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This chapter discusses the cases of postoperative blindness reported in the literature and the theories that attempt to explain the mechanisms involved. Although uncommon, alterations in vision and blindness after anesthesia for major surgical procedures, particularly cardiopulmonary bypass or spine surgery, are well documented, with an incidence varying between 0.05% and 1%. Accurate incidence data are unavailable because it is not known what percentages are reported. However, the large number of case reports over many years has provided some significant information. Although sustained compression of the eye is an important cause, postoperative visual loss may also occur, in an unrelated manner, because of ischemic optic neuropathy, central retinal artery or vein occlusion, or cortical blindness.

Purpose: To describe an obsessive-compulsive patient who developed blindness after self-inflicted repetitive optic nerve injury., Methods: Case report., Results: A myopic 46-year-old male became blind as a result of intermittent rubbing of his eyes, causing stretching of the optic nerves. Extensive ocular, neurologic and systemic work-ups were negative. Cerebral and orbital MR studies showed severe bilateral optic nerve atrophy. Psychiatric evaluation confirmed obsessive-compulsive personality., Conclusions: Self-inflicted optic nerve injury should be included in the differential diagnosis of progressive optic neuropathy in a young adult.

Minor blunt injury to the head and face may result in optic nerve contusion with secondary optic atrophy. The resulting visual loss is devastating for the individual. We report an uncommon but important complication that may result from an apparently trivial injury. Early identification and initiation of appropriate management may restore the individual's vision. Emergency physicians are often the first to see patients at risk of this complication yet there is little discussion of this injury in the emergency medicine literature.

Purpose: To report the clinical and pathologic findings in 3 cases of traumatic evulsion of the globe, during which the optic nerve and its sheath were disrupted at different locations and to varying extents., Methods: Case series (3 patients)., Results: We describe the clinical, gross, and microscopic pathologic findings in 3 globes that were traumatically evulsed from their orbits. The optic nerves and sheaths were disrupted at 2 different locations and in 2 distinct combinations. Two of these variations in discontinuity of the nerve and/or its sheath were unique. In 1 case, the eye and optic nerve sheath were evulsed without the nerve; in another case, the nerve and sheath were pulled from the posterior sclera at the lamina cribrosa., Conclusions: Traumatic evulsion of the globe may cause the optic nerve and its sheath to be disrupted at varying distances from the eye and may involve the optic nerve and its sheath together or separately. To the best of our knowledge, no cases have been reported in which orbital trauma caused the globe and optic nerve sheath to be removed together, leaving the nerve behind, or in which disruption of the optic nerve at the lamina cribrosa resulted in a complete posterior scleral defect. Three theories are proposed to explain possible mechanisms leading to optic nerve disruption during traumatic evulsion of the globe.

Purpose: To compare the efficacy of low-dose intravenous methylprednisolone or conservative treatment in the management of traumatic optic neuropathy., Methods: A non-randomized retrospective study of 21 patients (21 eyes) with traumatic optic neuropathy treated between October 95 and November 97 in a tertiary ophthalmology unit. Traumatic optic neuropathy was defined as traumatic visual loss with afferent pupillary defect in the absence of direct injury to the globe or optic nerve. The median follow-up period was one year. Nine patients were treated with 125-250 mg methylprednisolone 6-hourly intravenously for a mean of 3.3 days (range 2-5 days) and 12 patients were treated conservatively. Visual acuity (VA) was measured with a Snellen chart before and after treatment at each follow-up visit. Visual recovery was defined as an improvement of 2 or more Snellen lines one week post-injury or later., Results: The patients' mean age was 37.1 years (range 12-65 years). There were more males (90.5%) than females (9.5%). Traumatic optic neuropathy was in 12 right eyes and 9 left eyes. The cause of injury included traffic accidents (52.4%), falls (28.6%), assault (14.2%) and others (4.8%). The mean interval between the injury and steroid therapy was 3.6 days (range 1-11 days). Visual recovery was observed in 44.4% of eyes treated with methylprednisolone and in 33.3% treated conservatively (p = 0.673, Fisher's exact test)., Conclusions: Intravenous methylprednisolone at the dosage and duration used in this retrospective study did not significantly improve the visual recovery of eyes with traumatic optic neuropathy compared to conservative treatment. However, this small sample may not be sensitive enough to detect a small difference in visual recovery rates, and further studies with larger samples may be warranted.

