More than meets the eye: Point-of-care ultrasound diagnosis of acute optic neuritis in the emergency department

Optic neuritis (ON) is an inflammatory condition that causes demyelination and thickening of the optic nerve leading to acute/subacute vision loss. It is frequently associated with other conditions like multiple sclerosis, but is often misdiagnosed, which can lead to a suboptimal prognosis.Ultrasound is rarely utilized to help make this diagnosis, even though it can easily detect a thickened retrobulbar optic nerve sheath diameter.We describe four cases in which ultrasonographic measurement of the optic nerve sheath diameter aided in the diagnosis of ON.     

Ophthalmology update for primary practitioners. Part I. Update on optic neuritis

Optic neuritis is a common cause of acute visual loss. It is typified by sudden onset of visual impairment and pain with eye movements, followed by spontaneous recovery of vision over several months. Pathologically, optic neuritis is an acute demyelinating event affecting the optic nerve. Objective physical findings are typically few, including an afferent pupillary defect or Marcus-Gunn pupil, whereas subjective psychophysical findings abound (ie, diminished central visual acuity, color vision, decreased contrast sensitivity, and visual field abnormalities). These characteristics have made the diagnosis of optic neuritis based solely on clinical grounds disquieting to practitioner and patient alike. In addition, the fact that optic neuritis is often associated with multiple sclerosis as the first clinical manifestation of disease gives further reason for both patient and physician anxiety. The serious nature of visual loss and the consequences of making the diagnosis of optic neuritis has given rise to extensive testing and expensive treatments. This review is intended to explore our current state of knowledge with regard to (1) clinical presentation, (2) ancillary testing, (3) therapeutic intervention, and (4) associated disease, specifically the risk for multiple sclerosis in the patient who presents with an acute optic neuritis. Finally, a suggestion guide for informing the patient and addressing his or her concerns will be presented.     

Optic nerve atrophy and retinal nerve fibre layer thinning following optic neuritis: evidence that axonal loss is a substrate of MRI-detected atrophy

Magnetic resonance imaging (MRI) measures of brain atrophy are often considered to be a marker of axonal loss in multiple sclerosis (MS) but evidence is limited. Optic neuritis is a common manifestation of MS and results in optic nerve atrophy. Retinal nerve fibre layer (RNFL) imaging is a non-invasive way of detecting axonal loss following optic neuritis. We hypothesise that if the optic nerve atrophy that develops following optic neuritis is contributed to by axonal loss, it will correlate with thinning of the RNFL. Twenty-five patients were studied at least 1 year after a single unilateral attack of optic neuritis without recurrence, with a selection bias towards incomplete recovery. They had MR quantification of optic nerve cross-sectional area and optic nerve lesion length, as well as optical coherence tomography (OCT) measurement of mean RNFL thickness and macular volume, quantitative visual testing, and visual evoked potentials (VEPs). Fifteen controls were also studied. Significant optic nerve atrophy (mean decrease 30% versus controls), RNFL thinning (mean decrease 33% versus controls), and macular volume loss occurred in patients' affected eyes when compared with patients' unaffected eyes and healthy controls. The optic nerve atrophy was correlated with the RNFL thinning, macular volume loss, visual acuity, visual field mean deviation, and whole field VEP amplitude but not latency. These findings suggest that axonal loss contributes to optic nerve atrophy following a single attack of optic neuritis. By inference, axonal loss due to other post-inflammatory brain lesions is likely to contribute to the global MRI measure of brain atrophy in multiple sclerosis.     

Optic Neuritis Diagnosed by Bedside Emergency Physician−Performed Ultrasound: A Case Report

Background

Optic neuritis is an inflammatory demyelinating condition of the optic nerve that causes subacute visual loss. It is often the result of an underlying systemic condition, such as multiple sclerosis. Due to the possible long-term morbidity associated with this condition, it is essential that the emergency physician recognizes the diagnosis and expedites treatment.

Objective

This case report describes optic neuritis diagnosed at the bedside by emergency physician−performed ultrasound.

