视交叉以上视道疾病的视野改变50例分析

一眼来自视网膜鼻半侧的视神经纤维在视交叉处交叉到对侧,与来自对侧眼视网膜的颞半侧纤维会合组成视束,从此往上视道经过外侧膝状体、视放射直到视皮质;因此,视交叉以上视道的任何一段的病损,均将出现双眼在病灶的对侧半视野不同程度的缺损,     

人体视交叉的血液供养及双颞侧视野缺损

在黄斑区作一想象的垂直线,将视网膜分为鼻半及颞半;鼻半的纤维经视神经,在视交叉体部向对侧行去,与对侧眼的颞半的纤维组合成视束,视束绕过大脑脚往后进入外侧膝伏体,视纤维换元之后,成为视放射,直达视皮质.在视交叉体部的前外方为左右视神经,如果蝶鞍区的病变涉及到视交叉近端的视神经,可发生单眼的视野缺损,如一眼偏盲、中心暗点、甚至失明.在视交叉体部的后外方为左右视束的起端.如果蝶鞍区的病变涉及到近视交叉的视束,将发生双眼视野在病灶对侧的半个视野偏盲.除此上述情况之外,视交叉体部附近的病变,则经常发生双颞侧视野缺损.早在1884年 Vossius 首次提出了垂体病可及导致双颞侧视野缺损.其后的临床实践证实了这一观点.我们自己的临床观察也证实了这一观点,并且观察到通过手术或药物治疗可迅速改善或减除这些视野缺损.1948年Traquair 指出这种双颞侧视野缺损,首先系视交叉供血受阻碍所致.学者们对视交叉血液供应作了研究,以期证实 Traquair 的观点.协和医院眼科进行过1000余例视交叉部病例的3000余次视野检查.其中主要为垂体瘤病人(520例肢端肥大,185例泌乳素瘤及91例 ACTH 瘤)也都见到不同型样及不同程度的双颞侧视野缺损.临床的经验及疑点给我们提出以下七个问题.我们把这些问题,作为我们实验研究的背景,进行了两部分的研究.     

双眼原发性视神经萎缩并先天性双侧脑室及第三脑室积水一例

原发性视神经萎缩是指筛板以后的视神经、视交叉、视束以及外侧膝状体等部位的视路受到损害导致的神经节细胞纤维组织萎缩的一类病变。导致原发性视神经萎缩的病因较多,但原发性视神经萎缩伴先天性双侧脑室及第三脑室积水,目前却少有报道。我们将诊断的1例报告如下。患者,男性,     

联合应用磁共振弥散张量成像及质子密度加权成像对青光眼患者中枢神经系统视路的初步研究

[目的]使用磁共振成像观察伴双侧视野缺损的青光眼患者眼外中枢神经系统视路的改变.[方法]前瞻性研究.35名受检者纳入研究.其中,经眼科检查确诊伴双侧视野缺损的原发性慢性闭角型青光眼患者7例;伴双侧视野缺损的原发性开角型青光眼患者12例;正常对照者16人.采用GE SignaHD1.5T超导磁共振扫描仪及头部8通道相控阵头线圈进行扫描;应用弥散张量成像技术测量视路白质纤维束的部分各向异性(FA)及平均扩散系数(DCavg),并行纤维跟踪技术重建白质纤维束;应用冠状位质子密度加权成像技术测量外侧膝状体体积.由两位技术娴熟的神经放射学医生手工描绘感兴趣区,测量双侧视神经、视交叉、双侧视束、双侧视放射的平均FA值、平均DCavg值及双侧外侧膝状体体积.使用SPSS13.0软件进行统计学分析.[结果]不同组间双侧视神经、视交叉、双侧视束、双侧视放射比较,平均FA值差异有统计学意义(F=25.985,20.626,12.262,22.399,21.708,24.994,22.774;P＜0.05),而平均DCavg值差异无统计学意义(F=2.097,2.178,0.530,0.983,0.608,0.866,1.504;P＞0.05);不同组间外侧膝状体体积比较,差异有统计学意义(F=18.631,17.274;P＜0.05).[结论]青光眼患者存在眼外中枢神经系统视路的变性.     

