L8 Flashcards

1
Q

name the different structures involved in the subcortical pathway and the cortical pathway

NOTE the difference between the amount of structures involved

A

• Subcortical Vision:
Retinotectal Pathway = Retina → superior colliculis

Cortical Vision: Retinogeniculostriate Pathway = Retina → Thalamus (LGN) → Primary Visual Cortex

cortical has more structures involved

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2
Q

what do we already know about the cortical pathway

A

Cortical Vision = where and what

• We know that the retinogeniculostriate pathway is the target of ~90% of the axons in the optic tract.

• We know that subdivisions of this pathway provide the building blocks (e.g., form, colour, and motion
perception) that enable us to recognize and identify complex visual scenes.

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3
Q

If the activity of neurons in our cortical visual pathways account for so much of our visual processing and experience, then why do we have subcortical visual pathways?

• Subcortical visual pathways are phylogenetically older than cortical visual pathways (i.e., the cortical
visual system evolved after the subcortical visual system).

• Does the subcortical visual system (i.e., the retinotectal pathway) contribute to human experience and
behaviour?

A

things to think about

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4
Q

describe the organisation of the superior colliculis

A

The superior colliculus has a layered anatomical organization.

– Neurons that receive information from the retinal ganglion cells are located in the superficial layers
of the superior colliculi.

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5
Q

the superior colliculi sit on top of the cerebral aqueduct

A

j

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6
Q

a study used single cell recording in monkeys to map the receptive fields of neurons in the superficial layers of the superior colliculus

Before conducting the experiment, the monkeys were trained to fixate a spot of light that appeared on a screen in front of them.

Each time the monkey fixated the light, another stimulus was projected onto the screen and used to determine the receptive field of the cell under study.

At the site of each interesting cell, a small lesion was made by passing current through the electrode.

After mapping the receptive fields of many cells, what did they find

A

The superficial layers of the superior colliculi contain retinotopic maps of the visual field.

The retinotopic map in the left superior colliculus represents the right hemifield.
Note that, as with cortical visual pathways, projections from the nasal
hemiretinas to the superior colliculi cross the midline.

The retinotopic map is distorted, with more neurons devoted to analysis of the central portion of the visual field.

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7
Q

describe how the superior colliculis is retanotopicly mapped

A

The superficial layers of the superior colliculi contain retinotopic maps of the visual field.

The retinotopic map in the left superior colliculus represents the right hemifield.
Note that, as with cortical visual pathways, projections from the nasal
hemiretinas to the superior colliculi cross the midline.

The retinotopic map is distorted, with more neurons devoted to analysis of the central portion of the visual field.

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8
Q

the superficial superior colliculis contains a hemi map

what do the deeper layers contain

A

motor cells (for eye movement)

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9
Q

where is the central part of the visual field represented in the superior colliculis

A

more rostally

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10
Q

Unilateral removal of the visual areas in the cortex of the cat causes what

A

the cat to stop orienting towards visual stimuli in the contralateral hemifield.

eg after a right lesion the cat would stop responding to stimuli’s in the left visual field

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11
Q

what is the sprague effect

A

Sprague (1966) demonstrated that visual orienting responses can be restored in the cortically blind
hemifield by removing the contralesional superior colliculus or by cutting the fibers that connect the
two superior colliculi.

therefore the sparge effects = restoration of orienting toward the cortically blind hemifield

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12
Q

how was the sprague effect originally discovered

A

Originally this effect was explained by mutual inhibition between the two superior colliculi: Removal
of the superior colliculus contralateral to the cortical damage disinhibits the superior colliculus
ipsilateral to the cortical damage and therefore restores orienting toward the visual hemifield
contralateral to the cortical damage

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13
Q

how does the sprague effect work

A

Subsequent anatomical studies revealed that the Sprague effect actually results from cutting inhibitory fibers that originate in another nearby structure and project to the superior colliculus on the same side as the cortical lesion.

The first damage the cortical pathway of the cat and the effects are devastating (controlateral neglect) but then when they disinhibit the subcortical region of the visual cortex on the same side the cat is able to start orientating itself again

Therefore initially the subcortical area is not strong enough to orientate but when the normal suppression of the system is removed then the system is effective

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14
Q

what are some important points to note about the sprague effect

(really important to understand)

A
  1. removing visual cortex was devastating for the cat.
  2. subcortical visual pathways were unable to compensate for the damaged cortical visual
    pathways until the ipsilateral superior colliculus was released from normal inhibition (thus
    disinhibiting the subcortical visual pathway on the side of the cortical damage).
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15
Q

Visual cortex vs. superior colliculus damage

Researchers compared the effects of disrupting cortical vision versus disrupting subcortical vision

they did this by training rodents to do two tasks:

– Localization Task: Turn head toward a sunflower seed held in an experimenter’s hand.
– Discrimination Task: Run down a two-arm maze and enter the door behind which a sunflower
seed was hidden.

After training the rodents to do both tasks, half of the rodents received bilateral removal of visual
cortex and half of the rodents received transection of the input fibres to both superior colliculi.
– Group 1: bilateral removal of visual cortex
– Group 2: bilateral disruption of the retinotectal pathway

what did they find

A

The two lesions yielded a double dissociation:

Localization Task:
– Rodents with lesions in visual cortex performed normally.
– Rodents with lesions affecting the superior colliculus made no attempt to orient towards the seed
(however, whisker contact elicited rapid orienting).

