BACKGROUND: Traumatic optic nerve lesions (TONL) are probable but unpredictable consequence after severe midface or skull base trauma. Based on a previously described rat model, the authors developed a new model in order to simulate optic nerve crush during trauma on the optic canal. METHODS: To achieve a calibrated TONL, a microinjuring device was designed that made it possible to assess the correlation between a defined trauma and the neuronal degeneration in the rat retinal ganglion cell (RGC) layer. This device is based on a small dynamometer mounted onto a conventional micromanipulator. The supraorbital approach was chosen to expose the extracranial optic nerve. RESULTS: In this rat model (n=100, Wistar strain) the parameters of "force" and "time" could be precisely monitored during the experiment. The decrease in the mean number of retinal neurons (N) according to the pressure exerted (2-30 cN x mm(-2)) on the optic nerve was linear for 1, 6, and 15 minutes of injuring time; the decrease in N for varying injuring forces also appears to be nearly linear. CONCLUSION: The results show that this model provides a reliable method for studying quantitatively the anatomical effects of TONL on the RGC layer and the optic nerve itself, and may allow the design of treatment strategies following TONL.
BACKGROUND:Traumatic optic nerve lesions (TONL) are probable but unpredictable consequence after severe midface or skull base trauma. Based on a previously described rat model, the authors developed a new model in order to simulate optic nerve crush during trauma on the optic canal. METHODS: To achieve a calibrated TONL, a microinjuring device was designed that made it possible to assess the correlation between a defined trauma and the neuronal degeneration in the rat retinal ganglion cell (RGC) layer. This device is based on a small dynamometer mounted onto a conventional micromanipulator. The supraorbital approach was chosen to expose the extracranial optic nerve. RESULTS: In this rat model (n=100, Wistar strain) the parameters of "force" and "time" could be precisely monitored during the experiment. The decrease in the mean number of retinal neurons (N) according to the pressure exerted (2-30 cN x mm(-2)) on the optic nerve was linear for 1, 6, and 15 minutes of injuring time; the decrease in N for varying injuring forces also appears to be nearly linear. CONCLUSION: The results show that this model provides a reliable method for studying quantitatively the anatomical effects of TONL on the RGC layer and the optic nerve itself, and may allow the design of treatment strategies following TONL.
Authors: Rüdiger Zimmerer; Katrin Schattmann; Harald Essig; Philipp Jehn; Marc Metzger; Horst Kokemüller; Nils-Claudius Gellrich; Frank Tavassol Journal: Craniomaxillofac Trauma Reconstr Date: 2013-11-20