Vision Flashcards

1
Q

*Identify the major parts of the eye?

A

[cornea: transparent cells, does most of the refraction (bending) of light to bring image in focus on fovea; lens, transparent cells, does some refraction, and flexes to increase refraction, bringing close objects into focus; aqueous and vitreous humor, fluids of the respective anterior and posterior chambers; retina, CNS tissue containing rods, cones and ganglion cells, where transduction occurs; choroid, dark pigmented layer that absorbs light, part of inner choroid includes retinal epithelium layer; sclera: tough, outer covering of eye, white, and not present anteriorally (where cornea is)]

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2
Q

*Identify the layers of the retina from choroid?

A

[receptor layer (rods/cones), outer nuclear layer (cell bodies of rods/cones), outer plexiform (synapses with receptors and bipolars), inner nuclear (bipolars, amacrines), inner plexiform (synapse with bipolars, ganglion cells), ganglion cell layer]

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3
Q

Name 4 nuclei that receive input from retina?

A

[lateral geniculate nucleus (thalamus, conscious vision), suprachiasmatic hypothalamus (diurnal rhythms), superior colliculus (mesencephalon, eye/head movements), pretectal nucleus (mesencephalon, mediates light response reflex)]

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4
Q

What is the visual field?

A

[The area over which we can see at any given time… ~180 deg across, 110 deg up/down, it is divided into a left and right visual field… the right visual field is represented in the left visual cortex, the left visual field is represented in the right visual cortex]

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5
Q

What is the binocular visual field, and how big is it?

A

[The visual field observed by both eyes; in humans, the binocular field covers ~120 deg] To clarify the two above, the visual field includes the entire visual field seen by the left eye AND/OR right eye. The binocular field is the field seen by the right eye AND the left eye (some parts of our visual field can only be seen by the right eye, some can only be seen by the left eye(temporal monocular crescents).

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6
Q

What is a right homonymous hemianopsia?

A

[Loss of vision in the right visual field, most likely attributable to loss of left primary visual cortex. The left/right distinction is referenced to the visual field. Homonymous refers to the fact that it’s the same loss in each eye…in this case the left half (temporal side) of the left eye, the left half (nasal side) of the right eye. Heteronymous would mean it’s different between the two eyes… the classic being a pituitary tumor which pushes up and splits the chiasm…. crossing fibers (nasal retinae) are lost, but it would be the right half of the left eye and the left half of the right eye… referred to as a heteronymous hemianopsia (hemianopia). Hemianopia references a half visual field loss (cf quadranopsia … usually loss of upper (superior) or lower (inferior) quarter of visual field

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7
Q

What do you call loss of vision in the left eye?

A

[anopia of the left eye]

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8
Q

What is the retina?

A

[where transduction and initial visual processing occur; a layer of tissue at the back of the eyeball that is about the size of postage stamp and just as thick (160 um) that contains the rods, cones, bipolar cells and ganglion cells necessary for vision]

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9
Q

Name the major cell types of the retina?

A

[rods, cones, horizontals, amacrines and retinal ganglion cells]

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10
Q

What is the fovea?

A

[a specialization of the retina that exists as a ‘pit’, and is where the optic axis focuses light. It is pure cone (no rods), and these cones are tightly packed, ~10 um between cones. In the most central 2o , there are no blue cones, just red and green.. to minimize chromatic aberration].

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11
Q

Does the human fovea have any rods?

A

[no]

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12
Q

What is the range of wavelengths within the electromagnetic spectrum that constitutes the ‘visual’ spectrum?

A

[~400-700 nm]

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13
Q

*What color is at the bottom of a rainbow?

A

[blue, violet… because short wavelength bend more]

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14
Q

Is it true light travels through the ganglion cell layer of the retina to reach the rods and cones?

A

[yes… it probably seems stupid, but I wouldn’t 2nd guess evolution]

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15
Q

What vitamin is associated with rods/cones?

A

[vitamin A, an essential vitamin. Essential means you can’t make it, or you can’t make enough of it, so you need it in your diet; vitamins are organics that catalyze reactions. Retinal is a form of vitamin A that combined with opsin (a protein) constitutes rhodopsin]

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16
Q

Does light hyperpolarize or depolarize a rod/cone?

A

[hyperpolarize, decreasing the ‘dark current’, which controls the ‘drip’ rate of glutamate at the synapse]

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17
Q

*What happens when a photon hits a rod?

A

[The vitamin A (retinal) part of the rhodopsin molecule flips from cis to the more stable trans conformation. This form activates 100’s of transducin molecules which activate 100’s of phosphodiesterase molecules. The phosphodiesterase hydrolyzes cGMP which closes the dark current (decreased Na+ conductance), hyperpolarizing the rod and decreasing glutamate drip onto the bipolar cell]

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18
Q

What is the ‘dark current’?

