Case 3 Flashcards

1
Q

anatomy of the eye:

  • pupil
  • iris
  • cornea
  • sclera
  • extraocular muscles
  • orbit
  • conjunctiva
  • optic nerve
A
  • Pupil – this is the opening that allows light to enter the eye and reach the retina; it appears dark because of the light-absorbing pigments in the retina.
  • Iris – the pupil is surrounded by the iris, whose pigmentation provides the ‘eye colour’. The iris contains two muscles that can vary size of the pupil; one makes it smaller when it contracts, the other makes it larger.
  • Cornea – this is the glassy transparent external surface of the eye that covers the pupil and the iris.
  • Sclera – the cornea is continuous with the sclera, the ‘white of the eye’, which forms the tough wall of the eyeball.
  • Extraocular muscles – these are three pairs of muscles that insert into the sclera. The move the eyeball in the orbit. These muscles normally are not visible because they lie behind the conjunctiva.
  • Orbit – this is the bony eye socket in the skull, in which the eyeball sits.
  • Conjunctiva – this is a membrane that folds back from the inside of the eyelids and attachs to the sclera. The extraocular muscles lie behind this.
  • Optic nerve – this is the nerve responsible for vision. It carries axons from the retina, exits the back of the eye, passes through the orbit (optic foramen), and reaches the base of the brain near the pituitary gland where it decussates (optic chiasma) before reaching the primary visual cortex in the occipital lobe.
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2
Q

where do retinal blood vessels originate from?

A

the optic disc

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3
Q

where can the sensation of light not occur?

A

Sensation of light can’t occur at the optic disk because there are no photoreceptors here, nor can it occur where the large blood vessels exit because the vessels cast shadows on the retina.

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4
Q

macula

  • what is it
  • what’s it for
  • how’s it distinguished
  • what improves quality of central vision
A
  • yellow tissue at the centre of the retina, surrounding the fovea
  • it is for central vision
  • besides its colour, it’s distinguished by the relative absence of large blood vessels
  • the retinal blood vessels arc from the optic disc to the macula; this is also the trajectory of the optic nerve fibres from the macula en route to the optic disc
  • the absence of blood vessels improves the quality of central vision
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5
Q

what is the fovea?

A
  • dark spot about 2mm in diameter
  • at centre of retina
  • thinnest part of retina
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6
Q

what is defined as the nasal retina and temporal retina?

A

from the fovea, anything medial is the nasal retina and anything lateral is temporal retina
- optic disc is in the nasal retina

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7
Q

what colour does the retina appear and why?

A
  • orange

- due to the choroidal circulation under the photoreceptor layer

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8
Q

what brings about refraction of light? what is most responsible for it?

A
  • cornea and lens

- cornea is responsible for most of the refraction of light

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9
Q

how are light rays refracted by the cornea?

A
  • The light rays entering the eye are parallel rays.
  • The light rays that strike the curved surface of the cornea bend (as they enter the aqueous humor) so that they converge on the back of the eye; those that enter the centre of the eye pass straight to the retina.
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10
Q

what is the focal distance?

A

the distance from the refractive surface to the point where the parallel light rays converge

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11
Q

the more curved the cornea, the x the focal distance?

A

shorter

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12
Q

what is a dioptre?

A

the unit of the power of refraction

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13
Q

refractive power (dioptres) =

A

1/focal distance (m)

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14
Q

what does the cornea have a refractive power of? what does this mean in terms of focal distance?

A

42 dioptres

this means that the light rays striking it will be focused about 2.4cm (0.024m) behind it, about the distance from the cornea to the retina

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15
Q

what is the refractive power of the lens compared to the cornea?

A
  • it’s less

- about 12 dioptres

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16
Q

what is accomodation?

A
  • the refraction supplied by the lens is adjustable, allowing objects at various distances from the observer to be brought into sharp focus
  • the additional focusing power is provided by changing the shape of the lens = accommodation
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17
Q

describe how accommodation comes about

A
  • The ciliary muscle forms a ring around the lens.
  • For near vision, the ciliary muscle contracts and swells in size, thereby making the area inside the muscle smaller and decreasing the tension in the suspensory ligaments.
  • The lens becomes rounder and thicker because of its natural elasticity.
  • This increases the curvature of the lens, and thus its refractive power increases.
  • For viewing distant objects, relaxation of the ciliary muscle increases the tension in the suspensory ligaments, and the lens is stretched into a flatter shape, and its refractive power is reduced.
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18
Q

what does the pupillary light reflex do?

A

it aids the clarity of images formed on the retina

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19
Q

how does narrowing the pupil lead to sharper images? however what happens under conditions of dim illumination?

A

it reduces both spherical and chromatic aberration
(aberration = failure of rays to converge at one focus due to a defect in lens)
- spherical aberration = occurs due to increased refraction of light rays when they strike a lens
- chromatic aberration = the effect produced by the refraction of different wavelengths of light through slightly different angles, resulting in a failure to focus

  • reducing size of pupil also increases the depth of field - the distance within which objects are seen without blurring
  • however, a narrowed pupil also limits the amount of light that reaches the retina, and, under conditions of dim illumination, visual acuity becomes limited by the number of available photons rather than by optical aberrations.
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20
Q

what is the visual field?

A

the total amount of space that can be viewed by the retina when the eye is fixated straight ahead

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21
Q

what happens to the image of an object in the visual field?

A

it’s inverted on the retina

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22
Q

what is binocular and uniocular vision?

A
  • Binocular visual field is the visual field when both eyes are open.
  • With only one eye open the field is uniocular and is restricted inwards by the nose.
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23
Q

what is the most common visual field loss due to?

A

glaucoma

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24
Q

what is visual acuity? what does it depend on? what can be used to talk about visual acuity?

A

the ability of the eye to distinguish two nearby points

acuity depends on several factors - mainly on the spacing of photoreceptors in the retina and the precision of the eye’s refraction.

distance across the retina can be described in terms of degrees of visual angle. We can speak of the eye’s ability to resolve points that are separated by a certain number of degrees of visual angle.

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25
Q

what test is used to test visual acuity? what is normal?

A

the Snellen eye chart - tests our ability to discriminate letters and numbers at a viewing distance of 6 metres (20 feet)

normal vision = 6/6

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26
Q

describe the development of the retina

A

During development, the retina forms as an outpocketing of the diencephalon, called the optic vesicle, which undergoes invagination to form the optic cup.

- The inner wall of the optic cup forms the retina.
 - The outer wall gives rise to the retinal pigment epithelium (RPE).
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27
Q

what is retinal pigment epithelium (RPE)?

A
  • this epithelium is a thin melanin-containing structure that reduces backscattering of light that enters the eye
  • it also plays a critical role in the maintenance of photoreceptors, renewing photopigments and phagocytosing the photoreceptor discs, whose turnover at a high rate is essential to vision
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28
Q

what cells is the retina composed of?

A
  • photoreceptor cells (rods and cones)
  • bipolar cells
  • ganglion cells
  • horizontal cells
  • amacrine cells
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29
Q

what are the different layers called (outward to inward)

A
  • pigment epithelium
  • photoreceptor outer segments
  • outer nuclear layer
  • outer plexiform layer
  • inner nuclear layer
  • inner plexiform layer
  • ganglion cell layer
  • nerve fibre layer
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30
Q

where are the cell bodies of the photorecpetor cells located?

A

in the outer nuclear layer

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31
Q

where are the cell bodies of the bipolar cells, the horizontal cells and the amacrine cells located?

A

in the inner nuclear layer

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32
Q

where are the cell bodies of the ganglion cells located?

A

in the ganglion cell layer

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33
Q

what’s located in the outer plexiform layer?

A

the synaptic contacts between the photoreceptor cells, the bipolar cells and the horizontal cells

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34
Q

what’s located in the inner plexiform layer?

A

the synaptic contacts between the bipolar cells, the ganglion cells and the amacrine cells

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35
Q

what do both rods and cones have?

A
  • an outer segment composed of membranous disks that contain light-sensitive photopigment (photopigments absorb light, thereby triggering changes in the photoreceptor membrane potential)
  • an inner segment that contains the cell nucleus and gives rise to synaptic terminals that contact bipolar or horizontal cells
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36
Q

what is the life span of the membranous disks in the outer segment? what’s continuously being formed? what happens during life span?

A

12 days

  • new outer segment disks are continuously being formed near the base of the outer segment
  • during their life span, disks move progressively from the base of the outer segment to the tip, where the pigment epithelium plays an essential role in removing the expended receptor disks
  • shedding involves ‘pinching off’ a clump of receptor disks by the outer segment membrane of the photoreceptor
  • this enclosed clump of disks is then phagocytosed by the pigment epithelium
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37
Q

what blood vessels are photoreceptors supplied by?

A

choroidal blood vessels

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38
Q

what do the processes of horizontal cells enable?

A

lateral interactions between photoreceptors and bipolar cells that maintain the visual system’s sensitivity to luminance

they help integrate and regulate the input from multiple photoreceptor cells

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39
Q

what are the processes of amacrine cells?

A

they are postsynaptic to bipolar cell terminals and presynaptic to the dendrites of ganglion cells

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40
Q

were it retinal pigment epithelium found? what does it do?

A
  • it surrounds the tips of the outer segments of each photoreceptor
  • as well as being involved with the phagocytosis of expended membranous disks, it also regenerates photopigment molecules after they have been exposed to light
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41
Q

which cells in the retina are light-sensitive? how are cells influenced by light?

A

only the photoreceptors

all other cells are influenced by light only via the direct and indirect synaptic interactions with the photoreceptors:

  • direct synaptic interactions = photoreceptors > bipolar cells > ganglion cells > brain
  • indirect synaptic interactions = photoreceptor cells > bipolar cells (+ horizontal cells) > ganglion cells (+ amacrine cells) > brain
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42
Q

what are the only source of output from the retina?

