Traumatic Optic Nerve Research Articles

Epidemiological Trends of Traumatic Optic Nerve Injuries in the Largest Canadian Adult Trauma Center

There has been a paucity of information on the epidemiology of traumatic optic neuropathy (TON). This study documents epidemiology of TON over 2 decades in the largest level I adult trauma center in Canada. Data on all the trauma patients admitted to Sunnybrook Health Sciences Centre from 1986 to 2007 were collected in a prospective database. The aggregate data on optic nerve injuries including demographic data, etiology, Injury Severity Score (ISS), and associated head and facial injuries were recorded. These were analyzed using univariate and multivariate techniques to summarize the association of different variables with TON. During the study period, 0.4% of all trauma patients had TON. The respective demographics for TON group were as follows: male, 76%; median for age, 33.5 years; length of hospital stay, 14 days; ISS, 32; and case fatality, 14%. About two thirds of patients with TON had associated significant head injuries. Conversely, 2.3% of patients with head injury had TON. The relative incidence of TON per year has remained variable from 0% to 1.2%. Motorized vehicle accidents remained the main etiology of TON (63%), but fall had the highest relative frequency leading to TON. In univariate analysis, both ISS and significant head injury were associated with TON. In multivariate analysis, TON was associated with only nasoethmoid complex fractures and significant head injury. These data provide useful information on the frequency and etiologies of TON. It also highlights the importance of studies on better diagnostic tools for TON.

Traumatic optic nerve avulsion: A case report

Case report of a traumatic optic nerve avulsion. We report the case of a traumatic right optic nerve avulsion in an 11-year-old boy as a result of a contusion with a surfboard. On initial examination, the patient exhibited bilateral mydriasis with a right afferent pupillary defect. Visual acuity was no light perception. A moderate microhyphema was noted along with intraocular pressure of 12mmHg and no open globe. Fundus examination revealed retinal ischemia with white retinal edema, attenuated arteries and segmentally occluded vasculature. In place of the optic nerve, there was a hole with associated vitreous hemorrhage. Non-contrast CT and MRI demonstrated vitreous prolapse into the optic nerve sheath, which still appeared securely attached to the globe. Spectral domain OCT and visual evoked potentials confirmed disruption of the ganglion cell layer. While obvious in the presence of clear media, an avulsion may remain undetected in the case of associated vitreous hemorrhage. Orbital imaging may clarify the diagnosis. Although rare, optic nerve avulsions exhibit the same risk profile as open globe injuries and arterial occlusions.

Improved visual acuity by optic canal decompression after traumatic optic nerve injury: a case report

Improved visual acuity by optic canal decompression after traumatic optic nerve injury: a case report

Post-Injury Delivery of rAAV2-CNTF Combined with Short-Term Pharmacotherapy Is Neuroprotective and Promotes Extensive Axonal Regeneration after Optic Nerve Trauma

Recombinant adeno-associated viral (rAAV) vectors expressing neurotrophic genes reduce neuronal death and promote axonal regeneration in central nervous system (CNS) injury models. Currently, however, use of rAAV to treat clinical neurotrauma is problematic because there is a delay in the onset of transgene expression. Using the adult rat retina and optic nerve (ON), we have tested whether rAAV gene therapy administered at the time of injury combined with short-term pharmacotherapy has synergistic effects that enhance neuronal survival and regeneration. The ON was transected and a 1.5 cm segment of autologous peripheral nerve (PN) was grafted onto the cut end. At this time, bicistronic rAAV2 encoding ciliary neurotrophic factor (CNTF) and green fluorescent protein (rAAV2-CNTF-GFP) was injected into the injured eye. To provide interim support for axotomized retinal ganglion cells (RGCs) during vector integration and therapeutic transgene expression, rCNTF protein and a cyclic adenosine monophosphate (cAMP) analogue (CPT-cAMP) were injected intravitreally 3 and 10 days postoperatively. For comparison, another rAAV2-CNTF-GFP group received two intravitreal saline injections 3 and 10 days after the PN-ON surgery. A further PN graft group received only postoperative intravitreal injections of rCNTF plus CPT-cAMP. After 4 weeks, regenerating RGCs were retrogradely labelled by applying fluorogold to the distal end of each PN graft. Compared to saline-injected animals, both RGC survival and axonal regrowth were significantly higher in the rCNTF and CPT-cAMP injected rAAV2-CNTF-GFP group; approximately one third of the RGC population survived axotomy, and 27% of these regrew an axon. These values were also higher than those obtained in rats that received only rCNTF plus CPT-cAMP injections. Therefore, we show for the first time that rAAV-mediated gene delivery at the time of, or just after, neurotrauma is most successful when combined with temporary post-injury trophic support, and is potentially a viable treatment strategy for patients after acute CNS injury.

