High-dose steroid therapy of traumatic optic neuropathy may fail to protect the optic nerve permanently

Background: The optimal treatment of traumatic optic neuropathy (TON) is still unresolved due to the poor understanding of the pathology involved and the relatively small number of cases in the published clinical series. It is currently held that the results of conservative treatment with high-dose corticosteroids are similar to those obtained with surgical decompression. Purpose: To assess the late results of conservative treatment for traumatic optic neuropathy. Patients and methods: 15 patients (3 women and 12 men, age 14–64 years) who sustained a direct injury to the optic nerve as a consequence of closed head trauma. All were treated conservatively with high-dose dexamethasone therapy. Ten patients presented for follow-up examination 3–11 years after the injury, on average 5.3±2.4 years (SD). A full ophthalmologic examination and color-coded Doppler (CCD) study of the orbital vessels was performed in all subjects. Results: Full blindness of the affected eye, persisting since the injury, was noted in six patients. Their visual acuity did not improve in spite of vigorous treatment and their eyes remained without sight at the follow-up examination. The finding of an absence of flow in central retinal arteries at follow-up suggests structural damage to the nerve. Moreover, in five of these patients, distinct features of eyeball atrophy had evolved between the time of injury and the follow-up examination. Four patients, who on admission presented only with the ability to perceive light, responded to 2–3 weeks of steroid therapy with improvement of visual acuity to 3/50, 5/50, 5/10, and 5/7. After 4–6 years, however, the visual acuity of all of these patients had deteriorated, resulting in nearly total blindness in one case, light perception in two, and 1/50 in the fourth. Optic nerve atrophy was diagnosed in all of the affected eyes. Conclusion: Conservative treatment of TON, even if giving transient improvement in visual function, may not be reliable in providing permanent relief from the sequelae of traumatic optic neuropathy.     

Contusion of the optic nerve after minor blunt ocular trauma: case report and review of the literature

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.     

The role of vascular factors in the development of traumatic optic neuropathy in course of closed head injury

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.     

Ischemic optic neuropathy

Ischemic optic neuropathy (ION), based on vascular anatomy of the optic nerve, pathogenesis and clinical picture, consists of two distinct entities: anterior (AION) and posterior (PION) ischemic optic neuropathies. AION is due to interference with posterior ciliary artery supply to the optic nerve head and retrolaminar part of the optic nerve; it initially presents with visual loss and optic disc edema which progresses to optic atrophy in a month or two. PION is due to occlusion of nutrient arteries to the posterior part of the optic nerve; in this condition during the initial stages the optic disc is normal in spite of marked visual loss, but the atrophy develops later on. Their pathogeneses, causes, clinical pictures, diagnosis and management are discussed briefly.Some of the figures have been reproduced by courtesy of the British Journal of Ophthalmology (Figs. 2, 5, 7), American Academy of Ophthalmology and Otolarngology (Fig. 1) and Springer-Verslag (Fig. 8). This investigation was supported by Public Health Service Grant EY-01151.     

Posterior ischemic optic neuropathy. III. Clinical diagnosis

14 cases of posterior ischemic optic neuropathy (PION) were clinically analyzed, in whom we excluded known etiologies of optic nerve disturbances and confirmed the decreased blood supply to the posterior portion of the optic nerve. On the basis of our clinical findings, we have proposed the following criteria for the diagnosis of idiopathic PION: (1) sudden onset of unilateral visual disturbance in older patients; (2) normal optic disc, subsequently developing simple optic atrophy; (3) hypertensive and arteriosclerotic changes in the retinal vessels; (4) varying degrees of impaired vision, variable visual field defects; (5) associated systemic disease such as hypertension, diabetes mellitus, hyperlipemia, hypotension, etc.; (6) exclusion of other demonstrable causes of optic nerve disturbances, and (7) confirmation of abnormal hemodynamics in the posterior portion of the optic nerve by carotid angiography, ophthalmodynamography, ophthalmodynamometry and fluorescein fundus angiography.     