A

ganglion cells - no other retinal cell type projects an axon through the optic nerve

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43
Q

describe rod photoreceptors

A
  • these have a long, cylindrical outer segment, containing many disks
  • this makes them extremely sensitive to light
  • rods have a low spatial resolution
  • it is therefore specialised for sensitivity at the expense of resolution
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44
Q

describe cone photoreceptors

A
  • these have a shorter, tapering outer segment with fewer membranous disks
  • this makes them relatively insensitive to light
  • cones have a high spatial resolution - it is therefore specialised for acuity at the expense of sensitivity
  • the properties of cones allow humans to see colour
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45
Q

what happens as light intensity increases? what about at low levels of light? what is the names of the different types of vision involving different receptors?

A

• As light intensity increases, cones become more and more dominant in determining what is seen, and they are the major determinant of perception under relatively bright conditions.
• The response of an individual cone does not saturate at high levels of steady illumination.
• The contributions of rods to vision drops out nearly entirely in so called ‘photopic’ vision because their response to light saturates—that is, the membrane potential of individual rods no longer varies as a function of illumination because all of the membrane channels are closed.
 At the lowest levels of light, only the rods are activated – ‘scotopic’ vision.
 ‘Mesopic’ vision occurs in levels of light at which both rods and cones contribute.

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46
Q

people who have lost cone function are what?

A

legally blind

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47
Q

people who have lost rod function experience what?

A

night blindness

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48
Q

describe convergence of rod and cone cells and the ganglion cells - what does this mean in terms of spatial resolution and acuity?

A

• In most parts of the retina, rod and cone signals converge on the same ganglion cells depending on the level of illumination.
• The early stages of the pathways that link rods and cones to ganglion cells, however, are largely independent:
 Rod bipolar cells:
- These do not contact retinal ganglion cells.
- Instead, rod bipolar cells synapse with the dendritic processes of a specific class of amacrine cell that makes gap junctions and chemical synapses with the terminals of cone bipolar cells; these processes, in turn, make synaptic contacts on the dendrites of ganglion cells.
- Each rod bipolar cell is contacted by a number of rods, and many rod bipolar cells contact a given amacrine cell.
 Cone bipolar cells:
- Each retinal ganglion cell that dominates central vision (midget ganglion cells) receives input from only one cone bipolar cell, which, in turn, is contacted by a single cone.

  • Convergence makes the rod system a better detector of light, because small signals from many rods are pooled to generate a large response in the bipolar cell.
  • However, convergence reduces the spatial resolution of the rod system, since the source of a signal in a rod bipolar cell or retinal ganglion cell could have come from anywhere within a relatively large area of the retinal surface.
  • The one-to-one relationship of cones to bipolar and ganglion cells maximizes acuity.
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49
Q

are there more rod or cones in the human retina?

A

In the human retina, there are more rods (~90 million) than there are cones (~4.5 million). This means that the density of rods in the human retina is far greater than the cone density.

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50
Q

what happens in the fovea? how is this achieved?

A

In the fovea, the cone density increases dramatically reaching, at its centre, the highest receptor packing density anywhere in the retina.
 This high density is achieved by decreasing the diameter of the cone outer segments such that foveal cones resemble rods in their appearance.
 The increased density of cones in the central 300 μm of the fovea, called the foveola, is due to the absence of rods.

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51
Q

what allows the cone system to mediate high visual acuity?

A

The high cone density in the fovea, coupled with the one-to-one relationship with the bipolar cells and retinal ganglion cells, allows the cone system to mediate high visual acuity.

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52
Q

what does the exclusion of rods from the fovea and their presence in high density away from the fovea explain?

A

why the threshold for detecting a light stimulus is lower outside the region of central vision

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53
Q

what contributes to superior visual acuity in the fovea?

A

 The layers of cell bodies and processes that overlie the photoreceptors in other areas of the retina are displaced around the fovea, and especially the foveola.
 The retinal blood vessels are diverted away from the foveola. This central region of the fovea is therefore dependent on the underlying choroid and pigment epithelium for oxygenation and metabolic sustenance.

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54
Q

what is phototransduction?

A

when the photoreceptors convert, or transduce, light energy into changes in membrane potential

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55
Q

what happens to the membrane in a photoreceptor when there is light stimulation of the photopigment?

A

light stimulation of the photopigemtn leads to membrane hyperpolarisation rather than depolarisation

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56
Q

in the dark, what is the membrane potential of the rod outer segment? why is it like this? how maintained?

A

In the dark, the membrane potential of the rod outer segment is about -30mV.
 This depolarisation is caused by the steady influx of Na+ through special channels in the outer segment membrane.
 At the same time, K+ ions leave the inner segment, so as to balance the electrochemical gradient across the photoreceptor cell.
 The movement of positive charge (Na+ and K+ - diagram) across the membrane, which occurs in the dark, is called dark current.
 These gated sodium channels are simulated to open by an intracellular second messenger called cyclic guanosine monophosphate (cGMP).
 cGMP is produced continually in the photoreceptor by the enzyme guanylyl cyclase, keeping the sodium channels open.

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57
Q

how does light stimulation of the photopigment cause hyperpolarisation?

A

 Light stimulation of the photopigment activates G-proteins, which in turn activate an effector enzyme that reduces cGMP.
 This causes the cGMP-gated-Na+ channels to close, thus hyperpolarising the cell.

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58
Q

what is the relationship between luminance changes and the rate of transmitter release?

A

• There is a consistent relationship between luminance changes and the rate of transmitter release from the photoreceptor terminals.
• Transmitter release from the synaptic terminals of the photoreceptor is dependent on voltage-sensitive Ca2+/Na+ channels in the terminal membrane.
 In the dark, when photoreceptors are relatively depolarized, the number of open Ca2+/Na+ channels in the synaptic terminal is high, and the rate of transmitter release is correspondingly great.
 In the light, when receptors are hyperpolarized, the number of open Ca2+/Na+ channels is reduced, and the rate of transmitter release is also reduced.

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59
Q

what can the photopigment be thought of as? what’s it called?

A
  • thought of as a receptor protein with a pre-bound light absorbing ‘chromophore’
  • rhodopsin
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60
Q

what is the light absorbing ‘chromophore’ of rhodopsin called? what is it?

what is the receptor protein called?

how are the both of them linked?

A

retinal (11-cis retinal) - a substance derived from vitamin A
(all-trans retinol -> 11-cis retinal)

transducin (opsin)

opsin and 11-cis retinal are covalently linked

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61
Q

what happens to rhodopsin when light is absorbed? what is this called?

A
  • Absorption of light causes a change in the conformation of 11-cis retinal to all-trans retinal.
  • This activates opsin, causing it to be released from 11-cis retinal.
  • Opsin protein is constitutively active
  • Ligand = 11-cis retinal – acts as an ‘inverse agonist’ – keeps opsin in inactive state
  • Photoisomerization to all-trans (‘agonist’) and retinal dissociation triggers signalling

 The activation of opsin causes the activation of transducin, resulting in the conversion of GTP to GDP (by GTPase).
 GDP, along with phosphodiesterase (PDE) hydrolyses cGMP, thus reducing it’s concentration.
 This leads to the closure of the cGMP-gates-Na+ channels.
• Following isomerisation and release form the opsin protein, all-trans retinal is reduced to all-trans retinol.
• This process is called bleaching.

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62
Q

what type of protein in transducin? how does termination of its activity occur?

A

a G-protein

via GTPase activity

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63
Q

the restoration of retinal to a form capable of signalling photons is a complex process known as what? describe it

A

retinoid cycle:
 The all-trans retinol is transported out of the outer segment and into the retinal pigment epithelium.
 Enzymes convert it to 11-cis retinal.
 After it is transported back into the outer segment, the 11-cis retinal recombines with opsin in the receptor disks to form rhodopsin.

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64
Q

why is the recycling of rhodopsin needed?

A

for maintaining the light sensitivity of photoreceptors

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65
Q

what is signal amplification? why is it important?

A
  • One important feature of this biochemical cascade of transduction is signal amplification.
  • Many G-proteins are activated by each photopigment molecule, and each phosphodiesterase enzyme breaks down more than one cGMP molecule.
  • This amplification gives our visual system the ability to detect as little as a single photon, the elementary unit of light energy.
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66
Q

what happens to retinal sensitivity to light as levels of illumination increase?

A

sensitivity to light decreases, preventing the receptors from saturating and thereby greatly extending the range of light intensities over which they operate.

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67
Q

what are the three types of cones?

A

red, green and blue

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68
Q

explain the difference in cone cells

A
  • cones only contain a single photopigment
  • however, each type of cone differs in the photopigment it contains
  • each of these photopigments have a different sensitvity to light of different wavelengths
    • blue or ‘short’ wavelength (only 5-10% of cones, virtually absent at the fovea centralis)
    • green or ‘medium’ wavelength
    • red or ‘long’ wavelength
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69
Q

under normal conditions how can most people match any colour?

A

Under normal conditions, most people can match any colour by adjusting the intensity of three superimposed light sources generating long, medium, and short wavelengths.
 Colour vision is therefore trichromatic.

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70
Q

what do we perceive when all types of cones are equally active?

A

When all types of cones are equally active, as in broad-spectrum light, we perceive “white”.

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71
Q

what are colour vision deficiencies a result of?

A

 The inherited failure to make one or more of the cone pigments.
 An alteration in the absorption spectra of cone pigments.

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72
Q

what is dichromacy?

A

 This is because only two bandwidths of light are needed to match all the colours that these individuals can perceive. This is called dichromacy.
 The third colour category is simply not seen.

  • dichromats can match any colour they see with a mixture of no more than two pure spectral lights.
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73
Q

how is dichromacy inherited? what are the two forms?

A

Dichromacy is inherited as a recessive, sex-linked characteristic and exists in two forms:

  1. Protanopia – blindness to red light so blue and green cones are used.
  2. Deuteranopia – blindness to green light so blue and red cones are used.
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74
Q

why in most cases are the red and green pigments affected?

A

 This is because the red and green pigments show a high degree of sequence homology and lie adjacent to each other on the X chromosome, thus explaining the prevalence of colour blindness in males.
 In contrast, the blue-sensitive pigment gene is found on chromosome 7.

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75
Q

how long does dark adaption take? and what is it?