Role of endothelial progenitor cells in optic nerve injury of rats

To investigate the role of endothelial progenitor cells (EPC) in the injury of rat optic nerve. An experimental study. The rat model of optic nerve injury was created by fluid percussion brain injury device (FPI). On hundred and eight rats (108 eyes) were divided into 2 groups randomly. Each group was further divided into 9 subgroups by the time of injury (24 h before and 3, 12, 24, 48, 72 h, 1, 2 and 3 weeks after the injury). The number of circulating EPCs was measured, HE staining of the optic nerve, immunohistochemistry study of CD31 (markers of vascular endothelial cells) and flash-visual evoked potential (F-VEP) were observed at every time point. Two independent sample t-test was used for the comparison between the control group and the optic nerve injury groups at the same time point. The correlation between different items was analyzed by Pearson test. P value less than 0.05 was considered significant. The number of EPCs in normal rats was 46-52/200 000 monocytes. After traumatic optic nerve injury, the number of EPCs was (34 ± 4, 34 ± 5, 69 ± 9, 76 ± 6, 107 ± 9, 69 ± 7, 58 ± 6 and 56 ± 4)/200 000 monocytes at 3, 12, 24, 48, 72 h, and 1, 2 and 3 weeks. The difference of number of EPCs between the experiment and control groups was significant at 3, 12, 24, 48, 72 h and 1 and 2 weeks after the injury (t = 5.29, 2.90, -4.30, -7.61, -14.17, -5.74 and -2.79; P < 0.05). The number of CD31(+) cell in the optic nerve and surround tissues in normal rats was (7-9)/5 high magnification field. After the injury, the number of CD31(+) cell was 8.36 ± 1.52, 7.17 ± 1.10, 10.41 ± 1.92, 11.43 ± 1.58, 14.29 ± 2.03, 17.33 ± 1.47, 17.86 ± 1.22 and 18.13 ± 1.40 at different time points. The difference of number of CD31(+) cell between the experiment and control groups was significant at 48, 72 h, and 1, 2, and 3 weeks after the injury (t = 4.31, -7.61, -8.17, -10.08, and -10.79; P < 0.05). The number of microvessels in the optic nerve and surround tissues in normal rats was 6-9/5 high magnification field. After traumatic optic nerve injury, the number of microvessels was 7.54 ± 2.01, 8.52 ± 2.21, 11.02 ± 1.62, 15.40 ± 2.04, 18.39 ± 1.96, 23.21 ± 1.50, 22.78 ± 2.40 and 24.13 ± 2.51 at different time points. The difference of number of microvessels between the experiment and control groups was significant at 48, 72 h, 1, 2, and 3 weeks after the injury (t = 4.25, -7.74, -8.26, -10.28 and -11.49; P < 0.05). The latency period of P waves was decreased at 3 h and increased to above basic level at 24 h, and then tend to be stable. The difference of latency period of P waves between the experiment and control groups was significant at 3, 12, 24, 48, 72 h, 1, 2 and 3 weeks after the injury (t = 4.15, 3.74, 5.84, 6.08, 6.40, 6.52, 6.53 and 6.61; P < 0.05). The amplitude of F-VEP was decreased at 3 h and increased to the basic level at 12 h, then decreased to below the basic level gradually. The difference of the amplitude of F-VEP between the experiment and control groups was significant at 3, 24, 48, 72 h, 1, 2 and 3 weeks after the injury (t = 3.95, 4.14, 5.26, 5.78, 6.49, 6.72 and 6.23; P < 0.05). The number of EPCs was correlated with the number of CD31(+) cell, microvessels and F-VEP (r = 0.43, 0.41 and 0.43; P < 0.01). The present study showed that the number of EPCs in the blood increases significantly after traumatic optic nerve injury, and the cells can arrive the traumatic area to repair injured tissue and enhance angiogenesis.

