SD大鼠视神经不同程度损伤的闪光视觉诱发电位动态监测

目的　探索大鼠视神经不同程度损伤后闪光视觉诱发电位 (F VEP)的变化特征 ,为进一步研究间接性视神经损伤的修复提供实验基础和依据。方法　利用压力恒定的反向镊分别夹持大鼠视神经 6、30、6 0s,建立轻、中、重度视神经不完全损伤模型 ,记录正常及损伤后F VEP潜伏期和振幅的变化。结果　正常大鼠F VEP波形稳定 ,主波潜伏期 (L5b)为 5 3 6 7± 3 12ms,振幅 (A5 )为 17 83±5 91μV。视神经损伤后的大鼠F VEP与正常大鼠比较差异有统计学意义 (P <0 0 1)。损伤程度不同 ,F VEP的改变不同 ,损伤程度越重 ,伤后时间越长 ,潜伏期延迟越显著 ,波幅降低程度越大 ,F VEP的熄灭越早。结论　大鼠视神经损伤后F VEP的变化规律与神经的损伤程度一致 ,F VEP是客观反映其视神经功能的一项可靠指标     

高压氧治疗脑外伤并视神经损伤的疗效分析

目的通过观察不同压力和吸氧方式以及不同时机的高压氧治疗对脑外伤合并间接性视神经损伤患者疗效的影响，探讨一种对视神经损伤疗效高而不良反应小的高压氧治疗方案；同时，观察高压氧干预后对病程及疗效的影响。方法回顾性总结125眼间接性视神经损伤患者资料，根据是否实施高压氧治疗分A组（常规治疗组：67眼）和B组（高压氧治疗组：58眼）。根据治疗时机不同A组又分为≤3d治疗组37眼，4～7d治疗组21眼，〉7d治疗组9眼；B组又分为≤3d治疗组25眼，4～7d治疗组23眼，〉7d治疗组10眼，观察治疗后20d内的视力变化情况。近期疗效评定以20d时的治疗效果为准。结果高压氧治疗组总有效率明显高于常规治疗组（P〈0．01）；治疗压力0．1MPa（表压）者疗效明显高于治疗压力0．15MPa者（P〈0．01）；≤3d治疗组中A、B两组总有效率差异无统计学意义．而4—7d治疗组和〉7d治疗组中B组总有效率明显高于A组（P〈0．01，P〈0．05）；在B组中，≤7d治疗组较〉7d治疗组起效快（P〈0．01）；而在A组中，治疗时机对起效快慢影响不大。结论颅脑外伤合并视力障碍者在病情相对稳定的情况下应尽量在7d内实施高压氧配合下的常规治疗，这样可以提高有效率，起效快，有可能缩短疗程；其治疗压力不宜过高，0．1MPa较0．15MPa更为适宜，给氧应短时多次法。患者常规治疗必须在7d内实施，以提高有效率；如果早期治疗（≤7d）被延误，则不能单纯的行常规治疗，应采取高压氧配合下的常规治疗。     

经颅视神经减压治疗已失明的外伤性视神经损伤

目的 探讨已失明的外伤性视神经损伤的手术效果.方法 回顾性分析8例颅脑损伤合并视神经损伤患者的临床特点,比较经颅视神经管减压手术前后的视力变化.结果 7例有视神经管骨折(7眼),1例无视神经管骨折(2眼);视神经挫伤并视神经鞘膜下出血1例(1眼),视神经缺血坏死1例(2眼),视神经轻度水肿6例(6眼).4例(4眼)术后1个月视力得到改善.结论 经颅视神经管减压治疗外伤性视神经损伤安全有效.     

视神经炎多焦视觉诱发电位的初步研究

目的：研究视神经炎在多焦视觉诱发电位（ mfVEP）检查中按照不同离心度分布的各同心环的波形特征;追踪视神经炎发病后局部视神经损害情况及经治疗后的恢复情况,从而为视神经炎的诊断、疗效判定及预后监测提供客观依据。方法对30例（30只眼）单眼患轴性球后视神经炎患者进行多焦视觉诱发电位（mfVEP）和视野检测,采用同一个体的患眼治疗前后与健侧眼及15例（30只眼）正常对照组的比较方法,主要分析多焦视觉诱发电位（ mfVEP）的特征,按不同离心度的同心环进行分析,并与视野检测进行比较。结果患眼治疗前与对侧健眼比较：病变受累区域P波潜伏时相对对侧健眼对应区域延迟,振幅下降（ P＜0．05）。患眼治疗前后对比：患眼病变受累区域P波潜伏时有不同程度的改善,有统计学意义（P＜0．05）,振幅治疗前后有明显差异（P＜0．05）,治疗后均恢复正常。治疗后患眼与对侧健眼比较：P波振幅无明显差异（P＞0．05）;而潜伏时却仍有明显差异（ P＜0．05）,有统计学意义。患眼视野平均敏感度和平均缺损度已接近健侧眼。结论多焦视觉诱发电位（ mfVEP）可用于视神经炎的诊断及疗效判定,其在评价局部视神经损伤、追踪视神经损伤恢复情况较视野和传统VEP有明显的优势。     