A

The transmission from all-cone daytime vision to all-rod nighttime vision is not instantaneous; it takes about 20-25 minutes.

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76
Q

what factors affect dark adaption?

A

 Pupil dilation – this allows more light to enter the eye.
 Regeneration of unbleached rhodopsin.
 An adjustment of the functional circuitry of the retina so that information from more rods is available to each ganglion cell.

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77
Q

what happens when the dark-adapted eye goes back into bright light? and why?

A

Sensitivity to light increases greatly during this period.
 Because of this tremendous increase in sensitivity, when the dark-adapted eye goes back into bright light, it is temporarily saturated.

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78
Q

what happens after this temporary saturation? what does this involve?

A

• After this temporary saturation, light adaption begins.
• It involves reversing the changes in the retina that accompanied dark adaption.
• Role of calcium:
 cGMP-gated sodium channels also admit Ca2+ ions.
 In the dark, Ca2+ enters the cones and has an inhibitory effect on the enzyme (guanylyl cyclase) that synthesizes cGMP, thus closing the cGMP-gated channels.
 When the cGMP-gated channels close, the flow of Ca2+ into the photoreceptor is reduced; as a result, more cGMP is synthesized (because the synthetic enzyme is less inhibited), thereby allowing the cGMP-gated channels to open again.

 Essentially, when the channels close, a process is initiated that gradually reopens them even if the light level does not change.

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79
Q

what is the receptive field of a bipolar cell?
what does it consist of?
how does the response of a bipolar cell’s membrane potential to light differ between the two parts?

A

the area of retina that, when stimulated with light, changes the cell membrane’s potential

Two parts:

  1. a circular centre area of retina providing direct photoreceptor input, called the receptive field centre
  2. a surrounding area of the retina providing indirect photoreceptor input via horizontal cells, called the receptive field surround

• The response of a bipolar cell’s membrane potential to light in the receptive field centre is opposite to that of light in the surround! (on centre/off suround, or off centre/on surround)
 If illumination of the centre causes depolarization of the bipolar cell (an ON response - as light hyperpolarises, and on bipolar cells reverse the sign of the cone), then illumination of the surround will cause an antagonistic hyperpolarization of the bipolar cell. (as the surrounding cones becomes hyperpolarised too, so the horizontal cells are less excited so there is less of an inhibitory response to the centre cone, so more neurotransmitter released from centre cone, so on bipolar cell is less excited so hyperpolarisation?

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80
Q

centre ganglion cells

  • what do they respond to
  • what are the different types
  • how do they respond differently
  • what happens though
A

• Each ganglion cell responds to stimulation of a small circular patch of the retina, which defines the cell’s receptive field (RF).
 Turning on a spot of light in the RF centre of an ON-centre ganglion cell produces a burst of action potentials.
 Turning on a spot of light in the in the RP centre of an OFF-centre ganglion cell reduces the rate of discharge.

• Thus:
 ON-centre cells increase their discharge rate to luminance increments in the receptive field centre.
 OFF-centre cells increase their discharge rate to luminance decrements in the receptive field centre.

• However:
 In uniform illumination, the centre and surround cancel to yield some low level of response.

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81
Q

summarise the receptive field subregions and their on and off responses

A

ON center/OFF surround cell: Flashing small bright spot in the center subregion increases the cell’s response. Flashing a bright annulus in the surround subregion inhibits the cell’s response. There is little or no response to a large (full field) spot of light that covers both the center and the surround because excitation in the center cancels the inhibition from the surround, called lateral inhibition.

An OFF-center/ON-surround ganglion cell has the opposite arrangement. It gets inhibition from a small spot of light in the center, and excitation from an annulus in the surround.

  • both types are present in roughly equal numbers

http://www.cns.nyu.edu/~david/courses/
perception/lecturenotes/ganglion/ganglion.html

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82
Q

what are ganglion cells sensitive to?

A

differences between the level of illumination that falls on the receptive field centre and the level of illumination that falls on the surround = luminance contrast

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83
Q

why do receptive fields have overlapping distributions?

A

so that every point on the retina is analysed by severeal ON-centre and several OFF-centre ganglion cells

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84
Q

how is information about increases or decreases in luminance carried to the brain? what does this mean?

A
  • carried separately to the brain by the axons of these two different types of retinal ganglion cells
  • having separate luminance ‘channels’ means that changes in light intensity, whether increases or decreases, are always conveyed to the brain by an increased number of action potentials - this provides unambiguous information about both luminance increments and decrements
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85
Q

what do the ON- and OFF- centre ganglion cells synapse with? and what does depolarisation of those cells cause?

A
  • the terminals of ON and OFF- centre bipolar cells in the inner plexiform layer
  • depolarisation of the central bipolar cells causes the release of glutamate at their terminal synapse with the centre ganglion cells
  • glutamate binds to AMPA/kainite/NMDA receptors
86
Q

when there’s a dark stimulus, how do the different glutamate receptors on the different centre bipolar cells affect what happens to them?

what happens when there is a light stimulus?

A

ON- and OFF-centre bipolar cells express different types of glutamate receptors.

o OFF-centre bipolar cells have ionotropic receptors (AMPA and kainate) that cause the cells to depolarize in response to glutamate released from photoreceptor terminals.

o ON-centre bipolar cells express a G-protein-coupled metabotropic glutamate receptor (mGluR6). When bound to glutamate, these receptors activate an intracellular cascade that closes cGMP-gated Na+ channels, reducing inward current and hyperpolarizing the cell.
(ON-centre bipolar cells do the opposite, therefore the cone cell is depolarised as it’s dark, so the bipolar cell will be hyperpolarised)

• Normally, in a state of depolarisation (dark conditions), the photoreceptor terminals release glutamate, thus inhibiting the ON-bipolar cell but stimulating the OFF bipolar cell.
• Photoreceptors hyperpolarize in response to increased light, decreasing their release of neurotransmitter.
• Under these conditions:
 ON-centre bipolar cells contacted by the photoreceptors are freed from the hyperpolarizing influence of the photoreceptor’s transmitter, and they depolarize.
 In contrast, for OFF-centre cells, the reduction in glutamate represents the withdrawal of a depolarizing influence, and these cells hyperpolarize.

87
Q

horizontal cells

  • where are they found
  • what do they do
  • what effect does this have
A
  • these are cells that are found in the outer plexiform layer (their terminals) and in the inner nuclear layer (their cell bodies)
  • horizontal cells release their neurotransmitter directly onto the photoreceptor terminals in the outer plexiform layer
  • subsequently, this regulates the amount of neurotransmitter that the photoreceptors release onto bipolar cell dendrites
    - glutatmate release from photoreceptor terminals has a depolarising effect on horizontal cells
    - GABA release from horizontal cells has a hyperpolarising effect on the photoreceptor terminals
88
Q

describe the cascade effect when a small spot of light hit a photorecepotr supplying input to the centre of the ganglion cell’s receptive field? what happens with the addition of light to the surround?

A
  • A small spot of light centred on a photoreceptor supplying input to the centre of the ganglion cell’s receptive field produces a strong hyperpolarizing response in the photoreceptor.
  • Under these conditions, changes in the membrane potential of the horizontal cells that synapse with the photoreceptor terminal are relatively small, and the response of the photoreceptor to light is largely determined by its phototransduction cascade.
  • With the addition of light to the surround, however, the impact of the horizontal network becomes significantly greater; the light-induced reduction in the release of glutamate from the photoreceptors in the surround leads to a strong hyperpolarization of the horizontal cells whose processes converge on the terminal of the photoreceptor in the receptive field centre.
  • The reduction in GABA release from the horizontal cells has a depolarizing effect on the membrane potential of the central photoreceptor.
  • This causes an increase in the release of glutamate from the photoreceptor terminals, thus inhibiting the ON-centre ganglion cell but stimulating the OFF-centre ganglion cell.
89
Q

what are the different types of ganglion cells? what are the differences? what is each supplied by - cone or rod?

A

• Most ganglion cells in the retina have a centre-surround receptive field with either ON or an OFF centre.
• They can be distinguished as;
 Large M-Type Ganglion cells – 5% of population. [M = ‘magno’ = large]
 Smaller P-Type ganglion cells – 90% of population. [P = ‘parvo = small]
 The remaining 5% is made up of a variety of nonM-nonP ganglion cell types. These are less well characterised.

• M-type ganglion cells :
 Have larger receptive fields than P-type ganglion cells.
 Their axons conduct action potentials more rapidly in the optic nerve.
 They are more sensitive to low contrast stimuli.
 Respond to stimulation of their receptive field centres with a transient burst of action potentials, while P-type ganglion cells respond with a sustained discharge as long as the stimulus is on.

• P-type ganglion cells can transmit information about colour, whereas M-type ganglion cells cannot.

  • As a result, P-type ganglion cells are sensitive to differences in the wavelengths of light striking their receptive field centre and surround.
  • Although M-type ganglion cells also receive inputs from cones, there is no difference in the type of cone (red, green or blue) input to the receptive field centre and surround; the centre and surround of each M-type cell receptive field is driven by all cone types.
90
Q

what are colour-opponent ganglion cells? what are the two types of opponency? what are the concepts? give examples of opponency.

A
  • Some P-type ganglion cells and nonM-nonP cells are sensitive to differences in the wavelength of the light.
  • These colour-sensitive neurons are called color-opponent cells, reflecting the fact that the response to one wavelength in the receptive filed centre is cancelled by showing another wavelength in the receptive field surround.

• Two types of opponency are found:

  1. Red vs. Green
  2. Blue vs. Yellow

Concepts
• Either colour in the combinations above can be the ON-centre or the OFF-surround.
• The neuron responds to its ON –centre by firing action potentials.
• If the centre coloured stimulus encompasses the surround as well, the firing of action potentials still occurs, but with a dampened effect.
• The neuron is only inhibited when its corresponding colour lands on the OFF-surround.

  • White light encompasses all visible wavelengths; therefore, both the centre and the surround would be equally activated, thereby cancelling the response of the cell.
  • The lack of colour opponency in M-type ganglion cells is accounted for by the fact that both the centre and surround of the receptive field receive input from more that one type of cone.