Background: In some cases of closed head injuries after minor blunt trauma, an amaurosis can occur. Our knowledge concerning the pathophysiological mechanisms of traumatic optic neuropathy is limited. The aim of this study is to analyze the morphology of the optic canal in order to understand the effect of mechanical forces in the optic canal and the consecutive injuries., Methods: Forty-one optic canals from body donors were analyzed by light microscopic, polarization microscopic, immunohistochemical and scanning electron microscopic techniques., Results: In the optic canal, collagen fibrils of the dural sheath are organized in a scissor-like pattern. Within this collagen network multiple vessels are integrated. The main component of the extracellular matrix is collagen type I. The dural sheath and pial sheath are connected by collagen bundles. Parallel to these bundles, small vessels form anastomoses between the dural and pial vessel systems. In the arachnoidea, no blood vessels can be detected by immunohistochemical techniques., Conclusions: Based on morphological findings, the following pathophysiological mechanisms can be discussed in cases of blunt closed head injury with consecutive amaurosis: 1. Squeezing and rupture of nutritive vessels by transduction of shearing forces via the scissor-like collagen network. 2. Atrophy by pressure of the optic nerve after injury to the microvasculature followed by formation of microhematomas and reactive edema. 3. Direct injury of axons of the optic nerve by shearing forces within the optic canal. These mechanisms should be studied further in the future.

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.

Purpose: This study was undertaken to assess the pathogenesis of traumatic optic neuropathy as a consequence of closed head injury., Material and Methods: The clinical material comprised 34 patients (4 women and 30 men, age 14-70 years), who developed clinical symptoms of optic neuropathy after head trauma. A full ophthalmologic survey and colour Doppler examination of the orbital vessels were performed in all patients., Results: Full blindness of the affected eye, persisting since the injury, was noted in 20 patients. Orbital fracture was diagnosed in 15 person, but 4 patients among them had fracture of the optic canal bones. In 16 cases a retrobulbar hematoma was present. In 8 patients, who displayed no light perception after trauma, no flow was observed in the central retinal artery. In 18 other persons there was decreased of blood flow parameters. Only 6 patients had the normal flow in the orbital vessels., Conclusion: The reason of the development of optic neuropathy after head injury is not clear. Our results of the blood flow measurement in the orbital vessels suggest, that disturbance of circulation within the optic nerve is very serious factor in the pathogenesis of traumatic optic neuropathy.

Objective: To improve the level of diagnosis and treatment of optic nerve trauma at the canalicular segment., Method: Fifty-two patients with optic nerve trauma at the canalicular segment received decompression of optic canal through combined orbit, ethmoid and sphenoid approach., Result: The visual improvement rate of all 52 patients was 42.3%, 73.9% in 23 patients with secondary optic trauma and 17.2% in 29 patients with primary optic trauma. Patients's vision covered from 0.05 to 0.6 after six months., Conclusion: The advantages of decompression of optic nerve through combined orbit, ethmoid and sphenoid approach include easily operation and location, short approach, wide visual field and clear anatomy mark, so it is very safe and suited for those patients with dysplasia and osteosclerosis of ethmoidal or sphenoidal sinus. Orbital CT scan facilitates the diagnosis of optic canal fracture without false positive results. The curative effect is associated with the type of optic nerve trauma and the chance of surgery. Amaurosis shortly after trauma is a dangerous factor of poor prognosis, but it isn't impossible to improve vision if patients receive operation as early as possible.

The June COM. A 61 year old female presents with a three week history of increasing confusion, lethargy and headache. A neurological exam revealed disorientation, mild expressive aphasia, bilateral papilledema, and a right pronator drift. She had a craniotomy and resection of tumor. The tumor histologically was consistent with a solitary fibrous tumor displaying malignant features of hypercellularity, marked nuclear atypia, high mitotic activity, and a high proliferation index. This case is unique as the first malignant variant of solitary fibrous tumor to be reported intracranially.

