1. Vision

2. Visible light is part of the electromagnetic spectrum
Visible portion of electromagnetic spectrum (380 – 700 nm wavelength) has enough energy to make a reversible change in receptor molecules without permanently damaging them.

4. Image formation on the retina
Retinal image is inverted and reversed. Absence of receptors at optic disc creates blind spot in visual field about 15 degrees temporal to fixation point.

5. Diopter = 1/focal length in meters
Optical defects
Myopic eye is too long, focal point is in front of retina. Correct with concave lens.
Hyperopic eye is too short, focal point is behind retina. Correct with convex lens.
Eye increases in size for 15 years. Refractive errors decease .
Studies of experimental myopia in primates and chickens show retina controls growth of sclera and length of eye by detecting image blur. Retina can distinguish hyperopic blur from myopic blur though we can’t perceive difference.
Newborn axial length of eye = 17 mm, adult = 24 mm. Diopter = reciprocal of eyeball focal length in meters. For distant object, distance from center of lens and cornea to retinal image is meters. 1/0.017 = 58.8, so optical power of human eye at relaxed state is about 60 diopters.
Diopter = 1/focal length in meters
Relaxed eye ~ 60 D;

6. Chambers, iris and lens
Anterior and posterior chambers contain aqueous humor. Fundus of eye behind lens is filled with vitreous.
Ciliary muscle + ciliary processes = ciliary body
Aqueous humor is secreted into posterior chamber by highly vascularized folds, called ciliary processes, in secretory ciliary epithelium.

7. Aqueous humor and intraocular pressure
Aqueous humor is formed by ciliary processes and enters the anterior chamber through the pupil. Drains from the eye at the angle of the anterior chamber where it must pass through collection of tissue cords (trabecular meshwork) before entering canal of Schlemm. Intraocular pressure depends on the rate of aqueous production and the resistance to its outflow.
Warm entering aqueous is carried upward by convection currents before cooled by cornea.

8. Glaucoma
Optic neuropathy in which optic nerve deteriorates with progressive enlargement and cupping of optic disc.
There are several forms of glaucoma:
Primary open angle glaucoma. 80% of all cases; afflicts 1% of people over 40; most common optic neuropathy among elderly. Often, but not always, accompanied by elevated intraocular pressure that can stop axoplasmic flow as nerve passes through sclera. Structural change in trabecular meshwork impedes aqueous outflow. Lowering IOP does not arrest disease. Programmed optic nerve death?
Closed angle glaucoma. 10% of cases. Occurs when iris covers trabecular meshwork. Causes rise in IOP to > 40 mmHg that stops blood flow to optic nerve.
IOP > 21 mmHg = ocular hypertensive
IOP in 95% population < 21 mmHg; mean IOP =16.5 mmHg.

9. Why is glaucomatous disk so cupped?
Most distinctive feature of glaucoma is deeping and enlargement of optic nerve cup. Occurs even when intraocular pressure (IOC) is normal.
Loss of large diameter axons (other optic neuropathies affect mainly small axons)
Collagen fibers of sclera form meshwork through with optic nerve must pass. In glaucoma this lamina cribosa bends backwards. Due to defective collagen? IOC?
Glia cells do not proliferate to fill gaps, resulting from dead axons, as they do in other inflammatory or ischemic optic neuropathies

10. Accommodation and Presbyopia
Accommodation is the result of ciliary muscle contraction.
When ciliary muscle is relaxed, zonular fibers are under tension and pull outward on lens, flattening it. Unaccommodated eye is focused on distant objects.
When ciliary muscle contracts, it reduces pull of zonule fibers and lens becomes smaller and thicker. Due to elasticity of lens capsule. Change optical power 8 D.
Primary stimulus for accommodation is retinal image blur. Changes in image size and judgements of apparent distance can also act as stimulus.
Presbyopia: decreased accommodation amplitude with age. From 14 Diopters at 8 years to 1 D at 50 or 55 yr. No cure. Due to age related loss of elasticity.

11. The lens and cataracts
Lens is 90% protein, more than any other tissue in body. Transparency due to: 1) dense, uniform packing of crystallin protein molecules & 2) low water content maintained by ion pumping in epithelium.
Lens is formed of concentric layers of long, thin fibers in an elastic capsule.
Size of lens and number of fibers increase throughout life.
Cataracts are opacities in lens. Can occur at any age but most age related. Cause nearly 50% of blindness worldwide. Multiple risk factors. Dominant cause is UV radiation which alters protein structure. Treat by surgical removal of lens. Aphakic eye severely hyperopic so usually insert plastic or silicone intraocular lens
Na-K pumps transports Na inward, K out. Osmotic gradient moves water out of lens. Pump direction reverse of nerve.