Example: Red – Green Opponency
• In this example, we will have a red ON-centre and a green OFF-surround.
• The centre of the receptive field is fed mainly by red cones; therefore, the cell responds to red light by firing action potentials.
• Note that even a red light that bathes the entire receptive field is an effective stimulus. However, the response is reduced.

Example: Blue – Yellow Opponency
• In this example, we will have a blue ON-centre and a yellow OFF-surround (B+Y-).
• Blue light drives blue cones that feed the receptive field centre.
• Yellow light activates both red and green cones that feed the surround.
• Diffuse blue light would be an effective stimulus for this cell with a dampened response.
• Yellow light on the surround would cancel the response.
• Diffuse white light too would cancel the response.

91
Q

give a summary of light energy hitting photoreceptors to getting to the ganglion cells

A
  • Light energy is first converted into membrane potential changes in the photoreceptors.
  • Photoreceptor membrane potential is converted into a chemical signal (the neurotransmitter glutamate), which is again converted into membrane potential changes in the postsynaptic bipolar and horizontal cells.
  • This process of electrical-to-chemical-to-electrical signaling repeats again and again, until the presence of light or dark or color is finally converted to a change in the action potential firing frequency of the ganglion cells. This is done through the complex processes outlined above (receptive fields, colour opponency etc).
  • The information from the 125 million photoreceptors is funneled into 1 million ganglion cells.
  • In the central retina, particularly the fovea, relatively few photoreceptors feed each ganglion cell, whereas in the peripheral retina, thousands of receptors do. They develop a one-to-one relationship at the fovea.
  • This specialization ensures high acuity in central vision but also requires that the eye move to bring the images of objects of interest onto the fovea.
92
Q

upon exiting the eye, what happens to the fibres of the optic disc

A

they become myelinated - the fibre are unmyelinated in the retina to allow for better transmission of light onto the photoreceptors

93
Q

the optic disc is recognised as the site from which what (excluding optic nerve) enter and leave the eye?

A

ophthalmic artery and veins

94
Q

what is the appearance of the optic disc a useful gauge of? why?

A

‘intracranial’ pressure

The subarachnoid space surrounding the optic nerve is continuous with that of the brain; as a result, increases in intracranial pressure can be detected as papilloedema (swelling of the optic disc)

95
Q

describe the primary visual pathway

A

• Once past the chiasm, the ganglion cell axons on each side form the optic tract.
• The ganglion cell axons in the optic tract reach a number of structures in the diencephalon and midbrain.
• The major target in the diencephalon is the dorsal lateral geniculate nucleus of the thalamus.
• Neurons in the lateral geniculate nucleus send their axons to the cerebral cortex via the internal capsule.
• These axons pass through a portion of the internal capsule called the optic radiation and terminate in the primary visual cortex, (striate cortex, brodmann’s area 17, V1), which lies largely along and within the calcarine fissure in the occipital lobe.
 Ganglion cells that lie in the nasal division of each retina give rise to axons that cross in the chiasm.
 Ganglion cells that lie in the temporal retina give rise to axons that remain on the same side.

96
Q

describe the secondary visual pathway - what is each for?

A

• Optic nerve fibres reach the optic chiasm.
• Projections are given to:
 Superior colliculus
o Coordinates head and eye movements to visual (and other) targets.
 Pretectum
o Coordinates the pupillary light reflex.
o Afferent fibres terminate in the pretectal nucleus and pass to the Edinger-Westphal nucleus, which then project to the ciliary ganglion of the oculomotor nerve, causing contraction of the constrictor pupillae muscles.
 Hypothalamus (suprachiasmatic nucleus)
o These fibres are involved in the circadian cycle.
o The fibres that project here express their own light-sensitive photopigment (melanopsin).

97
Q

which are the fibres containing melanopsin? what are they capable of doing in the absence of signals from rods and cones? what does this mean for circadian rhythms?

A

The fibres containing melanopsin (fibres to Pretectum and hypothalamus) are capable of modulating their response to changes in light levels in the absence of signals from rods and cones. Therefore, the circadian rhythms are maintained even after the degeneration of photoreceptors.

98
Q

describe the decussation at the optic chiasm. why is it important?

A
  • The crossover of retinal ganglion cell axons within the chiasm isn’t linear (as seen in the diagram).
  • The fibres from the nasal division of the retina decussate within the chiasm.
  • The fibres from the nasal division of the retina form a structure called the anterior/ posterior knee of Willbrand.
  • This is significant when considering lesions of the visual pathways.
99
Q

lateral geniculate nucleus

  • what receives input from
  • organisation
  • role of striate cortex
  • imbalance in activity of eye leads to what
A
  • The lateral geniculate nucleus receives input from both eyes via ganglionic cell nerve fibres > optic chiasm > optic tract.
  • Although it receives input from both eyes, the axons terminate in separate layers, so that individual geniculate neurons are monocular, driven by either the left or the right eye.
  • Inputs from the left and right eyes remain segregated beyond the geniculate because the axons of geniculate neurons terminate in alternating eye-specific columns within cortical layer IV—the so-called ocular dominance columns.
  • Bringing together the inputs from the two eyes at the level of the striate cortex provides a basis for stereopsis, the special sensation of depth that arises from viewing nearby objects with two eyes instead of one.
  • Anything that creates an imbalance in the activity of the two eyes—for example, the abnormal alignment of the eyes during infancy (strabismus)—can permanently reduce the effectiveness of one eye in driving cortical neurons, and thus impair the ability to use binocular information as a cue for depth.
100
Q

what is the striate cortex?

A
  • part of the visual cortex that is involved in processing visual information
  • first cortical visual area that receives input from the lateral geniculate nucleus in the thalamus
  • named because it is ‘striated’ (layered)
101
Q

describe the organisation of the layers of the LGN and the neuronal populations

A

Layers of the Lateral Geniculate Nucleus
• It consists of 6 layers.
 Right eye = layers 2,3,5 of the RLGN
 Left eye = layers 1,4,6 of the RLGN

• The LGN is organised into 6 distinct neuronal populations occupying separate layers:
 Magnocellular neurons (the 2 ventral layers):
 These are located in layers 1 and 2.
 These are composed of large neurons.
 These are called the magnocellular layers because they receive information from the M-type (‘magno’) ganglion cell fibres.
 These neurons are important for high temporal resolution – location, speed and direction of a rapidly moving object.
 These neurons convey motion signals [remember: Magnocellular = Motion].

 Parvocellular neurons (the 4 dorsal layers):
 These are located in layers 3, 4, 5 and 6.
 These are composed of small neurons.
 These are called parvovellular layers because they receive information from the P-type (‘parvo’) ganglion cell fibres.
 These neurons are important for high spatial resolution vision – detailed analysis of the shape, size and colour of objects.
 These neurons receive information from red and green cones (red-green opponency).

 Koinicellular/ Interlaminar neurons:
 These are located between the magno- and parvocellular layers.
 These neurons receive information from blue and yellow cones (blue-yellow opponency).
• The axons of relay cells in the magno- and parvocellular layers of the lateral geniculate nucleus terminate on distinct populations of neurons in layer IV of striate cortex.
 The magnocellular layers of the LGN, conveying information about movement and gross spatial features, project mainly to layer 4Cα.
 The parvocellular layers of the LGN, carrying fine spatial information, terminate mainly in layer 4Cβ.
• The koniocellular fibres (and some pavocellular fibres), carrying information about colour, project to the superficial layers (layers II and III) of striate cortex, called blobs.

102
Q

what is the functional organisation of the striate cortex?

A
  • Cortical neurons respond vigorously to light–dark bars or edges, but only if the bars are presented at a particular range of orientations within the cell’s receptive field.
  • The responses of cortical neurons are thus tuned to the orientation of edges; the peak in the tuning curve (the orientation to which a cell is most responsive) is referred to as the neuron’s preferred orientation - The vertical columns are called orientation columns.
  • All edge orientations are roughly equally represented in visual cortex. As a result, a given orientation in a visual scene appears to be “encoded” in the activity of a distinct population of orientation-selective neurons.

• In each orientation column, there are two types of cell.
1. Simple cells - these respond to stationary bars of a certain orientation from a single visual field.
 These cells are monocular.
2. Complex cells - these are not direction sensitive but respond preferentially to bars of light of the same orientation as the simple cells, but moving across the receptive field, parallel to the preferred orientation.
 These cells are binocular.

• Each class of orientation-selective neuron transmits only a fraction of the information in the scene – the part that matches its filter properties (i.e. the orientation it is encoded for) – but the information from these different filters contains all the spatial information necessary to generate a faithful representation of the original image.

103
Q

pupillary constriction

  • afferent pathway
  • efferent pathway
A

• Afferent Pathway
 Light generates action potentials in optic nerve axons.
 Axons (some decussating at the chiasm) pass through each lateral geniculate body.
 Axons synapse at each pretectal nucleus.

• Efferent Pathway
 Action potentials pass to each Edinger-Westphal nucleus ‘bilaterally’ (thus effecting both eyes simultaneously) of the oculomotor nerve (CN III).
 This nucleus supplies preganglionic parasympathetic fibres to the ciliary ganglion.
 These cause the constriction of the concentric muscles (constrictor pupillae) in the iris, thus constricting the pupil.

104
Q

under normal conditions, what does light in one eye produce?

A

constriction of both the stimulated eye (the direct response) and the unstimulated eye (the consensual response)

105
Q

what’s the pathway for pupillary dilation?

A

Sympathetic impulses via fibres in the nasociliary (long ciliary) nerve pass to dilator pupillae (radial muscle).

 Sympathetic preganglionic fibres to the eye (and face) originate in the hypothalamus, pass uncrossed through midbrain and lateral medulla, and emerge from the spinal cord at T1 (close to the lung apex) to form the superior cervical ganglion at C2.
 Postganglionic fibres form a plexus around the carotid bifurcation.
 Fibres pass to the dilator pupillae (in the iris) and cause it to constrict, thus dilating the pupils.