外侧膝状体血管性损害的视野缺损

视路神经纤维有规则的空间排列,分析视路损害产生的特殊视野缺损常可对病变做出定位诊断。在诊断中最常用到的特征之一是视野缺损的相合性,即两眼视野缺损相同。视皮质损害的视野缺损的相合性最完全,视束损害其相合性最差。外侧膝状体位于视交叉后视路的前三分之一,该核前后病变产生不相合性视野缺损。在视野缺损的相合性与视路前后位置关系上,外侧膝状体血管性损害是个例外,它产生相合性视野缺损。报道5例外侧膝状体血管性损害,瞳孔对光反射均正常。例1、2表现为典型的楔形同侧偏盲,例1 CT扫描显示左后外侧丘脑缺血     

即早基因c-fos在视神经损伤大鼠外侧膝状体中的表达

目的研究大鼠视神经钳夹伤后外侧膝状体神经元的早期损伤反应。方法用70g压力的显微无创血管钳夹持SD雄性大鼠右侧视神经30s,于损伤后2h、1d、3d、7d、14d,采用c-fos和calbindin D-28k抗体行免疫组化和荧光双标检测外侧膝状体中的c-fos定位,用Western印迹法检测外侧膝状体中的c-fos表达量。结果在损伤眼同侧的外侧膝状体腹侧核内侧核团和中间核可见c-fos阳性细胞,损伤后2h开始出现,1d时达到高峰,3d时稍有减少,7d时明显减少,14d仍有少量c-fos阳性细胞。外侧膝状体的背侧核及对照组未见c-fos阳性细胞。Calbindin D-28k阳性细胞主要出现在外侧膝状体的腹侧核内侧核团和中间核内。75％-83％的c-fos都出现在calbindin D-28k阳性细胞的胞核中。结论大鼠的视神经钳夹伤诱导了即早基因c-fos在同侧外侧膝状体腹侧核内侧核团和中间核calbindin D-28k阳性投射神经元中的表达,它们可能在视神经急性损伤的病理过程中起重要作用。（中华眼科杂志,2005,41：321-324）     

视觉通路病变的视野判读要点

视觉通路的组成包括：视网膜、视神经、视交叉、视束、外侧膝状体、视放射及枕叶视觉中枢。视野检查是视觉通路疾病诊疗过程中不可或缺的重要辅助检查之一,用于早期发现视功能异常、鉴别视路疾病、了解疾病进展等。不同部位的损害可表现出不同形式的视野缺损,有些特征性的视野异常可帮助我们快速而准确地定位诊断。因此对视野检查结果的正确判读是神经眼科医师重要的基本技能之一。     

基于三维磁共振的眶内段视神经和视交叉准确截面积测量的标准操作规范

视神经是由视网膜神经节细胞发出的神经纤维构成,在视交叉部位鼻侧纤维交叉到对侧形成视束,要全面研究青光眼性中枢损害,视神经和视交叉的评估是一重要指标[1]。MRI具有软组织分辨率高、无辐射、任意断面成像等特点,特别是近年来扫描技术的发展,能清楚显示视神经解剖细节和微小病变,是视神经病变的最佳影像检查方法。用常规MRI证实原发性开角型青光眼(POAG)视神经萎缩,对人类活体青光眼前视路系统性研究尚少。以往文献多利用MRI测量视     

视神经病眼动脉血流速度的临床研究

视神经疾病为危害视功能的严重疾病,其发病机理尚在研究中。文献报道视神经血液供应不良常导致视神经萎缩。睫状后动脉(眼动脉的主要分枝之一)是筛板区和筛板前区视神经血液供应的唯一源泉,也是筛板后区视神经主要供血来源,而视盘、视盘周围的血液循环与眼内压和睫状后动脉灌注压密切相关。当眼压与血压的平衡失调,睫     

脑动脉硬化对视神经血供影响的形态学研究及其临床意义

目的 研究视神经动脉起源，数目，分布及相关动脉的病理变化，为视神经因为缺血所致视野缺损提供形态学依据。方法 在体视显微镜和手术显微镜下对100侧成人脑标本进行观察视神经动脉来源、数目和分布，对其中50—70岁年龄60侧脑标本的视神经和相关动脉做病理切片观察。结果 视神经动脉主要来源于颈内动脉、大脑前动脉和前交通动脉。其中单来源占3％(3侧)，双来源占68％(68侧)，三来源占29％(29侧)。病理切片观察动脉管壁有粥样硬化改变者占88．3％(53侧)，其中被硬化斑块阻塞眼动脉的占5．7％(3侧)，阻塞垂体上动脉的占7．5％(4侧)，小动脉管腔狭窄者占20．8％(11侧)。与小动脉阻塞相对应的视神经切片，可见有神经纤维萎缩，变性等病理改变。硬化的颈内动脉壁压迫视神经可以形成明显的压迹。结论 50岁以上导致视神经供血障碍脑动脉硬化不能除外。     

