Peripheral nerve injuries

Peripheral Nerve Injuries
Chye Yew Ng
MBChB(Hons) FRCS(Tr&Orth) British Diploma in Hand Surgery
European Board of Hand Surgery Diploma
Consultant Hand & Peripheral Nerve Surgeon
Fellowship Director, Upper Limb Fellowship
Wrightington Hospital

www.wrightington.com
Overview
Basic science
Classification of nerve injuries
Principles of nerve surgery
What (I think) you may be asked

Key Message
Not all nerve injuries are neurapraxia
Delay in treatment may lead to poorer outcome
Recognise nerve in danger:
Pain
Autonomic dysfunction
Tinel sign

Please draw the cross section of a nerve
Axon
Fascicle
Nerve
Endoneuriu
m
Epineurium
Perineurium
EpiPEn = Epi – Peri – Endo
A&E
Extrinsic & Intrinsic vascular supply
Longitudinal – Segmental - Interconnected

Degeneration & Regeneration
Lee & Wolfe. Peripheral nerve injury & repair. JAAOS 2000

Central Neuronal Death &
Neuroprotection
Neuronal death after peripheral nerve injury
Acetyl-L-carnitine
Arrests sensory neuronal death
Speeds up regeneration
N-acetyl-cysteine
Provides sensory and motor neuronal protection
Hart et al. Neurological Research 2008

Nerve Injury & Recovery
Motor
Proprioception
Touch
Temperature
Pain
Sympathetic
Recovery
Injury

Mechanoreceptors Characteristics
Meissner’s corpuscles
•Rapidly adapting
•Sensitive to light touch
Merkel’s discs
•Slowly adapting
•Pressure, texture
•Low frequency vibration
•Static 2PD
Pacinian corpuscles
•Rapidly adapting
•High frequency vibration
•Rapid indentations of skin
•Ovoid, 1mm in length
Ruffini terminals
•Slowly adapting
•Skin stretch
SubcutaneousCutaneous

Slowly Adapting Rapidly Adapting
Low
frequency
vibration
Merkel Meissner
High
frequency
vibration
Ruffini Pacinian

Nerve Regeneration
Order of return Sensory testing Histology PSSD
1
30Hz tuning fork
or
Moving touch
Meissner 1PM
2 Constant touch Merkel 1PS
3 Moving 2PD
Innervation
density quickly
adapting fibres
2PM
4 Static 2PD
Innervation
density slowly
adapting fibres
2PS

Mechanisms of Injuries
Crush / compression
Stretch / traction
Laceration / transection
Metabolic disturbance
Ischaemia
Radiation
Electrical injury
Thermal injury

Classification of Nerve Injuries
Seddon
BMJ
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in Continuity)
Neurotmesis
(Division of a nerve)
Brain
1943
• Localised
degeneration of
the myelin
sheaths
• Complete
interruption of
axons
• Preservation of
supporting
structures
(Schwann tubes,
endoneurium,
perineurium)
• All essential parts
destroyed
• Interruption can
occur without
apparent loss of
continuity

Neurapraxia Axonotmesis Neurotmesis
Motor
- - -
Sensory
+/- - -
Autonomic
+/- - -
NCS
Conduction block at the site
Distal conduction preserved
Loss of conduction both at
and distal to the lesion
Loss of conduction both at
and distal to the lesion
EMG No fibrillation Fibrillation ++ Fibrillation ++
Recovery
Days to weeks provided the
cause is removed
Months provided the cause
is removed
No recovery unless repaired

In clinical practice, how do you distinguish?
Axonotmesis versus Neurotmesis
Nature of injury
Serial observations
Exploration
Seddon BMJ 1942
(Imaging)

Sunderland
1951 I II III IV V
Focal
conduction
block
NO Wallerian
degeneration
Axonal
Disruption
Axon
+
Endoneurium
Disruption
Axon
+
Endoneurium
+
Perineurium
Disruption
Axon
+
Endoneurium
+
Perineurium
+
Epineurium
Disruption
Cross-innervation

Sunderland’s Classification
Grabb & Smith’s Plastic Surgery 6th edition. Chapter 9

Physiological Conduction Block
Type A
Intraneural circulatory arrest
Metabolic block with no nerve fibre pathology
Immediately reversible
Type B
Intraneural oedema
Increased endoneurial fluid pressure
Reversible within days or weeks