12. Optic disc, fovea and macula
choroid
Sclera OD
Fovea is fixation point in central retina and has highest acuity but low sensitivity. 1.5 mm diam. Occupies about 1 – 2 degrees visual space. At center of macula. Macula ~ 6 mm diam.. Has good acuity and occupies about 5 degrees of visual space.
Fovea

13. Age-related Macular Degeneration
Progressive loss of central vision due to gradual degeneration of the photoreceptors. First symptom is usually blurring of central vision when reading. Usually affects both eyes. Most common cause of vision loss in people over 55.
Causes of disease are unknown. Candidates include hereditary factors, cardiovascular disease, smoking, light exposure, nutrition—all may play a role.
10% AMD is exudative-neovascular (wet) form. Abnormal growth of blood vessels under macula leak blood into retina and damage photoreceptors. Rapid progression (months). Treat with laser therapy.
90% AMD non-exudative (dry) form. Gradual disappearance of retinal pigment epithelium over period of years. Loss of photoreceptors in affected areas. Patient usually retains some central vision. No treatment is available.
Affects six million people in US. There are also some hereditary forms of juvenile MD.

14. Rod and cone outer segment
Scotopic vision: High sensitivity; low spatial resolution. Starlight. Rods.
Mesopic vision: rods and cones; Moonlight
Photopic vision: Low sensitivity; high spatial resolution. Brighter than moonlight. Cones.
Normal vision depends mostly on cones.
Cones must capture 100 photons to produce response of 1 photo captured by a rod

15. Visual pigment
Phototransduction begins when a photon is absorbed by visual pigment in a receptor disk.
Photopigment contains a light absorbing chromophore, retinal (an aldehyde of vitamin A) coupled with one of several proteins called opsin.
Most studies on rods where photopigment is rhodopsin. Absorption of photon by rhodopsin molecule changes it from its 11-cis isomer to all-trans retinal. This triggers a sequence of biochemical events resulting in a receptor potential.

16. Phototransduction involves closing cation ion channels in outer segment membrane
1. Absorption of photon converts 11-cis retinal to all-trans isomer
Activated rhodopsin stimulates G protein, Transducin
Activated G protein activates enzyme that breaks down cyclic GMP
Intracellular [cGMP] drops, plasma membrane channels close, Na+ can’t enter; cell hyperpolarizes.
Amplifying cascade: 1 photon + 1 rhodopsin hydrolyze 250,000 cGMP per second

17. Biochemical cascade and light adaptation
Biochemical cascade initiated by photon capture greatly amplifies signal: Estimated that 1 light activated rhodopsin molecule can activate 800 transducin molecules. Each transducin molecule activates only 1 phosphodiesterase molecule but each of these may catalyze breakdown of up to 6 cGMP molecules. In this way absorption of one photon by a single rhodopsin molecule can cause about 200 ion channels to close and change the membrane potential about 1 mV.
Light adaptation. Magnitude of amplification varies according to level of illumination. Photoreceptors are most sensitive in dim light, less sensitive in bright light. This prevents them from saturating and extends the range of light intensities over which they can operate. cGMP-gated channels in outer segment are permeable to Ca2+ as well as Na+. As illumination increases, more channels close and intracellular [Ca2+] drops. This decrease triggers changes in phototransduction cascade that reduce sensitivity of receptor to light. Additional factors include neural interactions between photoreceptors and horizontal cells.

18. Structure of the Retina
Direct path: Receptor – Bipolar cell – Ganglion cell.
Indirect path: Receptor – Horizontal cell – Bipolar cell – Amacrine cell – Ganglion cell
Horizontal and Amacrine cells mediate lateral interactions
Retinal pigment epithelium contains melanin; prevents back-scattering of light; essential role in renewing photopigments and phagocytosing photoreceptor disks that are sloughed off and regenerated.
From Purves et al Neuroscience

19. Renewal of labeled amino acids in rods
Retinitis pigmentosa
Common hereditary retinopathy, affects 100,000 people in U.S. RP is group of hereditary eye disorders involving gradual degeneration of the photoreceptors. Main symptoms are night blindness, loss of peripheral vison, narrowing of retinal vessels and migration of pigment from disrupted retinal pigment epithelium into retina where it forms clumps near blood vessels.
Progressive death of rods, may be followed by loss of cones
Mutation may be X-linked or dominant or recessive autosomal gene. To date mutations identified on 30 genes. Many encode photoreceptor proteins. Pathogenesis is not well understood. Why do cones degenerate? Often protein that RP affects is not expressed in cones, e.g., rhodopsin.
Usually visual field deficits begin in mid periphery deg.from fovea—tunnel vision.
Normal phagocytosis of sloughed-off rod proteins by long processes of pigment epithelium
Dark clumps of pigment in retina
Renewal of labeled amino acids in rods

20. Color vision: 3 classes of cones
There are three types of cones with different photopigments that respond to Short, Medium or Long wavelengths.
Individual cones are colorblind. Can’t discriminate changes in wavelength from changes in luminance.
Color perception depends on comparing activity of ganglion cells from different classes of cones.
S M L