Background: Evulsion of the optic nerve is a rare form of traumatic optic neuropathy. It is a rupture of the optic nerve at the disc without damage of its sheaths occurring in association with a blunt skull trauma or a blunt bulbar trauma., Material and Methods: We searched the literature using Medline database for all articles with evulsion of the optic nerve. The bibliographies of the papers found therein were used to get a complete review. The data were analyzed with special regard to age, sex, mechanism of injury, and (if available) defects of visual field., Results: Sixty-three patients with a mean age of 22 years (range 4 to 60 years) were included in the study. In 22 patients (35 %) a partial and in 41 patients (65 %) a complete evulsion was present. In 31 patients (49 %) the cause was a small blunt object or finger that stroke the eye or entered the orbita. In 19 patients (30 %) a severe blunt skull trauma had occurred. The analysis of visual fields in eyes with partial evulsion of the optic nerve revealed a defect in the superior visual field in 6 of 12 patients and a defect in the inferonasal visual field in 3 of 12 patients., Pathogenesis: Our review suggests that the most common mechanism of injury is a severe rotation of the eye leading to rupture of the optic nerve fibers and an anterior displacement of the bulbus, possibly with deformation of the posterior eye walls.

Fiber tract lesions in the central nervous system (CNS) often induce delayed retrograde neuronal degeneration, a phenomenon that represents an important therapeutic challenge in clinical neurotraumatology. In the present study, we report an in vivo trauma model of graded axonal lesion of CNS neurons. Controlled by a newtonmeter device, we induced retrograde degeneration of adult rat retinal ganglion cells (RGCs) by graded crush of the optic nerve. The extent of secondary RGC death increased linearly with the applied crush force. Moreover, visually evoked potentials were used to characterize the consequences of controlled optic nerve lesion on the functional integrity of the visual projection. The presented model of fiber tract lesion closely resembles the clinical conditions of traumatic brain injury and could prove useful to screen for neuroprotective drugs based on both a morphological and functional read-out.

Purpose: To study the predictive value of the initial quantified relative afferent pupillary defect (RAPD) in patients with indirect traumatic neuropathy as it relates to final visual outcome., Methods: The RAPD was measured and quantified by neutral density filters in patients with unilateral indirect traumatic neuropathy. All patients were treated with megadose methylprednisolone by of the protocol established by the Second National Acute Spinal Cord Injury Study. Patients were followed twice daily during treatment and then at 3-month intervals., Results: Nineteen patients were enrolled over a 23-month period. Patients ranged in age from 12 to 78 years old; 18 of the 19 patients were male. No patient with an RAPD of 2.1 log units or greater had visual recovery to better than hand motion vision. The 7 patients with an initial RAPD of less than 2.1 log units showed improvement in their RAPD and were found to have vision of 20/30 or better during the follow-up period., Conclusions: In patients treated with megadose methylprednisolone with an initial RAPD of less than 2.1 log units, visual acuity improved to 20/30 or better; however, patients with an initial RAPD of 2.1 or greater showed little visual improvement. The initial quantified RAPD appears to have a predictive value related to final visual outcome.