106
Q

what happens to different types of relfex when there is optic nerve damage on one side?

A
  • ipsilateral direct reflex = lost
  • contralateral direct reflex = intact
  • ipsilateral consensual reflex = lost
  • contralateral consensual reflex = intact
107
Q

what happens to different types of relfex when there is oculomotor nerve damage on one side?

A
  • ipsilateral direct reflex = lost
  • contralateral direct reflex = intact
  • ipsilateral consensual reflex = intact
  • contralateral consensual reflex = lost
108
Q

what is the test for relative afferent pupillary defect? what happens and why?

A

Move torch quickly from pupil to pupil. If there has been incomplete damage to the afferent pathway, the affected pupil will dilate (slightly) when light is moved from the normal eye to the abnormal eye. This is because there is reduced afferent input from the affected eye and so the consensual pupillary relaxation response from the normal eye predominates. This is Marcus gunn sign.

  • Looking for afferent pupillary defects
  • In dark room, you shine light in one eye and then swing over to the other eye, then swing back to the first eye and swing back to the second eye
  • If there’s a defect in on the afferent pathways, when you swing to that eye both eyes will dilate, because is bilateral innervation, but when you swing back to normal eye both pupils constrict again
  • No light
  • Normal response to light – both pupils constrict
  • Positive RAPD (relative afferent pupillary defect) of right eye – both pupils dilate
109
Q

describe the convergence reflex and pathway

A

• Fixation on a near object requires convergence of the ocular axes and is accompanied by pupillary constriction.
• Afferent fibres in each optic nerve, passing through each lateral geniculate body, also relay to the convergence centre.
 This centre receives 1a spindle afferents from extraocular muscles.
• The efferent autonomic route is convergence centre to Edinger–Westphal nucleus to ciliary ganglion and pupils.

110
Q

where is information from the left half of the visual world represented?

A

Information from the left half of the visual world, whether it originates from the left or right eye, is represented in the right half of the brain, and vice versa.

111
Q

how is the retina subdivided? how is imaged formed? objects in the monocular portions of the visual hemifields are seen only by which part of retina?

A
  • The surface of the retina is subdivided by vertical and horizontal lines that intersect at the centre of the fovea.
  • The vertical line divides the retina into nasal and temporal divisions and the horizontal line divides the retina into superior and inferior divisions.
  • Corresponding vertical and horizontal lines in visual space intersect at the point of fixation and define the quadrants of the visual field.
  • The crossing of light rays diverging from different points on an object at the pupil causes the images of objects in the visual field to be inverted and left-right reversed on the retinal surface.
  • As a result, objects in the temporal part of the visual field are seen by the nasal part of the retina, and objects in the superior part of the visual field are seen by the inferior part of the retina.
  • Objects in the monocular portions of the visual hemifields are seen only by the most peripheral nasal retina of each eye.
112
Q

what are the extents of the viual fields, in terms of degrees?

A
  • Superior Field = 60 degrees above the line of sight
  • Inferior Field = 75 degrees below the line of sight
  • Nasal Field = 60 degrees medial to the line of sight
  • Temporal Field = 100 degrees lateral to the line of sight
113
Q

what is the superior field limited by? what happens with ageing?

A

The superior field is limited by the frontal bone. It becomes restricted with ageing because the frontal bone depresses slightly and the eye ball is withdrawn into the orbit.

114
Q

describe contralateral hemifield mapping

A
  • For the primary visual pathway, the map of the contralateral hemifield is established as such that information from the centre of vision (i.e. the fovea) is represented in the most posterior part of the striate cortex.
  • Information from the more peripheral regions of the retina is represented in progressively more anterior parts of the striate cortex.
  • Information from the upper visual field is mapped below the calacrine sulcus.
  • Information from the lower visual field is mapped above the calacrine sulcus.
115
Q

what is cortical magnification?

A
  • Cortical magnification refers to the fact that the number of neurons in the visual cortex responsible for processing the visual stimulus of a given size varies as a function of the location of the stimulus in the visual field.
  • Stimuli occurring in the centre of the visual field that have been detected in the fovea of the retina are processed by a very large number of neurons in the primary visual cortex of the occipital lobe, though these neurons handle only a very small region of the central visual field.
  • Conversely, stimuli detected in the peripheral visual field tend to be processed by a much smaller number of neurons in the primary visual cortex.
116
Q

is damage to central visual structures complete usually? expand

A

• Damage to central visual structures is rarely complete.
• As a result, the deficits associated with damage to the chiasm, optic tract, optic radiation, or visual cortex are typically more limited than those shown.
 This is especially true for damage along the optic radiation, which fans out under the temporal and parietal lobes in its course from the lateral geniculate nucleus to the striate cortex. Some of the optic radiation axons run out into the temporal lobe on their route to the striate cortex, a branch called Meyer’s loop.

117
Q

what is macular sparing? with what is it commonly found?

A

Injury to central visual structures can also cause ‘macular sparing’.
 Macular sparing is commonly found with damage to the cortex.
 Macula sparing is where the central 5-10 degrees is unaffected in an otherwise hemianopic defect.

118
Q

what is an anopia?

A

a defect in the visual field

119
Q

what are different types of partial anopia?

A

 Hemianopia – decreased vision/ blindness in half the visual field of one or both eyes, usually on one side of the vertical line.
 Homonymous heminopia – loss of half of the visual field on the same side in both eyes.
 Heteronymous heminopia: loss of half of the visual field on different sides in both eyes.
- Binasal heminopia – loss of field surrounding the nose.
- Bitemporal heminopia – loss of field closest to the temples.
 Quadrantanopia – decreased vision/ blindness in one quarter of the visual field.

120
Q

give a summary of the visual pathway

A

Each retina is divided into two halves; temporal and nasal. Axons from the retina form the optic nerve. At the optic chiasm, fibres from the nasal half of each retina decussate and join the uncrossed fibres from the lateral half of the retina (from the other eye) to form the optic tract. These fibres project to the lateral geniculate nucleus (LGN) of the thalamus, where they synapse with second order neurons. The second order neurons pass in the optic radiations to the striate cortex.
Some fibres bypass the LGN and project to the superior colliculus in the midbrain. Here the information is interpreted in conjunction with the afferent information from the somatosensory cortex, frontal eye field and the spinal cord. Efferent fibres project to the brainstem nuclei (pretectal nuclei > Edinger-Westphal nuclei) to bring about the pupillary light reflex and reflex movements of the eye, and to the spinal cord to initiate neck movement.
Other fibres bypass the LGN and project to the suprachiasmatic nucleus of the hypothalamus, and are involved in circadian rhythms.

121
Q

what do visual field tests assess?

A

the potential presence of blind spots (scotomas), which could indicate ocular pathology

  • Blind spot in temporal visual field at about 15 degrees eccentricity (due to optic disc)
122
Q

what is the most common type of visual field test called? describe the process

A

automated perimetry (Goldmann perimetry)

 This measures the response to the presence of objects in different areas in the visual field.
 The patient’s head is held still, usually with a chin rest inside a large bowl-like instrument.
 The patient stares at a source of light straight ahead.
 Random lights of different intensities are flashed in the peripheral visual field.
 The patient presses a button to indicate their response when they perceive the computer-generated light suddenly appearing in their field of vision.
 If they can’t see objects in an appropriate portion of their field of view, they may have a blind spot indicating vision loss.

GOLDMANN VISUAL FIELDS

  • Spots of different size and intensity allow isopters to be plotted
  • Isopters are lines joining points of equal sensitivity (circles around the macula I think?)

HUMPHREY VISUAL FIELD ANALYSER

  • Standard one that use now
  • Show visual field defects
123
Q

how far is the pituitary gland away from the optic chiasm? what does this mean in terms of tumours?

A
  • some distance away

- tumour needs to be quite large before it can interfere with the chiasm

124
Q

what are the two types of pituitary tumour?

A
  1. Hormone secreting:
     Patients with this type of tumour normally seek medical advice prior to occurrence of visual field defects.
     This is because the excessive secretion of hormones will bring about other systemic symptoms, which would result in the patient going to the doctor.
  2. Non-hormone secreting tumour:
     Vision loss will occur prior to any other systemic symptoms.
125
Q

after removal of the tumour, there is usually some recovery of visual field over what time period?

A

1-2 months

the quality of life of the patient is dependent on the pre-surgical severity

126
Q

what is the most frequent cause of diminished visual acuity?

A

refractive error: light rays entering the eye are not properly brought into focus on the retina

127
Q

in the absence of ophthalmic pathology, best-corrected visual acuity should equal what?

A

6/6 vision

128
Q

what are the different errors? what are they caused by?

A

Myopia (short-sightedness):
 This can be caused by the corneal surface being too curved, or by the eyeball being too long.
 The image of distant objects focus in front of the retina, instead of on the retina.

Hyperopia/Hypermetropia (long-sightedness):
 This can be caused by the corneal surface not being curved enough, or by the eyeball being too short.
 The image of near objects focus behind the retina, instead of on the retina.

Presbyopia:
 This is the normal ageing of the lens which leads to a change in the refractive state of the eye.
 As the lens ages it becomes less able to alter its curvature and this causes difficulty with near vision.
(long-sightedness caused by loss of elasticity of the lens)

129
Q

myopia

  • what is it
  • physiological - cause, onset, dioptre, treatment
  • pathological - cause, dioptre, predisposition, association, treatment
A

• Myopia is a common condition in which the refracting power of the eye at rest is too great in relation to the axial length of the eye; the focused image of an object lies anterior to the retina.
• Physiological Myopia
 Results from a mismatch between the refracting power of the eye and the axial length of the globe when neither of these components lies outside the normal range.
 Onset begins in the second decade and may progress through the third decade.
 Physiologic myopia is not thought to be heritable, but there appears to be an increased frequency of the disorder among higher socioeconomic groups and among those with greater academic training.
 Physiologic myopia usually ranges from about 0.5 to about 8.0 D, where the eye appears normal on physical and radiographic evaluation.
 Treatment – concave (minus)/ diverging lenses/spectacles.

