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Comparative Anatomy and Physiology of the Mammalian Eye
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
Embryologically, the retina is neuroectodermal in origin and forms first as an optic vesicle and later invaginates to form the optic cup. The posterior wall of the optic cup gives rise to the RPE, while the anterior wall gives rise to the remaining nine layers of the retina. The space between these layers that was present embryologically remains as a potential space and it is here, between the RPE and the sensory retina, that retinal detachments usually occur. In humans, the retina is mature at birth but, in many laboratory animals, the development of the retina continues postnatally. In the dog and cat, the retina is not mature until approximately 3 to 5 weeks centrally and 8 to 9 weeks peripherally.127,128 Once formed, the retina undergoes maturation from central to peripheral and, in most laboratory animals, this process is not complete until several days to weeks postpartum.
Ophthalmology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
A very rare developmental anomaly where the eye appears to be absent. Primary anophthalmos due to failure of the outgrowth of the optic vesicle, unassociated with an abnormality of the neural tube, is the most common type. This must occur during the first 2 weeks of development and is usually bilateral (but asymmetric), sporadic, and, in most cases, the child is otherwise well-formed.
Write short notes on the prenatal development of the lens. Use annotated diagrams where possible
Published in Nathaniel Knox Cartwright, Petros Carvounis, Short Answer Questions for the MRCOphth Part 1, 2018
Nathaniel Knox Cartwright, Petros Carvounis
The lens pit appears in the lens placode and deepens by a process of differential cellular elongation and multiplication (day 29). This causes the lens placode and the adjacent cells of the optic vesicle to buckle inward, transforming the latter into a two-layered optic cup.
Imaging-based Assessment of Choriocapillaris: A Comprehensive Review
Published in Seminars in Ophthalmology, 2023
Rohan Bir Singh, Tatiana Perepelkina, Ilaria Testi, Benjamin K. Young, Tuba Mirza, Alessandro Invernizzi, Jyotirmay Biswas, Aniruddha Agarwal
The development of human eye begins towards the end of the fourth week of gestation when the neural tube folds to form the two optic vesicles at the cranial end, which invaginates into optic cups.13 The mesenchymal layer surrounding the optic cups differentiates into internal and external layers, which further differentiate into choroid and sclera, respectively. The choroidal cells, such as the melanocytes, are derived from the neural crest cells, whereas mesoderm gives rise to the endothelial cells of the choroidal blood vessels. The choriocapillaris begins to differentiate during the fourth and fifth weeks. The increasing fenestrations, luminal enlargement, and basement membrane of the capillaries appear by the ninth week of gestation. The deposition of collagen between the basement membrane of the RPE and the capillaries appears in the subsequent 3 weeks.
Outcomes of the use of orbital hydrogel expanders in the management of congenital anophthalmia: CT-based orbital parameter analysis
Published in Orbit, 2022
Reem R. Alanazi, Silvana A. Schellini, Hailah Alhussain, Sahar Elkhamary, Rajiv Khandekar, Osama AlSheikh
Growth of the globe is essential for stimulating proper orbital and eyelid development before and after birth. However, in congenital anophthalmia, the optic vesicle fails to develop, resulting in micro-orbitism, congenital fornix atresia, constricted socket, phimotic lids, and reduced palpebral fissure.1 The absence of the eye in the orbit results in both orbital growth deficiency and ipsilateral reduction of the facial skeleton. Therefore, the presence of unilateral congenital anophthalmia coincides with orbital and facial asymmetry at birth, which increases further during orbital development. Consequently, the orbital volume, orbitomaxillary, zygomatic, and maxillary dimensions are smaller compared to the other side, resulting in a hemifacial microsomia and skeletal dysgnathia or, in the case of bilateral anophthalmia, to a complete facial microsomia.2,3 Hence, the treatment of congenital anophthalmia involves simultaneous expansion of the lids, soft tissues of the socket and orbital bones as soon as possible because early intervention can result in better outcomes.4
Aplasia of the Optic Nerve: A Report of Seven Cases
Published in Neuro-Ophthalmology, 2020
Yujia Zhou, Maura E. Ryan, Marilyn B. Mets, Hawke H. Yoon, Bahram Rahmani, Sudhi P. Kurup
Optic nerve aplasia (ONA) is a rare congenital condition characterised by the absence of optic nerve and disc, central retinal vessels, and retinal ganglion cells.1,2 There is no unified aetiology to the mechanisms of ONA. Proper proliferation and apoptosis of retinal ganglion cells (RGC) are important for the development of the optic nerve.3,4 ONA can be a result of primary agenesis or secondary degeneration of RGC during the third to fourth month of gestation due to failure of retinal angiogenesis.1,5 The optic vesicle starts to invaginate at the early stage of eye development and an optic fissure is formed to allow the hyaloid arteries to enter the retina. Failure of this process disrupts retinal vasculature, which is consistent with retinal abnormalities in ONA.3 It is suggested that the failure of neural retina formation may be responsible for disruption of optic nerve development and disorganisation of other ocular tissues in ONA.6 Pax-6 is expressed in the CNS, optic stalk, retinal progenitors, and RGC, and its mutations are likely disruptive to the optic nerve and other ocular structures.7