Case Report

This is a case report of a young man presenting with unilateral painful vision loss. Optic neuritis must be considered in the differential diagnosis of any young patient who presents with visual complaints without any other neurologic findings. This report is unique because there are very few cases describing the findings of optic neuritis on emergency physician−performed bedside ultrasound in the literature.

Conclusions

This article presents the case, describes diagnostic modalities, especially the use of ultrasound in its diagnosis, and the course of treatment for this particular condition.     

Two common neuro-ophthalmic problems. Optic neuritis and transient visual disturbances

Optic neuritis and transient visual disturbances are common and challenging neuro-ophthalmic problems. Optic neuritis may occur during the course of several neurologic and systemic disorders and is characterized by reversible central visual loss. In many patients, signs and symptoms of multiple sclerosis occur after an episode of optic neuritis. Although several risk factors for development of multiple sclerosis have been identified, the relationship between optic neuritis and multiple sclerosis is still controversial. Transient visual disturbances may take the form of visual loss or visual hallucinations. In many cases, the cause of transient visual loss is never found. Hallucinations of ocular origin, however, are easily diagnosed by a thorough eye examination.     

Myelin oligodendrocyte glycoprotein-specific T cell receptor transgenic mice develop spontaneous autoimmune optic neuritis

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system (CNS) that in many patients first presents clinically as optic neuritis. The relationship of optic neuritis to MS is not well understood. We have generated novel T cell receptor (TCR) transgenic mice specific for myelin oligodendrocyte glycoprotein (MOG). MOG-specific transgenic T cells are not deleted nor tolerized and are functionally competent. A large proportion (>30%) of MOG-specific TCR transgenic mice spontaneously develop isolated optic neuritis without any clinical nor histological evidence of experimental autoimmune encephalomyelitis (EAE). Optic neuritis without EAE could also be induced in these mice by sensitization with suboptimal doses of MOG. The predilection of these mice to develop optic neuritis is associated with higher expression of MOG in the optic nerve than in the spinal cord. These results demonstrate that clinical manifestations of CNS autoimmune disease will vary depending on the identity of the target autoantigen and that MOG-specific T cell responses are involved in the genesis of isolated optic neuritis.     

MRI of optic neuritis in a rat model

Neuritis of the optic nerve is one of the most frequent early symptoms of multiple sclerosis. There are only scarce data correlating magnetic resonance imaging (MRI) contrast alterations with the underlying pathology, that is inflammation, demyelination, and axonal damage. Here we studied optic neuritis in a rat model of experimental autoimmune encephalomyelitis by comparing in vivo MRI findings from multiple techniques (T1, T2, proton density, magnetization transfer) to histopathology. We further assessed a breakdown of the blood-brain barrier by using Gd-DTPA and indirectly estimated the intracellular accumulation of calcium as a consequence of axonal damage by using manganese-enhanced MRI. Hyperintensity on T2-weighted images and signal enhancement after Gd-DTPA were highly sensitive to lesions of the optic nerve but did not differentiate between mild, moderate, and severe damage. Signal reduction on T1-weighted images was less sensitive but correlated well with the severity of tissue damage. No significant changes in magnetization transfer ratio were observed. Manganese ions tended to accumulate in the central parts of the inflamed optic nerve. The resulting signal enhancement at 24 h after administration positively correlated with the severity of axonal loss. Thus, manganese might be an indicator of intracellular calcium accumulation that is known to be associated with axon damage. Although none of the methods alone distinguished between inflammation, demyelination, and reduced axon density, their specific capabilities should prove useful for future in vivo MRI studies of optic neuritis in both animal models and humans.     

药物与视神经管减压治疗急性球后视神经炎疗效观察

目的探讨药物与视神经管减压手术治疗急性球后视神经炎疗效。方法回顾1988～2005年收治双眼急性球后视神经炎54例108眼,经药物治疗与视神经管减压手术治疗（以下简称减压治疗）并观察其疗效。结果54例108眼经药物治疗16～20d有46例（85．19％）95眼（87．96％）视力恢复到0．5—1．2,但仍有8例（14．81％）13眼（12．04％）视力无光感～2m数指。选择视力最差的无光感～30cm数指的8例8眼施行减压治疗,术后药物继续治疗16～20d,术后8眼视力恢复到0．3～0．7。经3年观察,术侧眼视力0．5～1．0,眼底视乳头色正常;而未手术侧的5眼视力光感-20cm数指,眼底视乳头苍白,血管细小,呈鲜明对比,疗效迥然不同。结论①球后视神经炎经药物治疗,大多数病例视力恢复较好。②经药物治疗2—3周少数病例视力仍无光感一眼前指数,视乳头淡白,经CT或MRI检查排除颅内病变,而球后视神经明显增粗的重症病例,应行减压治疗,可恢复较好视力。     

