Evaluation of the Neuroprotective Effects of Methylprednisolone and Surgical Decompression in a Rodent Model of Traumatic Optic Neuropathy.

PURPOSE OF THE STUDY: Traumatic optic neuropathy (TON) is a rare but serious consequence of head injuries. The optimal therapy for TON remains controversial, and standardized recommendations are lacking. The most common therapies used are steroid administration and surgical decompression procedures. The aim of the present study was to compare two common conservative and surgical therapies in a rodent model with a standardized traumatic optic nerve lesion. MATERIALS AND METHODS: This study employed 59 male Wistar rats. After exposing the optic nerve, defined trauma was exerted on the optic nerve using a micromanipulator to trigger TON. Rats received either "megadose" methylprednisolone applied perioperatively or decompression via nerve sheath fenestration. The number of neurons was histologically evaluated in retinae explanted as whole mounts. Neuronal size was determined histomorphometrically. RESULTS: Neuronal loss was significantly lower following perioperative "megadose" steroid therapy (p = .017), especially in the central retinal area (p = .025). Compared to the control group without therapy, on average more than 400 neurons/mm2 were saved. In the central retinal area, more than 600 neurons/mm2 were rescued. In contrast, neuronal loss was not significantly affected by surgical decompression; however, this procedure was associated with a reduction in neuron size (p = .003). CONCLUSIONS: The present model revealed significant neuroprotective effects following administration of methylprednisolone for TON treatment. Mitigation of neuronal loss may result in functional benefits. Neuroprotective effects were not observed following surgical therapy, suggesting that this approach should be reserved for individual cases such as hematomas in the area of nerve envelopes.

Central resorption in an iliac crest transplant with microvascular anastomosis--report of 2 cases.

INTRODUCTION: The microvascular iliac crest flap is preferred for repair of segmental mandibular defects. Its viability and constant size are regarded as a great advantage for oral rehabilitation. PATIENTS: Two patients with oral cancer and recurrent keratocyst underwent mandibular reconstruction with an iliac crest transplant. Wound healing was uneventful. RESULTS: Several years after reconstruction we noticed complete absence of cancellous bone in the transplants. The cortical aspect consisted of vital bone. CONCLUSION: Secondary to changes in the blood supply after tissue transfer, microvascular bone transplants may develop complete medullary resorption. Substitution of this central bone is variable and may not happen at all.

Quantification of histological changes after calibrated crush of the intraorbital optic nerve in rats.

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.