Vision + Proprioception (wk 7)

Question 1

Describe the anatomy of the eye:

Answer 1

-White of the eye -> sclera
-Light passes through lens, then vitreous humour and then through to the retina to form an image
-Centre of the eye of the forvea and next to it is the optic disc, of which there is a blind spot

Question 2

Describe the lens of the eye:
-Including strength

Answer 2

-The lens is directly attached to the rest of the eye by zonular fibres which is connected to the ciliary muscle, where the lens is able to change shape.
-The lens -> Image formed on the eye is inverted and the brain must flip the image to make sense of it.
-Lens strength: diopteres-> The dioptere is a measure of lens focussing power. It is reciprocal of focal length. Power = 1/f D. 1D means focal point is 1m away. Both curvature and refractive index determine lens strength. Difference is refractive index between medium, combined with lens curvature determines lens strength (as measured in diopteres)

Question 3

Describe the optics of the eye:

Answer 3

-> Refraction occurs initially at cornea. Refractive index fixed at ~1.34. Further refraction caused by lens. Variable refractive index (mean ~1.41). Cornea and lens have similar refractive indices. However, most refraction occurs at the cornea (48D of total 58D) – provides the interface with the air (low refractive index).

Question 4

What is the accommodation of the lens?

Answer 4

Focal length is changed entirely by altering the shape of the lens: Accommodation achieved by ciliary muscle. Contraction of ciliary muscle relieves ligament tension on lens. Causes the lens to squash and this increases lens power and shortens focal length for closer objects.

Question 5

What is myopia?
-Normal sight, nearsightedness, nearsightedness corrected

Answer 5

(caused by eye ball being too long, or powerful cornea)
1. Normal sight -> Faraway object is clear (emmetriopia)
2. Nearsighted -> Eyeball too long (myopia)
3. Nearsightedness corrected

Question 6

What is hypermetropia?
-Normal sight, farsighted, farsightedness corrected

Answer 6

1. Normal sight -> Near object is clear (emmetriopia)
2. Farsighted -> Eyeball too short (hypermetriopia)
3. Farsightedness corrected

Question 7

What is presbyopia?

Answer 7

-> Normal range of lens accommodation ~12D. Lens seizes with age – no longer bulges when ciliary muscles contract. Near point moves further away.

Question 8

Describe the pupil
+ Pupillary muscles, benefits of smaller pupil size and pupil size

Answer 8

-The pupil -> Pupil diameter is first means of adaptation to changing light levels. Varies from ~2 to 8mm. Can alter the amount of light captured by ~16 times. This accounts for a very small portion of the eyes’ total light adaptation abilities.
-The pupillary muscles -> Pupil diameter controlled by 2 muscles – sphincter pupillae and dilator.
-Other benefits of smaller pupil size (besides less light reaching retina) -> Greater depth of field (more things in focus), reduced spherical aberration and reduced glare (scattering of light).
-Pupil size -> Reducing pupil size effectively, infinite depth of field and compensation for myopia.

Question 9

What is the retina?

Answer 9

-> Cannot simply observe another person’s retina directly; too much light absorbed. Ophthalmoscope: shines light directly onto subject’s retina. Adjustable lens used to being retina into focus. Optician can estimate spectacle strength based upon the ophthalmoscope lens required to being the retina into focus. Optic nerve carries all information from retina. Passes through optic disk ~15 degrees nasal. Results in blind spot.

Question 10

What are rids, cones, horizontals and bipolars?

Answer 10

-Rods, cones, horizontals and bipolars do not exhibit Action Potentials. Rods/cons modulate membrane potential of bipolars. Ganglion cells (and amacrine) change AP rate, taking signal to the brain.

Question 11

Describe the structure of the retina:

Answer 11

-> Design flaw? – Photoreceptors on the outside. Light must pass through other cells structures before reaching photoreceptors – scatter. Receptors being adjacent to pigment epithelium may help to minimise reflectance/scatter.

Question 12

What is the foveal retina?

Answer 12

Structures in front of foveal receptors are pushed to one side. Reduces light scatter/absorption, thereby increasing acuity. Black pigment epithelium minimises reflectance (true for whole eye, not just fovea).

Question 13

Describe rod and cone density:

Answer 13

-Rod and cone density -> No lens is perfect (including the eye). Acuity can be defined in the point spread function. Point spread function determines minimum separation of 2 points before they are perceived as separate entities. Density of photoreceptors in the human retina precisely tuned to the point spread function of eye optics.
-Rods and cones -> Photopigment contained within disks of outer segment. Disks continuously migrate outwards and are regenerated.

Question 14

What is photopigment?

Answer 14

Human photopigment is continuously bleached and regenerated. Receptors are saturated when all pigment is bleached – can no longer detect light.

