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Pathophysiology of nerve injury

Physiology
Anatomy
1. Schwann cells
a. Myelinated and unmyelinated nerve axons
b. Trophic factors (regenerative)
c. Enclosed in basal membrane
2. Layers
a. Endoneurium supporting cells
b. Perineurium blood nerve barrier
c. Epineurium undulation (movement)

Axoplasmic transport
1. Cell bodies produce protein & transport to neurons
2. Fast (membrane bound) & Slow (soluble) transport requires
energy and Ca2+
3. Antegrade (repair & synthesis) & Retrograde (recycling &
breakdown) direction

Injury to peripheral nerves


Neural (axons, Schwann cells, myelin)
Regeneration within 24h of injury
More organized regeneration
Restoration of function
2 main responses
Axonal
Segmental demyelination
degeneration
Slowing/ complete cessation of impulse condution

Response to injury
Wallerian degeneration (Distal to injury)

Changes in myelinated fibres


Axonal
Myelin sheath, Schwann
cell, macrophages
Granular
Partial collapse of myelin
disintegration
tube 48h after injury
(distal stump)
Granular
Production of myelin protein
amorphous

debris
Remnants of
Breakdown of myelin
axon
degeneration
Myelin becomes segmented
into ovoid
Myelin removal by Schwann
cells, hematogenous
macrophages
Schwann cell cytoplasm
shrinks
Ovoid segments in size
Schwann cells undergo
mitosis
Tightly packed Schwann cells
(distal stump)
Changes in unmyelinated fibres
Changes as in myelinated fibres
Myelin degeneration not seen
No prominent macrophage response
Schwann cell proliferation occurs

Proximal
end
degeneratio
n
Similar to
Wallerian
degeneration
Affects only
up to 2 nodes
of Ranvier
(from point of
injury)

Connective tissue (CT)


Proliferation of CT cells haphazardly
Repair by scar tissue
Anatomical continuity (rather than
restoration of function)

Cell body

End organs (muscle)

Chromatolysis (Nissl granules


breakdown)

RNA become more active form

protein production

axonal transport

Muscle
Atrophy
Neighbouring uninjured
nerve fibres may
innervate muscle fibres
that have lost nerve
supply
Change in muscle fibre
characteristics
Sarcolemma at N-M
junction looses folds
Nerve regeneration,
recover normal structure
Absense of innervations,
muscle atrophy,
irreversible fibrosis (2
years), motor end plate
degenerate completely
(18-24 months)

Cell body swell up


Nucleus pushed to periphery
Axonal stump (if lesion close to cell
body)
Death of cell body (no regeneration
possible) (if injury severe)

Sensory
Area shrinks due to
recovery from
neuropraxia (functional,
not anatomical defect)
Adjacent branches
supply anaesthetic area

Classification of Injury
Neuropraxia
Axonotmesis
Nerve conduction
Anatomical interruption of axon with no/partial
blocked (without
interruption to CT (preservation of perineural
anatomical
continuity)
interruption)
Loss of neurological
Fascicular alignment mostly preserved
function is
temporary
Full recovery takes
2 extends of injury are possible
place
Local segmental
Sunderland Grade 2
Sunderland Grade 3
Axon continuity is
Disrupt axon, myelin,
demyelination (most
disrupted
endoneurium
severe)
Myelin shealth continuity
Large diameter
may/may not be
fibres (most
preserved initially
susceptible)
Basement membrane is
Chance to recovery
No Wallerian
preserved
than Grade 2
degeneration
Wallerian degeneration
Continuity of basal
Distal segment
occurs 2 to axonal
lamina is lost (likelihood
retain nerve
damage in distal
of neuritis growing into
conduction capacity
Recovery in a few
segment (lead to
inappropriate distal
days (rarely longer)
breakdown of myelin)
segments higher)
Sunderland Grade
Recovery is sequentially
1 injury
from proximal to distal

Neurotmesis
Complete anatomical disruption (axon, surrounding
CT)

Sunderland Grade 4
Both axons, CT loose
continuity
Nerve not completely
severed
Interfascicular epineural
CT, perineurium
disrupted
Fascicular continuity is
lost (different from
axonotmesis)
Neurites caught in fibrous
tissue scars
May be in inappropriate
fasciculus when they find
distal stumps
Endoneural proliferation,
narrowing of distal
stumps, fibre diameter
will be smaller, function
compromised

Sunderland Grade 5
Nerve severed
completely
Neuroma formation (if
not repaired)

Neural regeneration
1. Reversal of chromatolysis
2. Axonal transport of materials
3. Axonal sprouting
a. Prolonged denervation prevent regeneration of axons
to enter appropriate tubes
b. Failure to enter due to
i. Scar formation
ii. Too long gap

Factors influencing prognosis


1. Age younger better
2. Site
3. Severity
4. Type
5. Tension
6. Sepsis
7. General factors condition, nutrition of patient
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. Tinels sign
2. Electrophysiology
a. Electromyography
b. Nerve conduction studies