CONTUSION INJURIES OF THE OPTIC NERVE

Indirect trauma to the optic nerve with secondary optic atrophy may result from minor trauma and has traditionally been associated with a poor visual prognosis. The case of a 32-year-old man who suffered a blow to his left supraorbital region and eyebrow in an automatic closing door is reported to draw attention to the uncommon but trivial nature of this injury which may result in profound visual loss. He suffered an initial inferonasal visual field loss which was related to vascular changes in the optic nerve head. Over the ensuing year there was deterioration in his central vision and visual field due to arachnoiditis.
Current trends in the management of optic nerve contusion injuries are discussed. There is currently a move towards primary medical management with high-dose corticosteroids as in this case; surgery is reserved for those patients who fail to respond to steroids or deteriorate as the steroid dose is reduced.     

Contusion injuries of the optic nerve

Indirect trauma to the optic nerve with secondary optic atrophy may result from minor trauma and has traditionally been associated with a poor visual prognosis. The case of a 32-year-old man who suffered a blow to his left supraorbital region and eyebrow in an automatic closing door is reported to draw attention to the uncommon but trivial nature of this injury which may result in profound visual loss. He suffered an initial inferonasal visual field loss which was related to vascular changes in the optic nerve head. Over the ensuing year there was deterioration in his central vision and visual field due to arachnoiditis. Current trends in the management of optic nerve contusion injuries are discussed. There is currently a move towards primary medical management with high-dose corticosteroids as in this case; surgery is reserved for those patients who fail to respond to steroids or deteriorate as the steroid dose is reduced.     

青盲一号方治疗中毒性视神经萎缩的疗效分析

目的:评价青盲一号方治疗中毒性视神经萎缩的临床疗效。方法:分析2013-01/2018-02于北京中医药大学东方医院眼科采用青盲一号方治疗的肝郁血虚型中毒性视神经萎缩患者7例13眼,随访6~24mo,观察治疗前后视力、视野、电生理及视网膜神经纤维层(RNFL)厚度等指标的变化,综合评估青盲一号方的临床疗效。结果:本研究纳入患者中乙胺丁醇中毒者5例10眼,酒精中毒者1例1眼,狂犬疫苗中毒者1例2眼。治疗前4例8眼患者行OCT检查示鼻侧与颞侧RNFL厚度已发生明显薄变,末次随访时各象限厚度仍呈下降趋势。至末次随访时,视力提高≥0.1者4眼(31%),提高0.06~<0.1者2眼(15%),提高0.04~<0.06者1眼(8%),提高0.01~<0.04者4眼(31%),视力无提高者2眼(15%);青盲一号方治疗显效3眼(27%),有效4眼(36%),无效4眼(36%),总有效率为64%。结论:青盲一号方能够延缓视神经萎缩的进展,可在一定程度上改善视功能,发挥视神经保护的作用。     

Long-term outcome after conservative treatment of indirect traumatic optic neuropathy

PURPOSE: To report the long-term outcome of patients with indirect traumatic optic neuropathy (TON) which showed useful vision for a short period after trauma. METHODS: A cohort of 12 TON patients treated with steroids megadose immediately after trauma was followed every 6 months for an overall period of 5 years. Other than a full neuro-ophthalmologic examination, each visit included quantitative Goldmann perimetry and pattern reversal visual evoked potentials. The results of each examination were compared with the visual function at baseline. The main outcome measures were visual acuity and visual field. Data were analyzed using the Wilcoxon signed-rank test. A p value of less than 0.05 was considered statistically significant. RESULTS: All patients showed a stable visual function 5 years after optic nerve trauma. There was no difference in visual acuity levels (p=0.65) and no visual field surface area between the visit at baseline and the last follow-up. However, a significant improvement in visual field extension (p=0.036) was observed after perimetry evaluation. CONCLUSIONS: This cohort of patients clearly demonstrates that the residual visual function found in the short term after TON is maintained for at least 5 years. These findings add further important clinical information for patients with TON. Furthermore, these data may be helpful to better quantify morbidity related to optic nerve trauma and its permanent sequelae.     

Don't get off the track

A 43-year-old man noted decreased vision after head trauma, with normal neuroimaging acutely. He had a left homonymous hemianopia, confirmed with hemifield visual evoked potentials, from trauma to the right optic tract. Four months after trauma, a magnetic resonance imaging of the brain showed atrophy of the right optic tract, and funduscopy revealed optic disk pallor with decreased retinal nerve fiber layer measures consistent with an optic tract syndrome.     