A

[an inward (depolarizing) current attributable to Na+ conductance when the rod/cone is in the dark]

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19
Q

In myopia (nearsightedness), the image is focused in front of the fovea?

A

[true, somewhere in the vitreous]

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20
Q

In presbyopia, the lens has lost its flexibility?

A

[probably true. This happens with age… older people (> 40) need convex (positive) lens to increase refraction bringing close objects into focus]

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21
Q

At the optic chiasm, the axons crossing are from the _______ retina?

A

[nasal]

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22
Q

Humans have 3 cone systems but can identify _____ hues?

A

[> 300].

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23
Q
  1. What are hues?
A

[separable colors; we can do this because the opsins associated with each cone system have broad absorption spectra and peak at different wavelengths… it is the relative activation of each of the 3 cone systems that allow us to name tens of hues]

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24
Q

*Are there tetrachromats?

A

[Among animals, goldfish and some finches. The 4th opsin is in the ultraviolet range. It is possible there are humans (certain women, there’s a genetic link) that are true tetrachromats. Among mammals, UV sensitivity is greatly diminished by the fact that the cornea absorbs most of UV light]

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25
Q

What is ‘color blind’?

A

[a defect in color discrimination. It is almost always a genetic defect, much more common in males. The most common, red-green, is interesting because although they still have 3 cone systems, the absorption spectra of red and green nearly perfectly overlap, thus the ratios of activation are nearly identical, and there’s no discrimination on the basis of wavelength…. In reality, most of these individuals can do a good job of color discrimination because different colors reflect light at different intensities… allowing discrimination on the basis of intensity/wavelength]

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26
Q

*What is a detached retina?

A

[a portion of the retina is displaced from the choroid. It is an emergency situation as it compromises the blood supply to the retina… it can be fixed by effectively ‘spot welding’ the retina back onto the eyeball with a laser. Because of the shape of the eyeball, very myopic people are more vulnerable than others]

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27
Q

What are cataracts?

A

[clouding of the lens (most common) or cornea that degrade vision. Risk factors are age, time exposed to sunlight, diabetes]

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28
Q

*What is the leading cause of blindness in the US?

A

[diabetic retinopathy (glaucoma is 2nd)]

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29
Q

*What causes blindness in diabetes?

A

[chronic high glucose levels in blood encourage breaking of capillaries and blood to pool on retina, disturbing vision… over time, this leads to poor vascularization of retina itself (in addition to the fact that the pooling of blood detracts from the optics)]

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30
Q

*What is optic neuritis?

A

[inflammation of optic nerve, associated with visual loss (compression on fibers) and pain associated with eye movement (the sheath of the optic nerve is innervated by the ophthalmic division of V). Optic nerve is CNS, and optic neuritis is the most common 1st episode of multiple sclerosis]

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31
Q

*What is glaucoma?

A

[increased intraocular pressure usually associated with a failure of the normal draining of aqueous humor in the eye. Blindness ensues due to chronic increased pressure on optic nerve. Age, family history and diabetes are major risk factors]

32
Q

What is the macula?

A

[The name given to the area around the fovea pit on the eyeball. It encompasses the central 5 deg and has a yellowish tint]

33
Q

Pituitary tumors are associated with which visual field defect?

A

[bitemporal heteronymous hemianopia, blocks the retinal fibers crossing at the chiasm]

34
Q

The layering of the lateral geniculate nucleus segregates retinal input?

A

[by eye and functional (magno/parvo) group]

35
Q

What are the optic radiations?

A

[the name given to axons from the LGN projecting to the visual cortex]

36
Q

What is Meyer’s loop?

A

[axons of LGN neurons representing the inferior retina (superior visual field). Meyer’s loop swings wide as it enters the internal capsule… very wide into temporal lobe. Because that area is more susceptible to stroke from occlusion of the middle cerebral artery, the contralateral superior visual field suffers (aka, ‘pie in the sky’ because this causes a loss of vision in the upper quadrant – a slice of pie shaped loss]

37
Q

Damage to Meyer’s Loop or the lower bank of the Calcarine sulcus yields ____?

A

[‘pie in the sky’, loss of vision in contralateral upper visual field, quandrantinopia]

38
Q

What is the ‘blind spot’?

A

[place on retina where optic fibers exit…aka, optic disk; it is located on nasal retina, if you close your left eye, it is ~20 deg lateral

39
Q

Which fibers cross at the optic chiasm?

A

[retinal axons from the nasal half of the retina]

40
Q

*What is the ‘line of decussation’?

