psychosocial skills but could include:
 Oxford scale
 Visual analogue scale
 Short form McGill pain questionnaire
Management / Interventions

Managing nerve damage can include the use of :

 Cryotherapy, Exercise

 Neurorehabilitation

 Surgery.