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Results for “Optic Nerve Injuries”

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At least 19 recordsLinked to original sources
PubMed1999

Bilateral optic nerve injury.

Bilateral optic nerve injury is a rare condition and is reported in 5-6 percent of all optic nerve injuries. However, there is no published series on bilateral optic nerve injury. Analysis of 31 cases of bilateral optic nerve involvement seen amongst 275 patients with optic nerve injury (11.5 percent) is discussed. Road traffic accident which is the most common cause of optic nerve injury, was recorded in 61 percent. Shotgun injury and blast in jury was the cause in 22.5 percent of cases. All the patients except 4 received steroids. Anterior cranial fossa fracture and opacity of paranasal sinuses were recorded in a third of the patients. Visual evoked potentials were recorded in 27 patients. Improvement in vision was noticed in 23 patients (74 percent). However, among the 62 eyes, 39 eyes showed improvement (62.8 percent). Possible reasons for better outcome in bilateral optic nerve injury are discussed.

Adolescent↗
PubMed1978

Clinical observations on the isolated optic nerve injury.

The optic nerve can be injured indirectly by blunt trauma to the frontoorbital region. The mechanism of injury is related to trauma of the nerve in the tight, bony optic canal. Neurovisual transmission in the canal is interrupted by pressure on the nerve. The conventional management includes careful observation and supportive treatment. Recent interest in this unique clinical problem has prompted the development of new techniques to decompress the injured optic canal extracranially; these approaches have produced encouraging results. Another dividend of the method has been the mapping of the optic nerve region under magnification using the operating room microscope. Any gain of vision, partial or complete, is well appreciated by the patient and the physician.

Craniocerebral Trauma↗
PubMed1988

Evidence of orbital deformation in indirect optic nerve injury. Weight lifter's optic neuropathy.

A 16-year-old boy developed monocular visual loss due to optic neuropathy following frontal head trauma. His trauma was unique in that it consisted of a static loading force to the brow, rather than the dynamic impact more commonly associated with blunt orbital injuries. This case demonstrates the role of isolated deformation of orbital bones in the pathogenesis of indirect optic nerve injury.

Adolescent↗
PubMed2002

Up-regulation of cytochrome oxidase in the retina following optic nerve injury.

The purpose of this study is to investigate the cytochrome oxidase (COX) activity in the retina and optic nerve following an optic nerve injury. The optic nerve crush of one eye was carried out in Balb/c mice. A semi-quantitative RT-PCR method was then adopted to evaluate the mRNA expression of cytochrome oxidase subunit 1 (COX1) in the retina after surgery. Up-regulation of COX1 mRNA in the retina was detected by RT-PCR at 24 hr following the optic nerve injury. Total retinal mitochondrial mass measured by fluorescent intensity of MitoTracker green was not altered following the injury. COX histochemistry performed on cryostat sections showed an elevated enzyme activity of COX in the retina and in the optic nerve. In the retina, elevation of the COX activity was observed in the retinal ganglion cell layer and the overlying nerve fibre layer. The increase of COX activity began from 24 hr after injury, peaked around day 3, and maintained up to 1 week after the operation. In the optic nerve, increase of COX activity was observed in regions distal to the crush line and distributed either randomly or in a cone shape. In conclusion, both the expression of COX1 mRNA in retina and the activity of COX in inner plexiform layer and retinal ganglion cell layer were elevated following optic nerve injury without affecting total retinal mitochondrial mass. These findings suggested that one of early responses in the retina and in the optic nerve after the optic nerve injury is to scale up the energy production.

Animals↗
PubMed1988

Transfrontal intradural microsurgical decompression for traumatic optic nerve injury.

Microsurgical decompression of the optic nerve was performed in 22 patients with traumatic optic nerve injury through a transfrontal intradural approach. When significant improvement is defined as an improvement of the visual acuity of 0.1 or more, 11 patients (50%) showed significant improvement and 7 patients (32%) showed non-significant improvement. Four patients who had been blind preoperatively, did not show any improvement. In cases with a preoperative visual acuity of 0.01 or more, significant improvement was obtained in 80% of the patients, and when the preoperative visual acuity was not nill but less than 0.01, 38% of patients showed significant improvement. We conclude that a transfrontal intradural microsurgical decompression is indicated, when the preoperative visual acuity is 0.01 or more and the time lag is less than 14 days after the injury.