• Pathological Myopia
 Pathologic myopia is a heritable condition in which the eye is abnormally long; the refracting apparatus is usually normal.
 Refractive error in pathologic myopia is usually greater than about 8.0 D.
 Patients with pathologic myopia are predisposed to retinal pathologies.
 Pathologic myopia may be associated with systemic disorders. Dilated fundus examination should be performed at frequent intervals, and patients should be alerted to symptoms of retinal detachment.
 Treatment – concave (minus)/ diverging lenses/spectacles.

130
Q

hyperopia

  • what is it
  • who normal in
  • cause in adolescents and adults
  • accommodation
  • symptoms
  • treatment
A

• The refracting power of the eye is insufficient to bring the focused image of an object onto the retina; the image lies posterior to the retinal plane.

  • Hyperopia is the normal condition in infants and young children.
  • Adolescent and adult hyperopia is not usually associated with anatomic abnormalities of the posterior segment.
  • Many patients with hyperopia are able to overcome their refractive deficiency by accommodating even when viewing at distance.
  • The ability to accommodate diminishes with age.
  • In addition to blurred vision, hyperopia may incite headaches in young adults because increasing effort is required to focus at intermediate distances.
  • Treatment - convex (plus)/ converging lenses/spectacles.
131
Q

how can colour vision be estimated? what is ‘red desaturation’?

A
  • Colour vision can be estimated by the patient looking at a red object (e.g. a red pen) with each eye.
  • If there is an optic nerve or tract lesion on one side the colour looks pink, dull or washed out with that eye. This is ‘red desaturation’.
132
Q

what is astigmatism?

A

a condition in which the corneal surface is asymmetric: light is refracted differently along different axes - light is refracted to multiple areas of the retina

  • it may be myopic in one plane and hypermetropic or emmetropic in the other plane
133
Q

in regular astigmatism, the steepest corneal axis lies how many degrees away from the flattest corneal axis?

how can regular astigmatism usually be corrected?

A

90 degrees - a configuration geometrically labelled an ellipsoid cap

with cylindrical and spherical spectacle lenses or with rigid contact lenses

134
Q

what may irregular astigmatism produce?

how is irregular astigmatism corrected?

A

an array of corneal configurations, usually owing to corneal ectasis, such as keratoconus (degenerative changes of the cornea that make it a more conical shape), or corneal scarring

irregular astigmatism is not correctable with spectacles but may be correctable with rigid contact lenses

135
Q

what is ambylopia? when does it develop?

A

functional reduction in visual acuity of an eye caused by disuse during visual development

it almost always develops before age 2

136
Q

what can occur in the affected eye if amblyopia is not detected and treated? why does it lead to this? what is needed for the visual system to develop properly?

A

Blindness can occur in the affected eye if amblyopia is not detected and treated before age 8.

  • The brain must simultaneously receive a clear, focused, properly aligned, overlapping image from each eye for the visual system to develop properly.
  • This development takes place mainly in the first 3 years of life but is not complete until about 8 years of age.
  • Amblyopia results when there is persistent interference with the image from one eye but not the other.
  • The visual cortex suppresses the image from the affected eye. If suppression persists long enough, vision loss can be permanent.
137
Q

what are causes of amblyopia?

A

 Strabismus can cause amblyopia because misalignment of the eyes results in different retinal images being sent to the visual cortex. Because the visual pathways are developed in adults, presentation of 2 different images results in diplopia rather than suppression of one image.
 Anisometropia (inequality of refraction in the 2 eyes, most often resulting from astigmatism, myopia, or hyperopia) results in different focus of the retinal images, with the image from the eye with the greater refractive error being less well focused.
 Deprivation amblyopia is caused by obstruction of the visual axis at some point between the surface of the eye and the retina (eg, by a cataract), this interferes with or completely prevents formation of a retinal image in the affected eye

138
Q

what is the treatment of amblyopia?

A

spectacles or contact lenses, cataract removal, patching

139
Q

what is strabismus (squint)?

A
  • if there is an imbalance in the extraocular muscles of the two eyes, the eyes will point in different directions
  • such a misalignment (in the horizontal plane) or lack of coordination between the two eyes is called strabismus
  • in most cases, strabismus is congenital
140
Q

what are the two types of strabismus?

A
  1. Esotopia (convergent squint) – the directions of gaze of the two eyes cross, and the person is said to be cross-eyed.
  2. Exotopia (divergent squint) – the directions of the gaze diverge, and the person is said to be wall-eyed.
141
Q

how do our bodies deal with strabismus?

A
  • children are able to avoid diplopia (double vision) by involuntarily suppressing one of the images
  • left and right images are sometimes suppressed alternately, in which case excellent vision may develop in each eye, but binocular vision does not develop in either situation
  • more frequently, one eye is constantly suppressed, preventing normal visual development in that eye
142
Q

what is the treatment for strabismus?

A
  • should be treated in early childhood

- involves the use of prismatic glasses, surgery to the extrocular muscles to realign the eyes or cycloplegic refraction

143
Q

what happens to strabismus without treatment?

A
  • Without treatment, conflicting images are sent to the brain from the two eyes, degrading depth perception (poor stereoacuity), and, more importantly, causing the person to suppress input from one eye.
  • The dominant eye will be normal but the suppressed eye will become amblyopic, meaning that is has poor visual acuity.
  • If medical intervention is delayed until adulthood, the condition cannot be corrected.
144
Q

what is the leading cause of blindness in the world?

A

cataract, or opacification (clouding) of the crystalline human lens

145
Q

who are cataracts seen in? what causes it?

A
  • It is usually a condition of the elderly (over 65 years of age). Nearly all patients older than 50 demonstrate some degree of degenerative lens changes when examined by slit lamp.
  • In most cases, there is normal ageing changes in which progressive yellowing of the lens nucleus (nuclear sclerosis) and hydration of the lens cortex are seen.
  • Genetic predisposition to senile cataract (cataract in old age) has been hypothesized but not proved.
  • Prolonged exposure to ultraviolet radiation has been shown to be cataractogenic.
  • Congenital and traumatic cataracts can occur from a variety of changes.
146
Q

what is treatment for cataract?

A

 Cataract surgery
 The lens is removed and replaced with an artificial plastic lens.
 Although the artificial lens cannot adjust its focus like the normal lens, it provides a clear image, and glasses can be used for near and far vision.

147
Q

what is glaucoma?

A

progressive loss of vision associated with elevated intraocular pressure

148
Q

what causes increase in intraocular pressure? and what causes gradual visual loss?

A
  • Aqueous humor is produced in the ciliary body and passes from the posterior chamber through the pupil into the anterior chamber.
  • Pressure in the aqueous humor plays a crucial role in maintaining the shape of the eye.
  • As this pressure increases (due to increased production or decreased drainage of aqueous humor), it compresses the retinal blood vessels, causing degeneration of the optic nerve.
  • The optic nerve axons are compressed, and vision is gradually lost from the periphery inward.
149
Q

by the time a person notices a loss of more central vision, what damage is done?

A

Unfortunately, by the time a person notices a loss of more central vision, the damage is advanced and a significant portion of the eye is permanently blind.

150
Q

what is essential with glaucoma? treatment?

A

Early detection and treatment with medication (eye drops) or surgery (trabeculectomy - small hole in sclera, followed by a trap-door in sclera) to reduce intraocular pressure are essential.

151
Q

primary open-angle glaucoma (POAG)

  • how common
  • what happens
  • screening method
  • treatment
  • risk factors
  • diagnosis
A
  • This is the most common form of glaucoma.
  • The anterior chamber angle anatomy appears normal, but aqueous outflow is reduced.
  • High intraocular pressures result from reduced outflow of aqueous humour through the trabecular meshwork/ canal of Schlemm.
  • Progressive visual field loss begins in the periphery and occurs so insidiously that affected individuals may be unaware until late in the disease course.
  • Intraocular tension measurement is an effective screening method.
  • Medical treatment attempts to reduce aqueous production by the ciliary body or to increase outflow through the trabecular meshwork (trabeculectomy) or uvea.

• Common risk factors include age, race (black Africans are greater risk), positive family history and myopia.
- Diagnosis is only made if the IOP is measured. Visual fields are performed and show a normal blind spot with scotomas.

152
Q

acute angle-closure glaucoma (AACG)

  • severity
  • what happens
  • risk factors
  • symptoms
  • treatment
A
  • This is an ophthalmic emergency.
  • This occurs due to reduced aqueous drainage as a result of the ageing lens pushing the iris forward against the trabecular meshwork.
  • People most at risk are hypermetropes (extreme long-sightedness) and women.
  • The attack is more likely to occur under reduced light conditions when the pupil is dilated.
  • AACG causes pressure build-up behind the iris, causing sudden onset of a red painful eye and blurred vision.
  • Patients become unwell with nausea and vomiting and complain of headache and severe ocular pain.
  • Prompt treatment – eye drops to reduce the intraocular pressure- is required.
153
Q

what are the different eye drops used to treat glaucoma?

A

• Prostaglandin Analogue (Laatanoprost/Xalatan) – reduce intraocular pressure by increasing the outflow of aqueous humor.
 These drugs increase the uveoscleral outflow mainly.
• Beta-blocker (Timolol) – reduce intraocular pressure by decreasing the production of aqueous humor.
 It increases the peripheral resistance and so there is less blood supply to the ciliary body, thus there is reduction in the production of aqueous humor.
• Carbonicanhydrase Inhibitor (Brinzolamide) – reduce intraocular pressure by decreasing aqueous humor production/secretion.
 Inhibition of this enzyme in the ciliary processes slows the formation of bicarbonate, and reduces sodium and fluid transport.