RGMA and neogenin protein expression are influenced by lens injury following optic nerve crush in the rat retina

The death and the failure of neurons to regenerate their axons after lesion of the central nervous system in mammals, as in the case of spinal cord injury and optic nerve trauma, remain a challenge. In this study, we focused on the repulsive guidance molecule A (RGMA) and its receptor neogenin. Since it was reported that RGMA+ cells accumulate in lesioned areas after spinal cord injury, brain trauma, and optic nerve crush, and curiously, anti-apoptotic effects of RGMA were also described, we investigated the role of RGMA and neogenin in the retina after optic nerve crush (ONC). We evaluated the spatial and temporal protein pattern of RGMA and neogenin in the rat retina without (non-regenerating model) or with (regenerating model) lens injury (LI). We investigated the presence of RGMA, neogenin and other proteins at up to nine time points (6 h-20 days post-surgery) by performing immunohistochemistry and Western blots. Independent of the treatment, RGMA protein was present in the nuclear layers (NLs), plexiform layers (PLs), nerve fiber layer (NFL), and in retinal ganglion cells (RGCs) of the rat retina. RGC and nerve fibers were always RGMA+. Further RGMA+ cells in the retina were blood vessel endothelial cells, astrocytes, Müller cells, and some microglial cells. The RGMA pattern for the specific retinal cells resembled those of previously published data. The neogenin pattern was congruent to the RGMA pattern. Western blots of retinal tissue showed further RGMA+ products only in LI animals. Furthermore, a higher amount of RGMA was found in the retinae of ONC + LI rats compared to ONC rats. Although a difference in the localization of RGMA is not obvious, the difference in the amount of RGMA is striking, the higher amount of RGMA in the retinae of ONC + LI rats compared to ONC rats indicates a role for RGMA during degeneration/regeneration processes. Our results are consistent with several reported neuroprotective effects of RGMA. Our new data showing the upregulation of RGMA after ONC in our regenerating model (plus LI) confirm these findings conducted in different settings.

An analysis on therapeutic effect of transcranial microsurgical decompression of optic canal treating optic nerve injury

Objective To analyse the therapeutic effect of transcranial microsurgical decompression of optic canal in treatment of traumatic optic nerve injuries. Methods Retrospective analysis of the operation timing, therapeutic effect and related factors affect of it in 27 cases.. Results Thirteen eases with the vision of no light perception, surgical effective rate is 23.1％, 11 cases with light perception, effective rate is 63.6％ ; hand movement effective rate is 100％. The total effective rate is 48.1％. without surgical complication. All of the effective patients undergoing operative within 2 weeks. Conclusion Simple optic nerve compression, the patients with beyond light perception vision, the therapeutic effect with early and fully decompression of optic canal is curative effect. Key words: Optic nerve injury ; Optic nerve decompression; Surgical approach

The application of anterior capsulectomy by scission in cataract surgery for lens subluxation

Objective To study the clinical efficacy of the application of anterior capsulectomy by scission in extracapsular cataract extraction (ECCE) for patients with lens subluxation. Methods 23 cases (23 eyes) with lens subluxation and cataract were treated by small incision ECCE combined with intraocular lens( IOL) implantation surgery. The scission was applied in anterior capsulectomy during operation. The cases were followed up for 6～24 months, 10.5 months in average. Results There were no expansion of lens detachment or increasement of vitreous prolapse during operation. The best corrected visual acuity (BCVA) of those cases were: 2 eyes ( 8. 70 % ) no less than 1.0,7 eyes ( 30. 43 % ) no less than 0. 5 and 16 eyes less than 0.5. Of those 16 eyes with BCVA worse than 0. 5,2 eyes were retinitis pigmentosa,7 eyes were ocular contusion combined with different degrees of retinal contusion, 2 eyes were traumatic optic nerve atrophy, 2 eyes were vitreous opaque ( obsolete hemorrhagic ) , 1 eye was traumatic macular hole and 2 eyes were high myopia( - 10.00 diopters or higher). Conclusion The application of anterior capsulectomy by scission is safe and satisfactory in small incision ECCE combined with IOL implantation surgery for lens subluxation. Key words: anterior capsulectomy; scission; lens subluxation; cataract surgery,small incision, manual