Purpose: The temporal series of molecular events that occur in dying retinal ganglion cells is poorly understood. We have examined the change in expression of a normally-expressed ganglion cell marker gene, Thy1, relative to the kinetics of cell loss caused by acute and chronic damaging stimuli., Methods: For acute experiments, mice were subjected to optic nerve crush or intravitreal injections of N-methyl-D-aspartate (NMDA) to induce ganglion cell death. RNase protection analysis was used to quantify Thy1 mRNA levels from total retina RNA and in situ hybridization was used to monitor the pattern of Thy1 positive cells. Changes in Thy1 expression were compared to the time course of cell loss induced by each treatment. To induce elevated intraocular pressure (IOP), the episcleral veins of rats were injected with hypertonic saline, which scleroses Schlemm's Canal and the trabecular meshwork. Elevated IOP was monitored every day for 35 days after which the animals were sacrificed and the retinas harvested for quantitative RT-PCR or fixed for in situ hybridization studies. Evaluation of glaucomatous damage caused by elevated IOP was determined from histological sections of the optic nerves of all rat eyes., Results: After optic nerve crush, Thy1 mRNA levels decreased within 24 h, although the number of expressing cells did not decline until 7 days. Both measures showed a loss of Thy1 well in advance of cell loss, which was detected by 2 weeks after surgery. This change in expression was not dependent on execution of the cell death program since a similar decrease was detected in Bax-/- ganglion cells, which are resistant to cell death induced by optic nerve crush. Thy1 mRNA levels and the number of expressing cells also decreased within 6 h after NMDA injection, in advance of cell loss, which was detected by 24 h. Similarly, elevated intraocular pressure was associated with a decrease in mRNA and expressing cells in a pressure-dependent manner. In moderately hypertensive rat eyes, the number of cells expressing Thy1 decreased before significant cell loss in the retina. Virtually no Thy1-expressing cells were detected in eyes with severe disease., Conclusions: Thy1 mRNA abundance and expressing cells, decreased in advance of detectable ganglion cell loss caused by three different modalities of damage. This change is independent of the committed step of cell death.

Background: The paranasal sinuses are intimately related to the orbit and consequently sinus disease or surgery may cause severe orbital complications. Complications are rare but can result in serious morbidity, the most devastating of which is severe visual loss., Methods: A retrospective review was undertaken of four cases of severe orbital trauma during endoscopic sinus surgery., Results: All the cases suffered medial rectus damage, one had additional injury to the inferior rectus and oblique, and two patients were blinded as a result of direct damage to the optic nerve or its blood supply., Conclusion: Some ophthalmic complications of endoscopic sinus surgery are highlighted, the mechanisms responsible are discussed, and recommendations for prevention, early recognition, and management are proposed.

A randomized, double blind study was carried out to compare the efficacy of dexamethasone and methylprednisolone in the treatment of indirect traumatic optic neuropathy. Twenty-one patients, 20 male and 1 female, were diagnosed as having suffered from indirect traumatic optic neuropathy. The time from injury to treatment was within 7 days. The average age was 26.38 +/- 11.89 years. The most common cause of injury was motor vehicle accident (MVA). Associated head and maxillofacial injury were reported 43.48 and 34.78 per cent, respectively. Before treatment, no light perception was detected in 19.05 per cent of the participants. Treatments were randomized: ten patients received dexamethasone intravenously for 72 hours and 11 methylprednisolone. The best corrected visual acuities (BCVA) were determined using the Snellen Chart before and 1, 2, 3, 7, 14 and 60 days after treatment. Three or more lines of improvement of the BCVA, were found in 70 and 67 per cent of patients treated with dexamethasone, and 45.45 and 33.33 per cent of patients treated with methylprednisolone, at 2 weeks and 2 months, respectively. There were no significant differences in age, cause of injury, injury to treatment interval, initial BCVA and visual improvement between the two groups.

Purpose: To raise the awareness of the rare complication of monocular blindness resulting from radiofrequency rhizotomy for trigeminal neuralgia., Methods: Case series from tertiary referral centers. Patients were referred after complaint of loss of vision., Results: We report three patients who had trigeminal neuralgia and underwent treatment by radiofrequency rhizotomy. Each developed complete loss of vision in one eye immediately after the procedure. One patient died of an unrelated cause, and pathologic analysis revealed changes compatible with acute trauma to the right optic nerve., Conclusion: Our third case confirms the hypothesis that traumatic optic neuropathy after trigeminal radiofrequency rhizotomy results from malpositioning of the rhizotomy needle through the inferior orbital fissure into the orbital apex rather than the foramen ovale.

