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1.
目的探讨经鼻内镜视神经减压术治疗外伤性视神经病的疗效及预后影响因素。方法对经鼻内镜视神经减压术治疗的105例外伤性视神经病患者的临床资料进行回顾性分析,采用单因素分析鼻内镜视神经减压术治疗外伤性视神经病疗效的影响因素。对有统计学意义的观察指标进行多因素Logistic回归分析。结果手术总有效率38.09%(40/105)。其中,术前尚存残余视力者有效率80.00%(20/25),术前不存在残余视力者有效率25.00%(20/80),差异有统计学意义(χ2=24.433,P0.05)。单因素分析显示,术前残余视力、伤后至手术间隔时间及筛蝶窦积血与手术效果存在明显的相关性(P0.05);多因素Logistic回归分析显示,术前无残余视力、伤后至手术间隔时间3d及筛蝶窦积血是影响经鼻内镜视神经减压术治疗外伤性视神经病疗效以及预后的危险因素(P0.05)。结论经鼻内镜视神经减压术治疗外伤性视神经病的临床疗效并不十分令人满意,特别是术前无残余视力、伤后至手术间隔时间3d及筛蝶窦积血的患者,手术疗效较差。术前针对患者临床特点制定相应的手术方案,对疗效及预后均有一定的积极作用。  相似文献   

2.
目的探讨鼻内镜视神经减压术治疗外伤性视神经病变的效果及预后的影响因素。方法选择112例神经病变病例,分析外伤性视神经病变治疗的相关因素。结果手术有效率达40.19%(45/105),术前是否存残余视力是决定术后疗效的主要因素,有残余视力和无残余视力的患者手术治愈率分别为80.65%(25/31)和25.93%(21/81),差异有统计学意义(P0.05)。单因素分析得出,术前残余视力、筛蝶窦积血及伤后至手术间隔时间与术后疗效之间存在相关性;多因素Logistic回归分析显示,术前残余视力、筛蝶窦积血及伤后至手术间隔时间是影响鼻内镜视神经减压术治疗的影响因素。结论单纯行鼻内镜视神经减压术治疗外伤性神经病变效果不明显,对无残余视力、伤后至手术间隔3d及筛蝶窦积血患者效果更差。术前应根据患者的临床情况制定个性化的手术方案,做到最大程度的积极治疗。  相似文献   

3.
目的探讨视神经管减压术治疗创伤性视神经损伤(TON)的疗效,评估相关预后影响因素,并分析视神经管不同部位骨折手术策略选择。 方法回顾性分析空军军医大学第二附属医院神经外科自2011年1月至2020年6月收治的58例TON后行视神经减压术患者的临床资料,采用单因素和多因素Logistic回归分析评价预后的潜在影响因素。根据视神经管骨折位置的不同,选择开颅视神经减压术和经鼻内镜减压术评估不同术式对不同骨折位置患者的术后视力改善情况的影响。 结果58例TON患者均行视神经减压术,33例患者术后视力得到改善(改善组),其中9例行开颅视神经管减压术,24例行经鼻内镜减压术;25例患者术后视力未得到改善(未改善组),其中8例行开颅视神经管减压术,17例行经鼻内镜减压术。单因素和多因素Logistic回归分析确定术前视力及视神经管是否骨折是术后视力改善的独立影响因素,有光感者有效率明显高于无光感者,无视神经管骨折患者术后改善率明显高于有视神经管骨折患者。35例单发视神经管骨折患者中,视神经管内下壁骨折使用经鼻内镜视神经减压有更好的预后,开颅减压则对于外上壁骨折更有益。 结论视神经管减压术治疗TON总体有较好的效果,尤其是对于术前尚存光感的患者。对于视神经管骨折患者应根据骨折位置选择合理的手术方式进行视神经减压。  相似文献   

4.
目的研究鼻内镜视神经管减压手术治疗外伤性视神经病变的疗效。方法选取于我院耳鼻喉科就诊的8例外伤性视神经病变患者进行观察治疗,予以鼻内镜视神经管减压手术,并研究鼻内镜视神经管减压手术治疗外伤性视神经病变的疗效。结果治疗后患者的视力状况得到明显改善,治疗前后差异具有统计学意义(P0.05)。患者伤后不同时机治疗的疗效各不相同,治疗3个月后的有效率(100%%)明显高于2周内的有效率(75%),差异有统计学意义(P0.05)。结论鼻内镜视神经管减压手术治疗外伤性视神经病变的疗效显著,创伤小、恢复快、手术时间短、并发症少,明显优于传统激素药物的治疗方法。  相似文献   