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Injury to the optic nerve can lead to axonal degeneration, followed by a gradual death of retinal ganglion cells (RGCs), which results in irreversible vision loss. Examples of such diseases in human include traumatic optic neuropathy and optic nerve degeneration in glaucoma. It is characterized by typical changes in the optic nerve head, progressive optic nerve degeneration, and loss of retinal ganglion cells, if uncontrolled, leading to vision loss and blindness. The optic nerve crush (ONC) injury mouse model is an important experimental disease model for traumatic optic neuropathy, glaucoma, etc. In this model, the crush injury to the optic nerve leads to gradual retinal ganglion cells apoptosis. This disease model can be used to study the general processes and mechanisms of neuronal death and survival, which is essential for the development of therapeutic measures. In addition, pharmacological and molecular approaches can be used in this model to identify and test potential therapeutic reagents to treat different types of optic neuropathy. Here, we provide a step by step demonstration of (I) Baseline retrograde labeling of retinal ganglion cells (RGCs) at day 1, (II) Optic nerve crush injury at day 4, (III) Harvest the retinae and analyze RGC survival at day 11, and (IV) Representative result.

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Injury to the optic nerve can lead to axonal degeneration, followed by a gradual death of retinal ganglion cells (RGCs), which results in irreversible vision loss. Examples of such diseases in human include traumatic optic neuropathy and optic nerve degeneration in glaucoma. It is characterized by typical changes in the optic nerve head, progressive optic nerve degeneration, and loss of retinal ganglion cells, if uncontrolled, leading to vision loss and blindness. The optic nerve crush (ONC) injury mouse model is an important experimental disease model for traumatic optic neuropathy, glaucoma, etc. In this model, the crush injury to the optic nerve leads to gradual retinal ganglion cells apoptosis. This disease model can be used to study the general processes and mechanisms of neuronal death and survival, which is essential for the development of therapeutic measures. In addition, pharmacological and molecular approaches can be used in this model to identify and test potential therapeutic reagents to treat different types of optic neuropathy. Here, we provide a step by step demonstration of (I) Baseline retrograde labeling of retinal ganglion cells (RGCs) at day 1, (II) Optic nerve crush injury at day 4, (III) Harvest the retinae and analyze RGC survival at day 11, and (IV) Representative result.

Traumatische Optikusneuropathie

Traumatic optic nerve neuropathy (TON) is defined as injury to the optic nerve with subsequent vision loss due to head or craniocerebral trauma. The treatment of this disease is the subject of controversial discussions. The purpose of the present study was to investigate pre- and immediate postoperative visual acuity in patients with unilateral TON and to compare the results with the time interval between trauma and surgical intervention. A total of 20 patients with unilateral TON and considerable vision loss were examined. All were treated with high dose corticoids and underwent microsurgical optic nerve decompression. Visual acuity was determined pre- and postoperatively. In long-term follow-up visual acuity was determined 3months postoperatively. Postoperatively, nine patients (45%) achieved an improvement in visual acuity of more than 0.4, and another three patients (15%) an improvement of ≥0.2. At 3months postoperatively another four patients achieved a further improvement of their visual acuity of >0.2. A decrease in visual acuity was not observed in any case, nor were major surgical complications. Factors which predict good prognosis for vision recovery include a short time interval between trauma and intervention, edema, and/or hematoma of the optic nerve sheath. Factors which predict a worse prognosis are a fracture line directly through the nerve canal, a time period between trauma and intervention of more than 24h, and initial complete amaurosis.

