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Anatomy
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
to oval white area Measures about 2 x 1.5 mm across. Major blood vessels of the retina radiate from the center of the nerve
Optic Nerve
Transmits
visual impulses from the retina to the brain. Visible part of the optic nerve is the optic disc, or optic nerve head.
Optic Nerve
ON
goes through the lamina cribrosa, a fibrous, sieve-like structure Lamina cribrosa forms the base of the physiologic cup, the depression in the disc.
Cup/Disc
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 0.3 or less
Optic Nerve
Peri
papilledema
Glaucoma
Optic atrophy
Macular Area
Straight ahead vision Best visual acuity Cones form a concentrated area known as the fovea, Fovea is center of the macula
Fovea
Located
2 1/2 disc diameters to the left of the disc, slightly ovalshaped blood vesselfree reddish spot
Macula
The
Macula
The
foveal pit, foveal slope, parafovea and perifovea is considered the MACULA area
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
AMD
Stargardts
Macular Disease
Macular Disease
Coats
CME
Macular Disease
Drusen
Macular hole
retina = circular field 6 mm around fovea Peripheral retina stretches to the ora serrata, 21 mm from the center of the optic disc.
Ora Serrata
Anterior
termination of the retina Junction of the retina and the ciliary body. Retina attaches to the choroid at ora serrata.
Retinitis Pigmentosa
Lattice Degeneration
Retinal tear
65-85%
of blood
20-30%
Retinal vessels
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
Anatomy by Layers
Bruchs Membrane
Separates the retina and choroid Permeable membrane Water-soluble nutrients diffuse from the choroid to the RPE and retina
Bruchs membrane
If Bruchs membrane compromised, nutrients such as vitamin A, 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 Bruchs membrane after it is first damaged by something else.
Subretinal neovascularization
SRNV
SRNV
AMD
Next layer near the choroid, furthest away from the vitreous Cells have varying amounts of melanin pigment Gives a granular appearance to the fundus.
of dark tissue absorbs excess light so that the photoreceptors can give a clearer signal (reduces scattering)
a role in "trimming" photoreceptors -- cones are "trimmed" at dusk, and rods are "trimmed" at dawn Move nutrients to (and waste from) the photoreceptors to the choroid. Bruch's membrane separates the choroid from the RPE.
Diseases of RPE
Central serous
Central serous
Central Serous
RPE
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
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
outer nuclear layer contains cell bodies of the rods and cones
outer plexiform layer (OPL) Connections between rod and cones, and bipolar cell dendrites
of bipolar cells Mller cells (synthesize and store glycogen) Amacrine cell bodies (act as condensers, as in an electric circuit)
station for the bipolar cells, to connect to ganglion cells. Amacrine cells also interact in networks to influence and integrate ganglion cell signals
Ganglion cell axons are fibers that carry electrical signal to the optic nerve
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
Flame hemorrhage
located in NFL
Layer right next to the vitreous. Forms a diffusion barrier between neural retina and vitreous humor.
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
Recap of 10 layers
Bruchs
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
patient with homozygous sickle cell disease and angioid streaks demonstrated heavy calcification and breaks in Bruch's membrane. We were unable to demonstrate iron deposition by histochemical techniques or transmission electron microscopy. 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.
Pseudoxanthoma
elasticum, PXE, is an inherited disorder that affects selected connective tissue in some parts of the body. Elastic tissue in the body becomes mineralized, that is, calcium and other minerals are deposited in the tissue. This can result in changes in the skin, eyes, cardiovascular system and gastrointestinal system.