5.
目的探讨经鼻蝶内窥镜视神经管减压手术对视神经损伤病人的治疗效果。方法回顾性分析我病区收治68例单侧视神经损伤的病人,男性48例,女性20例,年龄17~58岁,所有病例均行经鼻蝶内窥镜视神经管减压手术,手术时间为伤后24 h至47 d。术前眼球活动障碍5例,患侧眼屈光间质、眼底及对侧眼视力均正常。术前CT见额眶骨骨折63例,未见明显骨折5例,筛窦纸板骨折59例,视神经骨管骨折31例,筛窦积血57例,窦积血29例。结果术后3个月随访观察,本组68例病人中56例术后视力有不同程度提高。12例12眼无效。5例术前眼球运动受限的患者,术后3例眼球运动恢复正常。结论内镜下经鼻视神经减压手术,具有入路短,微创,康复快的特点。而且,由于重力作用,视神经减压后会自然下垂,减压效果远远大于其他手术入路。术中还可以发现影像及其他检查未明确的骨折。总之,内窥镜手术视神经管减压有其独特的优点。  相似文献   

6.
外伤性视神经损伤经颅手术时机选择   总被引:13,自引:3,他引:10  
目的分析外伤性视神经损伤后影响视力预后的因素,探讨适宜的手术时机。方法回顾性总结分析231例经颅视神经减压手术治疗外伤性视神经损伤患者的临床资料。根据病人术前视力情况分成2组,A组(无光感)171例;B组(光感以上)60例,每组根据伤后手术间隔时间长短再分为≤48h手术组和>48h手术组。术后随访1个月-6年。结果不同受力部位、术前FVEP检查结果对视力预后有影响(P<0.001);视神经管CT有无骨折对视力恢复影响无统计学意义(P=0.571)。A组伤后48h内手术的患者疗效明显高于48h后者(P=0.001),B组伤后48h内手术患者与48h后者的疗效差异无统计学意义(P=0.5047)。结论对颧骨或眉弓前方受力;视觉诱发电位检查P100潜伏期延长但未消失者应该积极考虑手术治疗;对完全失明患者亦不应放弃治疗,并尽可能争取在48h内手术,以挽救其视力;对有残存视力的患者可适当延长受伤至手术的时间。  相似文献   

7.
目的探讨神经内镜经筛蝶窦入路行视神经管减压术治疗创伤性视神经病变(TON)的临床效果。方法回顾性分析2013年12月至2018年2月上海交通大学附属第一人民医院神经外科连续收治的29例(32侧)TON患者的临床资料。术前视力:无光感15侧,光感14侧,指动3侧。所有患者均采用术中神经导航辅助神经内镜经筛蝶窦入路行视神经管减压术治疗。术前均行高分辨率头颅CT扫描,观察手术相关结构的解剖特点,术后观察患者的视力变化以及手术并发症情况。结果29例患者术后随访(5.2±1.1)个月(3~6个月)。术后视力:无光感10侧,光感4侧,指动4侧,指数5侧,最小分辨角的对数(logMAR)视力表≥0.02的9侧,手术有效率为59.4%(19/32)。无一例患者发生颈内动脉损伤、脑脊液鼻漏、嗅觉丧失等手术相关并发症。结论神经内镜经筛蝶窦入路视神经管减压术是治疗TON的有效手段,该手术入路解剖特点清晰,术中神经导航辅助有利于提高手术的安全性,减少手术相关并发症。  相似文献   

8.
目的探讨外伤性视神经病采用鼻内镜下视神经管减压术治疗的护理措施及效果。方法选取2014-08—2015-08我院收治的84例(84眼)外伤性视神经病患者,均采用鼻内镜下视神经管减压术治疗。按照随机数字表法分为干预组(针对性护理)与对照组(常规护理)。术后随访12个月,对比2组治疗及护理效果。结果干预前2组视力水平差异无统计学意义(P0.05);干预后2组视力水平均有所提升,干预组优于对照组,差异有统计学意义(P0.05);干预组有光感、无光感患者总有效率分别为92.6%(25/27)、73.3%(11/15),对照组为71.4%(20/28)、71.4%(10/14)。2组有光感患者总有效率差异有统计学意义(P0.05),无光感患者总有效率差异无统计学意义(P0.05);2组护理满意度差异有统计学意义(P0.05);所有患者术后均未出现并发症。结论外伤性视神经病患者采用鼻内镜下视神经管减压术治疗的过程中,辅以良好护理干预,能增强治疗效果,改善护理满意度。  相似文献   

