Besides cystoid macular edema due to a blood-retinal barrier breakdown, another type of macular cystoid spaces referred to as non-vasogenic cystoid maculopathies (NVCM) may be detected on optical coherence tomography but not on fluorescein angiography. Various causes may disrupt retinal cell cohesion or impair retinal pigment epithelium (RPE) and Müller cell functions in the maintenance of retinal dehydration, resulting in cystoid spaces formation. Tractional causes include vitreomacular traction, epiretinal membranes and myopic foveoschisis. Surgical treatment does not always allow cystoid space resorption. In inherited retinal dystrophies, cystoid spaces may be part of the disease as in X-linked retinoschisis or enhanced S-cone syndrome, or occur occasionally as in bestrophinopathies, retinitis pigmentosa and allied diseases, congenital microphthalmia, choroideremia, gyrate atrophy and Bietti crystalline dystrophy. In macular telangiectasia type 2, cystoid spaces and cavitations do not depend on the fluid leakage from telangiectasia. Various causes affecting RPE function may result in NVCM such as chronic central serous chorioretinopathy and paraneoplastic syndromes. Non-exudative age macular degeneration may also be complicated by intraretinal cystoid spaces in the absence of fluorescein leakage. In these diseases, cystoid spaces occur in a context of retinal cell loss. Various causes of optic atrophy, including open-angle glaucoma, result in microcystoid spaces in the inner nuclear layer due to a retrograde transsynaptic degeneration. Lastly, drug toxicity may also induce cystoid maculopathy. Identifying NVCM on multimodal imaging, including fluorescein angiography if needed, allows guiding the diagnosis of the causative disease and choosing adequate treatment when available.

除了由血视网膜屏障破坏引起的黄斑囊样水肿外，另一种称为非血管源性黄斑囊样病变 (NVCM) 的黄斑囊样间隙可以通过光学相干断层扫描检测到，但不能通过荧光素血管造影检测到。各种原因可能破坏视网膜细胞凝聚力或损害视网膜色素上皮细胞 (RPE) 和 Müller 细胞维持视网膜脱水的功能，从而导致囊样间隙形成。牵引原因包括玻璃体黄斑牵引、视网膜前膜和近视性中央凹劈裂。手术治疗并不总是允许囊样空间吸收。在遗传性视网膜营养不良中，囊样间隙可能是疾病的一部分，如 X 连锁视网膜劈裂症或增强型 S 锥综合征，或偶尔发生，如 bestrophinopathies、视网膜色素变性和相关疾病，先天性小眼畸形、无脉络膜血症、回旋萎缩和 Bietti 结晶营养不良。在 2 型黄斑毛细血管扩张症中，囊样间隙和空洞不依赖于毛细血管扩张症的液体渗漏。影响 RPE 功能的各种原因可能导致 NVCM，例如慢性中心性浆液性脉络膜视网膜病变和副肿瘤综合征。在没有荧光素渗漏的情况下，非渗出性老年性黄斑变性也可能因视网膜内囊样间隙而复杂化。在这些疾病中，囊样空间发生在视网膜细胞丢失的情况下。视神经萎缩的各种原因，包括开角型青光眼，由于逆行跨突触变性而导致内核层中出现微囊样空间。最后，药物毒性也可能诱发囊样黄斑病变。在多模态成像上识别 NVCM，