Papilledema: clinical clues and differential diagnosis.

The term "papilledema" describes optic disc swelling resulting from increased intracranial pressure. A complete history and direct funduscopic examination of the optic nerve head and adjacent vessels are necessary to differentiate papilledema from optic disc swelling due to other conditions. Signs of optic disc swelling include elevation and blurring of the disc and its margins, venous congestion, and retinal hard exudates, splinter hemorrhages and infarcts. Patients with papilledema usually present with signs or symptoms of elevated intracranial pressure, such as headache, nausea, vomiting, diplopia, ataxia or altered consciousness. Causes of papilledema include intracranial tumors, idiopathic intracranial hypertension (pseudotumor cerebri), subarachnoid hemorrhage, subdural hematoma and intracranial inflammation. Optic disc edema may also occur from many conditions other than papilledema, including central retinal artery or vein occlusion, congenital structural anomalies and optic neuritis.     

Corticosteroid therapy for the treatment of optic neuritis

Optic neuritis is frequently the first clinical sign of multiple sclerosis (MS). Study results indicate that methylprednisolone pulse therapy reduces the rate of development of MS over a two year period. Patients also experience quicker recovery of vision. This short duration therapy presents immediate and intense nursing care challenges. Coordination of care between three departments at the University of Michigan Medical Center enables many patients to complete IV [intravenous] pulse therapy at home. Although coordination is challenging for providers, ambulatory care and home care benefit patients and their families with potential healthcare cost savings.     

31例儿童视神经炎的临床特点和转归分析

目的:总结儿童视神经炎(ON)的临床特点和预后。方法:回顾性分析2007年1月至2013年1月我院确诊为ON的患儿共31例(52眼)的临床资料及随访结果,比较不同临床特征对ON转化为多发性硬化(MS)或视神经脊髓炎(NMO)的影响。结果:10例(32.3%)病前1~3周有上呼吸道感染史,21例(67.7%)双眼起病,初诊视力下降至≤0.1共29眼(55.8%),13例(41.9%)出现视乳头炎;治疗后视力恢复至≥1.0者共21眼(40.4%)。平均随访时间为43.6月(12~84月),9例(29.0%)在随访期间转化为MS或NMO,其中6例诊断为MS,3例诊断为NMO。2组复发比例差异有统计学意义(P=0.015)。结论:儿童ON双眼起病多见,视力下降严重,治疗后恢复良好。     

Optic neuritis with concurrent etanercept and isoniazid therapy

OBJECTIVE: To report a case of optic neuritis associated with concurrent etanercept and isoniazid therapy. CASE SUMMARY: A 55-year-old man diagnosed as having rheumatoid arthritis had received treatment with nonsteroidal antiinflammatory drugs, sulfasalazine, oral methotrexate, leflunomide, and deflazacort. Four months prior to admission, he had a Disease Activity Score of 6.06; treatment with etanercept was considered. Three months prior to admission, because of evidence of latent tuberculosis, isoniazid 300 mg once daily and pyridoxine 50 mg once daily were prescribed. Treatment with subcutaneous etanercept 25 mg twice weekly was started 5 days after isoniazid was initiated. Two weeks prior to admission, the patient developed blurred vision in his left eye. Ten days later, his vision worsened and he was hospitalized. The visual acuity in both eyes was 0.7, and a campimetric examination was compatible with optic neuritis. Magnetic resonance imaging of the brain revealed lesions suggesting demyelinating lesions. The clinical course was consistent with bilateral optic neuritis. Etanercept was stopped, and isoniazid was replaced with rifampin 600 mg once daily. The patient was treated with intravenous methylprednisolone hemisuccinate 1 g/day for 5 days followed by oral prednisolone, resulting in a minor subjective improvement in left eye visual acuity. He then received oral prednisone for 3 weeks, slowly tapering to discontinuation. DISCUSSION: No physiologic factors could have predisposed this patient to develop optic neuritis. He was not diagnosed with a demyelinating disease or underlying systemic condition. The optic neuritis was unlikely to be an early manifestation of multiple sclerosis based on the clinical course and the negative results of the imaging tests. Furthermore, there was a close temporal correlation between the drug exposure and the onset of symptoms. After discontinuation of etanercept and isoniazid therapy, the patient's general condition improved. Use of the Naranjo probability scale indicated a possible relationship between optic neuritis and combined etanercept-isoniazid therapy. CONCLUSIONS: Patients initiated on etanercept and isoniazid should be closely monitored for the development of adverse neurologic signs and effects. If optic neuritis is determined, etanercept and isoniazid should be discontinued immediately.     

