Peripheral Nerve Injuries – Management

Indications for Surgery

Sunderland I – neuropraxic
Sunderland II – axonotmetic
Sunderland III – perineurium preserved
Sunderland IV – incomplete disruption of perineurium
Sunderland V – neurotonmesis

The trick is in distinguishing the Sunderland I, II, and III injuries from the IV and V, and recognizing what the surgery can actually accomplish.
– Clinical examination
– Electrophysiologic testing

Closed injury – the lesion in continuity
Open injury – laceration or blast

? Role for early exploration ?
– less scarring makes the dissection easier
– intraoperative evaluation of the anatomy, and possibly with
electrophysiologic means, the function of the nerve
– early repair with potential for faster recovery

– Is it worth the risk of operating on those who will
improve on their own?

Timing of Surgery

Biological considerations:

– Wallerian degeneration – axons, endoneurial tubes, cell bodies
– Motor end plates – 12-24 months
– Muscle – atrophy and suicide genes
– Sensory end-organs – undefined survival time
– Axonal regenerative capacity – 2.5 cm per month

EMG changes – transient fibrillation potentials – spontaneous fibrillations (membrane instability)

Technical considerations:

– Type of injury – laceration, crush, avulsion
– Type of wound – open or closed
– Condition of open wound – clean, contaminated

For sharp transections in a clean environment – immediate repair

For contaminated wounds – initial debridement and tagging of ends, followed by secondary repair.

For closed injuries – 3-6 months of observation.

The outcomes of all methods of treatment, including neurolysis, nerve repair, and nerve grafting, deteriorate after 6 months.

Surgical Management

Mobilization – the 2.5 cm gap

Epineurial repair with 9-0 or 10-0 monofilament suture

Fascicular repair versus epineurial repair?

Nerve Loss
– tension causes gapping, increased intraneural fibrosis, and decreased blood flow
– methods of closing gaps
– how much is too much tension?
– mind the 2.5 cm threshold!

Nerve Grafts
– sural nerve
– lateral antebrachial cutaneous nerve
– medial antebrachial cutaneous nerve

Beyond the surgeon’s control:
– patient age
– level of injury

Current and Future Possibilities

Coaptation Techniques

– CO2 laser and argon laser welding
– fibrin gluing

Nerve Conduits

– bone
– silicone
– vein ? + Schwann cells or neurotrophic factors
– artery
– polyglactin 910
– collagen


– immunologic rejection vs immungenicity
– irradiation, lypholization, freeze-drying – all reduce antigenicity
– cyclosporin and FK506 – immunosuppression
– effect on allograft Schwann cells

FK506 – Tacromilus

– promotion of functional nerve recovery

Enhancement of Nerve Regeneration

Full recovery of function after nerve transection is rare.
Motor end-plates have a finite life span after dennervation – the axonal growth must reach the target organs in time.
Neuronal survival is critical.


Neurotrophic Factors

Nerve Growth Factor – NGF
– multiple and varied effects inside and outside the nervous system
– receptor mRNA is upregulated after experimental injury
– motor neurons lack trkA receptors; unlikely that NGF will have much effect on motor nerve injuries

Brain Derived Neurotrophic Factor – BDNF
– growth and survival factor for motor neurons, prevents natural apoptosis
– strong evidence to support its role in axonal and neurite regeneration in motor neurons in particular.

Neurotrophin 3 – NT-3
– role in CNS regeneration (spinal cord)
– sensory and parasympathetic neurons
– motor neuron survival
– motor endplates

Enhancement of Nerve Regeneration

Neurotrophin 4/5 (NT-4/5)
– survival of motor neurons
– modulates neurmuscular junction in axotomized motor neurons
– increased ability of motor neurons to innervate skeletal muscle fibers

Ciliary Neurotrophic Factor (CNTF)
– neurite

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