Peripheral Nerve Injuries

Nerves can be injured by:

1- ischemia
2- compression
3- traction
4- laceration
5- burning
Damage varies in severity from transient
and quick recovery to complete
interruption and degeneration
 Transient ischemia
Acute nerve compression causes:
- numbness and tingling within 15 minutes
- Loss of pain and sensibility after 30 min
- Muscle weakness after 45 min
Relief of compression is followed by intense
paresthesia lasting up to 5 min (the familiar pins
and needles after a limb goes asleep)
Feeling is restored within 30 seconds
Full muscle power after about 10 min
Changes are due to transient anoxia and leave no
trace of nerve damage
Tourniquet application during surgery
 Neurapraxia
Reversible physiological nerve conduction block
Loss of some type of sensation and muscle
power
Followed by spontaneous recovery after a few
days or weeks
Due to mechanical pressure causing segmental
demyelination
Seen typically in crutch palsy, Saturday night
palsy and the milder tourniquet palsy
 Axonotmesis
Literally: axonal interruption
More severe nerve injury
Typically after closed fractures and dislocations
There is loss of conduction but the nerve is in continuity
and neural tubes are intact
Distal to the lesion and a few mm retrograde, axons
disintegrate and are resorbed by phagocytes (called
Wallerian degeneration)
Takes only a few days and is accompanied by marked
proliferation of Schwann cells and fibroblasts lining the
endoneurial tube
Degenerative target organs (motor end plates and
sensory receptors) gradually atrophy
If they are not reinnervated within 2 years they will never
recover
 Axonotmesis
Axonal regeneration starts within hours of nerve
damage
Encouraged by neurotropic factors produced by
Schwann cells distal to the injury
Numerous fine unmyelinated tendrils grow from
the proximal stump and find their way into the
cell-clogged endoneurial tubes
Axonal processes grow at a speed of about
1mm per day
Larger fibers slowly acquiring a new myelin coat
Eventually they join to end organs which enlarge
and start functioning again
 Neurotmesis
Division of the nerve trunk
Or more severe injury without actual cut
Recovery will not occur
Rapid Wallerian degeneration
Endoneurial tubes are destroyed and scarring
occurs that prevents regenerating axons from
entering the distal segment and regain their
target organs
Instead they form a “neuroma” at the site of
injury
Neuroma: regenerating fibers mingling with
proliferating Schwann cells and fibroblasts in a
jumbled knot
 Neurotmesis
Even after surgical repair:
- Many new axons fail to reach the distal
segment
- Those that do may not find suitable
Schwann tubes
- Or may not reach the correct end organ in
time
- Or may remain incompletely myelinated
- Function may be adequate but never
normal
 Classification of Nv. Inj.
First degree Injury: transient ischemia and
neuropraxia. Reversible
Second degree Injury: axonal degeneration.
Preserved endoneurium. Regeneration can lead
to complete or near complete recovery without
the need for intervention
Third degree Injury: disrupted endoneurium.
Intact perineurial sheaths and limited internal
damage. Fibrosis and crossed connection limit
recovery. Good chances for axons to reach their
targets
 Classification
Fourth degree injury: only the epineurium
is intact nerve trunk is still in continuity but
damage is severe. Recovery is unlikely.
The injured segment should be excised
and the nerve repaired or grafted
Fifth degree injury: the nerve is divided
and will have to be repaired.
 Clinical Features
Acute nerve injuries are easily missed esp. when
ass. with #s and dislocations
Always test for nerve injuries following any
significant trauma
Look for accompanying vascular injuries
Ask for P&N, weakness. Examine injured limb
systematically for neurology
Accurate mapping
Plastic pen test: dry skin
Repeat examination on intervals
 Clinical features
chronic
Smooth and shiny anaesthetic skin in
smooth and shiny
Clues of diminished sensibility such as
cigarette burns.
Wasted muscle groups and fixed postural
defromities
Assessment f nerve recovery
How severe was the lesion
How well is the nerve function now
Examination of power and light touch
Motor recovery is slower than sensory
recovery
Assessment: degree of injury
Low energy injury: neuropraxia, recovery
anticipated
High energy injury: third and fourth
degree, recovery is less predicted
Open injury or very high energy closed
injury: nerve is probably divided and early
exploration is called for.
