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
– 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)
– 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.
Mobilization – the 2.5 cm gap
Epineurial repair with 9-0 or 10-0 monofilament suture
Fascicular repair versus epineurial repair?
– 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!
– sural nerve
– lateral antebrachial cutaneous nerve
– medial antebrachial cutaneous nerve
Beyond the surgeon’s control:
– patient age
– level of injury
Current and Future Possibilities
– CO2 laser and argon laser welding
– fibrin gluing
– vein ? + Schwann cells or neurotrophic factors
– polyglactin 910
– 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.
SPEED and SURVIVAL
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)