Retinal Anatomy



Retina and Areas
 Optic

nerve  Macula  Central/peripheral retina  Retinal Vasculature  Choroidal Vessels

Normal Retina
 The

retina is approximately 0.5 mm thick and lines the back of the eye.

Normal Retina .

Normal Retina .

Normal Retina .

Normal Retina .

Normal Retina .

Normal retina .

Optic Nerve and Vessels  Circular to oval white area  Measures about 2 x 1.  Major blood vessels of the retina radiate from the center of the nerve .5 mm across.

or optic nerve head. .  Visible part of the optic nerve is the optic disc.Optic Nerve  Transmits visual impulses from the retina to the brain.

Optic Nerve  ON goes through the lamina cribrosa. the depression in the disc. sieve-like structure  Lamina cribrosa forms the base of the physiologic cup. . a fibrous.

Cup/Disc .

3 or less  .1 to 0.9  Normal 0.  Scale from 0.C/D ratio Rim of ON is compared in size with the cup to get C/D ratio.

Optic Nerve  Peri = around  Papillary = ON  Peripapillary = area of the retina around ON.  papilledema .

Optic Nerve disease  Optic disc drusen  Glaucoma .

Optic Nerve Disease  Optic disc pit  Optic nerve hypoplasia .

Optic Nerve Disease  Optic atrophy  Leber’s optic neuropathy .

Fovea is center of the macula .Macular Area     “Straight ahead” vision Best visual acuity Cones form a concentrated area known as the fovea.

 slightly ovalshaped  blood vesselfree reddish spot .Fovea  Located 2 1/2 disc diameters to the left of the disc.

Macula  The center of the fovea is known as the foveal pit .

parafovea and perifovea is considered the MACULA area  A yellow pigmentation to the macular area is known as the macula lutea. .Macula  The     whole foveal area foveal pit. foveal slope.

Macula lutea  Yellow pigmentation  Acts as a short wavelength filter.  (Lens also a filter)  Protective mechanism for avoiding bright light and especially UV irradiation damage .

Macular Disease



Macular Disease

Best’s juvenile, adult

Macular Disease



Macular Disease


Macular hole

Central and Peripheral Retina  Central retina = circular field 6 mm around fovea  Peripheral retina stretches to the ora serrata. . 21 mm from the center of the optic disc.

 Retina attaches to the choroid at ora serrata. .Ora Serrata  Anterior termination of the retina  Junction of the retina and the ciliary body.

Peripheral Retinal Disease  Retinitis Pigmentosa  Sickle Cell Retinopathy .

Peripheral Retinal Disease  Lattice Degeneration  Retinal tear .

2 sources of retinal blood supply  CHOROIDAL BLOOD VESSELS  65-85% of blood flow  Nourishes outer retina (photoreceptors = rods and cones) .

2 sources of retinal blood supply  CENTRAL RETINAL ARTERY  20-30% blood flow  Nourishes inner retinal layers  Has 4 main branches .

Retinal vessels  Arteries cross over veins  Arteriole narrowing in hypertension .

Arteriole Disease  CRAO  BRAO .

Vein Disease  CRVO  BRVO .

Choroid  Layer in-between the retina and the sclera  Mainly composed of blood vessels  Function is to supply nourishment to the outer portion of the retina .

Choroidal Disease  Choroidal neovasc  Chorioderemia .

Anatomy by Area  Optic nerve  Macula  Central/peripheral retina  Retinal Vasculature  Choroidal Vessels .

Anatomy by Layers .

Bruch’s Membrane    Separates the retina and choroid Permeable membrane Water-soluble nutrients diffuse from the choroid to the RPE and retina .

nutrients such as vitamin A.Bruch’s membrane If Bruch’s membrane compromised. might not be able to reach rods and cones.  Drusen deposits of extracellular material  Provide space for SRNV by lifting up the RPE  .

.Subretinal neovascularization  SRNV  SRNV  abnormal vessels develop and penetrate Bruch’s membrane after it is first damaged by something else.

Subretinal neovascularization  SRNV  SRNV  AMD correlates with a thickening of the membrane with extra-cellular material .

Retinal Pigment Epithelium .

.Retinal Pigment Epithelium    Next layer near the choroid. furthest away from the vitreous Cells have varying amounts of melanin pigment Gives a granular appearance to the fundus.

Retinal Pigment Epithelium  RPE  layer of dark tissue  absorbs excess light so that the photoreceptors can give a clearer signal (reduces scattering) .

cones are "trimmed" at dusk.  Bruch's membrane separates the choroid from the RPE. .Retinal Pigment Epithelium  Plays a role in "trimming" photoreceptors -. and rods are "trimmed" at dawn  Move nutrients to (and waste from) the photoreceptors to the choroid.

