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Mouth and throat, face, and the five senses
Published in Frank J. Dye, Human Life Before Birth, 2019
Early in development, even before the anterior neuropore (the opening at the cephalic end of the neural tube) has closed, a pair of lateral outpocketings arise from the walls of the forebrain (the portion destined to become the diencephalon). These optic vesicles grow out toward the overlying ectoderm on the sides of the developing head. As they do this, the portion of each closest to the wall of the brain constricts to form a relatively narrow optic stalk. Each optic vesicle develops a ventro-lateral inpocketing, which converts it into a two-layered optic cup with a break in its wall (called the choroid fissure). This fissure is carried back along the optic stalk to provide a pathway for the growth of the optic nerve toward the brain (Figure 17.7). The optic cups give rise to the retinas. The inner layer of the cup—the nervous layer—develops photoreceptor cells (called rods and cones), which receive light energy and change it into nerve impulses. The outer layer of the cup—the pigmented layer—becomes increasingly pigmented as development proceeds, so as to absorb light not intercepted by the nervous layer.
Head and Neck
Published in Rui Diogo, Drew M. Noden, Christopher M. Smith, Julia Molnar, Julia C. Boughner, Claudia Barrocas, Joana Bruno, Understanding Human Anatomy and Pathology, 2018
Rui Diogo, Drew M. Noden, Christopher M. Smith, Julia Molnar, Julia C. Boughner, Claudia Barrocas, Joana Bruno
The bilayered retina is an outgrowth of the brain and ganglion cells located in this tissue send axons beneath the optic stalk and into the brain as the optic nerve (CN II) (Plate 3.14; see also Section 3.5.7). The glial cells that support the olfactory and optic nerves are of the type that surrounds CNS structures and therefore are not damaged by demyelinating diseases that target Schwann cells (e.g., multiple sclerosis).
Growth of the Orbit
Published in D. Dixon Andrew, A.N. Hoyte David, Ronning Olli, Fundamentals of Craniofacial Growth, 2017
In relation to the developing eye, neural crest cells from the diencephalic region of the forebrain migrate rostrally, dorsal to the expanding eye vesicle, then stream caudally around the optic stalk. Prosencephalic crest cells invade the frontonasal process and form the bulk of the mesenchyme of the maxillary process (Le Lievre, 1978; Newgreen and Erickson, 1986), which also receives crest cells migrating from the mesencephalic area (Noden, 1973). The various processes which make up the embryonic face in the human are described by (among others) Duke-Elder and Cook (1963). The developing optic vesicles are widely separated by the median frontonasal process, and between the 6 and 12 mm stage come each to be flanked above and in front by the lateral nasal process (separated now from the median nasal process of the frontonasal by the olfactory pit), and below by the maxillary process. As maxillary and lateral nasal processes meet and fuse, deep to the line of fusion lies a solid rod of cells, the anlage of the nasolacrimal duct. By 16 mm, the maxillary processes have extended to meet in the anterior midline, forming a continuous shelf underlying the eye. “The swinging forwards of the axes of the orbits with a consequent swing of the visual axes is essentially due to the forward extension of the maxillary processes” (Duke-Elder, loc. cit). The eyefields migrate from a lateral head position at 7 weeks to a frontal position at 8-9 weeks (Burdi et al, 1988). At 9 weeks or 40 mm crown-rump length “eyefield migration subsides ... [and] the angle between the left and right optic axes stabilizes at their 71- to 68-degree postnatal values” (Figure 10.1). The bony orbit is formed from the mesenchyme surrounding the developing eye, derived from neural crest, as outlined above, invading the frontonasal and maxillary processes — frontal bone (both mesodermal and ectomesenchyme), maxilla, ethmoid, zygoma, nasal, and lacrimal. The precise contributions of mesenchyme to the sphenoid bone and its wings seem less certain.
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
A de novo mutation in PITX2 underlies a unique form of Axenfeld-Rieger syndrome with corneal neovascularization and extensive proliferative vitreoretinopathy
Published in Ophthalmic Genetics, 2020
Stephanie N. Kletke, Ajoy Vincent, Jason T. Maynes, Uri Elbaz, Kamiar Mireskandari, Wai-Ching Lam, Asim Ali
The role of PITX2 in retinal development is not fully elucidated and the association of ARS with bilateral progressive proliferative vitreoretinopathy has not been reported. Pitx2 knockout zebrafish have disorganized, irregular branching and patterning of the hyaloid vessels and small retinas (26). A case of persistent hyperplastic primary vitreous (PHPV) has also been reported in a patient with Peters anomaly caused by a c.649 C > A mutation in PITX2 (27). There is evidence that PITX2 drives the differentiation of the periocular mesenchyme (POM), a specific neural crest cell population that plays a role in optic stalk differentiation, embryonic fissure closure and vascular angiogenesis (28). Pitx2 expression has been demonstrated in the mouse POM at embryonic stage E10.5 and in the mesenchyme around the retina and cornea at E15.5 (29). PITX2 also regulates neural crest-derived pericytes, which stabilize ocular blood vessels during development (30). PITX2 downstream effectors may similarly play a role in normal retinal angiogenesis; however, the mechanism by which this leads to proliferative vitreoretinopathy is unclear. It is notable that proliferative vitreoretinopathy was observed in the left eye at 1 year prior to any posterior segment surgery. In comparison, it may be argued that retinal surgical procedures in the right eye contributed to the progression of the vitreoretinopathy to some extent.