Background: The care of indirect traumatic optic neuropathy is still treated differently. Special diagnostic and therapeutic difficulties exist in comatose patients without definable visual acuity and in patients with complex failure of the visual field with central visual acuity still receiving sufficiently., Method: The total collective of optic nerve decompressions within the period between January 1992 and August 2000 was comprised of 66 patients. 18 of these 66 patients (average age: 40.5 years) were comatose and required critical care. 3 of the 48 consciousness-clear patients showed post-traumatically different defects of the visual field with a visual acuity of 0.3, 0.4 and 1.0. The indication for surgical decompression in both groups was based on the ophthalmological findings and the CT-finding of traumatization of the optic nerve, or the orbit apex respectively., Results: During the subsequent postoperative examinations (on average 12.3 months postoperatively) five patients within the group of the unconscious patients showed a normal visual acuity (0.9-1.0), 3 patients a visual acuity of 0.7, 0.4 and 0.3 and one a visual acuity of 0.1. Six patients remained amaurotic. Three patients died from the general consequences of injury. Improvement of visual field and correction of stereoscopic function occurred in all patients, operated on primarily because of the described visual defects., Conclusions: Due to these results the indication for the decompression of the optic nerve should find special consideration in comatose patients and in cases of severe restriction of the visual field.

Objective: To investigate the efficacy of early optic nerve decompression in comatose and conscious patients with indirect traumatic optic neuropathy., Study Design: Retrospective analysis of 65 optic nerve decompressions., Methods: The total collective of optic nerve decompressions comprised 65 patients treated within the period between February 1987 and December 1998. Thirteen of these 65 patients (average age, 32 y) were comatose and required critical care treatment, so visual acuity could not be measured. The indication for surgical decompression in all patients was based on the ophthalmological examination and the finding on computed tomography (CT) scan of a lesion inside the optic nerve canal or the orbit apex, respectively., Results: In the comatose patients the time interval between trauma and surgery was 16.1+/-12.1 hours (mean +/- standard deviation). During the subsequent postoperative examinations (on average, 12.3 mo postoperatively) five patients showed a normal visual acuity (20/20), two patients a visual acuity of 20/30 and 20/50, and one a visual acuity of 20/200. Three patients (three eyes) remained amaurotic. Two patients died of the general and severe consequences of injury. The beneficial visual acuity results achieved within the group of comatose patients were equivalent to those achieved within the group of patients who were conscious during the preoperative examination. The success rate, defined as an improvement of three lines with a final visual acuity of at least 20/1000, was 57.7% versus 61.5%., Conclusion: The results confirm our concept of early decompression of the optic nerve, based on close interdisciplinary cooperation and the ophthalmological findings.

The curve of visual evoked potentials was observed and compared with changes of visual acuity and visual field during a 24-month period in a group of 39 patients with optic nerve injury as a result of mild cerebral trauma. Results of the study showed great improvement of visual acuity and visual field after treatment, and slower and continuous improvement of visual evoked potentials. The main abnormality of visual evoked potentials is the shortening of amplitude, which is recorded to gradually recede after treatment in half of the patients. Authors conclude that the shortening of amplitude can be partially explained by the edema and the compression of fibers in the optic canal. Also, they emphasize that in this type of optic nerve injury visual acuity testing is the best indicator of the promptness and scope of the injury, while visual field research presents the best method for following later delicate changes of visual function.

Endoscopic sinus surgery has become the standard of care for the surgical management of chronic sinus disease. Sinus disease and its surgical treatment carry the risk of orbital complications, irrespective of the approach. Orbital complications associated with sinus surgery include nasolacrimal duct damage, extraocular muscle injury, intraorbital hemorrhage/emphysema, and direct optic nerve damage, resulting in blindness. The finding of an unequal pupil at the end of a procedure would be a cause of considerable concern, but it is most likely due to the topical contamination of the eye with a mydriatic pharmacological agent commonly used in endoscopic sinus surgery.