Optic Nerve Blindness Following Blunt Forehead Trauma

Seven cases of sudden monocular blindness following frontal head trauma are presented. The average age of these patients was 18 years. Four of the seven patients underwent transethmoid-sphenoid nerve decompression with only one of the four achieving a minor return of vision. None of the three out of six patients who failed to respond to megadose steroids regained vision with optic nerve decompression. Three out of six patients had return of good vision with megadose steroids without optic nerve decompression. Two of these three patients had a delayed loss of vision. One of the three patients with visual return developed visual loss again following a facial fracture reduction, which again responded to megadose steroids without optic nerve decompression. Another patient had visual return on steroids but also required removal of a subperiosteal hematoma to obtain near normal vision. This case differs from our other cases in that subperiosteal hematoma is an unusual complication of these injuries and caused the optic nerve compression in the orbital apex in this case. Review of the literature and our clinical and experimental findings suggest that the etiology of the indirect optic nerve injury is secondary to a stretching, tearing, torsion, or contusion of the nerve caused not only from the momentum of the eyeball and orbital contents being absorbed by the fixed canalicular portion of the optic nerve but also by skeletal distortion caused by forces remote from the initial impact. This is well illustrated by the holographic findings. These injuries cause direct injury to the nerve or vascular compromise from tearing, thrombosis, hematoma, or compression of the small nutrient vessels supplying the optic nerve. Megadose steroids appear to be useful in some cases of traumatic monocular blindness secondary to blunt facial trauma and as an adjunct to or an indication for surgery in others. The authors' recommended indications for optic nerve decompression (transethmoid-sphenoidotomy with removal of the medial wall of the optic canal) following blunt trauma are (1) delayed visual loss following frontal head trauma unresponsive to 12 hours of megadose steroid therapy and (2) initial return of vision with megadose steroids followed by visual decrease while on steroids or with the tapering of steroids.     

Optic nerve atrophy after vitrectomy for diabetic retinopathy: its systemic and local risk factors

PURPOSE: To evaluate the incidence and risk factors of optic nerve atrophy after vitrectomy for diabetic retinopathy. SUBJECTS AND METHODS: Clinical charts of 48 eyes of 40 patients who underwent vitrectomy for diabetic retinopathy were retrospectively reviewed. The relationship between postoperative optic nerve atrophy and patients' physical condition was statistically analyzed. RESULT: Postoperative optic nerve atrophy, distinct from glaucomatous optic nerve atrophy, occurred in 5 eyes (10.4%). Its incidence was correlated with higher plasma creatinine concentration (p=0.001), proliferative diabetic retinopathy (p= 0.046), and retinal white vessel formation (p= 0.007). Maintenance of the best postoperative visual acuity was difficult in the patients with optic nerve atrophy. CONCLUSION: Patients with proliferative diabetic retinopathy accompanied by renal dysfunction were at high risk of optic nerve atrophy after vitrectomy.     

Analysis of the Peripapillary Retinal Nerve Fibre Layer Thickness Using Optical Coherence Tomography in Traumatic Optic Neuropathy

The aim of the study is to evaluate the change in thickness of the retinal nerve fibre layer following acute traumatic optic neuropathy using optical coherence tomography. Twenty-eight patients who had unilateral decreased visual acuity and who were diagnosed with traumatic optic neuropathy were evaluated. Twelve eyes in the 28 patients who had trauma to the orbit or head resulting in traumatic optic neuropathy were serially examined every 2 weeks for 6 weeks and again at 12 and 24 weeks after the trauma. The progressive axonal change in retinal nerve fibre layer thickness was examined with disc optical coherence tomography. The mean age of the 12 patients was 48.58?±?21.64 years. The mean retinal nerve fibre layer thickness at the second week after trauma was 95.03?±?5.93 μm; this mean thickness decreased sequentially over the next 6 months and was 50.61?±?5.99 μm at 24 weeks after trauma. Retinal nerve fibre layer thickness decreased at a faster rate during the first 6 weeks after trauma than in any other period, and the rate of this decrease became stable 6 months after the trauma. The superior and inferior portions of the optic disc showed greater reductions in retinal nerve fibre layer thickness than other areas. The authors conclude that in cases of traumatic optic neuropathy, retinal nerve fibre layer thickness decreased sequentially for 6 months. Most of this decrease occurred during the first 6 weeks after trauma.     

Hypovolemic ischemic optic neuropathy.

