Pilon Andrew, Newman Tricia, Messner Leonard V
Illinois Eye Institute, Chicago, Illinois, USA.
Optom Vis Sci. 2006 Jul;83(7):415-20. doi: 10.1097/01.opx.0000218430.40132.68.
Diffuse optic nerve excavation and focal rim loss mimicking an optic pit have never been reported to predispose patients to serous detachments despite their relative frequency among patients with glaucoma. Recent reports of idiopathic macular schisis detachments occurring in the setting of elevated intraocular pressure without evidence of a contributing comorbidity have caused some to speculate that alternative mechanisms exist with the capacity to engender these retinal complications. Experimental simian research has unveiled the capacity of chronically elevated intraocular pressure to yield conduction portals between the posterior hyaloid face and the subretinal space by inducing microscopic fractures in the inner-limiting membrane. To our knowledge, this is the first case report providing objective evidence of an idiopathic neurosensory detachment resulting from a fractured inner-limiting membrane arising in the setting of chronically elevated intraocular pressures.
A 34-year old black man presented with transient eye pain and fluctuating vision in his left eye with his current spectacle prescription. A 2-year history of right eye blindness from glaucoma was uncovered. Funduscopic evaluation revealed a broad neurosensory detachment in the setting of an excavated optic nerve in the patient's right eye. Optical coherence tomography confirmed the hydrodynamic separation of the sensory retina from the retinal pigmented epithelium and permitted visualization of a fractured inner-limiting membrane with a contiguous communication between the posterior hyaloid face and the subretinal space at the nasal limit of the detachment. Fluorescein angiography studies identified the absence of chorioretinal vascular compromise contributing to the minimal expansion of the dye into serous cavity late into the study. No optic pit was discernible using optical coherence tomography imaging or fluorescein angiography.
Although glaucomatous damage of the optic nerve has rarely been shown to predispose an individual to serous complications within the macula, recent reports attest to its pathogenic capacity and propose a theory to explain their infrequent clinical coexistence. This case provides additional support for the mounting evidence to support the role of a compromised inner-limiting membrane in inducing a macular detachment in the setting of chronically elevated intraocular pressure without evidence of preexisting optic pits.
弥漫性视神经凹陷和类似视盘小凹的局灶性边缘缺失,尽管在青光眼患者中相对常见,但从未有报道称其会使患者易患浆液性视网膜脱离。最近有报道称,在眼压升高且无相关合并症证据的情况下发生特发性黄斑劈裂性视网膜脱离,这使得一些人推测存在能够引发这些视网膜并发症的其他机制。实验性猕猴研究揭示了长期眼压升高通过在内界膜诱导微小骨折,从而在玻璃体后表面和视网膜下间隙之间产生传导通道的能力。据我们所知,这是第一例报告,提供了客观证据,证明在长期眼压升高的情况下,因内界膜骨折导致特发性神经感觉性视网膜脱离。
一名34岁黑人男性,因目前佩戴眼镜视力矫正,出现左眼短暂眼痛和视力波动。发现有右眼因青光眼失明2年的病史。眼底检查显示患者右眼视神经凹陷,伴有广泛的神经感觉性视网膜脱离。光学相干断层扫描证实感觉视网膜与视网膜色素上皮之间存在流体动力学分离,并显示在脱离的鼻侧边界处有内界膜骨折,玻璃体后表面与视网膜下间隙之间有连续的通道。荧光素血管造影研究表明,脉络膜视网膜血管无损害,在研究后期染料极少渗入浆液腔。使用光学相干断层扫描成像或荧光素血管造影均未发现视盘小凹。
尽管很少有证据表明青光眼性视神经损害会使个体易患黄斑部浆液性并发症,但最近的报道证实了其致病能力,并提出了一种理论来解释它们在临床上罕见共存的原因。该病例为越来越多的证据提供了额外支持,这些证据支持在长期眼压升高且无既往视盘小凹证据的情况下,受损的内界膜在诱发黄斑脱离中的作用。