PERIPHERAL NERVE INJURY

DR. ASHISH GOHIYA

Assistant Professor
Dept. of Orthopaedics
Gandhi Medical College
Bhopal
 ANATOMY
 Peripheral nerves are bundles of axons
conducting afferenat & efferent impulses.
 Each axon is elongated process of a nerve cell
(Neuron).
 Cell bodies of
 motor neuron – Ant horn cell
 sensory neuron – dorsal root ganglia.

 Single neuron may supply 10 – 1000 fibres.

ANATOMY
ANATOMY
 ANATOMY
 Myelinated  Unmyelinated
– All motor axons – Small diameter (crude
– Large sensory axons touch )
– (touch, pain – Efferent sympathetic
proprioception)

 Nodes of Ranvier  No nodes

 Faster conduction  Slower conduction
ANATOMY

 Endoneurium – covers
axon.
 Perineurium – covers
fascicles
 Epineurium – covers
nerve trunk
 BLOOD SUPPLY OF NERVE
 Blood vessels run in the
epineurium.
 Become endoneurial
capillaries after
penetrating.
 Sympathetic supply to
vessels by same nerve.
(cause for RSD)
 MODE OF NERVE INJURY
 Ischemia
 Compression
 Traction
 Laceration
 Burn.
NERVE INJURY HEALING
 SEDDON CLASSIFICATION

NEUROPRAXIA AXONOTMESIS NEUROTMESIS

•Axonal
interruption •Division of nerve trunnk
•Physiological conduction
block •Nerve in continuity •Endoneurial tube

•Segmental demyelination •Axon disintegrate – destroyed to variable

phagocytosis – Wallerian length
•Crutch pasly
degeneration •Regenerating
Saturday nerve palsy
•Regeneration at the rate fibres+schwann
Tourniquet palsy cells+fibroblasts
of 1 mm / day
=Neuroma

Transient Ischemia
 SUNDERLAND CLASSIFICATION

Sunder
Seddon Epineurium Perineurium Endoneurium Axon Outcome
land

1 Neuropraxia + + + Block Good

2 Axonotmesis + + + _ G / fair

Axonotmesis
3 + + _ _ F /poor

Axonotmesis
4 + _ _ _ Poor

5 Neurotmesis _ _ _ _ Poor
 CLINICAL FEATURES
Highindex of suspicion.
Symptoms
– Numbness
– Paraesthesia
– Muscle weakness
Signs
– Abnormal posture
– Weakness
– Loss of sensation
– Sudomotor changes (plastic pen test)
 ASSESSMENT

 Degree of injury
 Tinels sign
(advancing at rate of 1
mm\day)
 EMG
– Denervation potential at
3 weeks
– Does not distinguish
between axonotmesis
and neurontemesis.
 ASSESSMENT

Level of function
– Sensory
Two point discrimination

(innervation density)
Threshold test

– Motor
Medical Research Council Scale

(0-5 grades)
 TREATMENT

Expectant
– Dynamic splints
– Passive manipulation
– Drugs ??
 Steroids
 methylcobalamine
 TREATMENT

Nerve Exploration
 Indications
– Type of injury suggest that nerve is divided.
– If recovery is delayed
 Vascular injury, unstable fracture
contaminated soft tissue, tendon injury are
dealt before nerve injury.
 TREATMENT
Primary Repair
 Sooner the better.
 Ragged ends –pared.
 Use microscope and
10\0 suture.
 Suture epineurium.
 Fascicular repair.
 Avoid tension on suture
line.
 Splinting.
 TREATMENT

Delayed Repair
 Indications
– Closed injury not improving at expected time
– Late presentation and missed diagnosis
– Failed primary repair
 Nerve Explored – scarred segment resected
-nerve mobilized –transposition (if req.) -
graft (if req.).
 TREATMENT

Nerve Grafting
 Used to bridge gaps.
 Sural nerve most commonly used.
(single\cable).
 Vascularised grafts also used.
 TREATMENT

Nerve Transfer
 Indicated forroot avulsions of brachial plexus.
 Spinal accessory to suprascapular nerve.
 Intercostal nerves to musculocutaneous nerve.
 TREATMENT
Tendon Transfer
 Motor end plate must have degenerated
(i.e. 18 – 24 months after injury)
 Assess
– Muscles – lost
– Muscles – available
 Donor Muscle
– Expendable
– Adequate power
– Synergistic
 Transferred tendon
– Routed subcutaneously
– Straight pull
 PROGNOSIS
DEPENDS ON
 TYPE OF LESION
 LEVEL OF LESION
 TYPE OF NERVE
 SIZE OF GAP
 AGE
 DELAY IN SUTURE
 ASSOCIATED LESION
 SURGICAL SKILL