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Retinal Anatomy

Retinal Anatomy

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Published by: Sean Scoggins on Apr 26, 2012
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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 .

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

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.

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

Cup/Disc .

3 or less  .C/D ratio Rim of ON is compared in size with the cup to get C/D ratio.  Scale from 0.1 to 0.9  Normal 0.

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.

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

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. .

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

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.  Drusen deposits of extracellular material  Provide space for SRNV by lifting up the RPE  . might not be able to reach rods and cones.

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) .

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

Diseases of RPE  Central serous  Central serous .

Central Serous .

Sensory Retina: Rods and Cones RPE .

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

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.

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

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 .

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

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

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

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 .

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. patient with homozygous sickle cell disease and angioid streaks demonstrated heavy calcification and breaks in Bruch's membrane. .

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

The retinal pigment epithelium is a singlecelled layer that lies between the retina and the choroid . Essentially. The leakage occurs through a defect in the tissue layer known as the retinal pigment epithelium. 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). It was first described in ophthalmology more than one hundred years ago. it is an "idiopathic disorder" which means that the precise cause is unknown.

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

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

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

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

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

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

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

. since they operate best under high luminance conditions (i. . 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.e. 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). daytime).

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

the bipolar cells. to connect to ganglion cells. different varieties of horizontallyand vertically-directed amacrine cells.Inner Plexiform Layer  Functions as a relay station for the verticalinformation-carrying nerve 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. somehow interact in further networks to influence and integrate the ganglion cell signals.  In addition.

 Choriodal neovasc  Choriodal neovasc .

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