视神经损伤后修复再生的GAP-43原位杂交和免疫细胞化学动态研究

目的研究和探讨视神经损伤后的自然修复再生和脑源性神经营养因子及睫状神经营养因子互补辅助再生的GAP-43mRNA原位杂交组织化学和分子神经生物学变化特征，寻找视神经有效再生的新途径。方法用猫作为实验对象，术前动物被分为四组：①正常对照组；②单纯球后视神经1／2截断组；③视神经1／2截断并定时玻璃体内注射生理盐水对照组；④视神经1／2截断并定时玻璃体内注射脑源性神经营养因子和睫状神经营养因子复合因子辅助再生组。动物模型制做为以眶外侧入路方法手术开眶，暴露眼球后视神经，在眼球后5mm处准确行视神经的1／2截断术。术后四组动物共同在正常视环境中饲养4～8个月，视神经1／2截断并玻璃体内注射脑源性神经营养因子和睫状神经营养因子辅助再生组，在术后即日注射脑源性神经营养因子和睫状神经营养因子复合液（10ng），并在以后每周注射脑源性神经营养因子和睫状神经营养因子复合液2次。在视神经损伤后第4个月和第8个月后将动物处死行外侧膝状体的GAP43免疫细胞化学和原位杂交组织化学检测。结果在视神经损伤4个月时，四组的外侧膝状体的损伤眼相应输入层GAP43免疫阳性神经元的细胞数密度和积分光密度比较为：正常对照组与视神经1／2截断组和视神经1／2截断并定时玻璃体内注射生理盐水对照组比较都有显著差异性（P均〈0．001），而与视神经1／2截断并定时玻璃体内注射脑源性神经营养因子和睫状神经营养因子复合因子辅助再生组比较有显著差异性（P〈0．01）；视神经1／2截断并定时玻璃体内注射脑源性神经营养因子和睫状神经营养因子复合因子辅助再生组与视神经1／2截断并定时玻璃体内注射生理盐水对照组和视神经1／2截断组比较都有显著差异性（P均〈0．001），在视神经损伤8个月时，四组的外侧膝状体的损伤眼相应输入层GAP43免疫阳性神经元的细胞数密度和积分光密度比较为：正常对照组与视神经1／2截断组和视神经1／2截断并定时玻璃体内注射生理盐水比较都有显著差异性（P均〈0．001），而视神经1／2截断并定时玻璃体内注射脑源性神经营养因子和睫状神经营养因子复合液组比较也有差异（P〈0．05）；视神经1／2截断并定时玻璃体内沣射脑源性神经营养因子和睫状神经营养因予复合液组与视神经1／2截断并定时玻璃体内注射生理盐水组和视神经1／2截断组比较都有显著差异性（P均〈0．01）。损伤第4个月和第8个月时外侧膝状体的损伤眼相应输入层的GAP43 mRNA原位杂交阳性信号积分光密度和数密度经计算机图像分析及统计学处理发现原位杂交组织化学图像分析结果与免疫细胞化学图象分析结果相一致。结论①视神经1／2损伤后可以施加条件因素辅助再生，脑源性神经营养因子和睫状神经营养因子对促进视神经损伤后的再生有调节局部微环境和互补促生长作用；②原位杂交组织化学实验观察也证实了视神经1／2损伤后的复合神经营养因子辅助视神经再生具有显著的拮抗损伤效应。     