21. Color blindness Trichromats (Normal)
Most people can match any color by adjusting the intensity of three superimposed light source producing S, M and L wavelengths
About 8% of men and only 0.5% of women are color blind
Dichromats Can match colors with only two lights ; don’t see third color category
Protanopia– no red cones; x chromosome
Deuteranopia– no green cones; x chromosome
Tritanopia– no blue cones; chromosome 7 (rare)
Anomalous trichromats
Red or green gene is replaced by hybrid gene that has intermediate spectral sensitivity. (protanomalous if it is red gene; deuteranomalous if it is green gene that is abnormal)
Genes for red and green lie adjacent each other on X chromosome and high degree of sequence homology; probably evolved recently maybe from duplication of single ancestral gene. Purves Neurosci p 248

22. Central visual pathways
Retinal projections:
Pretectal area of midbrain
Pupillary light reflex
Superior colliculus
Saccadic eye movements
Multimodal maps of visual space
Lateral geniculate nucleus
Cortical feedback, filters transmission to cortex
Part of pathway for conscious visual perception

23. Most ganglion cells go to the lateral geniculate nucleus
Axons from nasal half of each retina cross in optic chiasm.
Each optic tract ‘looks’ at contralateral visual field
Parvocellular layers
Parvo
Parvo layers get small ganglion cells form and color; Magno layers get large ganglion cells, movement
Magnocellular layers

24. Optic radiation to visual cortex
Lateral ventricle
Lateral geniculate n.
Meyer’s Loop
Field of left eye
Field of right eye
LGN
Optic radiation
Calcarine sulcus
In left cerebral hemisphere
Nolte p. 434

25. Left visual cortex contains right half of visual field of both eyes
Seen only by right eye
Inferior field
Calcarine sulcus
Field of left eye
Field of right eye
Fovea
Superior field
Nolte p. 436

26. Primary visual cortex is organized into columns
Color sensitive regions RE LE
Ocular dominance columns
Orientation columns

27. Ophthalmic artery anurism
Visual Field Defects
Visual field of
Ophthalmic artery anurism
Pituitary tumor
Lesion in Myer’s Loop

28. Visual deprivation and amblyopia
Amblyopia is diminished visual acuity due to failure to establish appropriate cortical connections early in life.
Strabismus (misalignment of eyes) can cause double vision and is most common cause of amblyopia. In some individuals brain suppresses input from one eye which may become effectively blind. Early surgical correction of extraocular muscle length important.
During development, axons of cells in the lateral geniculate compete for synaptic space on cells in visual cortex. This critical developmental period, when cortical synapses are being formed, lasts several years in children. Visual deprivation of one eye during part of the critical period (due to congential cateracts, or amblyopia caused by strabismus) can result in few cortical cells responding to the deprived eye which may become permanently functionally blind.
Visual deprivation after the end of the critical period when synapses for both eyes have been established does not affect vision.
See Purves pp 568. For example, closing one eye of a kitten during first 3 months abolishes ocular dominance columns in visual cortex. Almost no cells respond to previously closed eye, which is permanently behaviorally blind. Same procedure on adult does not affect cortical dominance columns. In undeveloped tropics millions of people are affected by parasitic eye infections (e.g., ‘river blindness’ caused by a nematode) can cause cateracts or corneal opacity in one or both eyes and blindness, but vision recovers if opacity removed before child is 4 mo

29. Temporal parvocellular pathway analyses form and color
Lesions of the temporal vision-related cortical pathway cause inability to name and identify familiar objects, symbols, words, colors etc. For example: Prosopagnosia

30. Prosopagnosia: inability to identify familiar faces
Lesion of lingual, fusiform and parahippocampal gyri. Right side only or bilateral. Caused by stroke, tumor, demyelination or atrophy.
Cannot recognize familiar face. Know face is a face and if sad or happy, but not whether they have seen it before. Cannot learn to recognize new face.
Cannot distinguish between members of other classes of objects either.
Can tell knife from fork but not different knives, farmer can’t recog individual cows, bird watcher cant identify birds, car buff cant differentiate between models.
Bilateral inferior occiptiotemporal lesions

31. Magnocellular parietal pathway analyzes motion
Lesions of parietal vision-related cortex pathway cause visual illusions and deficits related to the distribution of visual attention and perception and manipulation of items in space. Examples: Hemispatial or unilateral neglect Akinetopsia

32. Hemispatial or unilateral neglect
Disorder of spatially directed attention caused by lesion of right posterior parietal region. Body centered instead of visual field centered.

33. Self protraits after right posterior parietal lesion
2 mo
3.5 mo
6 mo
9 mo

34. Akinetopsia: inability to detect motion
Lesion in visual area V5 (MT) in parieto-occipital cortex which contains neurons sensitive to motion but not orientation or wavelength. Sees moving objects but does not perceive them as in motion.
See Trobe neurology of vision p 342.