Diseases of RPE  Central serous  Central serous .

Central Serous .

Sensory Retina: Rods and Cones RPE .

 The cones are located in the central visual area (macula) and are responsible for color vision .Rods and Cones  The rods and cones are right above the RPE  Photoreceptors: specialized nerve endings convert light into electrochemical signals.

Rods and Cones  Rods designed to operate under dim light  Not directionally selective like the cones.  Cones ignore blurred off-axis light  Only use sharp high-contrast images produced by axial light .

Retinitis Pigmentosa  Degeneration of rods  Loss of peripheral vision .

External Limiting Membrane .

Outer Nuclear Layer  The outer nuclear layer contains cell bodies of the rods and cones .

 and bipolar cell dendrites .Outer Plexiform Layer  The outer plexiform layer (OPL)  Connections between rod and cones.

Inner Nuclear Layer  Contains:  Nuclei of bipolar cells  MÜller cells (synthesize and store glycogen)  Amacrine cell bodies (act as condensers. as in an electric circuit) .

to connect to ganglion cells.Inner Plexiform Layer  Relay station for the bipolar cells.  Amacrine cells also interact in networks to influence and integrate ganglion cell signals .

Ganglion Cell Layer  Ganglion cell axons are fibers that carry electrical signal to the optic nerve .

Nerve Fiber Layer  Located above the ganglion cell layer  Fibers radial to the optic nerve  Distribution plays role in VF defect patterns  Major blood vessels embedded in this layer .

Nerve Fiber Pattern .

Blood vessels in NFL  Flame hemorrhage  located in NFL .

 Forms a diffusion barrier between neural retina and vitreous humor.Internal Limiting Membrane  Layer right next to the vitreous. .

Internal Limiting Membrane  Wrinkling of the ILM can cause distorted central VA .

 Time-sensitive delicate and difficult operation .ILM  Standard surgery for  Membrane Peel macular pucker or macular hole repair  Peeling away the ILM with microsurgical forceps.

ILM  New technique  Removes the abnormal macular tissue and wrinkled ILM  Fluid pressure lifts ILM and separates tissue  Also smoothes underlying distorted retinal layer  Fluidic Internal Limiting Membrane Separation .

Recap of 10 layers  Bruch’s membrane is between the RPE and choroid  RPE responsible for absorbing excess light so that the photoreceptors can give a clearer signal  Rods and cones convert light into electrical signals .

.Recap of 10 layers  Nuclear layers and plexiform layers internal circuits in the retina: transmit info to other neurons  Gangion cell layer final retinal station  Nerve fiber layer ganglion axons form the optic nerve  Internal limiting membrane diffusion barrier between neural retina and vitreous humor.

Neovascularization  neovasc  New blood vessels .

Blood in front of retina .

. patient with homozygous sickle cell disease and angioid streaks demonstrated heavy calcification and breaks in Bruch's membrane. These studies suggest that calcification rather than iron deposition is the major factor leading to brittleness of Bruch's membrane in patients with hemolytic anemia and angioid streaks. We were unable to demonstrate iron deposition by histochemical techniques or transmission electron microscopy.

PXE. Elastic tissue in the body becomes mineralized. cardiovascular system and gastrointestinal system. that is. is an inherited disorder that affects selected connective tissue in some parts of the body. . calcium and other minerals are deposited in the tissue. This can result in changes in the skin. eyes. Pseudoxanthoma elasticum.

it is an "idiopathic disorder" which means that the precise cause is unknown. The retinal pigment epithelium is a singlecelled layer that lies between the retina and the choroid . Central serous chorioretinopathy is a retinal disorder which affects the macula. Central serous is associated with an elevation (detachment) of the macula due to leakage of fluid from the circulation behind it (choroidal circulation). The leakage occurs through a defect in the tissue layer known as the retinal pigment epithelium. Essentially. It was first described in ophthalmology more than one hundred years ago.

When energy is absorbed by the chromophore (in the form of a photon) it "unbends" the molecule. Photopigment is a complex of two molecules: opsin and the chromophore. vitamin A.e. the all-trans isomer is converted back into the 11-cis form so that vision is possible again .  Photopigment contained in the disk membranes of the outer segment absorbs photons and undergoes a biochemical change.. Opsin is a protein. the chromophore is the part affected by light -. This process is called photo-isomerization. Ultimately.. which is why your mom encouraged you to eat carrots).e. adn converts it to an all-trans configuration. i. When retinal is bound to opsin it is in the so-called 11-cis configuration (i.called retinal (a derivative of retinol. the molecule is "bent").