视神经半截断后神经营养因子辅助再生的动态电生理学研究

目的探讨视神经损伤后的自然修复再生和脑源性神经营养因子及睫状神经营养因子互补辅助再生的图形视觉诱发电位变化特征,寻找视神经有效再生的新途径.方法用猫作为实验对象,术前动物随机分为四组：正常对照组、球后视神经半径截断组、视神经半径截断并定时玻璃体内注射生理盐水对照组和视神经半径截断并定时玻璃体内注射脑源性神经营养因子和睫状神经营养因子复合因子辅助再生组.经眶外侧入路手术开眶行视神经半径截断术.术后四组动物共同在正常视环境中饲养1、4和8个月,复合因子辅助再生组在术后即日注射脑源性神经营养因子和睫状神经营养因子复合液（10 ng）,并在以后2次/周注射等量脑源性神经营养因子和睫状神经营养因子复合液.在视神经损伤后1、4和8个月,3次行视神经半径动态检测.结果在视神经半径截断损伤后1个月时,与正常对照组相比,视神经半径损伤各组的图形视觉诱发电位N1-P1振幅显著降低（P＜0.001）,P1潜时延迟（P＜0.001）;视神经半径截断组和生理盐水对照组与复合营养因子辅助再生组比较,图形视觉诱发电位的N1-P1振幅也出现了降低和P1潜时的延迟（P均＜0.01）.在视神经半径损伤后第4个月时,视神经半径截断组和视神经半径切断并定时玻璃体内注射生理盐水对照组与正常对照组比较,其图形视觉诱发电位的P1潜时显著延迟（P均〈0.001）和N1-P1幅度显著降低（P均〈0.001）.而复合因子辅助再生组与正常对照组比较图形视觉诱发电位的P1潜时具有显著性（P〈0.05）,但与视神经损伤后1个月时同组动物的图形视觉诱发电位测试结果比较出现了恢复型曲线图谱并差异有显著性（P〈0.01）.在视神经损伤8个月后,视神经截断组和生理盐水对照组图形视觉诱发电位的P1潜时还是显著延迟和N1-P1幅度显著降低,未见明显的恢复型曲线图出现.复合因子辅助再生组图形视觉诱发电位的P1潜时和N1-P1幅度与视神经损伤后4个月时图形视觉诱发电位测试的结果比较差异具有显著性 （P〈0.01）,与视神经半径截断组和生理盐水对照组比较差异具有显著性（P均〈0.01）,与正常对照组比较其图形视觉诱发电位的P1潜时未见延迟（P〉0.05）,但N1-P1幅度还低于正常对照组（P〈0.05）.结论动态观察图形视觉诱发电位变化结果说明,1/2损伤的视神经在复合神经营养因子的互补作用下可促进其修复再生和恢复视觉信息的传导功能.     

葛根素注射液联合鼠神经生长因子治疗视神经挫伤

目的：探讨葛根素注射液联合鼠神经生长因子（mNGF）治疗视神经挫伤的临床疗效。方法：70例（70只眼）视神经挫伤的住院患者随机数字法分为2组,治疗组35例（35只眼）采用葛根素注射液联合鼠神经生长因子治疗,同时应用激素治疗;对照组35例（35只眼）除不用葛根素外其他治疗不变。治疗21天后根据患者视力、VEP观察治疗前后的视神经挫伤变化情况评定临床疗效。结果：治疗组的总有效率为88．57％,高于对照组的65．71％,治疗后两组总有效率比较差异有统计学意义（P〈0．05）,治疗组疗效明显优于对照组。结论：葛根素注射液联合鼠神经生长因子治疗视神经挫伤安全、有效。值得临床推广应用。     

鼠神经生长因子治疗视神经挫伤的研究

目的：观察鼠神经生长因子对视神经挫伤的临床疗效。方法：随机将视神经挫伤患者40例（42眼）分为两组,治疗组20例（21眼）,对照组20例（21眼）。治疗组主要采用鼠神经生长因子30μg,用2.0mL0.9%氯化钠溶液或注射用水溶解,肌肉注射,1次/d,平均治疗21d,同时给予改善微循环及激素类药物治疗。对照组除不加用鼠神经生长因子外,其他用药同治疗组。结果：主要疗效观察指标为视力、VEP,治疗组总有效率为80.95%,对照组为52.38%,两组比较有显著性差异（χ2=3.875,P〈0.05）。结论：鼠神经生长因子对视神经挫伤的治疗具有肯定疗效,安全性高,值得推广。     

视神经减压术治疗创伤性视神经损伤的手术时机(国内文献分析)

