Development of the eye

In the human embryo, the eye starts developing at about 3 weeks of pregnancy. The eye is formed from multiple embryonic tissues interacting with each other in close connection - neural (relating to nervous system) tissue for the retina, which also gives rise to parts of the brain, ectodermal (relating to the outermost cell layer) tissue for the lens and the eyelids which also gives rise to skin; mesodermal (relating to the middle cell layer) tissue for the iris, uvea (middle part of the eye), eye vasculature (the arrangement of blood vessels) and muscles of the eye. Genes such as PAX6 play an important part in controlling development. Neural cells form two spherical balls at the side of the head. These indent to form the optic cups. Specialised cell layers in the optic cups (neural and mesoderm) develop into the retina, choroid and uvea of the eye. The surface ectoderm is pinched off and incorporated in the optic cup to form the lens. At about 7 weeks of development, each optic cup fuses below from the centre going forwards and backwards to form ball shaped structures. The developing eye blood supply (the hyaloid vasculature) disappears just before birth to be replaced by a mature vascular system derived from blood vessels of the head and neck. As growth continues, the eyes move to the centre of the face. The eyelids fuse at the beginning of the second trimester (4th month) and reopen at the beginning of the 6th month (third trimester). Since the eye is formed from multiple tissues, disorders of the eye and brain (optic nerve hypoplasia and absence of optic chiasm), eye and skin (syndermatotic cataracts) are not uncommon.

Further development of the eye takes place during pregnancy with connections established between the eye and the primary visual cortex (the visual area) in the occipital lobe (one of the five lobes) of the brain. Further refinement in visual development takes place when the primary visual cortex forms connections with associated visual areas throughout the brain for detailed analysis of images. Abnormalities of focus (refractive error), alignment (squint) and obstruction to vision (cataract) will prevent normal visual maturation and cause poor vision (amblyopia).

During pregnancy eye growth can be disrupted due to various factors such as excessive intake of alcohol, drugs (foetal alcohol syndrome), infections (e.g. rubella causing cataract; toxocara (a genus of nematode parasites) or toxoplasma (a genus of intracellular parasites) causing inflammation and retinal scars). The newborn eye may show congenital abnormalities because of arrested embryonic development e.g. anophthalmos (absence of an eye), microphthalmos (an unusually small eye), coloboma (a cleft-like defect) & aniridia (almost complete absence of the iris), abnormal development such as congenital cataract and genetic dysfunction such as retinoblastoma (malignant tumour of the retina). In prematurely born infants, there may be persistence of embryonic tissues, which are programmed to disappear before birth such as nasolacrimal duct obstruction (causing tears to run down the affected side), persistent pupillary membrane (a middle cell layer attached to the rim or front of the iris), persistence of hyaloid vasculature (the developing eye blood supply) and primary hyperplastic posterior vitreous –PHPV (where the vitreous is replaced by a thick mass behind the lens). Finally, brain damage due factors such as lack of oxygen at birth can lead to poor vision i.e. cerebral visual impairment (CVIU), the commonest cause of visual impairment in the developed countries.

Visual development in children

All infants are born with an immature visual system. At birth, there is an established structural template from the eye to the brain with basic visual functions. Normal visual experience from very early life is essential for further visual development. Visual development is rapid in the first few months to approximately 18 months of life. There is further development at a slower pace for the next 5-7 years of life. Though each visual function (e.g. contrast, motion, shape recognition, colour & depth perception) has a separate developmental pattern, they are interlinked, with the development of one facilitating the development of the other. Visual development can be disrupted by abnormal visual experience. The severity of visual impairment is dependent on the age at which it occurs and the nature of the disease process. Early detection and appropriate treatment during the critical period of visual development often leads to a partial or complete recovery of disrupted visual development.

Development of visual skills