Central serous chorioretinopathy is a retinal disorder which affects the macula. It was first described in ophthalmology more than one hundred years ago. Essentially, it is an "idiopathic disorder" which means that the precise cause is unknown. 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. The retinal pigment epithelium is a singlecelled layer that lies between the retina and the choroid
Photopigment contained in the disk membranes of the outer segment absorbs photons and undergoes a biochemical change. Photopigment is a complex of two molecules: opsin and the chromophore. Opsin is a protein; the chromophore is the part affected by light -- called retinal (a derivative of retinol, i.e., vitamin A, which is why your mom encouraged you to eat carrots). When retinal is bound to opsin it is in the so-called 11-cis configuration (i.e., the molecule is "bent"). When energy is absorbed by the chromophore (in the form of a photon) it "unbends" the molecule, adn converts it to an all-trans configuration. This process is called photo-isomerization. Ultimately, the all-trans isomer is converted back into the 11-cis form so that vision is possible again
The isomerization of 11-cis retinal to all-trans begins the process of phototransduction. Interestingly, 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 activates an enzyme called phosphodiesterase. Phosphodisterase, in turn, breaks cGMP into its inactive form, which causes Na+ channels (which are open in the resting state) to close. Closing Na+ channels hyperpolarizes the neuron. 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. Since receptors are so small, the receptor potential is still large at the axon terminal in the inner segment. Thus, most retinal neurons transmit information using only graded potentials. Some amacrine cells and all ganglion cells use action potentials
Stargardt
In
1997, Foundation researchers isolated the gene for stargardt disease. The ABCR gene produces a protein involved in energy transport to and from photoreceptor cells in the retina. Mutations in the ABCR gene, which cause stargardt disease, produce a dysfunctional protein that cannot perform its transport function. As a result, photoreceptor cells degenerate and vision loss occurs
Bests disease
Stage 1: Initially a recording of eye movements and eye position identifies abnormal electrical potential. Eyes will be tested resting or moving in dark and light conditions. Stage 2: Usually occurs between 10-25 years of age. Typical yellow spots, sometimes accompanied by material leaking into a space by the retina can be observed; an observation called "egg-yolk" lesion. Stage 3: When part of the lesion becomes absorbed, this is identified as stage three. Even at this stage there may be little effect on vision. Stage 4: At this stage, when the "egg-yolk" breaks up in a process referred to as "scrambled-egg", sight will probably be affected. Stage 5: The fifth and final stage is when the condition causes the most severe sight loss.
All vertebrate retinas are composed of three layers of nerve cell bodies and two layers of synapses. 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. Dividing these nerve cell layers are two neuropils where synaptic contacts occur
PXE
PXE affects the retina of the eye. The first changes, visible only during an ophthalmologic examination, are called "peau d'orange" because the retina looks like the skin of an orange. Characteristic irregular streaks, called angioid streaks, may develop later. Neither peau d'orange nor angioid streaks affect the vision. Both appear before vision loss is noticed. Mineralization of the highly elastic membrane behind the retina (Bruch's membrane) can lead to cracking, called angioid streaks. Small blood vessels beneath this layer take advantage of these breaks in the membrane and grow through the membrane. This is called neovascularization. Sometimes these blood vessels leak and bleed. This bleeding results in the loss of central vision. While people with PXE may lose so much vision that they become legally blind, almost all people with PXE continue to have peripheral vision.
Photoreceptors
The rod and cone outer segment membranes are constantly being replenished (like fingernails, they just keep growing). This is why the pigment epithelium must trim off the excess, a process known as
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). 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, if you've got lots of light to begin with: true for cones, since they operate best under high luminance conditions (i.e., daytime).
Inner Segment: Photoreceptor inner segments contain the nucleus, support organelles (mitochondria, ribosomes, endoplasmic reticulum, synaptic vesicles, etc), and the axon terminal (where neurotransmitter is released). The capture of individual photons by the photopigment molecules in the disk membranes is what initiates neural signalling. Photoreceptors are actually specialized hair cells, and the inner and outer segments are connected by the cilium. 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. Cone inner segments are actually exquisitely engineered waveguides (i.e., fiber optic structures) which capture light and funnel it into the outer segment. Because these inner segment waveguides capture light shining straight on them better than light from shallower angles, we can measure what is called the Stiles-Crawford effect, published in 1933.
Functions as a relay station for the verticalinformation-carrying nerve cells, the bipolar cells, to connect to ganglion cells. In addition, different varieties of horizontallyand vertically-directed amacrine cells, somehow interact in further networks to influence and integrate the ganglion cell signals. 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.
Choriodal neovasc
Choriodal neovasc