Adolescent↗
PubMed1987

Recovery of vision after presumed direct optic nerve injury.

Immediate loss of light perception after direct optic nerve injury is usually irreversible. Our patient sustained presumed direct optic nerve injury because of a shotgun injury with loss of light perception, absent pupillary response, and absent visual-evoked potential. A small pupillary response was noted 12 days after injury, light perception returned by 15 days, and visual acuity was 20/100 at 4 months. A variety of pathophysiologic mechanisms may lead to visual loss after direct optic nerve injury. It is important to recognize that blindness is not always permanent in these cases despite the results of initial clinical and electrophysiologic testing.

Adolescent↗
PubMed1990

Does optic nerve injury require decompression?

Forty patients with indirect optic nerve injury were prospectively analysed. Ultimate outcome on conservative management were correlated to their visual evoked potential (VEP) finding and the need for optic nerve decompression was questioned. An associated indirect optic nerve injury was observed in 2% of all head injuries. Ethmoid fracture was recorded in 2 patients and optic canal fracture was recorded in one patient. CT scanning for optic canal and for the orbit revealed abnormality in none of these patients. All the patients were managed conservatively and received intravenous dexamethasone for 48 hours followed by oral prednisolone therapy. Optic nerve decompression was not undertaken. VEPs were present in 18 patients of whom 4 had normal VEPs. Twenty patients had visual improvement. Amongst the patients with positive VEPs 89% had visual improvement. It is concluded that VEP study may help in avoiding unnecessary decompression of the optic nerve.

Adolescent↗
PubMed1999

Spontaneous axonal regeneration after optic nerve injury in adult rat.

Optic nerves of adult rats were crushed 2 mm behind the eye to examine the ability of retinal ganglion cells (RGCs) to regenerate their axons. Some animals were treated with the immunophilin ligands FK 506 or GPI 1046 for up to 4 weeks. After 10 days to 16 months, regenerating RGC axons were visualized using anterograde tracing and/or electron microscopy. A small proportion of RGC axons regenerated across the lesion site and grew very slowly along the entire optic nerve. Immunophilin ligands had no obvious effect. The regenerating axons were about 0.2 microm in diameter, and usually in clusters surrounded by astrocyte processes. Thus, some CNS axons can spontaneously regenerate long distances within degenerate white matter and this slow regeneration is not accelerated by immunophilin ligands.

Animals↗
PubMed1999

[A pathological study on indirect optic nerve injury in rabbit eyes].

OBJECTIVE: To study the pathological changes after indirect optic nerve injury. METHODS: Animal models (72 rabbits, 144 eyes) for intracanalicular optic nerve injury was developed by keeping the optic canal intact. The pathological changes of optic nerve were observed under light microscope and transmission electron microscope and the number of myelinated axons was enumerated by computer-aided image analyzer. The data were analyzed by using variance of SAS software. RESULTS: The model contributed much valuable information regarding nerve edema, loss of myelin, myelin regeneration and changes of axons. The edematous area in the optic nerve injury was reduced (P < 0.01) by treating with prednisone. The counted number of myelinated fibers showed more in the group treated by prednisone than that in the group without treatment. CONCLUSIONS: Significant changes of optic nerve after indirect injury are edema, demyelination and the change of axon amount. The effects of prednisone on reducing these pathological changes are demonstrated in this study.

Animals↗
PubMed1993

Gangliosides attenuate axonal loss after optic nerve injury.

Gangliosides have been shown to be capable of protecting nerve tissue from mechanical and biochemical insults and promoting their repair. The present study provides morphologic evidence that monosialogangliosides attenuate the degenerative process at the distal stump of the rat optic nerve after crush injury. Injured rat optic nerves were treated for 7 days after injury with daily intraperitoneal injections of monosialogangliosides (30 mg/kg/day), and compared with untreated injured controls with respect to the number of viable axons 2 and 4 weeks after injury, as indicated by transmission electron microscopy. After 2 weeks, the mean number of viable axons in the treated optic nerves (n = 5) was slightly higher than in the controls (n = 5). Four weeks after injury, although the absolute number in both the experimental and the control groups had dropped, it was about seven-fold higher in the treated animals (1696 +/- 1149, n = 7) than in the untreated animals (216 +/- 65, n = 6); this difference was statistically significant. These findings, which offer some insight as to how monosialogangliosides affect injured nerves, may have important implications for treatment in cases of optic nerve injury.