急性颅脑损伤并发视神经损伤的诊治探讨

目的：探讨急性颅脑损伤并发视神经损伤的病因、损伤机制及其诊治经验。方法：总结2009-02-2011-06我院收治的72例颅脑损伤并发视神经损伤病例,其中手术治疗45例,非手术治疗27例,采用焦氏评价法评价视力。结果：手术治疗病例总有效率84.4%,其中术前视力完全丧失病例有效率为46.2%,术前视力残存病例有效率为100%。非手术治疗病例总有效率63.0%,其中治疗前视力残存病例有效率77.8%,视力完全丧失病例有效率33.3%。结论：视神经损伤总体预后较差,早期诊断和及时治疗是提高视力的关键,有手术指征的应尽早手术治疗。     

Allergic neuritis: an experimental disease of rabbits induced by the injection of peripheral nervous tissue and adjuvants

In experimental allergic encephalomyelitis (EAE), produced by injecting rabbits with whole rabbit spinal cord together with tubercle bacilli and mineral oil, lesions comparable to those seen in the central nervous system are found in the nerve roots, spinal ganglia, and peripheral nerves. When special fractions of bovine white matter are used as antigen in rabbits, the same distribution of lesions is seen but peripheral nerve involvement is relatively less frequent. When rabbit sciatic nerve or spinal ganglia are used as antigen in rabbits, lesions occur only in the roots, ganglia, and peripheral nerves. Lesions are not produced in the central nervous system, nor is there a meningitis. This disease picture has been called experimental allergic neuritis (EAN). The antigenicity of rabbit nerve is not impaired by autoclaving. Sciatic nerve of other mammalian species produces the same disease in rabbits as does rabbit nerve. Optic nerve, used as antigen, produces the typical picture of EAE, not EAN. The optic nerves are not affected in EAN, whereas they commonly contain lesions in EAE. There are differences of symptomatology, referable to the difference in distribution of lesions, between EAE and EAN. The spinal fluid of EAE shows an increase both in the number of cells and in the total protein content. In EAN, the same changes in protein are observed, but usually the cell count remains normal. The cell count appears to be related to the involvement of cerebral and spinal meninges, which is an almost invariable accompaniment of EAE. The skin tests and serologic studies made with homologous and heterologous antigens were essentially non-contributory, apparently as a consequence of the diversity of antigens present in the inoculated materials. The similarity between EAN and certain of the human polyneuritides is indicated and discussed.     

Automatic Optic Nerve Measurement: A New Tool to Standardize Optic Nerve Assessment in Ultrasound B-Mode Images

Transorbital sonography provides reliable information about the estimation of intra-cranial pressure by measuring the optic nerve sheath diameter (ONSD), whereas the optic nerve (ON) diameter (OND) may reveal ON atrophy in patients with multiple sclerosis. Here, an AUTomatic Optic Nerve MeAsurement (AUTONoMA) system for OND and ONSD assessment in ultrasound B-mode images based on deformable models is presented. The automated measurements were compared with manual ones obtained by two operators, with no significant differences. AUTONoMA correctly segmented the ON and its sheath in 71 out of 75 images. The mean error compared with the expert operator was 0.06 ± 0.52 mm and 0.06 ± 0.35 mm for the ONSD and OND, respectively. The agreement between operators and AUTONoMA was good and a positive correlation was found between the readers and the algorithm with errors comparable with the inter-operator variability. The AUTONoMA system may allow for standardization of OND and ONSD measurements, reducing manual evaluation variability.     