Quadruple sectoranopia

Quadruple sectoranopia is a rare campimetric syndrome involving upper and lower, homonymous, congruent field blind sectors sparing a horizontal zone. Ischemia or infarction of the lateral parts of the lateral geniculate body, supplied by the distal part of the anterior choroidal artery, accounts for the visual field defect. Ganglionic nerve fiber atrophy matched to the visual field defect may be found if the lateral geniculate body dysfunction involves infarction. The four cases reported so far involve the following etiologies: a case of surgical ligation of the distal part of the anterior choroidal artery during cerebral meningioma removal, two cases of stroke with anterior choroidal artery infarction, and a case of vascular steal with anterior choroidal artery blood flow being shunted away from the lateral geniculate body by an arteriovenous malformation. If lateral geniculate body infarction is not solely involved, partial recovery may occur, ischemic quiescent neuronal areas being able to resume their activity following ischemia resolution.     

Acute visual loss: just the beginning?

A 47-year-old man presented with sudden visual loss, optic disk edema, retinal ischemia, and limited upgaze in the left eye. Initial MRI revealed thickened, enhancing left optic nerve. Extensive work-up for an inflammatory and infiltrative etiology was positive only for Borrelia burgdorferi IgM by Western blot. Six weeks later the patient had numbness and weakness on his left side. MRI showed enhancing lesions extending from the left optic nerve to the optic chiasm, along the visual pathways bilaterally, mainly on the right side from optic tract to lateral geniculate body and pulvinar. Stereotactic biopsy of the right pulvinar lesion revealed glioblastoma. The tumor progressed rapidly, and the patient died 11 weeks after the onset of first symptoms.     

Zinn-Haller arterial ring observed by ICG angiography in high myopia

AIMS—To delineate the entire Zinn-Haller arterial ring angiographically in vivo.
METHODS—382 highly myopic eyes (210 patients) with refractive errors greater than −8.25 D were examined using indocyanine green (ICG) videoangiography. A control group of 80 eyes (40 patients) had refractive errors within plano +/− 3 D.
RESULTS—The Zinn-Haller ring was visible in 206 of 382 highly myopic eyes (53.9%) by ICG angiography. Although only a part of the Zinn-Haller ring was visible in 162 of 206 eyes, in the remaining 44 eyes it was observed almost completely around the optic nerve head. No anastomotic channels between lateral and medial short posterior ciliary arteries were filled by ICG angiography. In 22 of the 44 eyes (50.0%) the Zinn-Haller ring was supplied by branches of the lateral and medial short posterior ciliary arteries; in seven eyes, it was supplied only by the lateral short posterior ciliary artery; and in seven eyes, it was supplied only by the medial short posterior ciliary artery. In none of the control subjects was the Zinn-Haller ring visible by ICG angiography.
CONCLUSIONS—The Zinn-Haller ring observed by ICG angiography was not a complete collateral circle between lateral and medial posterior ciliary arteries. Also, the patterns in supply vessels to the Zinn-Haller ring varied. ICG angiography made possible the detailed observation of the Zinn-Haller ring in human eyes in vivo.

Keywords: Zinn-Haller circle; blood flow; optic nerve head; myopia     

视神经鞘减压术有关动脉的应用解剖

目的为视神经鞘减压术提供有关动脉解剖学资料。方法采用显微解剖和血管铸型技术对30个甲醛固定成人尸头和4个新鲜尸头视神经的鞘动脉等进行观察。结果鞘动脉可分为视神经管内支和眶内支。眶内支主要来自眼动脉第2段，占63．33％，也可发自眼肌动脉干等，其入鞘点多在眶内部鞘的后1／3段的上面或内侧面。管内支多从眼动脉的内侧壁发起，行于视神经腹侧面，以1支者多见，占61.67％，2支者占11.67％，3支者占5.00％。结论管内视神经鞘切开部位在鞘的外上壁或内上壁较安全，眶内鞘切开部位选在鞘的外侧面较好。     

2',3'-cyclic nucleotide 3'-phosphohydrolase activity in rat visual pathways with experimental allergic encephalomyelitis

The enzyme 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) is one of the important markers for myelin synthesis or demyelination. We measured the CNPase activities in the visual pathway tissues of Lewis strain rats with experimental allergic encephalomyelitis (EAE) induced by inoculation of myelin basic protein from the brain. The enzyme activities in the retina, optic nerve, optic chiasma and lateral geniculate body were reduced to about 50-80% of that of controls at 15 days after myelin basic protein inoculation when symptoms of EAE were most severe. However, the activities recovered at 19 days except in the retina when the symptoms of EAE disappeared. Furthermore, the activities of the optic nerve and chiasma increased to a level higher than that of the controls at this time. By histopathological study, infiltration of inflammatory cells and focal demyelination were found in the optic nerve and lumbar spinal cord at 15 days after myelin basic protein inoculation. It was considered that the reduction of CNPase activity and its recovery and increase reflect demyelination and activation of oligodendroglia for remyelination, respectively.     