Animals↗
PubMedDate not supplied

Delayed recovery from indirect optic nerve injury. A report of two unusual cases.

Two patients with indirect optic nerve injury are reported. In one, head injury was minor, while in the second, the head injury was severe. Both the patients had immediate type of optic nerve injury with complete visual loss. CT scans for the orbit and optic canal were normal. Visual evoked potentials (VEP) repeatedly performed in the first 6-8 weeks were absent in both the patients. Onset of visual recovery was very late, in first case it was noticed after 12 weeks and in the second case visual recovery started after 8 weeks. Both the patients had partial visual recovery.

Adolescent↗
PubMed2004

[Transcranial optic nerve decompression for optic nerve injury].

OBJECTIVE: To discuss the operative indications and advantages of transcranial optic nerve decompression in treatment of optic nerve injury resulted from skull base fracture. METHODS: The data, such as the site of impact, vision, ocular movement, characteristic of CT, and pathologic changes during operation, and the extent of operative decompression of 118 patients with optic nerve injury. According the site of impact on the head, 87 of lateral superciliary arch type, 18 of medial superciliary arch type, and 13 of zygomatic type, undergoing transcranial optic nerve decompression were analyzed retrospectively. The patients were followed up for 6 months after operation. For the purpose of evaluation, the postoperative outcome of visual acuity was classified into five grades: blindness, hand movement, finger count, light perception and visual acuity > 0.05. The visual acuity improvement reaching one grade or more was defined as effective. The improvement of visual field was also considered effective. RESULTS: After follow-up of 6 months, effect was shown in 35 out of the 72 patients with pre-operative blindness (48.6%), and all the 46 patients with residual vision (100%). The total effective rate was 68.6%. The post-operative effective rate was 64.4% in patients with lateral superciliary arch type, 83.3% in patients with medial superciliary arch type injury and 76.9% in patients with zygomatic type injury. CONCLUSIONS: Transcranial optic nerve decompression is worthy recommending to the patients with traumatic optic neuropathy. The operative indications include patients with residual vision; patients with bilateral optic nerve injury; and patients with blindness less than 3 days.

Adolescent↗
PubMed1986

Optic nerve injury after sudden traumatic rotation of the eye. A case report.

Optic nerve injury is regularly accompanied by signs of local facial or ocular injury, fractures or unconsciousness. The energy of the blow is thought to be delivered to the optic nerve directly by stretching and tearing and by shock wave forces and secondarily as sequelae of contusion. A case is described in which optic nerve injury is caused by a sudden traumatic duction of the eyeball, with all signs of local or systemic contusion missing. During observation the primarily healthy optic nerve head developed subtotal optic atrophy. This case strengthens the belief that the optic nerve is particularly vulnerable to stretching, tearing and torsion.

Blindness↗
PubMed2003

Delayed optic nerve decompression for indirect optic nerve injury.

OBJECTIVE: To test the efficacy of delayed optic nerve decompression in traumatic optic nerve injury. STUDY DESIGN: Critical analysis of Proforma-based, prospectively accrued data of all cases with injury to surgery interval of greater than 2 weeks. METHODS: Thirty-five cases with a median injury to surgery interval of 56 days (range, 16-374 d). Surgical decompression was undertaken only in cases that continued to have poor vision after treatment with steroids in conventional doses (1 mg/kg prednisolone). Pre- and postoperative visual acuity measurements were converted to the logMAR scale of visual acuity and the percentage of visual improvement was calculated. RESULTS: Surgery was universally unrewarding in all 9 cases with persistent and complete blindness of greater than 2 weeks and no response to steroid therapy. Of the cases with some residual vision, 20 of 26 cases improved (mean percentage improvement, 41.0 +/- 5.7%). Cases were categorized on the basis of the injury to surgery interval into groups of 2 weeks to 2 months, 2 months to 4 months, and greater than 4 months. No significant difference was demonstrated in the probability or quantum of improvement in these groups (P =.97). CONCLUSIONS: Optic nerve decompression remains useful as a salvage procedure for conventional dose steroid failed cases of traumatic optic neuropathy. In cases that are not completely blind, vision can be improved even when surgery is undertaken a few months after the injury.

Adolescent↗
PubMed2001

[Relationship between operative time and therapeutic effectiveness after the optic nerve injuries].