154
Q

retinal detachment

  • what does it cause
  • what is it usually secondary to
  • what does the shadow correspond to
  • what happens following a tear
  • symptoms
  • treatment
A
  • This causes a painless progressive visual field loss.
  • This is usually secondary to trauma or diabetes.
  • The shadow corresponds to the area of detached retina.
  • Following a tear in the retina, fluid (from the vitreous space) collects in the potential space between the sensory retina and the pigment epithelium.
  • Symptoms - sudden onset of floaters often associated with flashes of light prior to the detachment.
  • Treatment – laser surgery to scar the edge of the retinal tear, thereby attaching the retina to the back of the eye.
155
Q

retinitis pigmentosa

  • what is it
  • cause
  • symptoms
  • what happens clinically
  • treatment
A

• Retinitis pigmentosa (RP) is characterized by progressive vision loss due to a gradual degeneration of photoreceptors.
• There is no known cause, but there is clearly a strong genetic component.
• The photoreceptor cells appear to die by apoptosis:
 Loss of rods may lead to early night blindness and constricted visual fields.
 Loss of cones may affect central visual acuity.
• Symptoms – the first sign is usually a loss of peripheral vision and night vision.
• Clinically, retinal atrophy is accompanied by constriction of retinal vessels and optic nerve head atrophy (“waxy pallor” of the optic disk) and the accumulation of retinal pigment around blood vessels, thus accounting for the “pigmentosa” in the disease’s name.
• Treatment - oral supplements of vitamin A palmitate. This slows the course of the disease, although the disease is slowly progressive over decades already.

156
Q

age-related macular degeneration (AMD)

  • what happens
  • cause
  • risk factors
  • types
  • treatment
A
  • In this condition, patients only lose their central vision.
  • The cause is unknown but risk factors include increasing age, smoking, hypertension, hypercholesterolemia and ultraviolet exposure.
  • There are two types of AMD: dry and wet

Non-exudative (Dry) Macular Degeneration
• There is painless and progressive loss of vision.
• With age, lipofuscin deposits (drusen) are found between the retinal pigment epithelium (RPE) and Bruch’s membrane.
• Drusen may be hard or soft and there may be focal RPE detachment.
• Not all patients with these changes will be affected visually but some develop distortion and blurring of their central vision.
• Extensive atrophy of RPE can occur (geographic atrophy).

Exudative (Wet) Macular Degeneration
• This accounts for only 10% of the cases.
• It occurs with the development of abnormal subfoveal choroidal neovascularisation in the region of the macula and causes severe central visual loss.

• Treatment:
 Laser surgery can sometimes minimise further vision loss, but the disease currently has no known cure.
 Vitamins C and E – this slows the progression of the disease.
 β carotene - this slows the progression of the disease.
 Zinc and copper - this slows the progression of the disease.

157
Q

what are the main feature of perception?

A

 Perception is knowledge based and partly learned.
 Perception is inferential - We perceive the whole person and not half a person.
 It is categorical – We like to categorize what we see.
 Perception is relational - what we see as small or large depends on the context.
 Perception is adaptive – we tend to perceive significant things better than insignificant.

158
Q

how do we recognise what is perceived? different types of processing

A

 Bottom-up processing – The perceptual system is assumed to analyse a stimulus into a set of features and then the brain matches/compares it to other sets already existing in the brain. If a match occurs, then recognition occurs.
 Top-down processing – The context creates expectancy and sets up what is known as “perceptual set”. We “see” what we expect, or want to see, and recognition occurs.
 Both mechanisms together – In trying to read a page of poor handwriting we may use both processes: puzzling out what each letter looks like, as well as guessing meaning from the context.

159
Q

how do we influence perception?

A

 We control perception by paying attention to different aspects of our environment.
 Attention is the directing and focusing of perception.
 It may be:
- Selective – we attending more to stimuli that are changing, repeated, intense and personally meaningful.
- Divided or focused – Our ability to divide attention is limited, although it can be improved with practice.
- Negatively affected by stress and fatigue.

160
Q

what is stigma? what are the different types?

A

• Stigma involves a negative evaluation of and associated lowering of respect for individuals because of some personal characteristic, which may be physical or behavioural.

  • Stigma – branding or marking.
  • Enacted Stigma – societal reaction produces discriminatory experiences (non-sufferers treat the stigmatised individual differently).
  • Felt Stigma – expected societal reactions can change self-identity (individual feels embarrassed or shamed regardless of what others do or feel).
  • Curiosity Stigma
161
Q

how is disability typically assessed?

A

• Disability is typically assessed by measures of activities of daily living (ADL), which assess the person’s ability to perform everyday self-care or mobility activities.
• These measures assess activities that virtually everyone would wish to perform and, therefore, do not include activities that may be important for particular individuals.
• There are two main methods of assessment;
 Self-report
 Observation

162
Q

what’s the difference between orthoptist and ophthalmologist?

A

3 year degree course for orthoptist, ophthalmologist is a medical doctor

163
Q

how many bones is the bony orbit made up of?

A

7

164
Q

where do all rectus muscles originate from?

A

annulus of Zinn/common tendinous ring = apex of orbit

  • Oval shaped thickening of the periosteum at the orbital apex
  • Encloses the optic canal and part of the superior orbital fissure
165
Q

where is the equator of the eye?

A

line that bisects the eyeball that’s in the coronal plane and separates the anterior and posterior

166
Q

what lies above the annulus of Zinn?

A

Lying above the annulus of Zinn on the lesser wing of the sphenoid are the origins of the levator palpebrae superioris and superior oblique muscle

167
Q

what are the three rotations of the eye? what do they involve?

A
  • Yawing (around vertical axis) (side-to-side)
  • Rolling (sagittal)
  • Pitching (transverse) (up and down)
Pitching:
-	Elevation 
-	Depression 
Rolling 
-	Intorsion 
-	Extorsion (superior sclera initially moving outwards) 
Yawing 
-	Abduction (to the lateral orbit) 
-	Adduction (to medial orbit)
168
Q

what are intorsion and extorsion?

A
intorsion = rotation inwards 
extorsion = rotation ouwards
169
Q

what are the actions of extraocular muscles from their primary positions?

A
  • Extraocular muscles normally pull in more than one plane
  • Extraocular muscles normally do not act alone
  • Lateral rectus abducts the eye
  • Medial rectus adducts the eye
  • Superior rectus elevates, intorts and adducts the eyeball
  • Inferior rectus depresses, extorts and adducts the eyeball
  • Inferior oblique elevates, abducts and extorts the eyeball
  • Superior oblique depresses, abducts and intorts the eyeball
  • In relation to insertion on eyeball, all the origins of these muscles on apex is medial
  • Therefore, all rectus muscles pull medially
  • Therefore superior, inferior and medial rectus are all going to some extent adduct the eyeball
  • Not the case for lateral rectus, as it abducts it
170
Q

what happens when your eye is abducted and adducted to a certain number of degrees?

A
  • When eye is abducted to 23* superior & inferior rectus pull eye vertically
  • When eye is adducted to 51-55* superior & inferior oblique pull eye vertically
171
Q

if they eye cannot abduct or adduct, what is there a problem with?

A
  • If the eye cannot abduct there is a problem with the lateral rectus
  • If the eye cannot adduct there is a problem with the medial rectus
172
Q

how do you test muscles that produce vertical movements?

how do you test superior & inferior rectus muscles?

how do you test superior & inferior oblique muscles?

A

place eyes into secondary positions

  • Abduct eyes to test superior and inferior rectus muscles as when eye is abducted to 23* the rectus muscles pull the eye vertically
  • Adduct eyes to test inferior (elevate) and superior oblique (depress) muscles as when eye is adducted to 51* the oblique muscles pull the eye vertically
173
Q

why is binocular vision important?

A
  • Binocular vision importance in terms of depth perception

- If you’re looking at a close object, you need to overlap visual fields more than if you’re looking at a distant object

174
Q

binocular vision

  • what are versions
  • what are vergences
A

Versions:

  • The eyeballs move in the same direction
  • The lines of sight of each eyeball remain parallel
  • E.g. supraversion (up), infraversion (down), dextroversion (right) and levoversion (left)

Vergences:

  • The eyeballs move in opposite directions
  • The lines of sight of each eyeball do not remain parallel
  • E.g. convergence and divergence
  • E.g. infravergence and supravergence
  • (when you look at something further away your eyes diverge compared to a closer object when they converge)
175
Q

which of the nerves supplying the eye has parasymapthetic fibres?

A

oculomotor

176
Q

what do the cranial nerves III, IV and VI all pass through? and through what do they leave the cranial cavity?

A

they all pass through the cavernous sinus and leave the cranial cavity through the superior orbital fissure

177
Q

what are the main oculomotor nuclei?

A
  • Somatomotor nuclei
  • SR (superior rectus), MR, IR, IO & LPS (nucleus divided into subnuclei which each deal with a different muscle – each with one of these muscles)
  • Receives fibres from superior colliculus – therefore supplied by information from visual cortex
  • Receives fibres (internuclear neurones) from medial longitudinal fasciculus – therefore connected to nuclei of IV, VI and VIII
  • Important for co-ordinating eye movements
  • There’s the main oculomotor nuclei and a Edinger-Westphal nucleus
178
Q

what does the oculomotor nerve supply? and with which fibres?

A

Superior branch:

  • Superior rectus (contralateral nucleus)
  • Levator palpebrae superioris (both left and right)

Inferior branch:

  • Medial rectus (cell body in ipsilateral nucleus)
  • Inferior rectus (ipsilateral)
  • Inferior oblique (ipsilateral)
  • Ciliary muscle for accommodation *
  • Smooth muscles of the iris for pupil constriction*
  • parasympathetic fibres from E-W nuclei; all others from main nuclei
179
Q

Edinger-Westphal nuclei

  • type
  • where
  • recieves what fibres
A

Aka E-W or accessory parasympathetic nuclei

  • Visceral motor nuclei parasympathetic
  • Posterior to main nuclei
  • Nuclei receive corticonuclear fibres for accommodation reflex
  • Also receive fibres from pretectal nucleus for direct and consensual light reflexes
180
Q

what’s the link between oculomotor nerve and ciliary nerves?

A
  • Fibres synapse in ciliary ganglion
  • Postganglionic fibres in short ciliary nerves (which pierce the sclera go on to innervate structures in the eye – intraocular muscles)
181
Q

what’s the autonomic function of the oculomotor nerve?