9.
目的观察经颅视神经管减压术治疗外伤性视神经损伤临床效果。方法收集我2012-06—2015-01采用经颅视神经管减压术治疗外伤性视神经损伤的患者30例,观察术后视力恢复情况,评价手术疗效。结果术前14例无光感者术后4例无变化,10例恢复光感,有效率71.4%;术前10例有光感者,术后2例无变化,4例恢复至眼前手动,4例恢复至眼前数指,有效率80%;术前6例眼前手动,术后4例眼前数指,2例视力恢复至0.1,有效率达80%。术后随访时间为1个月。结论对于外伤性视神经损伤患者,一旦诊断明确后尽早采用经颅视神经减压管减压手术,可有效帮助患者改善视力,具有一定优越性。当然手术时机的选择及术中视神经的充分减压尤为重要。  相似文献   

10.
目的探讨神经内镜经鼻筛蝶窦入路视柱磨除视神经管扩大减压术治疗外伤性视神经病变(TON)的可行性和治疗效果。方法回顾性分析2018年3月至2022年10月宁波大学附属李惠利医院神经外科连续收治并行手术治疗的43例TON患者的临床资料。采用神经内镜经鼻筛蝶窦入路进行常规视神经管减压手术24例(对照组), 应用神经内镜经鼻筛蝶窦入路视柱磨除视神经管扩大减压术式19例(试验组)。比较两种不同术式的手术时长、术中出血量及住院时长等, 术后观察患者的视力变化以评估手术的有效性, 安全性评估指标为手术相关并发症的发生情况。结果对照组的手术时长为56.3~103.5 min[(76.6±23.4)min], 试验组为75.1~121.6 min[(93.2±17.9)min], 差异有统计学意义(t=2.55, P=0.009)。两组间术中出血量及住院时长的差异均无统计学意义(均P>0.05)。对照组的术前视力:无光感6例、光感10例、眼前手动6例、眼前指数2例;术后3个月, 无光感5例、光感7例、眼前手动7例、眼前指数3例、LogMAR视力表≥0.02 2例, 手术有效比例为9/24。试验组术...  相似文献   

11.
One optic tract underwent prolonged degeneration after enucleating one eye. Crushing the remaining optic nerve at a later time resulted in regeneration to both tectal lobes. However, density of the tectal projection through the degenerated optic tract was directly related to the duration of optic tract degeneration.  相似文献   

12.
Compressive optic neuropathy is a rare condition that may be caused by trauma or non-traumatic events. Endoscopic techniques have evolved to provide an easier surgical approach to decompression. The aim of this study was to determine the endoscopic anatomy of the orbital apex and to identify the optimal targets for endoscopic optic nerve decompression. We report five patients with endoscopic optic nerve decompression: two with traumatic optic neuropathies, two with fibrous dysplasias, and one with chordoma. For these lesions, the major treatment concern was removal of the bony structures around the optic nerve. All compressive lesions were removed effectively via an endoscopic endonasal route. Following endoscopic optic nerve decompression, three patients had markedly improved visual acuity and fields of vision, one patient had improved fields of vision without change in visual acuity, and one patient had improved visual acuity alone. There were no operative complications. Adequate exposure of the intracanalicular portion of the optic nerve was essential for effective decompression, and to achieve this, decompression of the roof as well as medial wall of the intracanalicular portion was critical. We conclude that endoscopic optic canal decompression is a minimally invasive, safe, and efficient treatment for compressive optic neuropathy regardless of etiology.  相似文献   

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14.
Primary mitochondrial DNA (mtDNA) mutation at the nt 11778 site in Leber's hereditary optic neuropathy (LHON) has been reported to be present in patients with ethambutol-induced optic neuropathy. To study further this association between LHON and ethambutol-induced optic neuropathy, we tested ethambutol-induced optic neuropathy patients for the presence of the mtDNA mutations at nucleotides (nt)–11778, nt–14484, nt–3460, nt–15257, nt–9438, nt–9804, nt–13730, and nt–14459 in 24, 15, 8, 6, 5, 5, 5, and 5 patients respectively. However, none of the ethambutol-induced optic neuropathy patients was found to exhibit any pathogenic LHON mtDNA mutation. In conclusion, we found no evidence of any association between ethambutol-induced optic neuropathy and the LHON mutations. Received: 21 January 2002, Received in revised form: 26 August 2002, Accepted: 30 August 2002 Correspondence to Jeong-Min Hwang, M. D.  相似文献   