OBJECTIVE: To understand the relationship between the operative opportunity and effectiveness in the optic nerve injuries. METHOD: Twenty-three cases with optic nerve injuries were undertaken optic canal decompression. RESULT: The visual acuity in 13 cases were improved after the operation, and progressed about 0.233 averagely. The average time from injuries to operations was (12.90 +/- 16.77) d (3-22 d) in ineffective group. 7 cases of hypoactivity of eyeball recovered in 8 cases. CONCLUSION: The optic nerve decompression should be done after the patients were treated with megadose of steroid for 48 hours and did not recover. The time had better be no more than 7 days.

Adolescent↗
PubMed1994

Optic nerve injury alters basic fibroblast growth factor localization in the retina and optic tract.

Basic fibroblast growth factor (bFGF) is thought to be a trophic factor for several classes of neurons. Its distribution changes in response to cortical neural injury. We have determined the effect of injury to the optic nerve on localization of bFGF in the rodent retina and visual pathways. Our observations were confirmed by using different antisera and monoclonal antibodies. While photoreceptors normally contain virtually no bFGF, crushing the optic nerve causes a striking increase, over a period of several weeks, in the amount of bFGF in retinal photoreceptors. Since photoreceptors do not synapse directly upon the injured ganglion cells, intermediary cells must participate in the cascade of events that results in the elevated bFGF. In light of the observation that exogenous bFGF protects photoreceptors from photodamage (Faktorovich et al., 1992), this increase in bFGF in photoreceptors may explain, in part, why crushing the optic nerve protects photorecptors against photodamage (Bush and Williams, 1991). Whereas bFGF is constitutively found in glia in the optic nerve, little bFGF is found in glia in the optic tract. However, damage to the optic nerve increases bFGF in astrocytes in the optic tract. This change occurs within days, suggesting that a relatively direct signal may intervene between the injured axon and the adjacent glial cells. Thus, despite the fact that the optic nerve and optic tract are contiguous structures through which axons of retinal ganglion cells project, the glial elements in these structures express distinct properties, because of differences in either glial subclasses or microenvironment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Methylprednisolone treatment does not influence axonal regeneration or degeneration following optic nerve injury in the adult rat.

BACKGROUND: Methylprednisolone (MP) is often used to treat optic nerve injury. However, its effects in experimental crush injury have not been extensively evaluated. METHODS: Adult Sprague-Dawley rats were subjected to a standardized optic nerve crush injury. Animals were treated either with 30 mg/kg MP intravenous bolus followed by subcutaneous injections every 6 hours for 48 hours, or with a drug vehicle alone. RESULTS: The injury resulted in a partial loss of neuronal nuclei-labeled retinal neurons and a corresponding degeneration of axons distal to the injury. EDI-labeled macrophages accumulated at the site of lesion, phagocyting FJ-labeled axonal debris. Regenerative fibers expressing growth associated protein-43 were seen proximal to the lesion, but did not traverse the glial scar. Analysis of optic nerve function using visual evoked potentials showed typical signals in intact animals, which were abolished after injury in MP-treated and untreated animals. CONCLUSIONS: We did not detect any effects of MP on retinal cell survival, macrophage activity at the site of injury, axonal degeneration/regeneration, or visual function. These experimental results provide a physiologic underpinning for the lack of efficacy demonstrated in a large trial of MP treatment of clinical optic nerve injury.

Animals↗
PubMed1989

The conditioning effect of optic nerve injury upon axonal regrowth from adult rat retinal ganglion cells explanted in vitro.

An in vitro assay was used to determine the effects of conditioning nerve lesions on the regeneration of adult rat retinal ganglion cell (RGC) axons from retinal explants. Following the conditioning lesion (CL) of unilateral optic nerve transection, maximal regrowth was seen from RGC explanted from ipsilateral retinae 10 days post-CL. Explants from this group initiated axonal regrowth earlier and a greater percentage regrew axons when compared with explants from normal rats. Axonal regrowth from explants of retinae contralateral to CL was also seen earlier than normal. In further experiments, the effects of both exposure of the optic nerve sheath in the orbit and the incision of the dura without injury to optic nerve axons were studied. The conditioning effect of a dural incision was found to be the same as that of optic nerve transection, whilst exposure of the optic nerve sheath had no conditioning effect on RGC axonal regrowth in vitro.

Animals↗