Morphological and functional changes of the optic nerve following traumatic optic nerve injuries in rabbits

Abstract

Abstract. The aim of the present study was to investigate the morphological changes of the optic nerve following traumatic injuries and decompression at different times after injury, and to observe the changes of the visually evoked potentials, to identify the relevant associations between surgical opportunity and the clinical effect of traumatic optic nerve injuries. Rabbits were chosen as the animal model for the study. All the rabbits were randomly divided into five groups (A-E), representing the normal control, decompression in 48 h, in 1 week, in 2 weeks and non-decompression groups, respectively. The pattern reversal visual evoked potentials (P-VEP) and morphological changes of the optic nerve were observed. The P-VEP of each healthy rabbit revealed typical NPN contours, while NPN waves in the injured rabbits were low and flat. The latent period of the P-wave was lengthened and the amplitude was reduced. The differences of the latent period and amplitude pre-and post-trauma were statistically significant. The morphological changes were also assessed. In the normal control group, the astrocytes of the optic nerve exhibited a cylindrical form and were arranged evenly on the vertical section. The neural fibers were arranged neatly, were even following application of a dye, and the cross section exhibited a normal configuration of the blood vessel. For the 48-h decompression group, the arrangement of the astrocytes was even on the vertical section, and vacuoles, slight swelling of the nerve, exudation around the blood vessel and a small amount of astrocytic hyperplasia were observed in the damaged area. In the non-decompression group there were large areas of necrosis, clear nerve demyelination, serious exudation around the blood vessel and astrocytic hyperplasia were observed. In conclusion, the optic nerve decompression is beneficial to protect the visual function in indirect optic nerve injuries. Visual function may be improved by decompression in 48 h compared to 2 weeks. In order to prevent secondary axon injury and to protect visual functions, the decompression should be performed as soon as possible.

A Novel Mouse Model of Traumatic Optic Neuropathy Using External Ultrasound Energy to Achieve Focal, Indirect Optic Nerve Injury

“…The crush model causes local destruction of tissue ultrastructure and alteration of vascular plexus surrounding the globe and nerve 18 . Moreover, the model does not quantify the force applied to achieve injury 19 , and the degree of injuries are variable depending on the individual performing the procedure. In addition to severing the blood supply to the posterior segment of the globe 14 , the optic nerve transection 14 technique shares many of the drawbacks of the crush model in that optic nerve exposure and direct physical contact are needed to induce injury.…”

Possible role of miR-204 in optic nerve injury through the regulation of GAP-43

“…Optic nerve injury results from damage to the optic nerve in craniocerebral trauma, with the majority of cases caused through an indirect mechanism (1). Optic nerve injury is commonly the result of ocular surgical injury, which refers to the complete or partial loss of the optic nerve due to the effect of external force or through direct contact with tools (2). The progressive death of retinal ganglion cells (RGCs) is a major cause of irreversible visual impairment following optic nerve injury.…”

Tumor Necrosis Factor Inhibition in the Acute Management of Traumatic Optic Neuropathy

“… 2 The most common animal model used to simulate optic nerve injury is optic nerve crush (ONC). 16 , 17 While this model effects RGC loss, 18 it requires direct contact with the optic nerve—a less common etiology for clinical TON. 5 Using sonication shock as a means to induce TON (sonication-induced TON [SI-TON]), 19 we established an injury model that closely approximates the indirect clinical mechanism in TON.…”