The role of activated macrophage in the repair of traumatic optic nerve injury

Objective To explore the role of activated macrophage in the repair of traumatic optic nerve injury in an animal model of incomplete traumatic optic nerve injury with lens damage. Methods One hundred and twelve healthy New Zealand big ear white rabbits were divided into two groups (experimentaland control groups) randomly. According to the different time points (one, four, seven, ten, 14, 21 and 28 days), each group was further divided into seven subgroups, each subgroup had eight rabbits. Traumatic optic neuropathy and lens damage were induced in one eye of each rabbit by fluid percussion brain injury device (FPI);those eyes were the experimental group. The eyes of control group only had traumatic optic neuropathy. The functional and morphological changes of retina and optic nerve were evaluated by histopathology and flash-visual evoked potential (FVEP). Results FVEP P100 latency was (42.74± 5.83)ms, P100 amplitude was (7.98 ± 2.15) μV before optic nerve injury was induced. One day after the injury,the P100 latency increased and the P100 amplitude reduced significantly. The P100 latency reached the longest at ten days after injury, and then recovered gradually. The P100 amplitude reached the lowest at seven days after injury, and then recovered gradually. The histopathological examination showed activated macrophages were not detected in the retina and optic nerve at day one after the injury, then they increased gradually and reached their peak (91.25 ±-6.91) at day ten, and decreased after that, the difference was statistically significant (F= 21. 277, P= 0. 000);retinal ganglion cell axon regeneration began at day seven after the injury with an average of (6.38± 1.85). The axons increased gradually and reached their peak (49.63±2. 50) at day 28, and the changes were significant (F=7. 711, P=0. 000). Conclusions Incomplete optic nerve injury can recover gradually if there is lens damage at the same time. Activated macrophage may playan important role in this recovery process. Key words: Optic nerve injuries; Macrophages; Animal experimentation

Regeneration of optic nerve

The optic nerve is part of the central nervous system (CNS) and has a structure similar to other CNS tracts. The axons that form the optic nerve originate in the ganglion cell layer of the retina and extend through the optic tract. As a tissue, the optic nerve has the same organization as the white matter of the brain in regard to its glia. There are three types of glial cells: Oligodendrocytes, astrocytes, and microglia. Little structural and functional regeneration of the CNS takes place spontaneously following injury in adult mammals. In contrast, the ability of the mammalian peripheral nervous system (PNS) to regenerate axons after injury is well documented. A number of factors are involved in the lack of CNS regeneration, including: (i) the response of neuronal cell bodies against the damage; (ii) myelin-mediated inhibition by oligodendrocytes; (iii) glial scarring, by astrocytes; (iv) macrophage infiltration; and (v) insufficient trophic factor support. The fundamental difference in the regenerative capacity between CNS and PNS neuronal cell bodies has been the subject of intensive research. In the CNS the target normally conveys a retrograde trophic signal to the cell body. CNS neurons die because of trophic deprivation. Damage to the optic nerve disconnects the neuronal cell body from its target-derived trophic peptides, leading to the death of retinal ganglion cells. Furthermore, the axontomized neurons become less responsive to the peptide trophic signals they do receive. On the other hand, adult PNS neurons are intrinsically responsive to neurotrophic factors and do not lose trophic responsiveness after axotomy. In this talk different strategies to promote optic-nerve regeneration in adult mammals are reviewed. Much work is still needed to resolve many issues. This is a very important area of neuroregeneration and neuroprotection, as currently there is no cure after traumatic optic nerve injury or retinal disease such as glaucoma, which affect retinal ganglion cells and optic nerve axons.