Homonymous hemianopsia in brain tumors

Homonymous hemianopsia may be caused by tumors in the region of the optic tract, the lateral geniculate body, the optic radiation, and the visual cortex. Tumors are responsible for about two-thirds of the temporal lesions and about one-half to one-third of the parietal and occipital lesions. With brain tumors a chronological sequence of two groups of signs and symptoms is the rule: first the focal symptoms corresponding to the tumor lesion in a defined cerebral area, later the distant effects of the increasing volume of the tumor, which lead to the general signs of increased intracranial pressure. The different types of homonymous hemianopia in tumor lesions along the suprachiasmatic pathway (optic tract, lateral geniculate body, temporal lobe, parietal lobe, occipital lobe) are described and discussed. The general neurological signs and symptoms are briefly reviewed. Demonstration of important cerebral diagnostic examination methods (plain X-ray, electroencephalogram, computer tomogram, nuclear magnetic resonance, angiography). Differential diagnosis of brain tumors (hematomas, abscesses, granulomas, parasites etc.).     

Acrylamide effects on the macaque visual system. II. Retinogeniculate morphology

Oral acrylamide dosing for 6-10 weeks produced axonal swellings with neurofilament accumulation in the distal optic tract and lateral geniculate nucleus of macaques. No swellings were seen in the retina or optic nerve. Monkeys that were killed 6-8 months after similar dosing showed a marked neuronal degeneration in the visual pathways that was more pronounced after two than after a single period of exposure. This degeneration was characterized by the following: loss of ganglion cells in central retina with relative sparing of other retinal neurons; disproportionate degeneration of temporal to central optic nerve and the dorsal optic tract; and neuronal atrophy in parvocellular layers of the lateral geniculate nucleus, with relative sparing of magnocellular layers. The pattern of neuronal loss suggests that one type of retinal ganglion cell or its axon may be especially vulnerable to damage by acrylamide. The selective neuronal damage produced by acrylamide may help explain the nature of the visual dysfunction associated with this intoxication.     

Mn^2＋在活体眼增强磁共振视路示踪成像的量效和时效关系研究

背景近年来基于Mn^2＋作为神经示踪剂的功能磁共振成像（MRI）技术使得活体示踪视神经成为可能,但其应用的最佳浓度及示踪视神经的动态过程的研究报道较少。目的探讨不同浓度Mn^2＋在活体兔眼增强磁共振视神经示踪成像的量效和时效关系。方法48只青紫兰兔经左侧眼球上方距角巩膜缘1～1．5mm处玻璃体腔内分别注入不同浓度的MnCI2溶液（0．5、1、2、5、10、15、20、40mmol／L）25μl,右眼不进行任何注射作为对照。分别于注射后4、6、8、12、24、48、96、168h用1．5T超导MRI对兔头颅进行扫描,观察兔眼玻璃体腔注射后视神经、视交叉、对侧视束、外侧膝状体和上丘视觉传导通路的MRI显像情况,计算出上述部位的信噪比（SNR）,分析Mn^2＋作为MRI视路示踪剂的最佳有效浓度和最佳显像时间。结果左眼玻璃体腔内注射0．5～1mmol／LMnCl2溶液后24h可见视神经显影较右眼视神经略增强,但双侧SNR值比较差异无统计学意义（t=1．17、t=0．95,P〉0．05）。左眼玻璃体腔内注射2mmol／L的MnCl,24h后,左侧视神经的SNR值明显高于右侧,差异有统计学意义（t=8．43,P〈0．05）,但左侧外侧膝状体和上丘无明显强化显影,与右侧相比差异无统计学意义（t=0．04、t=0．22,P〉0．05）。左眼玻璃体腔注射10～40mmol／LMnCl,24hMRI视神经信号最强,此后随时间延长MRI信号逐渐减弱,168h后消失。视神经MRI图像的SNR值与玻璃体腔注入Mn“浓度呈正相关,（1,=66．234＋24．269lnx,F=374．15,P=0．000,R^2=0．984）。Mn^2＋在视觉通路的转输速度为（3．32＋0．19）mm／h。结论兔玻璃体腔注射25μl5—40mmol／L的MnCl,溶液24h,MRI能够清晰地显示整个视觉传导通路的信号增强,视路信号增强的程度呈MnCl,剂量依赖性并随着时间的延长呈现先增强后衰减的动态变化过程。     

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.