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Pathophysiol ogy of nerve injury

Physiology
Anatomy Axoplasmic transport
1. Schwann cells 1. Cell bodies produce protein & transport to neurons
a. Myelinated and unmyelinated nerve axons 2. Fast (membrane bound ) & Slow (soluble) transport – requires energy and
b. Trophic factors (regenerative) Ca2+
c. Enclosed in basal membrane 3. Antegrade (repair & synthesis) & Retrograde (recycling & breakdown)
2. Layers direction
a. Endoneurium – supp orting cells
b. Perineurium – blood nerve barrier
c. Epineurium – undulation (moveme nt)

Injury to peripheral nerves

Neural (axons, Schwann cells, myelin) Connective tissue (CT)
Regeneration – within 24h of injury Proliferation of CT cells haphazardly
More organized regeneration Repair by scar tissue
Restoration of function Anatomical continuity (rather than restoration of
2 main responses function )
Axonal Segmental demyelination
degeneration
Slowing/ complete cessation of impulse con dution

Response to injury
Wallerian degeneration (Distal to injury) Proximal end Cell body End organs (muscle)
degeneration
Changes in myelinated fibres Similar to Chromatolysis (Nissl granules breakdown) Muscle
Axonal Myelin sheath, Schwann cell, Wallerian • RNA become more active form Atrophy
macrophages degeneration • ↑ protein production Neighbouring uninjured nerve
Granular Partial collapse of myelin tube – • ↑ axonal transport fibres may innervate muscle
disintegration 48h after injury Affects only up fibres that have lost nerve
(distal stump) to 2 nodes of Cell body swell up supply
Granular Production of myelin protein ↓ Ranvier (from Change in muscle fibre
amorphous debris point of injury) Nucleus pushe d to periphery characteristics
Remnants of axon Breakdown of myelin ↑ Sarcolemma at N-M junction
degeneration Axonal stump (if lesion close to cell body ) looses folds
Myelin becomes segmented into Nerve regeneration, recover
ovoid Death of cell body (no regeneration normal structure
Myelin removal by Schwann cells, possible) (if injury severe) Absense of innervations,
hematogenous macrop hages muscle atrophy, irreversible
Schwann cell cytoplasm shrinks fibrosis (2 years), motor end
Ovoid segments ↓ in size plate degenerate completely
Schwann cells undergo mitosis (18-24 months)
Tightly packed Schwann cells (distal
stump) Sensory
Area shrinks due to recovery
Changes in unmyelinated fibres from neuropraxia (functional,
Changes as in myelinated fibres not anatomical defect)
Myelin degeneration not seen Adjacent branches supply
No prominent macrop hage response anaesthetic area
Schwann cell proliferation occurs
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Classification of Injury
Neuropraxia Axonotmesis Neurotmesis
Nerve conduction blocked Anatomical interruption of axon with no/partial interruption to CT Complete anatomical disruption (axon, s urrounding CT)
(without anatomical (preservation of perineural continuity)
interruption)
Loss of ne urological Fascicular alignment mostly preserved Sunderland Grade 4 Sunderland Grade 5
function is temporary Both axons, CT loose continuity Nerve severed completely
Full recovery takes place 2 extends of injury are possible
Local segmental Sunderland Grade 2 Sunderland Grade 3 Nerve not completely severed Neuroma formation (i f not
demyelination (most Axon continuity is disrupted Disrupt axon, myelin, repaired)
severe) endoneurium Interfascicular epineural CT,
Large diameter fibres Myelin shealth continuity perineurium disrupted
(most susce ptible) may/may not be preserved Fascicular continuity is lost
No Wallerian initially (different from axonotme sis)
degeneration Basement membrane is Chance to recovery ↓ than Neurites caught in fibrous
Distal segment retain preserved Grade 2 tissue scars
nerve conduction capacity Wallerian degeneration occurs Continuity of basal lamina is May be in inappropriate
Recovery in a few days 2° to axonal damage in distal lost (likelihood of neuritis fasciculus when they find distal
(rarely longer) segment (lead to breakdown of growing into inappropriate stumps
Sunderland Grade 1 myelin) distal segments higher) Endoneural proliferation,
injury Recovery is sequentially from narrowing of distal stumps,
proximal to distal fibre diameter will be smaller,
function compromised

Neural regeneration Factors influencing prognosi s

1. Reversal of chromatolysis 1. Age – younger better
2. Axonal transport of materials 2. Site
3. Axonal sprouting 3. Severity
a. Prolonged denervation prevent regeneration of axons to enter 4. Type
appropriate tubes 5. Tension
b. Failure to enter due to 6. Sepsis
i. Scar formation 7. General factors – condition, nutrition of patient
ii. Too long gap 8. Timing of repair – earier better

Nerve injury & Wallerian degeneration Nerve regeneration

Tests of regeneration
1. Clinical
a. Reassess motor, sensory, autonomic function
b. Examinte scar tissue and neuroma
c. Tinel’s sign
2. Electrophysiology
a. Electromyography
b. Nerve conduction studies