Objectives: This is a retrospective descriptive case study which will look into the spectrum of ophthalmic involvement in cases with orbital and eye injuries after cranio-facial trauma and to analyse the visual and motility outcome., Material: One hundred and four cases with ophthalmic involvement after cranio-facial trauma that were referred to and seen in the eye department of a tertiary teaching hospital in Singapore between 1991-97 were included in the study., Methods: The case records of 104 such patients were traced. The demographic data, the mode of injury, the type of fracture sustained and presence of serious eye injury were noted. The details about visual acuity, significant diplopia and enophthalmos at the first and last visits were charted. Presence of traumatic optic neuropathy including the type of treatment given was recorded., Results: There was a male preponderance (82%). The industrial accidents were 21%, only next to road traffic accidents, which constituted approximately 36.5%. The predominant types of fractures seen were blow-out orbital fractures, complex fractures comprising of Le-Fort II, III, panfacial and fronto-basilar skull fractures. Diplopia was the most common presenting feature (40%) with visual acuity disturbance (23% having <6/60) as the next most common finding. Traumatic optic neuropathy was seen in 20% of patients and serious eye injury was present in 9% of patients. The incidence of traumatic optic neuropathy was significantly higher (p<0.001) in patients with complex fractures and fronto-basilar fractures, as compared to the blow-out and zygomatico-maxillary fractures. Analysis of final results indicated 15% as having significant diplopia in one or more gazes and 12.5% as having a vision of <6/60., Conclusion: Diplopia and visual acuity disturbances seem to be the most common ophthalmic presentations in cranio-facial trauma. A significant number of patients suffer from poor vision and significant diplopia despite treatment., (Copyright 2000 European Association for Cranio-Maxillofacial Surgery.)

A case of visual loss following cranio-maxillofacial trauma is reported. The patient had a sudden partial blindness associated with a fracture of the roof, medial and lateral orbital walls. Access to the orbit was achieved through a transethmoidal approach using the Howarth-Lynch medial incision and resecting the bone fragments which impinged on the optic nerve. The patient had total return of visual acuity, without surgical complications. The role of orbital and optic decompression in the management of patients with traumatic optic neuropathy is discussed. Its indications are controversial and the procedure should be considered only within the context of the specific needs of the individual patient.

A 16-year-old female presented with unilateral blindness in her right eye 2 months after blunt head trauma. Optic nerve edema was demonstrated by funduscopic examination, ultrasonography, and magnetic resonance imaging and failed to respond to medical treatment. Delayed post-traumatic blindness may be a severe complication of head trauma. The late appearance leads to delayed diagnosis and resulting unresponsiveness to treatment. Patients who experience head trauma that could involve the optic nerves should undergo ultrasonography of the optic nerves. An abnormal finding should be followed by an intensive evaluation to determine possible damage.

Purpose: To describe a patient with optic nerve avulsion after being struck in the eye with a golf club., Methods: A 10-year-old male was hit in the left eye by a golf club. The patient underwent full ophthalmoscopic evaluation and neuroimaging., Results: The patient had no light perception in the left eye when first seen. Avulsion of the optic nerve with vitreous hemorrhage was apparent on examination. Computed tomographic imaging of the brain and orbits revealed no abnormalities., Conclusions: Optic nerve avulsion from golf-related injury is more likely to occur when the impact site is between the globe and the orbital rim. Rupture of the globe is more likely to occur with direct impact to it.

McCune-Albright syndrome (MAS) is a disease of noninheritable, genetic origin defined by the triad of café-au-lait pigmentation of the skin, precocious puberty, and polyostotic fibrous dysplasia. This syndrome, which affects young girls primarily, has also been reported with other endocrinopathies, and rarely with acromegaly and hyperprolactinemia. The fibrous dysplasia in MAS is of the polyostotic type and, apart from the characteristic sites such as the proximal aspects of the femur and the pelvis, the craniofacial region is frequently involved. A male patient with MAS presented with juvenile gigantism, precocious puberty, pituitary adenoma-secreting growth hormone and prolactin, hypothalamic pituitary gonadal and thyroid dysfunction, and polyostotic fibrous dysplasia causing optic nerve compression. Visual deterioration and its surgical management are presented.

Optic nerve avulsion secondary to a basketball injury is a rare complication. The patient underwent a vitrectomy for a non-clearing vitreous hemorrhage. The nerve was partially avulsed with multiple choroidal ruptures in the fovea. It was concluded that optic nerve disorders rarely occur after basketball injuries. Patients with a dense vitreous hemorrhage may benefit from a vitrectomy although the vision will be limited by the optic nerve disorder.