A

[an imaginary line in the retina that bisects the fovea. Axon of ganglion cells on the nasal side cross at the chiasm, axons of ganglion cells on the temporal side of the retina do not cross. The vertical meridian of the visual field is represented by the line of decussation]

41
Q

What is the optic nerve?

A

[The fiber bundle containing the axons of retinal ganglion cells from one eye (there’s about a million axons/eye). The optic nerve ends at the optic chiasm. Retinal axons more central are part of the optic tract].

42
Q

Where is the blind spot in the visual field?

A

[~20 deg temporal (lateral) of the fovea, which is the point of gaze]

43
Q

How do you find the fovea on an ophthalmoscope?

A

[find the place where there’s no blood vessels.. on the temporal side of the optic nerve head]

44
Q

Where is the fovea represented in primary visual cortex?

A

[at the occipital pole]

45
Q

What is macular sparing?

A

[preservation of central visual field following extensive damage to primary visual cortex. It occurs either because of anastomoses from unaffected arteries, or because there is a small amount of nasotemporal overlap at the vertical meridian and the fovea is double-represented in both hemispheres]

46
Q

Why are rods more sensitive to light?

A

[First, there’s more of them, lots more (~19:1 rods:cones). Second, they have more opsin, a lot more, so better chance to catch a photon. Also, the single photon signal is better amplified in rods. A single photon will suppress the dark current by 4% in a rod vs 0.06% in a cone! Finally, the geometry of a rod is more conducive to catching a photon than a cone]

47
Q

Give 3 names for primary visual cortex?

A

[area 17, V1, striate cortex]

48
Q

Identify differences between the layers of neurons in the lateral geniculate nucleus?

A

[differences by eye, functional group (magnocellular/parvocellular), on center/off center]

49
Q

Among magnocelluar/parvocellular neurons, which is color opponent?

A

[parvocellular]

50
Q

Is it true that magnocellular neurons only receive rod input?

A

[No. magnocellular are not color opponent (they’re referred to as ‘broad-band’, that is different from not receiving input from cones; they do receive cone input!]

51
Q

Which picks up light better, rods or cones? Why?

A

[rods, they have a lot more opsin/rod, hydrolyze much more cGMP (shutting off the dark current), are bigger, have better geometric design, show extensive convergence on bipolar cells, and, quite frankly, there’s just a whole lot more of them than there are cones]

52
Q

Why are there no blue cones in the fovea?

A

[minimizes chromatic aberration]

53
Q

What is chromatic aberration?

A

[distortions in optics attributable to the fact that different wavelengths of light bend more than others… think ‘rainbow’]

54
Q

Why is the choroid black?

A

[To minimize reflection of light which would lead to diffraction, and degraded images.

55
Q

What is the cost/benefit of a small pupil?

A

[minimizes diffraction or scattering of light to yield better optics (good), let’s in less light (bad]

56
Q

*When the lasik procedure flattens the cornea, does that add or subtract refractive power?

A

[subtracts]

57
Q

Most of the refraction done by the eye is done by the _______?

A

[cornea, by far. The unit is diopters, and our optics is powerful: 58 diopters, with ~50 of those diopters attributable to corneal refraction]

58
Q

What is by far the most common receptive field design in the retina?

A

[ concentric, on center-off surround, off-center on surround]

59
Q

Which cell type is responsible for constructing the antagonistic ‘surround’ of the concentric cell?

A

[horizontal cells]

60
Q

Which cell type is slower to respond to a changing contrast, on-center or off-center? Why?

A

[on-center, because the on-bipolar glutamate receptor reverses the sign of light (light hyperpolarizes rods/cones, reducing glutamate drip) and involves a metabotropic glutamate receptor, mGluR6…. Truth be known… it only slows things down by 2-3 msec compared to the ionotropic AMPA receptor associated with off-center cells]

61
Q

How does the concentric design facilitate vision?

A

[it reduces redundancies in visual scenes by keying on differences rather than similarities across their receptive field; in addition, the concentric design will exaggerate signals at contrast borders by displaying maximal output on one side of the edge and minimal output on the other side of the edge depending on the polarity of concentric cell ]

62
Q

*If we lost all of our off-center or on-center cells, could we still see ok?

A

[ yes, one or the other is enough… you’d just have issues with contrast sensitivity… effectively the ability to discriminate shades of gray placed next to each other]

63
Q

What is the ‘duplicity’ theory of vision?

A

[the idea that rods are for night vision, cones for day vision; it extends to other aspects of vision: color vision = cones, foveal vision = cones, detection of light = rods]

64
Q

Do our rods ‘work’ in daylight?

A

[probably not…. They’re all saturated from too much light]

65
Q

*What does 20/20 mean?