大鼠急性甲醇中毒视神经损伤实验研究

目的探讨大鼠急性甲醇中毒视神经损伤时间窗及程度。方法用SD大鼠经口灌注甲醇,灌注后分不同时段处死大鼠取血测甲醇浓度、取视神经做病理检查。结果LD50从2h开始出现较为明显的损伤,4h后程度最重。LD0损伤最重的时间段在8h后。不论是LD0、LD50在损伤程度达到最严重之后,连续观察24h、48h、72h随着血液中甲醇浓度的降低,视神经的损伤仍然明显地持续存在。结论急性甲醇中毒对视神经早期（0.5h）就有损伤,损伤程度和剂量浓度有关,视神经的损伤最严重出现在血液中甲醇浓度高峰值的4h后,随时间推移甲醇在大鼠体内的继续弥散,致使损害迁延。     

Les douleurs dans la sclérose en plaques

Pain is present in around 2/3 of patients with multiple sclerosis. It can be classified as: central neuropathic (either continuous or paroxysmal), headaches, musculoskeletal, related to optic neuritis and related to disease modifying treatments. Defining acurately the type of pain is mandatory to give the most adapted treatment. Despite pharmacological treatments currently available, several patients are not relieved and the development of new treatments is still necessary.     

B型超声在球后视神经炎诊断中的作用

目的探讨B型超声在球后视神经炎诊断中的应用价值。方法应用美国Alcon Digital超声系统,对30例（48只眼）临床诊断球后视神经炎病人行B型超声检查。观察视盘及视神经横断面的形态,对视神经直径进行生物测量。结果B型超声检查发现视神经异常44只眼,其中视神经直径增大38只眼,伴视盘水肿22只眼,伴视神经鞘膜积液18只眼;视神经直径变小6只眼。超声检查阳性率达91．7％。结论B型超声对球后视神经炎的诊断具有重要的临床应用价值。     

视神经管减压术联合单唾液酸四己糖神经节苷脂对外伤性视神经损伤的疗效观察

目的观察视神经管减压术联合单唾液酸四己糖神经节苷脂（GM-1）对外伤性视神经损伤的治疗效果。方法回顾2006年1月~2011年1月在本院行视神经管减压术治疗的20例外伤性视神经损伤患者的临床资料,其中11例患者联合应用GM-1 100 mg＋5%GS 250 mL,静脉滴注,1次/d,连用2周后,40 mg＋5%GS 250 mL,静脉滴注,1次/d,再连用2周;随访6~12个月,观察患者的视力恢复情况。结果单独手术组和手术联合GM-1组患者的术前一般情况及伤情无明显差异,单独视神经管减压术的9例患者中无改善2例,有效4例,显效2例,特效1例,总有效率77%手术联合GM-1组的11例患者中视力无改善2例,有效3例,显效4例,特效2例,总有效率81%,视力恢复程度优于单独手术组。结论尽早行视神经管减压术清除骨片和血肿对视神经的压迫,及剪开视神经鞘膜和总腱环给受损的视神经纤维释放足够的空间,对视神经的功能恢复起到了关键作用;联合应用单唾液酸四己糖神经节苷脂可以明显促进受损视神经的修复,提高患者的视力恢复程度。     

急性视神经炎54例临床分析

目的：探讨急性视神经炎的病因和疗效。方法：回顾性分析我科1996年10月至2007年10月收治的急性视神经炎患者54例（81眼）的临床资料。结果：急性视神经炎病因较多，其中多发性硬化占9%。及时采用以静脉滴注甲基强的松龙为主的综合治疗后，治愈率为62%，总有效率为93%。结论：急性视神经炎病因众多，及时诊断治疗是提高视功能的关键。