Closing Na+ channels hyperpolarizes the neuron. the receptor potential is still large at the axon terminal in the inner segment. breaks cGMP into its inactive form. Thus. Some amacrine cells and all ganglion cells use action potentials . Since receptors are so small. most retinal neurons transmit information using only graded potentials. the result of transducing light energy is photoreceptor hyperpolarization. The exact chain of events is: isomerization of photopignemt breaks apart a molecule called transducin. in turn. Light stimulation thus causes less transmitter to be released at the synapse! The hyperpolarization of the outer segment spreads to the inner segment by electrotonic conduction. Phosphodisterase. which activates an enzyme called phosphodiesterase. Interestingly.  The isomerization of 11-cis retinal to all-trans begins the process of phototransduction. which causes Na+ channels (which are open in the resting state) to close. in contrast to other neurons.

which cause stargardt disease. The ABCR gene produces a protein involved in energy transport to and from photoreceptor cells in the retina.Stargardt  In 1997. As a result. photoreceptor cells degenerate and vision loss occurs . Foundation researchers isolated the gene for stargardt disease. produce a dysfunctional protein that cannot perform its transport function. Mutations in the ABCR gene.

sometimes accompanied by material leaking into a space by the retina can be observed. Stage 3: When part of the lesion becomes absorbed. an observation called "egg-yolk" lesion. Stage 4: At this stage.Best’s disease      Stage 1: Initially a recording of eye movements and eye position identifies abnormal electrical potential. Typical yellow spots. Stage 2: Usually occurs between 10-25 years of age. sight will probably be affected. this is identified as stage three. Stage 5: The fifth and final stage is when the condition causes the most severe sight loss. Eyes will be tested resting or moving in dark and light conditions. Even at this stage there may be little effect on vision. . when the "egg-yolk" breaks up in a process referred to as "scrambled-egg".

Dividing these nerve cell layers are two neuropils where synaptic contacts occur . The outer nuclear layer contains cell bodies of the rods and cones. the inner nuclear layer contains cell bodies of the bipolar. horizontal and amacrine cells and the ganglion cell layer contains cell bodies of ganglion cells and displaced amacrine cells.Nerves and Synapses  All vertebrate retinas are composed of three layers of nerve cell bodies and two layers of synapses.

Characteristic irregular streaks. Both appear before vision loss is noticed. called angioid streaks. Small blood vessels beneath this layer take advantage of these breaks in the membrane and grow through the membrane. Neither peau d'orange nor angioid streaks affect the vision. While people with PXE may lose so much vision that they become legally blind. called angioid streaks. The first changes. This is called neovascularization. Mineralization of the highly elastic membrane behind the retina (Bruch's membrane) can lead to cracking. visible only during an ophthalmologic examination. are called "peau d'orange" because the retina looks like the skin of an orange. almost all people with PXE continue to have peripheral vision. This bleeding results in the loss of central vision. Sometimes these blood vessels leak and bleed. may develop later.PXE  PXE affects the retina of the eye. .

Photoreceptors The rod and cone outer segment membranes are constantly being replenished (like fingernails.  This is why the pigment epithelium must trim off the excess. a process known as  . they just keep growing).

if you've got lots of light to begin with: true for cones.Stiles-Crawford Effect    Cones are more sensitive (by a factor of 10) to light which enters the eye from the center of the pupil (axial light) than they are to light entering from the margins of the pupil (off-axis light). .e. Light which enters through the center of the pupil forms sharper images than light which enters from the sides of the pupil This evolutionary strategy of "ignoring" (by being less sensitive) the blurred image produced by off-axis light in favor of the sharp high-contrast images produced by axial light works. daytime). since they operate best under high luminance conditions (i..

endoplasmic reticulum. and the axon terminal (where neurotransmitter is released).  Inner Segment: Photoreceptor inner segments contain the nucleus. Stiles-Crawford Effect: For light to reach the outer segment (and be absorbed by a photopigment molecule) it must first pass through the inner segment. The capture of individual photons by the photopigment molecules in the disk membranes is what initiates neural signalling. Cone inner segments are actually exquisitely engineered waveguides (i. ribosomes. synaptic vesicles. Photoreceptors are actually specialized hair cells. support organelles (mitochondria. fiber optic structures) which capture light and funnel it into the outer segment. etc). ..e. Because these inner segment waveguides capture light shining straight on them better than light from shallower angles. published in 1933. we can measure what is called the Stiles-Crawford effect. and the inner and outer segments are connected by the cilium.

. to connect to ganglion cells. the bipolar cells.  It is at the culmination of all this neural processing in the inner plexiform layer that the message concerning the visual image is transmitted to the brain along the optic nerve.  In addition. different varieties of horizontallyand vertically-directed amacrine cells.Inner Plexiform Layer  Functions as a relay station for the verticalinformation-carrying nerve cells. somehow interact in further networks to influence and integrate the ganglion cell signals.

 Choriodal neovasc  Choriodal neovasc .

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