 Tinel’s sign
Peripheral tingling or dysaesthesia provoked by
percussing the nerve
In neuropraxia: TS is negative
In axonotmesis: TS is positive at the site of injury
bec. Of the sensitivity of the sprouts of the
regenerating axons. TS will then advance after a
delay by 1 mm per day
Failure of TS to advance suggests 4th or 5th
degree injury and early exploration is needed
Slow advancement and poor muscle group
response suggest unlikely recovery and the
need for exploration.
 EMG: electromyogram
Denervation potentials at the third week if
muscle looses its nerve supply
This excludes neuropraxia
But dose not differentiate between axonotmesis
and neurotmesis: this remains a clinical
distinction
If one waits too long to decide then the target
muscle may have failed irrecoverably and the
answer hardly matters
 Assessment: the level of nerve
function
Two point discrimination is a measure of
innervation density
Threshold tests: measure the threshold at
which a sensory receptor is activated.
They are more useful in nerve
compression syndrome where individual
receptors fail to send impulses centrally,
here two point discrimination is preserved
 Motor power assessment
Graded on the Medical Research Council scale:
0 no contraction
1 a flicker of activity
2 muscle contraction but unable to overcome
gravity
3 contraction able to overcome gravity
4 contraction against resistance
5 normal power
 Prognosis
Type of lesion: neuropraxia always recover fully,
axonotmesis may or may not, neurotmesis will not
unless the nerve is repaired
Level of the lesion: the higher the worse
Type of the nerve: purely motor or purely sensory
recover better than mixed nerves because there is less
likelihood of axonal confusion
Age: children do better
Delay in suture: a most important adverse factor. The
earlier the better. After a few months recovery following
suturing become less likely
Ass. Lesions: even if nerve recovers well, they may
prohibit limb recovery
Surgical techniques: if no experience; transfer
Regional survey
 Brachial plexus injuries
Stab or traction
Traction: supraclavicular 65%, infraclavicular
25%, combined 10%
SC: motorcycle injuries
IC: # dislocation of the shoulder, in 25% the
axillary artery is also torn
# of the clavicle rarely damage the plexus
Preganglionic vs. postganglionic
PG: can’t recover and surgically irreparable
Mild lesions (neuropraxia): recover
spontaneously but may need months to recover
fully
 Clinical features
level of the lesion
Upper plexus: (C5, C6): shoulder abductors and
external rotators and the forearm supinators are
paralysed. Sensory loss of the outer aspect of
the arm and forearm
Pure lower plexus are rare: paralysed intrinsic
hand muscles and weak wrist and finger flexors.
Loss of sensation in the ulnar forearm and hand
If the entire plexus is damaged, the whole limb is
paralysed and numb
 Pre or post ganglionic
Pre (root avulsion): crushing or burning
pain in an anaesthetic hand. Paralysis of
scapular muscles or diaphragm. Horner’s
syndrome. Severe vascular injury. Ass.
Injuries of the cervical spine. Spinal cord
dysfunction.
Histamine test: positive in preganglionic
MRI shows pseudomeningiocele due to
root avulsion
Obstetrical Brachial Plexus Injuries
Excessive traction on brachial plexus
during childbirth
Upper root injury: Erb’s palsy: overweight
babies with shoulder dystocia at delivery
Complete plexus injury: Klumpke’s palsy:
usually after breech delivery of smaller
babies.
 clinical
Erb’s: C5, C6 and sometimes C7
abductors and external rotators of the shoulder
and supinators are paralysed
The arm is held to the side internally rotated and
pronated
Klumpke;s: less common, more severe. The arm is
flail and pail. All finger muscle are paralysed.
Vasomotor impairment and unilateral Horner’s
X-rays should be taken to exclude #s of the
shoulder or clavicle
 management
Paralysis may recover completely: most
Erb’s. a reliable indicator is the return of
biceps activity by the third month. Absence
of biceps recovery dose not completely
rule out later recovery.
May improve
May persist
Consider operative if no biceps recovey
after 3 months