目的总结不同手术时机对视神经管减压术疗效的影响。方法以关键词"创伤性、视神经损伤、手术时机"检索三大中文数据库,严格按照诊断标准筛查病例,最后收录了16篇国内关于视神经管减压术治疗外伤性视神经损伤的文献报道,通过目前公认的视神经损伤恢复标准判定方法:"无光感、光感、眼前手动、眼前指数、视力表0.04以上",术后与术前视力相比提高1个等级视为有效,分析了这16篇(共670例683眼)文章,讨论选择不同时机行视神经管减压术病例的术后疗效。结果670例683眼中外伤后3d以内手术组,手术有效率77.3%;3～7d手术组,手术有效率65.8%;>7d手术组,手术有效率30%,三组之间相比有统计学意义(P<0.01)。结论外伤性视神经损伤在明确诊断下,如有手术指征并且病人全身条件允许,越早行视神经减压术效果越好。外伤后3d以内手术效果最佳。     

颅脑外伤合并视神经损伤35例临床分析

目的分析颅脑外伤合并视神经损伤的损伤机制及治疗效果。方法回顾分析颅脑外伤合并眼视神经损伤35例的临床资料。对其诊断及非手术和手术治疗结果进行了探讨。结果颅脑外伤合并视神经损伤总体预后较差,早期的诊断及及时有效的综合治疗是提高视力的关键。结论治疗颅脑外伤合并视神经损伤,眼科和神经外科医生需密切配合,掌握救治视神经损伤的最佳时机。     

外伤性视神经病变与视力预后相关的因素

 目的 分析影响外伤性视神经病变(traumatic optic neuropathy,TON)患者与视力预后相关的因素。方法 采用回顾性病例对照研究。对96例(97眼) TON患者的临床资料进行分析,通过单因素分析初步筛选出影响因素,再将这些因素纳入多因素分析( Logistic 回归分析),筛选出影响视力预后的因素。结果 经过激素或激素联合手术治疗,44眼(43.14%)视力得到改善。单因素分析结果显示:受伤时间距离治疗时间、伤后是否有光感、是否合并视神经管骨折、是否行视神经管减压术、是否存在蝶窦/筛窦积血、是否昏迷,两组间的视力预后有统计学差异。多因素分析显示:受伤时间≥2 d(OR=0.233),合并蝶窦/筛窦积血(OR=0.307)是视力改善的危险因素,伤后有光感(OR=14.866)是视力改善的保护因素。结论 TON视力预后与多种临床因素有关,是否手术对于预后无明显影响。明确影响视力预后的危险因素和保护因素,有利于临床医师制定合理的临床策略,指导治疗。     

视神经炎的MRI表现及与视觉诱发电位的相关性研究

目的 探讨诊断视神经炎的有效MR检查序列、MRI表现及其与视觉诱发电位(VEP)的相关性.方法 对98例(154只眼)诊断为视神经炎、视神经乳头炎、多发性硬化、视神经脊髓炎的视力下降患者MRI资料进行分析,并与VEP结果及临床视力表现做x2检验、秩和检验和一致性分析.结果154只患眼中56条视神经增粗,76条形态不变,22条变细.MR短时间反转恢复(STIR)序列显示132条视神经呈异常高信号.异常信号累及范围包括视神经球壁段7条,眶内段135条,管内段109条,颅内段97条,视交叉受累56例,视束受累23条.54例行钆喷替酸葡甲胺(Gd-DTPA)增强枪查者,87只患眼中74条视神经强化.98例患者共196只眼中,视力下降同时视神经MRI信号异常者132只眼,视力正常、视神经MRI信号正常者26眼,MRI与视力表现之间的一致率为80.61%(Kappa=0.453,P＜0.01).住获得VEP结果的175只眼中,视力下降同时VEP异常者129只眼,视力正常、VEP正常者30只眼,VEP与视力表现之间的一致率为90.86%(Kappa=0.731,P＜0.01);视神经MRI信号异常及VEP异常者117只眼,MRI信号正常、VEP正常者24只眼,MRI表现与VEP之间的一致率为80.57%(Kappa=0.460,P＜0.01).结论MR STIR序列和Gd-DTPA增强扫描联合脂肪抑制技术有助于视神经炎定位和定性诊断,VEP有助于视神经炎的诊断和亚临床病灶发现,MRI结合VEP能提高视神经炎诊断的准确率.     

