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Organisation of visual pathways

  • Left eye sees pink region, right eye sees blue region. They don't completely
  • There is a substantial region that is binocular (carnivores = binocular, prey = eyes on side of head)
    • If we copy the normal procedure and do left eye in right brain and vice versa, there will be significant separation between similar/related information
    • Therefore we split the lot down the middle, and have our left visual field to right brain, right visual field to left brain
      • Reorganisation is in the optic chiasm
      • Then information goes to lat. geniculate nuc. of thalamus back to optical radiation to occipital lobe

Two distinct pathways arise in retina

  • midget ganglion and parasol ganglion cells from particular parts of retina
    • parasol cells = lower resolution, big receptive fields (can't determine colour - mixed cone input), and are fast transmission
    • midget cells = higher resolution, small receptive fields (can determine colour), and are slow transmission

Lateral geniculate nucleus

  • 6 layers, to preserve the different inputs
    • ipsilateral inputs - 2, 3, 5
    • contralateral inputs - 1, 4, 6
    • M (parasol) cells - 1, 2
    • P (midget) cells - 3, 4, 5, 6

Visual deficits arising from LGN lesions

  • The only thing the M pathway is good for is flicker.

The optic radiation

  • Two different paths per hemifield, depending on whether we're looking at upper or lower parts of the field
    • Hence overall we have 4 quadrants
    • Also, the central area of the visual field has a large cortical representation
      • This corresponds to the relative distribution of rods and cones in the eye (i.e. high vs low resolution)
    • To deal with our world, we look around and stitch together a quilt of the world.

The site of a lesion on the visual pathway determines its effect on the visual field

  • Macula sparing
    • it's a large area of cortex (harder to damage it)
    • several independent blood supplies to that area of cortex
    • therefore more likely to lose peripheral vision over macular vision

Visual information goes to other parts

  • Recall lecture on sleep - some goes to suprachiasmic nucleus
  • We also have superior colliculus for orienting responses
  • Pretectum for pupillary reflex
    • This is the circuitry for the pupillary light reflex which does not involve LGN or visual cortex
    • Key: this innervation is bilateral, so see the results of the pupillary light reflex test on next slide
    • Note involvement of Edinger Westphal nucleus of the occulomotor nerve

Effect of damage to different segments of pupillary light reflex

Illusion: celebrities

  • Don't understand how it works
  • ?Combination between 1) peripheral low acuity vision 2) ability to interpret things in time etc

Primary visual cortex

  • Area 17, V1
  • Visuotopic organisation
  • Depending on the layer of thalamus where the visual cortex input comes from, we get ocular dominance columns
  • Neurons at the zone where the two ocular dominance columns are where binocular neurons are (the neurons for determining your binocular vision)
  • Strabismus in development = use one eye only, we see that one set of stripes is very much bigger than the other.
    • Therefore cortex remodels early on depending on its environment
    • If you don't correct it by age 6-7, the cortex is mapped and can't be changed
  • The cortex has neurons that are responsive to different orientations of lines
    • This allows us to recognise faces, letters etc. This recognition begins in the primary visual cortex, and gets more complex (up to faces) in associative cortices etc.
    • All these processes are very environmentally sensitive. E.g. cat raised in environment of only vertical lines, they can't detect horizontal lines (those neurons have not been maintained and so were lost)
      • This matters because astigmatism (where the eyes aren't round), gives a cylindrical distortion, so you tend to get either more vertical or horizontal cells
        • --> unbalanced cortical representation. Therefore you need to correct it early


  • Cortical blindness that arises during development. Locked in around age 7-9
    • Therefore correct strabismus early, otherwise they'll never be able to see normally in that eye because they lose their cortical neuronal representation, even if the defect is corrected later.

Extrastriate visual areas are arranged in streams

  • P cells project to V1 then to temporal lobe (for high acuity vision)
  • M cells project to V1 then to parietal lobe (for flicker)
  • M cell pathway is much faster than the P cell pathway. This is useful as the M cell pathway guides eye movement.
    • This way we know where to look/read before we have seen it (e.g. a tiger in your periphery, then you look at it to see which way it's moving etc).
  • Prosapognosia = due to temporal lobe damage. That is for recognition of faces.
  • Mismatch of communication between the M and P pathways is thought to contribute to dyslexia. The visual system does work in isolation, but the two parts don't talk to each other properly.
  • Temporal lobe lesions = hard to determine what an object is (reading, face recognition)
  • Parietal lobe lesions = hard to determine where an object is in space. Damage to MT = can't detect motion.
  • Overall, temporal lobe = "what"
    • Parietal lobe = "where".