Question 15

Describe the process of photopigment bleaching:

Answer 15

• Two molecules combine to form photopigment: retail and opsin. Combined molecule (in rod cells) is called rhodopsin (‘unbleached’ state).
• Light photon interacts with rhodopsin causing configurational change
• Retinal and opsin part company (‘bleached’)

Question 16

Describe cell membrane hyperpolarised (via G protein):

Answer 16

• Released opsin activated enzyme phosphodiesterase (PDE) (via transducing G protein)
• PDE converts cGMP to GMP (cGMP normally opens Na+ channels)
• Closure of Na+ channels causes hyperpolarisation of cell because K+ continues to leak out

Question 17

Describe the process of how neural output of ganglion cells are modified:

Answer 17

• Rod/cone hyper-polarisation results in less neurotransmitter release (glutamate)
• Modulates membrane potential of bipolar cell
• Changes firing rate of ganglion cell (bipolar can be excitatory or inhibitory)

Question 18

What is the visual range of luminance?

Answer 18

Human vision functions across ~10 15 units of luminance. The eye can detect single photons and work in bright sunlight.

Question 19

What is photopic vision?

Answer 19

-Suited for high luminance
-Cones only
-Low sensitivity/ high acuity
-Foveal and peripheral

Question 20

What is mesopic vision?

Answer 20

-Intermediate luminance e.g. dusk
-Rods and cones
-Intermediate sensitivity/ acuity
-Foveal and peripheral

Question 21

What is scotopic vision?

Answer 21

-Low light only
-Rods only
-High sensitivity/ low acuity
-Non-foveal

Question 22

What are the 4 mechanisms of adaptation to luminance:

Answer 22

1. Pupil size
2. Switchover between rods and cones
3. ‘Dark adaptation’ -> Bleaching/ regeneration of photopigment
4. ‘Field adaptation’ – aka light adaptation. Automatic gain control within photoreceptor (calcium release mechanism)
   +Adaptation is a constant trade-off between sensitivity versus activity

Question 23

Rods versus cones:

Answer 23

-> Rod cells inherently more sensitive than cones, by ~1 order of magnitude. But a much bigger difference in sensitivity comes from high convergence of rods onto ganglion cells (via bipolar cells). At the extremes: 1 cone ->1 ganglion cell (fovea) and 75,000 rods -> 1 ganglion cell (periphery). Degree of convergence can be altered in different light conditions e.g. under mesopic conditions, rods and cones may converge together

Question 24

What is the distribution of rods and cones in the retina?

Answer 24

-> Foveal vision entirely dependent upon cones. Therefore, foveal acuity very poor at night. The acuity is greatest at fovea.

Question 25

What is dark adaptation (aka bleaching)?

Answer 25

-> Copes with large changes in light. Visual sensitivity gradually increases over ~20 minutes in dark (i.e. threshold reduces). Photopigment progressively regenerates (following bright light at time zero). First drop is through cone sensitivity then the second drop is due to more photopigment regenerating

Question 26

What is field adaptation (aka ‘light adaptation’)?

Answer 26

-Field adaptation (aka ‘light adaptation’) -> Very quick change in sensitivity (within seconds) when background luminance changes. Copes with fast (relatively small) changes in light. Prevents response saturation at high light. Involves an automatic gain control process. May involve several mechanisms, but mainly due to altered calcium release within photoreceptor.

Question 27

What is lateral inhibition?
(visual processing at the level of the retina)

Answer 27

-> Lateral inhibition mediated by horizontal cells. It is presented as a centre-surround field and doesn’t matter whether it is inhibited or excited. Includes bipolar and horizontal cells and receptors. Retinal ganglion cells respond to edges. Centre-surround receptive fields emphasize edges.
-> There is also contrast illusion. Eyes see difference in objects/images through spatial change and not the actual image.

Question 28

What is colour vision: theoretical 1 channel receptor system?

Answer 28

Responds purely to stimulus intensity. One degree of freedom. No discrimination except brightness. A monochrome system. Single channel system is unable to clearly discriminate colour.

Question 29

What is theoretical 2 channel receptor system?

Answer 29

Responds to 2 aspects of stimulus intensity. Two degrees of freedom. Can discriminate colours. All outputs can be described by 2 numbers.

Question 30

What is the 3 channel system?

Answer 30

-> Fraction of light absorbed by different cones – sensitivity.

Question 31

What is the spectral sensitivity of cones?

Answer 31

Fraction of light absorbed by different cones – sensitivity.

Question 32

What is the colour triangle?

Answer 32

-> Assume constant intensity (luminance) for all wavelengths. Any colour can be ‘dialled up’ by a combination of red, green and blue. Colour can be defined by 2 factors – saturation and hue. Saturation defines strength of colour. Pure red is fully saturated and white is fully unsaturated. Hue defines the colour itself. No wavelengths can stimulate green cones alone without activating red or blue cones.

Question 33

What is neutral processing of colour?

Answer 33

-> Colour processing largely takes place in the retina itself. Ganglion cells generally don’t respond to red, green or blue alone, but combinations. Colour oppency is a combination of spatial opponency and colour oppency.

Question 34

What is colour oppency?