急性甲醇中毒致视力损害临床研究

目的探讨急性甲醇中毒致视力损害的临床特点及预后。方法收集2014年4—8月收治的7例急性甲醇中毒致视力损害住院患者的临床资料。急诊住院后患者均进行视力和眼底检查,给予经纠正酸中毒、激素冲击及大剂量B族维生素辅助治疗,并对患者进行随访,探讨患者临床特点及预后情况。结果患者均急性起病,病程早期伴有全身中毒症状,同时,出现双眼不同程度的视力下降。视力下降3 d内达顶峰,7例患者14眼视力从无光感至0.5,均有色觉改变。急性期眼底视盘大致正常,病变部位以球后部视神经受累为主。随访2个月,除2例因代谢性酸中毒死亡外,其余5例患者视力均有不同程度改善。结论急性甲醇中毒可导致严重的视神经损害,全身症状重,预后差。     

Optic nerve hyperintensity on T2-weighted images among patients with pituitary macroadenoma: correlation with visual impairment

PURPOSE: Visual acuity (VA) disturbance other than field defect is important in evaluating patients with pituitary macroadenoma. The purpose of this study was to evaluate MR imaging appearances of optic nerves in patients with pituitary macroadenoma and to ascertain whether visual impairment was correlated with abnormality in optic nerve signal intensity. PATIENTS AND METHODS: Twenty-seven patients with pituitary macroadenoma were examined. Optic nerves were evaluated on T2-weighted images and correlations of signal intensity abnormality with VA disturbance, visual field disturbance, degree of optic chiasm compression, pathologic findings of surgical specimen, and disease duration were statistically analyzed. Correlations between recovery of VA after treatment and the above-mentioned factors were also determined. RESULTS: Coronal T2-weighted images demonstrated unilateral optic nerve hyperintensity lesions in 9 patients. Bilateral signal intensity abnormality of the optic nerve was seen in 5 patients. Signal intensity abnormality of the optic nerve was seen at the site of compression and in the ventral side of the tumor. These patients did not demonstrate signal intensity abnormality posterior to the tumor. Presence of such signal intensity abnormalities was correlated with the degree of optic chiasmal compression and with VA disturbance. Recovery of VA after treatment was correlated with disease duration. CONCLUSION: Hyperintensity of the optic nerves ventral to the pituitary macroadenoma was associated with VA impairment. Recovery of VA after treatment was correlated with disease duration. MR imaging of the optic nerves can provide valuable information for management of pituitary macroadenoma.     

经颅多普勒监测和尼膜同对脑外伤后脑血管痉挛的作用

目的　分析脑外伤后脑血管痉挛 (CVS)的发生规律及经颅多普勒 (TCD)监测CVS的作用 ,并评价尼膜同对脑外伤后CVS的治疗价值。　方法　将 72例脑外伤后CVS患者分为治疗组 (尼膜同治疗组 30例 )和对照组 (42例 ) ,分别于伤后第 1,3,7,14天通过TCD对双侧大脑中动脉 (MCA)及颈内动脉 (ICA)颅外段进行脑血流速度监测 ,并评价其意识情况和预后 ,分析尼膜同对脑外伤后CVS患者预后的影响。　结果　伤后 1～ 3d已开始出现血管痉挛 ,3～ 7d达峰值 ,14d时明显减轻 ;治疗组血管痉挛的程度明显低于对照组 (P <0 .0 5 ) ,并且其意识情况和预后均明显好于对照组 (P <0 .0 5 ) ;血管痉挛程度越重 ,病情越重 ,预后越差。　结论　TCD是监测脑外伤后早期CVS的有效方法 ,尼膜同对纠正脑外伤后CVS有显著疗效。     

MRI of optic nerve and postchiasmal visual pathways and visual evoked potentials in secondary progressive multiple sclerosis

We studied the relationship between abnormalities shown by MRI and functional disturbances in the visual pathway as assessed by the visual evoked potential (VEP) in 25 patients with established multiple sclerosis (MS); only 4 of whom had a history of acute optic neuritis. Optic nerve MRI was abnormal in 19 (76 %) and is thus useful in detecting subclinical disease. Optic nerve total lesion length and area on the STIR sequence was found to correlate significantly with prolongation of the VEP latency. This may reflect a predominantly demyelinating rather than inflammatory origin for the signal change in the optic nerve. Received: 21 July 1997 Accepted: 1 April 1998     