BACKGROUND: Ischemic optic neuropathy refers to an acute event of ischemia, or decreased blood flow, to the optic nerve resulting in varying degrees of vision loss and visual field defects. Typically this disease affects the elderly population who experience systemic diseases that compromise the blood flow efficiency of the optic nerve head (e.g., giant-cell arteritis, hypertension, diabetes, etc.). However, cases of blood loss to the optic nerve, secondary to traumatic injuries or surgeries, have also been shown to result in ischemic optic neuropathy, regardless of age. It seems that in these cases, the resulting anemia and hypotension play contributing roles in the development of ischemic optic neuropathy. METHODS: A 41-year-old black man came to us with optic nerve head pallor O.S., count-fingers vision O.S., positive afferent pupillary defect O.S., and a central scotoma O.S. after being hospitalized and treated for a stab wound to his left neck that severed his left carotid artery at the bifurcation. RESULTS: This patient had been seen in the Optometry Clinic two years before the stab-wound incident. At that time, he had 20/20 vision in his left eye and no remarkable neurological deficits. His ocular presentation after the traumatic hypovolemic event was probably a direct result of the hypoperfusion to the left optic nerve head. This patient was diagnosed with a hypovolemic, or blood loss-related, ischemic optic neuropathy (O.S.). CONCLUSIONS: Patients who experience large amounts of blood loss due to trauma, surgery, internal bleeding, etc. and report vision loss should be screened for possible optic nerve ischemia. As eye care providers, when we are presented with patients who have optic nerve head atrophy, we should inquire about events that may have precipitated blood loss, potentially triggering ischemic optic neuropathy.     

Avulsion of the optic nerve: two case studies

Avulsion of the optic nerve is a rare and serious injury. The authors report two cases of optic nerve avulsion. The first one concerns a 5-year-old boy who presented ocular trauma after falling on the handlebars of a bicycle. His visual acuity was light perception in the right eye, and his right pupil was unresponsive to light. The anterior segment was normal. The ophthalmoscopic examination showed a total separation of the optic nerve head from the sclera with peripapillary hemorrhage. The second case concerns a 30-year-old man who was hit in the right eye with a stick. On admission, he had no light perception in the right eye, a right afferent pupil defect, a small laceration of the right lower eye lid and no abnormalities on the anterior segment. The fundus examination showed a mild vitreous hemorrhage. Ocular ultrasonography showed vitreous hemorrhage coming directly from the optic nerve head in a mushroom pattern. A CT scan of the orbit revealed a thickened optic nerve. Color Doppler ultrasonography documented slowing of blood flow in the central retinal artery. The two patients received 1 mg/kg/day of prednisone for 2 weeks. No improvement was noted. Optic nerve avulsion is often caused by sudden and forceful rotation of the eye with tearing of the optic nerve as it exits the globe. The nerve can be partially or totally avulsed. The prognosis is usually poor.     

Use of instenon in complex treatment of patients with optic nerve atrophy caused by craniocerebral trauma

Instenon, a combined nootropic agent, was used on the step-type basis within a complex treatment of optic nerve atrophy caused by craniocerebral trauma. Our study revealed that instenon, when used within a complex treatment of a partial optic nerve atrophy caused by craniocerebral trauma, improved the visual acuity in 85.7% of patients and it expanded the total visual field in 76.2% of patients, whereas the routine therapy ensured the related improvements in 58.9% and 61.5% of patients, respectively. Besides, the drug provided for a better retinal electric sensitivity and for a better optic nerve conduction in 73.8% of cases versus 64.1% of cases with basic therapy. Increased velocity parameters in the ocular-artery blood flow were registered in 77.1%, of patients who received instenon, by duplex scanning.     

Moderate to severe obstructive sleep apnoea patients is associated with a higher incidence of visual field defect

PURPOSE: To compare the visual fields (VFs) and optic nerve head changes between obstructive sleep apnoea (OSA) in normotensive patients and an age-matched non-OSA population. DESIGN: Case-control study. PARTICIPANTS: A total of 41 ethnic Chinese patients diagnosed with moderate to severe OSA referred from the Sleep Laboratory, ENT Department, Tuen Mun Hospital. A total of 35 age-matched non-OSA subjects recruited from the Ophthalmology Department, North District Hospital. METHODS: Comprehensive ophthalmological and systemic history, complete ophthalmological examination, including central-30 computerized perimetry for all studied patients. MAIN OUTCOME MEASURES: Polysomnographic data, VF indices, optic disc changes. RESULTS: In the OSA arm, VF indices were significantly subnormal and the incidence of suspicious glaucomatous disc changes was four times higher than that of the control arm. None of the studied patients suffered from any form of anterior segment complications. CONCLUSIONS: Moderate to severe OSA is associated with a higher incidence of VF defect and glaucomatous optic nerve changes.     