A
  • Lens accommodation by innervating ciliary muscles
  • Innervate the constrictor pupillae
  • constrict using parasympathetic fibres
  • pupillary constriction happens when objects become nearer
182
Q

what’s the accommodation reflex?

A
  • Lines of sight converge (need to overlap fields more to obtain binocular vision)
  • Pupils constrict (to prevent spherical aberration – so less light waves scattering off the coroid and hitting the retina in the peripheral parts of it and distorting the image that you see)
  • Change focal length by altering shape of lens
183
Q

what happens to see near object?

A

(with objects nearer us we want to refract the light waves more)

  • Ciliary muscles contracts
  • Tension removed from suspensory ligaments
  • Tension removed from lens
  • Lens bulges antero-posteriorly (bends light waves more so they hit the retina)
184
Q

trochlear nerve nuclei

  • originate from
  • where located
  • what fibres does it receive
A
  • Originate from neuronal cell bodies at the border of pons and midbrain
  • Located in grey matter surrounding cerebral aqueduct
  • Receives fibres from superior colliculus – therefore supplied by information from visual cortex
  • Receives fibres from medial longitudinal fasciculus – therefore connected to nuclei of III, VI and VIII
  • Receive corticonuclear fibres from both cerebral hemispheres

TROCHLEAR NERVE: MOTOR FUNCTION
- Innervates: superior oblique only (contralateral nucleus)

185
Q

abducens nerve nuclei

  • originate from
  • what fibres does it receive
A
  • Originates from neuronal cell bodies beneath floor of fourth ventricle
  • Receives fibres from superior colliculus – therefore supplied by information from visual cortex
  • Receives fibres from medial longitudinal fasciculus – therefore connected to nuclei of III, IV and VIII
  • Receive corticonuclear fibres from both cerebral hemispheres
  • Internuclear neurones to contralateral main oculomotor nucleus via MLF important
186
Q

what is diplopia? what happens? what may it indicate?

A

double vision

don’t precisely overlap our visual fields

  • Fatigue
  • Cranial nerve dysfunction (e.g. lesions)
  • Raised intracranial pressure
  • Cerebellar (coordinates contractions of skeletal muscles) dysfunction
  • Blow-out fractures of the orbit
187
Q

describe sensory coding

A

SENSORY CODING

  • The activity of axons in sensory nerves ‘codes’ information from the sense organs
  • anatomical coding
  • temporal coding

ANATOMICAL CODING

  • Different nerves represent different sensory modalities
  • Distinctions between stimuli of the same modality (e.g. arising from different spatial locations)

TEMPORAL CODING
- Rate of firing of axons represents (‘encodes’) stimulus intensity

188
Q

what is psychophysics? what used to measure?

A
  • The systematic study of the relation between the physical characteristics of stimuli and the sensations they produce

Used to measure:
• Absolute threshold
-minimum level of a stimulus that can be detected
• Difference threshold (‘just-noticeable difference’)
-minimum detectable difference between 2 stimuli

189
Q

what can perception be influence by unconsciously?

A

higher-level cognitive processes such as expectations

190
Q

what are Gestalt principles of grouping?

A
  • The adjacency/proximity principle
  • elements of a visual scene that are close are grouped together
  • The similarity principle
  • similar elements are perceived as belonging together
  • Good continuation
  • elements that smoothly follow a line tend to belong together
  • The law of closure
  • missing information is supplied to close or complete a figure
  • The principle of common fate
  • elements on the same movement trajectory belong together
191
Q

what are models of pattern perception?

A
  • Templates
  • stored visual memories of patterns compared with visual input
  • Prototypes
  • flexible, idealised stored patterns compared with visual input
  • Feature detection models
  • distinctive features model Geons (certain no. of shapes that any shape can be constructed from)
192
Q

what is limited capacity resource?

A
  • We don’t attend to everything that our sensory system detects even though this can have fatal consequences
  • Our capacity for conscious processing of information is limited – selective attention is responsible for allocating this limited resource of awareness
193
Q

what are different types of shifting attention?

A

Can be ‘bottom-up’ or ‘top-down’:

  • Bottom-up = reflexively/automatically, e.g. in response to a stimulus appearing suddenly
  • Top-down = consciously controlled movement
194
Q

are there many cones outside of the macula region? how does density of rods change?

A

Density of rods decreases as you go more peripheral of retina – so more peripheral retina becomes less sensitive to light

Very few cones outside of the macula region

195
Q

what is the horizontal raphe?

A

if there’s a ganglion cell on one side of this line, its axons will stay on the same side as the horizontal line and go to the optic disc

HORIZONTAL RAPHE

  • Visual field abnormalities that do not cross the horizontal midline are of retinal origin (compare with lesions originating in brain)
  • E.g. glaucoma – problem with nerve in the eye
196
Q

what are ganglion cell photoreceptors?

A
  • 1% ganglion cells are also photoreceptors – melanopsin based – they’re not involved with vision itself (visual acuity) but they have other roles
  • They project to all 4 subcortical regions
  • Concerned with:
  • circadian rhythms
  • pupil responses
  • adaptive responses to overall lighting conditions
197
Q

what is Meyer’s loop?

A

where fibres from inferior retina enter the temporal lobe (the fibres loop forward before they go backward)

198
Q

describe binocular vision. when do you get monocular vision? what creates binocular vision?

A
  • Binocular vision gives you depth perception and stereopsis (the single perception of a slightly different image from each eye)
  • Due to decussation in optic chiasm
  • You get monocular vision if you go out to the far periphery of the visual field
  • Eyes are aligned so image in nasal field of one eye matches image in temporal field in the other eye – creating binocular visual field
199
Q

what would superonasal retinal detachment lead to?

A

inferotemporal visual field defect

200
Q

which fibres does the pituitary gland tumour usually press? what does this cause?

A

the decussating fibres (nasal retina) so you’re losing temporal visual field = bitemporal hemianopia

201
Q

homonymous hemiasnopia - what usually causes it?

A

HOMONYMOUS HEMIANOPIAS (RETROCHIASMAL LESIONS)

  • Visual field defect in the temporal side of one eye and the nasal of the other
  • Right homonymous hemianopia – may be a lesion of the optic tract
  • Lesion in visual cortex – can sometimes get a degree of sparing of macular vision
202
Q

homonymous quadrantanopia - what usually causes it?

A
  • Just affecting one of the four quadrants
  • Superior visual field loss – optic radiations in Meyer’s loop (temporal lobe) affected
  • Inferior visual field loss – optic radiations in parietal lobe affected
203
Q

what is the difference between visual field defects caused by lesiosn of the visual cortex compared with those from the optic tracts?

A
  • The nerves that represent corresponding points in the 2 eyes (points which view the same object) get closer and closer together as they pass through the visual pathway
  • Lesions of the visual cortex, therefore, often produce perfectly congruous (identical in both eyes) visual field defects while those from the optic tracts often produce incongruous defects
204
Q

give a summary of visual field defects

A
  • Bitemporal hemianopia
  • Homonymous hemianopia
  • Homonymous quadrantanopia
  • Homonymous hemianopia with central sparing
  • Damage to optic nerve -> loss of field in one eye
  • Damage to retina -> loss of field in one eye
  • Lesion affecting chiasm typically leads to bitemporal visual field loss
  • Retrochiasmal lesion (behind the chiasm in the visual pathway) -> homonymous hemianopia
  • Lesion of Meyer’s loop -> homonymous quadrantanopia
  • Lesion in visual cortex -> homonymous hemianopia with central sparing
205
Q

what’s the vasculature of the retinal layer? what is it disrupted by?

A
  • Retinal
  • supplies inner retina
  • disrupted in glaucoma
  • Choroidal
  • supplies photoreceptors
  • disrupted by retinal detachment
206
Q

what is the phototransduction cascade? why is it important?

A

OPSIN PROTEIN SIGNAL AMPLIFICATION: THE PHOTOTRANSDUCTION CASCADE
Photon absorption -> G-protein (transducen) dissociation -> phosphodiesterase activation -> closure of cGMP-gated channels
- Cascade allows huge signal amplification allows meaningful response to single photon absorption
- Each activated opsin can activate lots of transducen, each activated transducen can activate lots of phosphodiesterase, each phosphodiesterase can hydrolyse lots of cGMP, which causes a big change in membrane conductance, even with absorption of a single photon of light

207
Q

what captures more photon, rods or cones?

A
  • Rods capture more photons
  • They have larger signal amplification
  • They are more sensitive
208
Q

what types of synapses are sign inverting and sign conserving?

A

Sign inverting – inhibitory synapses

Sign conserving – excitatory synapses

209
Q

what type of receptors do ‘on’ and ‘off’ bipolar cells have?

A
  • ‘on’ bipolar cells have metabotropic glutamate receptors

- ‘off’ bipolar cells have ionotropic glutamate receptors

210
Q

whaen are on and off centre ganglion cells excited?

A
  • On centre ganglion cells: excited when light intensity in centre of receptive field higher than surround
  • Off centre ganglion cells: excited when light intensity in centre lower than surround
211
Q

how colour works?

A
CENTRE:SURROUND – RED:GREEN COLOUR 
Green:
-	400nm 
-	Balance of inhibitory input > excitatory 
-	Ganglion cell inhibited by ‘green’ 
Red:
-	600nm 
-	Balance of inhibitor input < excitatory 
-	Ganglion cell excited by ‘red’ 

BLUE: YELLOW COLOUR
- Ganglion cell connected to blue cone by ON bipolar and red & green cones by OFF bipolar

Blue:
-	430nm 
-	Balance of inhibitory input < excitatory 
-	Ganglion cell excited by ‘blue’ 
Yellow:
-	570nm 
-	Balance of inhibitory input > excitatory 
-	Ganglion cell inhibited by ‘yellow’
212
Q

what does firing pattern of ganglion cells tell you?

A
  • Does not simply report the amount of light falling on the photoreceptors
  • Rather encodes ‘visual information’:
  • spatial contrast in ‘grey scales’ (centre:surround) and/or colour
  • movement in a particular direction
  • local motion
  • ‘brightness’ (luminance)