Discrimination Task:
– Rodents with lesions in visual cortex showed severely impaired performance: The animals could run down the maze and had sufficient motor capabilities to enter one of the doors, but they could
not discriminate horizontal from vertical stripes.
– Rodents with lesions affecting the superior colliculus performed normally.

therefore disrupting subcortical vision impaired their ability to orient toward the position of a stimulus, while disrupting cortical vision disrupted object discrimination.

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16
Q

what does bilateral removal of visual cortex cause

A

disrupting cortical vision disrupted object discrimination.

17
Q

what does bilateral disruption of the retinotectal pathway cause

A

disrupting subcortical vision impaired their ability to orient toward the position of a stimulus

18
Q

the results from the rodents provide compelling evidence for dissociable functions of the rodent’s subcortical visual system and cortical visual system.

However, we cannot assume that the same division of functions occurs in humans. why

A

Perhaps during the evolution of more complex visual systems, cortical areas took over functions that had depended on subcortical areas.

eg 90% of vision = cortical and 10% = subcortical therefore we clearly rely on one system more than the other

19
Q

Cortical is for complex images and subcortical is simple

A

j

20
Q

In humans, the contribution of subcortical pathways to vision in the absence of cortical pathways can
be assessed after a stroke involving primary visual cortex.
• If we physically disrupt visual processing via the retinogeniculostriate pathway, then we can assess any
visual abilities that remain and assume that they can be attributed to processing via subcortical
pathways.

A

j

21
Q

what is perimetry testing

A

a visual feild test

22
Q

Complete damage of V1 within one hemisphere will render the patient…

A

hemianopic.

partial blindness or a loss of sight in half of your visual field

23
Q

when someone is hemianopic what is happen to their visual information

A

The rods and cones still fire, and information is transmitted to the lateral geniculate nucleus of the
thalamus, but the patient is not aware of visual stimuli when they appear in the region normally
represented by the damaged cortex.

24
Q

what is a scartomia

A

blind spot

25
Q

the extent of a scartoma can be mapped using what

A

by a perimetry test, which involves presenting
a small spot of light at random locations across the visual field while the patient fixates on a central
stimulus. The patient reports whether they detected the spot of light.
• When the light falls outside the scotoma, detection is immediate.
• When the light falls within the scotoma, the patient fails to detect the light

26
Q

Unilateral Primary Visual Cortex Damage Unilateral Primary Visual Cortex Damage Causes Contralesional Hemianopia

A

k

27
Q

If cortically blind rodents can still locate (orient towards) sunflower seeds, then perhaps humans have residual vision in the absence of V1 as well.
• In order to test this, Weiskrantz (1986) used a task that, unlike perimetry testing, did not require
explicit report but rather tapped into the patient’s implicit knowledge of his hemianopic field.

what does this mean

A

Explicit = asking if they saw it (consciously aware of the stimulus)

Implicit = aware of the stimulus but not consciously aware (eg guess where you think the light might be)

28
Q

Task: When a tone sounds, move your eyes to the location of the light.

what would you find with someone that had blindside

A

The results showed that responses on
control trials were random, but when the
spot of light appeared up to 20 into the
blind field, responses were highly
correlated with the position of the light.
• Weiskrantz named this residual vision,
which occurs in the absence of awareness,
blindsight.

29
Q

in blind site where can we hypothesise the visual information is being processed given that V1 (where and what) has been cut)

A

The fact that visual stimuli presented in the cortically blind hemifield affected behaviour indicates that
the visual stimuli were, to some extent, processed.

• Although the stimuli that appeared in the cortically blind hemifield were not processed to the point of
conscious awareness, the degree of processing that did occur must have involved a pathway other than the retinogeniculostriate (assuming that striate cortex was completely dysfunctional).

Given that the superficial layers of the superior colliculus contain a retinotopic map, one can
hypothesize that, when the stimulus appeared within the cortically blind hemifield, it activated the
retinotectal pathway and that activity in this pathway led to the above chance performance.

30
Q

Residual Vision without Primary Visual Cortex?

A

The ‘blindsight’ capabilities of patients who are
rendered cortically blind after damage to primary visual
cortex suggest that the subcortical visual pathway in humans
may play an important role in orienting toward visual
stimuli.

31
Q

The ‘blindsight’ capabilities of patients who are
rendered cortically blind after damage to primary visual
cortex suggest that the subcortical visual pathway in humans
may play an important role in orienting toward visual
stimuli.

what is a way to test this

A

there is a fixation point and then when a light appears they move their eyes as fast as they can to that spot

sometimes there was a distraction stimulis which would slow the eye movement down if they could see it

when this distraction stimulus was in their scotoma their eye movement to the target was still slowed down therefore indicating they they are unconsciously aware of the distraction stimulus

therefore The increase in reaction time associated with a distractor in
the cortically blind hemifield may be explained by
competing activation by the distractor via the retinotectal
pathway

32
Q

Unilateral damage to primary auditory cortex (A1)

• Unlike the effects of unilateral damage to primary visual cortex, after unilateral damage to primary auditory cortex a surprising degree of normal auditory function is retained. why is this

A

• The relatively minor impact of unilateral damage to primary auditory cortex (in the context of contralesional stimulation) can be easily explained by the fact that, unlike visual information, auditory information is transmitted to both ipsilateral and contralateral primary auditory cortex.

therefore their is auditory information from one ear happening on both sides of the brain

33
Q

not all auditory information crosses the midline (i.e., each of your ears projects auditory information to both hemispheres of your brain.).

what is the consequence of this

A

Consequently, damage to primary auditory cortex in one hemisphere does not result in cortical
deafness (for input to the contralateral ear). Indeed, the deficit that results from unilateral damage to
primary auditory cortex is minor.