Causes of visual disability in children and young adults

PURPOSE: Blindness and visual disability is a great problem all over the world. Loss of visual acuity in children requires special attention. The aim of the study was to determine the causes of uni- and bilateral low vision in children and young adults. Patients were from our clinic and from the School for the Blind and Visually Impaired in Lodz. MATERIAL AND METHODS: The study group included 271 patients aged from 3 months to 21 years, visually disabled and with uniocular reduction of visual acuity to 25% or less. RESULTS: The commonest cause of low visual acuity in the group was optic nerve atrophy (22%) due to perinatal hypoxia. Other important causes were retinopathy of prematurity (17%) and congenital abnormalities of the eye globe (11%). The main causes of uniocular low vision were anisometropia and strabismus. CONCLUSIONS: The main cause of visual impairment and disability in the study group from our region was optic nerve atrophy. Retinopathy of prematurity was also frequently seen in the handicapped children and was responsible for severe visual loss. Anisometropia and strabismus were predominant causes of uniocular visual deterioration, but not of visual disability.     

原发性青光眼患者术后低视力及康复效果观察

目的 :了解原发性青光眼术后低视力患者远近矫正视力及应用助视器后的矫正视力 ,研究针对造成低视力的相关因素所进行康复治疗的效果。方法 :对 10 4例原发性青光眼患者 16 5只眼术后近期 (第 4周 )裸眼及矫正远近视力进行分析 ,分析导致低视力的病因 ,并观察给予相应助视器矫正后的视力康复情况。结果 :16 5眼中有 38眼为低视力 ,主要病因为青光眼性视神经萎缩、眼底病变、并发性白内障、角膜病变等。应用助视镜后 ,76 .3%的低视力眼的矫正远视力和 84.2 %的矫正近视力可提高到有用视力。结论 :助视镜的应用仍是较为可靠、有效的康复治疗方法之一 ,但仍需改进     

Ophthalmoscopic findings in 3 patients with panarteritis nodosa and review of the literature

BACKGROUND: Ocular involvement in panarteritis nodosa (PAN) has been reported to occur in 10 to 20% of patients. In 3 patients with acute visual disturbance we point out unusual findings. PATIENTS: Case 1. A 40-year-old man initially presented with papilledema together with partial optic atrophy in both eyes, later polyneuropathy, gangrene of the toes and myalgic pains developed. Caliber changes in the small arteries in the liver were seen angiographically and recognized as signs of PAN. Under treatment with cyclophosphamide und prednisone no relapse occurred during a follow-up of 2 years. Case 2. In a 67-year-old man who suffered from arterial hypertension and coronary heart disease, central retinal artery occlusion occurred, at first in the left and then later in the right eye. The clinically suspected diagnosis of PAN (arterial hypertension, myalgia, polyneuropathy) was confirmed by a muscle biopsy. During a follow-up of 4 years--including treatment with prednisone and cyclophosphamide--no relapse occurred. Case 3. A 16-year-old adolescent with throbbing headaches and a thickened right temporal artery reported visual disturbances. These were due to an inflammation of choroidal vessels of the right eye appearing as an initial sign of PAN. Histology revealed a necrotising arteritis of the temporal artery. He presented with signs of Raynaud's disease, cachexia and arterial hypertension. Multiple vasculitic changes were detected by aorto-arteriography. Five months after the visual deterioration an anterior spinal artery syndrome with quadriplegia developed. After a follow-up of 2 years and treatment with prednisone und cyclophosphamide, he still had paralysis of both legs. The visual acuity was 1.0 in each eye. CONCLUSION: PAN should be considered in differential diagnosis in patients with acute inflammatory signs of the optic nerve head, the choroid and/or the retina together with general signs of the disease. If the disease is suspected, a muscle biopsy is indicated.