Answer 34

-> Three oponent channels in retinal output. May explain why yellow is percieved to be a ‘primary’ colour, along with RGB. Also explains impossible colours: can have bluish-green (turqouise) but nit yellowish-blue or reddish-green.

Question 35

What is colour constancy?

Answer 35

-> Colours tend to look the same despite large changes in the wavelength of illuminating light. Multiple mechanisms – highly stimulated colour channels will tend to adapt and become less responsive and contextual cognitive cues (e.g. bananas are generally yellow)

Question 36

What are disorders of colour vision?

Answer 36

-> Monochromats – rod type (vv rare) and cone type (vv rare). Dichromats – 2 lights: Protanopes no red 1% men, Deuteranopes no green 1% men, Tritanopes no blue very rare both. Anamalous trichomats – 6% men, 0.5% women.

Question 37

What is the concept of receptive field?

Answer 37

-> The ganglion cell is the final output of the retina. Each ganglion cell may respond to many photoreceptors. Shine a light on the retina to determine the ganglion receptive field from the ganglion cells. Some photoreceptors excite the ganglion cells, some inhibit. Forms a centre-surround shape, causing lateral inhibition. This is good for edge detection.

Question 38

What are visual pathways?

Answer 38

-> Left visual field enters right brain. Optic nerve splits at optic chiasm. Information relayed to visual cortex via the lateral geniculate nucleus (in thalamus).
-> Exact location of blindness can be used to diagnose anatomical site of lesion.

Question 39

What is proprioception?

Answer 39

-> Proprius (‘one’s own’, ‘individual’) and perception. The sense of the relative position of neighbouring parts of the body. Vestibular sensation sometimes included.
-The importance of proprioception for movement and balance:

Question 40

What is the physiology of proprioception:
-Joint capsule receptors

Answer 40

-> Ruffini, Paciniform, Golgi-type and free nerve endings contained with joint capsule. Historically thought to be the main source of joint position sense. However, modern evidence suggests minimal role for joint capsule – ‘Animal recordings suggest joint capsule afferents provides ambiguous information, mainly acting as limit detectors (injury prevention?’)

Question 41

What is the muscle spindle?

Answer 41

-> Bundle of thin muscle fibres contained within a capsule. Situated in parallel with main ‘extrafusal’ muscle, but generates no useful force. Wrapped around by a pair of sensory axons that detect muscle stretch. Gamma motor neurons cause active contraction of spindle (‘alpha’ motor neurons innervate the main body of muscle). Detects -> static length of muscle (i.e. position) and rate of change of muscle stretch (i.e. velocity). Joint angles can be calculated from changes in muscle length signalled by spindles.

Question 42

Describe the muscle spindle in its activation:

Answer 42

-> Central part of muscle spindle is non-contractile. Stretch-sensitive ion channels in sensory axons are activated when muscle is stretched.
* ~400 spindles in soleus muscle
* Primary endings -> signal position and velocity. Transmitted via 1a afferents. Sensitive to vibration.
* Secondary endings -> position only, via group II afferents
* Gamma fibre -> contractile element of spindle. No useful force output – purely intended to keep spindle taught
* Alpha-gamma coactivation -> maintains sensitivity of spindle in the face of changing muscle length

Question 43

How does alpha-gamma coactivation maintain spindle sensitivity?

Answer 43

-> 1a spindle afferent continuously fires to signal muscle length. Contraction of main muscle (via alpha motor neurons) causes spindle to slacken – this causes a drop in firing rate and a loss of sensitivity. Gamma activation contracts the spindle to keep it taught, thus maintaining sensitivity.

Question 44

What is the golgi tendon organ?

Answer 44

-> Indirectly contributed to joint rotation sense – signals force and heaviness. May be important when muscle movement is ambiguous (e.g. concentric vs eccentric contraction). Situated between muscle and tendon – unlike spindles, Golgi are in-series with muscle. When golgi tendon organ is stretched (usually because of muscle contraction), the 1b afferent axon is compressed by collagen fibres and its rate of firing increases.

Question 45

Muscle spindles v golgi tendon organ:

Answer 45

Muscle spindles -> parallel arrangement and length recorder
. Golgi tendon organ -> series arrangement and tension recorder.

Question 46

Describe motor performance following sensory loss:

Answer 46

-> Sequential finger movements in a patient with severe peripheral sensory neuropathy. In the absence of vison, movement accuracy degrades over time

Question 47

Describe the interaction with other senses (vestibular):

Answer 47

-> Galvanic Vestibular Stimulation (GVS) – Vestibular information must be interpreted in the context of neck orientation. Illusions of neck orientation cause vestibular information to be reinterpreted.

Question 48

Describe proprioception, ageing and falls:

Answer 48

-> Ankle proprioception declines with age. However, proprioception-falls link not strong

Question 49

What is the interaction of muscle sensation and strength:

Answer 49

-> Strongest and weakest subjects studied separately. No difference in lower limb sensory function. Sway disproportionally increased by eye closure in weaker subjects. Not due to weakness per se, but an inability to utilise proprioceptive signals.