Over a 10-year period the authors have performed 92 transethmoidal optic nerve decompressions for the treatment of visual loss due to various pathological processes, including 45 cases of trauma, 32 cases of neoplasm, 2 cases of bacterial pansinusitis, 5 cases of sphenoethmoidal mucocele, 4 cases of aspergillosis (all were immunocompetent patients), 2 cases of Wegener's granulomatosis, and 2 cases of sarcoidosis. Forty-eight patients (52%) had preoperative visual acuity of light perception or better, and in 44 patients (48%) the preoperative vision was no light perception. Sixty-five patients (71%) achieved improvement of vision postoperatively. Twenty-four patients (26%) had no change in vision and 3 patients (3%) had deterioration of vision after surgery. The mean percentage of improvement was 40.7% +/- 6.9% in the trauma group, 61.6% +/- 23.2% in the neoplasm group, 66.4% +/- 25.2% in the infectious/mucocele group, and only one patient in the inflammatory group had slight visual improvement from no light perception to counting fingers. Extracranial optic nerve decompression can result in the improvement of visual function in some patients with optic nerve injury from various causes.

Introduction: Isolated trauma of the optic nerve usually occurs in association with blunt skull trauma involving fractures of the skull and optic canal, but rarely occurs from blunt ocular trauma., Case Report: A 7-year old boy fell and struck his left eye against a toy antenna. The initial examination revealed a visual acuity of 0.2 and slight edema of the optic nerve head. Perimetry revealed a defect in the superior and nasal visual fields. CT and MRI scans of the orbit were normal. Nine months after the injury, vision had improved to 1.0. On examination, optic nerve atrophy had developed and perimetry continued to display a defect in the superior visual fields., Discussion: The mechanism of optic nerve damage secondary to trauma can be classified as primary or secondary. Primary damage occurs as a result of external forces at the moment of trauma, e.g., rupture of nerve fibers or of capillary vessels. Secondary damage may not be present initially, but may occur later on and results from compromised blood supply to the optic nerve, e.g., following edema or angiospasm. In our patient, it is not clear whether the damage was primary or secondary., Conclusion: Damage to the optic nerve can be caused by blunt skull trauma and, rarely, also by blunt ocular trauma. This fact is of importance when considering legal and reimbursement issues.

Optic nerve decompression is a procedure that is now receiving increasing clinical attention. However, there are currently no standardized treatment protocols in the therapy of traumatic or pressure insults to the nerve. The present retrospective study was designed to report our experience with microscopic endonasal transethmoid-sphenoid optic nerve decompression in 24 unilateral trauma cases and 11 unilateral skull base tumor patients. In general preoperative visual acuities in the trauma patients were worse than in the tumor patients. Following surgery, 9 of 11 tumor patients (82%) had at least some improvement of their vision, including 5 complete recoveries. In the group with traumatic visual impairment, 16 of the patients had no light perception preoperatively. Postoperatively, 13 patients (54%) had at least some improvement, with 4 patients regaining normal or near normal vision. Compared to other techniques and approaches, our technique is a minimally invasive procedure for optic nerve decompression, reducing unnecessary operative trauma to nasal structures, skin incisions or even craniotomy and frontal lobe retraction.

Objective: To find a better method to treat traumatic optic neuropathy., Methods: Fourteen cases were treated by transnasal endoscopic sphenoethmoidal optic canal decompression in clinic., Results: Nine of them had their visual acuity improved from NLP, HM, FC/50 cm, HM, NLP, LP, NLP, HM, NLP to 0.2, 0.3, 0.3(+2), 0.4, 0.06, 0.3, 0.1, 0.7, 0.12 after the operation. The clinical anatomy, attentions during operation, merits of operative approaches were discussed., Conclusion: Transnasal endoscopic sphenoethmoidal optic canal decompression is a good method for treatment of post-traumatic optic neuropathy.