Lundborg
1988
Physiological
conduction
block
Myelin
damage
Axonal
damage
Axon
+
Endo
damage
Axon
+
Endo
+
Peri
damage
Axon
+
Endoneuriu
m
+
Perineurium
+
Epineurium
damage
Type
A
Type
B
Sunder
land
1951
I II III IV V
Seddon
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in
Continuity)
Neurotmesis

Lundborg
1988
Physiological
conduction
block
Myelin
damage
Axonal
disruption
Axon
+
Endo
Axon
+
Endo
+
Peri
Axon
+
Endoneuriu
m
+
Perineurium
+
Epineurium
Type
A
Type
B
Sunder
land
1951
I II III IV V
Seddon
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in
Continuity)
Neurotmesis
Non-
degenerative
Degenerative

Lundborg
1988
Physiological
conduction
block
Myelin
damage
Axonal
disruption
Axon
+
Endo
Axon
+
Endo
+
Peri
Axon
+
Endoneuriu
m
+
Perineurium
+
Epineurium
Type
A
Type
B
Sunder
land
1951
I II III IV V
Seddon
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in
Continuity)
Neurotmesis

Sunderland ‘VI’
Grabb & Smith’s Plastic Surgery 6th edition. Chapter 9

Nerve in Danger!
Pain, Pain, Pain
• Burning
• Severe
Autonomic dysfunction
• Absence of sweating
• Smoothness & dryness of skin
Tinel sign
• Distal to Proximal
• Regenerating touch fibres

George Bonney 1986

Nerve Surgery
Neurolysis
Nerve repair
Nerve grafting
Nerve transfer

Neurolysis
External
Internal

Nerve repair

Prerequisites for Nerve Repair
Skeletal stability
Healthy tissue bed
Healthy nerve ends
No undue tension
Adequate soft tissue coverage

Epineurial versus Group Fascicular Repairs
Epineurial
Less exact
Simple
Group Fascicular
Better alignment
More dissection (scarring)
The functional results of group fascicular repair
has not been shown to be more superior than that
of epineurial repair.

Which of the following is false regarding fibrin glue?
a) Fibrin glue is nontoxic and does not block axon regeneration
b) It may be used in combination with suture repair
c) The outcome of fibrin glue repair is inferior to that of suture
repair
d) The common components of fibrin sealants include
fibrinogen, thrombin and calcium chloride
e) It has low tensile strength
Tse & Ko. Nerve glue for upper extremity reconstruction. Hand Clinics 2012

Prognostic Factors of Outcomes
•AgePatient
factor
• Level of injury (distal vs
proximal)
• Type of nerve (pure vs mixed
functions)
• Condition of nerve ends
Injury
factors
• Delay to repair
• Length of gap
Surgical
factors

Nerve Grafts/Conduits
Autologous Source
Nerve autograft
Vein (+/- muscle)
Off-the-shelf
Type I collagen
Caprolactone
Polyglycolic acid (PGA)
Processed nerve
allograft
Lin et al. Nerve Allografts & Conduits in Peripheral Nerve Repair. Hand Clinics 2013
Kaushik & Hammert. Options for Digital Nerve Gap. JHSAm 2015

A 35 year-old male presented with numbness along the radial border of his
right index finger 9 months after he sustained a cut in his first web. After
surgical exploration and debridement, there is a 3.5cm nerve defect in the
radial digital nerve.
What is the most appropriate surgical reconstructive option?
a) Flexion of digit to achieve primary repair before gradual distraction
b) Type I collagen nerve conduit
c) Autologous vein graft
d) Posterior interosseous nerve graft
e) Polyglycolic acid (PGA) conduit

Principles of Motor Nerve Transfers
Donor nerve near target motor end plates
Expendable donor nerve
Pure motor donor nerve
Donor-recipient size match
Donor function synergy with recipient function
Motor re-education improves function
Mackinnon SE, Novak CB. Hand Clin 1999

Peripheral Nerve Injury Service
Tel: 01257 488285
Fax: 01257 256476
Email: nerve@wwl.nhs.uk
We treat
Adult traumatic brachial plexus injuries
Nerve injuries following trauma/surgery
Recurrent/persistent entrapment neuropathies
Painful scarred nerve or neuroma
Brachial neuritis / Parsonage Turner syndrome
Benign nerve sheath tumour

Peripheral nerve injuries

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