Redefining tissue engineering for nanomedicine in ophthalmology

Working at the nanoscale means to completely rethink how to approach engineering in the body in general and in the eye in particular. In nanomedicine, tissue engineering is the ability to influence an environment either by adding, subtracting or manipulating that environment to allow it to be more conducive for its purpose. The goal is to function at the optimum state, or to return to that optimum state. Additive tissue engineering replaces cells or tissue, or tries to get something to grow that is no longer there. Arrestive tissue engineering tries to stop aberrant growth which, if left uncontrolled, would result in a decrease in function. Nano delivery of therapeutics can perform both additive and arrestive functions influencing the environment either way, depending on the targeting. By manipulating the environment at the nanoscale, the rate and distribution of healing can be controlled. It infers that potential applications of nanomedicine in ophthalmology include procedures, such as corneal endothelial cell transplantation, single retinal ganglion cell repair, check of retinal ganglion cell viability, building of nanofibre scaffolds, such as self-assembling peptides, to create a scaffold-like tissue-bridging structure to provide a framework for axonal regeneration in the case of optic nerve reconnection or eye transplantation, and ocular drug delivery. Examples of potential arrestive therapies include gene-related treatment modalities to inhibit intraocular neovascularization and to block retinal cell apoptosis. Looking towards the future, this review focuses on how nanoscale tissue engineering can be and is being used to influence that local environment.

The effect of ginkgo biloba on the rat retinal ganglion cell survival in the optic nerve crush model

To investigate the effect of ginkgo biloba on the retinal ganglion cell survival in a rat optic nerve crush model. Twenty-four Sprague-Dawley rats were divided randomly into a study group of 12 animals receiving intraperitoneal injections of ginkgo biloba and a control group of 12 animals receiving intraperitoneal saline injections. All injections were performed 1 hr before the optic nerve crush and daily afterwards. For each animal, the right optic nerve was crushed closely behind the globe for 60 seconds using a microclip with 40 g power. The left optic nerve was kept intact. At 23 days after the optic nerve crush, the retinal ganglion cells were labelled retrogradely by injecting 3% fluorogold into both sides of the superior colliculus of the brain. At 4 weeks after the optic nerve crush, the animals were killed. Photographs taken from retinal flat mounts were assessed for the number and density of the retinal ganglion cells. The survival rate, defined as the ratio of the retinal ganglion cell density in the right eye with the optic nerve crush divided by the retinal ganglion cell density in left eye without an optic nerve trauma, was significantly (p=0.035) higher in the study group with ginkgo biloba than in the control group (60.0+/-6.0% versus 53.5+/-8.0%). The results suggest that intraperitoneal injections of a ginkgo biloba extract given prior to and daily after an experimental and standardized optic nerve crush in rats were associated with a higher survival rate of retinal ganglion cells.

Prevalence of ocular and orbital injuries in polytrauma patients.

Polytrauma patients usually suffer from both life-threatening injuries, where early intervention is mandatory in order to prevent mortality from uncontrollable haemorrhage-especially during the "golden hour", and secondary injuries of lower priority which receive delayed referral or treatment. Non-life-threatening injuries can sometimes be overlooked and so remain untreated until a much later stage. The aim of this study was to investigate the incidence of eye (ocular and orbital) injuries in polytrauma (injury severity score >15) patients and describe their complexities and outcomes. Over a 10-year period (1991-2001), all polytrauma patients admitted in our institution were evaluated. Patients with ocular and orbital injuries were identified and their records were retrospectively analyzed. Out of a total of 2,985 polytrauma patients, 222 (7.5%) met the inclusion criteria. Forty-one case notes were not retraceable. The files of 181 patients were therefore available for review. The mean age of this group of patients was 33years (3-84) with a sex ratio (male: female ratio) 5:1. The types of eye injuries encountered were orbital wall fractures (61%), periorbital swelling or hematoma (46%), sub-conjunctival hemorrhage (23%), periorbital lacerations (22%), optic nerve trauma (11%) and penetrating eye injuries (6%). Visual impairment resulted in about 67% of survivors, including loss of eye in 24%. Diplopia requiring intervention was seen in 24% of the cases. Polytrauma patients are at high risk for vision-threatening injuries, and an early multidisciplinary approach is essential for early detection and treatment.

Perioperative visual loss in ocular and nonocular surgery.

