The Eye
Time period: weeks 3–10
Introduction
The development of the eye begins
around day 22 with bilateral invaginations of the neuroectoderm of the
forebrain (Figure 47.1).
As the neural tube closes these
invaginations become the optic vesicles and remain continuous with the
developing third ventricle (Figure 47.1). Contact of these optic vesicles with
the surface ectoderm induces the formation of the lens placodes (Figures
47.1 and 47.2).
As the optic vesicle invaginates
it forms a double‐walled structure, the optic cup (Figure 47.2). At the
same time the lens placode invaginates and forms the lens vesicle which
lies in the indent of the optic cup and is completely dissociated from the
surface ectoderm. Epithelial cells on the posterior wall of the lens vesicle
lengthen anteriorly and become long fibres that grow forwards. It takes about 2
weeks for these fibres to reach the anterior cell wall of the vesicle. These
are primary lens fibres (Figure 47.3). Secondary lens fibres form from
epithelial cells located at the equator of the lens and are continuously added
throughout life along the scaffold made by the primary fibres from the centre
of the lens. These cells elongate and eventually lose their nuclei to become
mature lens fibres. This occurs in early adulthood.
In the optic cup there is an
outer layer that develops into the pigmented layer of the retina and an inner
layer that becomes the neural layer.
The posterior four‐fifths of the
inner neural layer (Figure 47.4) consists of cells forming the rods and cones
of the photoreceptive layer. Deep to this are the neurons and supporting
cells. Deeper again lies a fibrous layer comprising the axons of these neurons,
with axons leading towards the optic stalk that will develop into the optic
nerve.
The anterior one‐fifth of the
inner layer remains one cell thick. It becomes parts of the iris and ciliary
body (Figure 47.5). Ciliary muscle forms from mesenchyme that covers this
part of the optic cup and is internally connected to the lens by the suspensory
ligament. The complete iris forms from the inner retinal layer, the
pigmented outer layer and a mesenchymal layer sandwiched between them, becoming
the sphincter and dilator muscles.
The optic cup remains attached to
the forebrain via the optic stalk (Figure 47.2). Axons from the
photoreceptor cells and other neurons within the retina run along the inner
wall of the optic stalk.
Within the optic stalk is a
groove, the choroid fissure (Figure 47.6), and within this lie the
hyaloid blood vessels formed from invading mesenchyme. The number of neurons
running through the optic stalk increases and during week 7 the choroid fissure
closes forming a tunnel for the hyaloid artery which becomes the central artery
of the retina (Figure 47.6). Continually increasing numbers of neurons fill the
stalk and the lumen of the optic stalk is obliterated. By week 9 it is the optic
nerve.
Meninges
The choroid and sclera of
the eye are comparable to the pia mater and dura mater of the brain,
respectively. They develop from the loose mesenchyme that surrounds the
posterior part of the developing eye. The choroid is highly vascular and
pigmented whereas the sclera is tougher and more fibrous. The sclera is continuous
with the dura mater that surrounds the optic nerve (Figure 47.6).
Loose mesenchyme surrounding the
anterior part of the developing eye is split by vacuolisation, forming the
anterior chamber. An inner iridopupillary membrane is created that degenerates,
leaving open communication between the two fluid‐filled spaces of the anterior
and posterior chambers (Figure 47.7). The outer portion is continuous with the
sclera and becomes the cornea.
The cornea has three parts: an
epithelia layer from ectoderm, the mesenchyme part mentioned above and another
epithelial layer that lines the anterior chamber. Neural crest cells contribute
to the sclera and the cornea.
Extraocular muscles include the
inferior and superior oblique, medial, lateral, inferior and superior rectus
and levator palpebrae superioris muscles. These muscles may develop from
paraxial mesoderm of somitomeres 1–4 or from mesenchyme near the prechordal
plate (a thickening of endoderm in the embryonic head) and are innervated by CN
III, IV and VI.
Clinical relevance
Neonatal vision is tested in the
24 hours after birth and again at 6 weeks. Many abnormalities of the eye cause
blindness, but not all. Most affect vision to some degree and as newborn
infants’ eyes are not aligned and an intermittent squint can develop, it is
important that these tests are carried out.
Congenital cataracts can
be caused by infection, such as rubella during pregnancy, or by hereditary
factors, but often there is no known cause. Cataracts may be identified from a
squint, difficulty in focusing or from the child holding his or her head at an
odd angle to see, and in a few cases a clouding in the lens of the eye. Congenital
glaucoma is generally inherited and caused by an increase in intraocular
pressure through excess fluid. It presents as watering of the eye with dilated
pupils, irritability, and the cornea may be hazy. Treatments are aimed at
decreasing the pressure through increasing the drainage of fluid from the eye
or decreasing fluid production.
Coloboma is caused by
incomplete closure of the choroid fissure. There are varying degrees, and
usually only a cleft in the iris is left, which tends not to affect vision. The
cleft can affect the eyelid, ciliary body, retina, choroid, lens or even the
optic nerve, which would affect vision and can cause blindness in the most
severe cases. There is currently no treatment.
Albinism affects
pigmentation in the skin, hair, iris and retina,
and is diagnosed from an eye
examination. The lack of pigment in the iris and retina can lead to numerous
eye conditions including macular hypoplasia, optic nerve ystagmus, light
sensitivity and overall poor vision.