混合晶状体蛋白对大鼠视神经损伤后视网膜神经节细胞的保护作用

目的观察混合晶状体蛋白对Long Evens大鼠视神经切断伤后视网膜神经节细胞(retinal ganglion cells,RGCs)存活的作用。方法于视神经切断伤前7 d逆行标记RGCs。将成年Long Evens大鼠20只,随机分成4组,分别为正常对照组和视神经切断伤后1,2,3周组,每组5只。视神经切断后即刻右眼经玻璃体腔注射浓度为1×10~(-4)g/L的混合晶状体蛋白5μl(实验眼),左眼注射等渗盐水5μl(对照眼),分别于伤后1,2,3周对实验动物行RGC计数。结果视神经切断伤后1周RGCs数明显下降。混合晶状体蛋白作用眼RGCs数在视神经切断伤后1、2、3周分别下降为正常对照组的71%、32%和15%,但均显著高于参渗盐水作用眼(P＜0．01)。结论视神经切断伤后玻璃体腔注射可溶性混合晶状体蛋白能够保护RGCs,延缓其死亡,这种作用可以持续到视神经切断伤3周以后。     

Hyperintense Optic Nerve due to Diffusion Restriction: Diffusion-Weighted Imaging in Traumatic Optic Neuropathy

BACKGROUND AND PURPOSE:Abnormal signal intensity of the optic nerve due to diffusion restriction may be seen in traumatic optic neuropathy. In addition to evaluating optic nerve hyperintensity on diffusion-weighted imaging, we compared the group differences of ADC values between the injured and uninjured contralateral nerve and identified the relation between measured ADC values and admission visual acuity.MATERIALS AND METHODS:We retrospectively evaluated 29 patients with traumatic optic neuropathy who underwent MR imaging with DWI. Uninjured contralateral optic nerves were used as controls. Two attending radiologists, blinded to the side of injury, independently reviewed the DWI for the presence of signal-intensity abnormality and obtained ADC values after manually selecting the ROI.RESULTS:Hyperintensity of the optic nerve was demonstrated in 8 of the 29 patients, with a sensitivity of 27.6% (95% CI, 12.8–47.2) and a specificity of 100% (95% CI, 87.9–100). ADC values were obtained in 25 patients. The mean ADC in the posterior segment of the injured nerve was significantly lower than that in the contralateral uninjured nerve (Welch ANOVA, F = 9.7, P = .003). There was a moderate-to-strong correlation between low ADC values and poor visual acuity in 10 patients in whom visual acuity could be obtained at admission (R = 0.7, P = .02). Patients with optic nerve hyperintensity presented with worse visual acuity.CONCLUSIONS:Hyperintensity of the optic nerve due to diffusion restriction can serve as a specific imaging marker of traumatic optic neuropathy. When paired with reduced ADC values, this finding may be an important surrogate for visual acuity.

Traumatic optic neuropathy (TON) is an acute injury of the optic nerve (ON), typically presenting with severe impairment of visual function. TON is often classified on the basis of the location of the injury. Anterior ON injury is usually associated with ON head avulsion and disruption of circulation at the ON head. These patients present with intraocular hemorrhage and disruption of anatomy at the ON head on funduscopy. Posterior TON involves the nerve at a site proximal to where the ophthalmic artery enters the ON.¹ Clinical diagnosis of posterior TON is based on the presence of a relative afferent pupillary defect, decreased visual acuity (VA), normal funduscopic examination findings, and no apparent intraocular pathology.^2–4 The focus of this study was limited to posterior TON. Contusion, necrosis, concussion, hemorrhage, nerve fiber tears, and infarction due to vascular thrombosis or spasm have all been implicated as potential mechanisms of TON.^5,6 Specific causes include motor vehicle collisions, falls, assaults, blunt force effects of penetrating trauma, and surgical mishaps in and around the optic nerve, with a reported high prevalence among young men.⁷The architecture of the orbit facilitates transfer of impact forces from facial trauma to the region of the optic canal, where the nerve is vulnerable to injury due to the shearing effect between its fixed and mobile portions.^7–9 The concept of primary and secondary injury in TON has been proposed by Walsh.¹⁰ Primary injury results from immediate shearing of the retinal ganglion cell axons of the nerve. Secondary injury occurs from a complex biochemical cascade of events that follows the primary injury, resulting in edema of the ON within the inflexible optic canal.¹¹ Edema of the nerve in the optic canal produces a compartment syndrome, resulting in nerve ischemia due to compression of the pial vascular plexus.^12,13Conventional MR imaging findings are normal in most patients with TON.^3,5 An earlier study with DTI in TON showed decreased axial diffusion and ADC values in the posterior segment of the injured ON.³ In this retrospective study, we aimed to determine the ability of abnormal signal intensity of the ON due to diffusion restriction on DWI to diagnose TON, compare the group differences of ADC values between the injured and uninjured contralateral nerves, and identify the relation between the measured ADC values and admission VA.