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Following complete optic nerve injury in a lizard, Ctenophorus ornatus, retinal ganglion cell (RGC) axons regenerate but fail to restore retinotectal topography unless animals are trained on a visual task (Beazley et al. [ 1997] J Comp Neurol 370:105-120, [2003] J Neurotrauma 20:1263-1270). Here we show that incomplete injury, which leaves some RGC axons intact, restores normal topography. Strict RGC axon topography allowed us to preserve RGC axons on one side of the nerve (projecting to medial tectum) while lesioning those on the other side (projecting to lateral tectum). Topography and response properties for both RGC axon populations were assessed electrophysiologically. The majority of intact RGC axons retained appropriate topography in medial tectum and had normal, consistently brisk, reliable responses. Regenerate RGC axons fell into two classes: those that projected topographically to lateral tectum with responses that tended to habituate and those that lacked topography, responded weakly, and habituated rapidly. Axon tracing by localized retinal application of carbocyanine dyes supported the electrophysiological data. RGC soma counts were normal in both intact and axotomized RGC populations, contrasting with the 30% RGC loss after complete injury. Unlike incomplete optic nerve injury in mammals, where RGC axon regeneration fails and secondary cell death removes many intact RGC somata, lizards experience a "win-win" situation: intact RGC axons favorably influence the functional outcome for regenerating ones and RGCs do not succumb to either primary or secondary cell death.  相似文献   

18.
In young people, the most frequent cause of isolated monocular visual loss due to an optic neuropathy is optic neuritis. We present the case of a 27 year old woman who presented monocular visual loss, excruciating orbital pain and unusual temporal headache. The initial diagnosis of optic neuritis revealed later to be a posterior ischemic optic neuropathy (PION). In this case, PION was the first unique presentation of a non-traumatic carotid dissection, and it was followed 24 h later by an ischemic stroke.Sudden monocular visual loss associated with a new-onset headache are clinical symptoms that should immediately prompt to a carotid dissection.  相似文献   

19.
Trans‐synaptic degeneration could exacerbate neurodegeneration in multiple sclerosis (MS). We aimed to assess whether anterograde trans‐synaptic degeneration could be identified in the primary visual pathway in vivo. Diffusion tensor imaging (DTI) was used to assess the optic radiations in 15 patients with previous optic nerve inflammation and 9 healthy volunteers. A probabilistic atlas of the optic radiations was created from healthy diffusion tractography data. Lengthwise profiles for DTI parameters (axial [λ||], radial [λ?] and mean diffusivity [MD], fractional anisotropy [FA] and the angle of deviation of the principal eigenvector [α]) were analyzed for patients and controls. Patients also underwent multifocal visual evoked potential (mfVEP) assessments to characterize the latency and amplitude of cortical potentials. Correlations were performed between mfVEP latency and amplitude in the left and right visual hemi‐fields and DTI parameters in the contra‐lateral optic radiations. Patients displayed a significant decrease in λ|| within the body of both optic radiations, which significantly correlated with loss of mfVEP amplitude. Abnormal λ? and FA were detected bilaterally throughout the optic radiations in patients but the abnormality was not associated with amplitude reduction or latency prolongation of the mfVEP. An abnormal α value was observed in the left optic radiations of patients, and the α value in the body of the optic radiations also correlated with mfVEP amplitude loss. The assocation between bilateral DTI abnormalities within the optic radiations and loss of afferent electrical activity could indicate anterograde trans‐synaptic degeneration occurs following optic neuritis. Hum Brain Mapp 33:2047–2061, 2012. © 2011 Wiley Periodicals, Inc.  相似文献   

20.

Introduction

Hereditary optic neuropathies, resulting from retinal ganglion cell degeneration, are a heterogeneous group of diseases ranging from asymptomatic forms to legal blindness.

State of knowledge

Two most frequent phenotypes are Kjer's disease, an autosomal dominant optic atrophy caused by OPA1 gene mutations, and Leber's disease due to maternally inherited mitochondrial DNA mutations.

Prospects and conclusion

Both optic neuropathies usually isolated are sometimes associated with extraocular symptoms, especially neurological symptoms, thus justifying a systematic neurological evaluation and brain imaging.  相似文献   

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