Incidence estimates for perioperative vision loss (POVL) after nonocular surgery range from 0.013% for all surgeries up to 0.2% following spine surgery. The most common neuro-ophthalmologic causes of POVL are the ischemic optic neuropathies (ION), either anterior (AION) or posterior (PION). We identified 111 case reports of AION following nonocular surgery in the literature, with most occurring after cardiac surgery, and 165 case reports of PION following nonocular surgery, with most occurring after spine surgery or radical neck dissection. There were an additional 526 cases of ION that did not specify if the diagnosis was AION or PION. We also identified 933 case reports of central retinal artery occlusion (CRAO), 33 cases of pituitary apoplexy, and 245 cases of cortical blindness following nonocular surgery. The incidence of POVL following ocular surgery appears to be much lower than that seen following nonocular surgery. We identified five cases in the literature of direct optic nerve trauma, 47 cases of AION, and five cases of PION following ocular surgery. The specific pathogenesis and risk factors underlying these neuro-ophthalmic complications remain unknown, and physicians should be alert to the potential for loss of vision in the postoperative period.

Longterm follow‐up of children with traumatic optic nerve avulsion

We report the longterm follow-up of children with optic nerve avulsion (ONA) caused by traumatic events. The remarkable differences in courses and outcomes may elucidate the spectrum of ONA-associated symptoms and injuries. During the last 15 years, three children with ONA were referred to our department. These cases are presented with special attention to their longterm follow-up. Two patients suffered from complete ONA after head injury. The third patient presented with partial ONA caused by a bicycle accident. Longterm follow-up varied between 7 and 15 years. In the first patient, a pale swollen retina without any visible retinal vasculature was observed early in the course of follow-up. The retina later completely detached. In the second patient, extended fibroglial scarring occurred and an extremely large epiretinal membrane formed and was finally released spontaneously into the vitreous. The third patient developed only mild fibroglial scarring and retinal pigment epithelium hyperplasia. The optic nerve head in this patient came to resemble a morning glory disc. Optic nerve avulsion can adopt different courses and outcomes in different patients. Final visual outcome seems to depend on the degree of visual acuity immediately after injury. Substantial intraocular architecture changes can occur as a result of ONA.

Optic nerve trauma with unilateral edema as a result of head injury

We encountered a patient who suffered a head injury that translated to the optic nerves, leading to dramatic unilateral right optic nerve edema. The decedent was a 20-year-old unsecured passenger in a convertible. The car collided with a pickup truck. The patient survived for 8 h. At autopsy, a comminuted skull fracture involving the right frontal bone including the right orbital plate was found. The right optic nerve measured 1.2 cm in diameter, compared to only 0.4 cm for the left optic nerve. Microscopically, the right optic nerve was markedly edematous, but the nerve fibers and nuclei were viable and intact. The dramatic difference in size between the right and left optic nerves can be attributed to several mechanisms. The survival interval was essential for the asymmetrical swelling to take place. Optic nerve trauma is relatively rare in head injuries, reported to be present in 0.5% of automobile accidents and assaults. Other causes of optic nerve trauma and edema include tumors, osteopetrosis, or reaction to a peripheral hemodialysis shunt.

Clinical value of endoscopic optic nerve decompression in posttraumatic optic neuropathy patients with no light preception

Objective To investigate the clinical value of endoscopic optic nerve decompression in traumatic optic neuropathy patients with no light perception (NLP). Methods 13 NLP patients with traumatic optic neuropathy were performed endoscopic decompression of optic nerves basing on the Messerklinger technique and the clinical data were retrospective analyzed.Results Seven of 13 patients with NLP improved at least one grade after three to twelve months follow-up period and the total effective ratio was 54% (7/13). Six patients showed no change and one patient was lost during follow-up.Based on the duration from loss of vision to operation after trauma, all 13 patients were divided into 3-7 d group, 8-14 d group,15-21 d group and above 21 d group.In the analysis of the data of different groups, there was no difference in effect among groups (P＞0.05 ). Conclusion Potential benefit could be achieved from endoscopic decompression of optic nerve even for traumatic optic neuropathy patients with no light perception. Key words: Optic nerve trauma; Endoscope; Decompression; Surgery