A

[Designation for normal acuity. You can see at 20 feet what normal people see at 20 feet. It is an average… so one can do better, e.g., one can 20/15: meaning they can see at 20 feet when normal people have to be at 15 feet… in myopia, it’s worse … e.g., 20/200… you can see at 20 feet what normal people can see at 200 feet]

66
Q

*What is astigmatism?

A

[distortions in image formation that occur with orientation… ideally, a line should be in focus at all angles.. in astigmatism it does not. Not to worry: cylindrical lenses can ‘fix’ astigmatism. If you wear contacts, they put little weights on the lenses so the orientation of the contacts is standard and the cylindrical lens will correct the astigmatism; when I had lasik, they charged me an extra $300 per eye to engage software that would ‘sculpt’ my cornea to make the astigmatic correction]

67
Q

Do our cones ‘work’ in dim light?

A

[hardly…. Hence we have neither color vision, nor foveal vision under dim illumination, and ~30% of our visual cortex is turned off in scotopic (dim-light) conditions!]

68
Q

Can we detect a single photon?

A

[Not really… if you were in a room devoid of light, and a single photon showed up..that’s not enough… 9 photons of the optimal wavelength (~570 nm) that impinge ~20 deg off fovea (area of peak rod density)… that’s enough of reliable detection in the dark-adapted eye. If you’re curious why we can’t detect a single photon, it’s because rods and cones are ‘trigger happy’ and sometimes just go off on their own creating noise… a pulse of 9 photons delivered to the right place, at the right wavelength (~500 nm) in the dark-adapted eye will go above the noise level]

69
Q

The eye works over how many orders of magnitude of light?

A

[12!…. from dimmest light to bright sunlight]

70
Q

What is contrast?

A

[a measure of local variation in luminance]

71
Q

What is luminance?

A

[brightness, the number of photons hitting a given area over time; our visual system keys on contrast, not luminance, much more efficient]

72
Q

What is ‘magnification factor’ in vision?

A

[the idea that visual cortex in particular has greatly increased space devoted to central (foveal) vision…. e.g., 10% of our visual cortex is devoted to processing the central 1% of our visual field. In truth, this magnification is much ado about nothing… if one calculates the faction of ganglion cells ‘serviced’ by area the magnification factor goes ‘poof’… i.e., the fovea has a ton of ganglion cells… therefore, it only fair that they should get 10% of visual cortex. The density of ganglion cells in the periphery is much less…. It’s only fair..]

73
Q

What is a ‘scotoma’?

A

[a ‘blind spot’ in our visual field. We all have one in each eye where the optic nerve head exits. We aren’t aware of this because the blind spot in one eye is ‘covered’ by the other eye. However, there’s more. When we close 1 eye, we’re also not aware of a ‘blind spot’. Why It’s relatively small, and our visual cortex fills in what it ‘thinks’ should be there based on the scene near the blind spot. In cortical (stroke) or retinal (diabetes) it’s common to have scotomas… and our visual system is insidious in how it covers up our blind spot. Most people are surprised, if not shocked when told they have big (10-20 deg) holes in their visual field.]

74
Q

*What is stereopsis?

A

[It’s the amazing ability to view depth by virtue of the fact that nature deliberately misaligns retinal ‘wires’ (via LGN) from the 2 eyes onto some neurons in visual cortex. As a result, some binocular (both eye) responses only occur when objects are ‘closer than’ the point of gaze, and some responses only occur when objects are ‘further than’ point of gaze. Wheatstone (1838) first speculated the brain might do this, and built the first stereoscope based on these principles. One must have overlapping visual fields from both eyes (binocular) to have stereopsis, but that is not sufficient. Approximately 10% of the population is stereoblind… i.e., no stereopsis, and most would be surprised that they didn’t have it. It’s not that important….I mean if you close one eye, the world doesn’t suddenly go flat… there’s plenty of monocular cues that tell us about depth, independent of stereopsis. Stereopsis likely only comes into play for fine discriminations.. e.g., shooting 3-pointers, threading needles].

75
Q

Where in the visual system does one first observe binocular cells?

A

[in the traditional retina-geniculo-striate system, primary visual cortex – prior to that, all representation in the visual field is from one eye only; we rate the cells on a scale of 1-7, 1 if it responds to light presented to the contralateral eye only, 4 if equal, 7 if it responds to light presented to the ipsilateral only… ocular ‘dominance’, the degree to which a cell is dominated by input from one eye or the other is a columnar property]

76
Q

What is transduction?

A

[conversion of one form of energy into another. For the nervous system, the conversion of some form of energy into electricity, the commodity of the nervous system]

77
Q

What is a sensor?

A

[in neurospeak, a specialized neuron of support cell specifically designed]