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Axonal Misdirection in a Femoral Nerve Neuroma in Continuity Injury Model
Jacob D. Alant, MBChB, FRCS(C); Joanne Forden; Rajiv Midha, MD, MSc, FRCS(C)
Department of Clinical Neurosciences, University of Calgary., Calgary, AB, Canada
Background: The management of traumatic neuroma-in-continuity (NIC) injuries poses ongoing challenges to peripheral nerve surgeons. NIC lesions are characterized by disruption of the internal nerve architecture, often as a consequence of high compression and traction forces. Axonal misdirection with non-specific reinnervation, frustrated regeneration and axonal attrition, are believed to be among the anatomical substrates that underlie the poor functional recovery and neuropathic pain associated with these devastating injuries. We hypothesized that unlike crush injuries, NIC injuries would result in axonal misdirection and attrition, similar to transection injuries. We applied our novel NIC injury model to rat femoral nerves to investigate this hypothesis.
Methods: A malleus nipper (MN) was modified and calibrated to exert a range of intense uniform compression forces. Histological NIC features were reproduced in vivo when sub-transection compression forces were applied to nerves with 3-second malleus nipper compression and optimized in combination with simultaneous 50g traction with a spring scale hooked around the nerves (Fig.1). 42 male Lewis rats were randomized into one of 7 groups for left femoral nerve surgeries (Fig.2). At 28 days, Fast Blue and Di-
I were respectively applied distally, to the main motor and sensory divisions of the nerves for retrograde labeling of spinal cord motor neurons. Distal nerve segments were also harvested at this time for histomorphometry. 13 days later spinal cords and femoral nerves were harvested for longitudinal cryostat sectioning, counting of fluorescently labeled neurons and histological evaluation of injury zones.
Results: Characteristic histological NIC features were demonstrated in the MN, MN+50g and (MN+50g)x2 groups. Misdirection of motor axons, motor neuron counts (attrition) and percentage neural tissue in the motor division of the (MN+50g)x2 group showed statistically significant differences compared to the SHAM and CRUSH groups, similar to the TRANSECTION and TRANSECTION+REPAIR groups (Fig.3+4).
Conclusion: Our results further characterize this injury model by confirming a high degree of axonal misdirection and attrition in severe NIC injuries, similar to transection injuries. This is consistent with long held theories, although previously unproven in the absence of a relevant experimental model.
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