Traumatic neuroma-in-continuity (NIC) injuries result in profound neurological deficits, and its management poses the most challenging problem to peripheral nerve surgeons. The absence of a clinically relevant experimental model continues to handicap our ability to investigate ways of better diagnosis and treatment for these disabling injuries. The aim of this project was to develop and refine a clinically relevant small animal NIC injury model to allow us to better understand this injury and the anatomical substrates for the associated poor functional recovery. An intense focused compression force in combination with a small traction force produced histological features and functional deficits consistent with NIC injuries in rat nerves. The methods were refined to identify a small NIC force window that is to be targeted to reproduce these injuries. With these methods the detrimental role of axonal attrition and misdirection on functional recovery was confirmed to characterize and validate this new model.