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Perception

• Chris Rorden• Lecture 8: Vision and perception

• Low level visual deficits:• Visual field defects

• Blindsight• Achromatopsia :: cortical colorblindness (V4)• Akinetopsia :: motion perception (MT/V5)• Agnosias :: apperceptive, associative, prosop- (FFA)

• ‘How’ versus ‘what’

www.mricro.com

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Vision

Human vision: Lots of real-estate

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Visual Pathway

Each eye sees both left and right visual field.

Ipsilateral information crosses over at optic chiasm.

Some connections to superior colliculi.– Reflexive eye movments

Others go to thalamus (lateral geniculate nuclei) and then cortex.

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Visual Defects

Field defects reveal anatomical injury

A. Monocular blindnessB. C. Bitemporal hemianopiaD. Homonymous

hemianopiaE. Upper quadrantanopiaF. Lower quadrantanopiaG. Homonymous

hemianopia

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V1

Primary visual cortex (V1) lies in calcarine fissure.

Complete damage leads to Homonymous hemianopia.

Partial damage leads to scotomas

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V1 – retinotopic mapping

V1 is retinotopic: distorted spatial map of visual scene

Fovea has massively over represented.

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V1 damage and blindsight

People with damage to V1 fail to report objects presented in their field defect.

However, when forced to guess, they can accurately point to location of unseen visual stimulus!

Can also accurately report direction of motion. Weiskrantz et al., 1974Weiskrantz et al., 1974

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Implications of Blindsight

V1 is crucial for conscious awareness. What explains blindsight? Why do only 20% of

V1 patients show blindsight?– Incomplete damage to V1? Islands of spared tissue

(Gazzaniga, 1994).– Typically seen in people who had injury while young

– neural plasticity?– Small number of indirect connections to later cortical

visual centers?– Visual connections to colliculi?

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The visual processing stream

Three major streams of vision:1. Subcortical

2. Dorsal

3. Ventral

Different streams do different things…

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Cortical visual processing

M-ganglion cells

P-ganglion cells

MagnoLGN

ParvoLGN

V1

V1

V2

V2

V3

V4

MTV5

ITcortex

ParietalDorsal system is fast, but color blind.Helps with motor control (Where/How).

Ventral system is slow, but detailed.Helps with object identification (What).

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Achromatopsia :: V4

Achromatopsia is usually caused by bilateral damage to V4 - lingual and fusiform gyri (occipitotemporal junction) and is characterized by an inability to identify or discriminate colour

Still able to perceive form and motion

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Akinetopsia (Motion Blindness)

Zilles reported first case of akinetopsia. Pure cases are rare, as requires bilateral injury.

– Case LM - akinetopsia 43 yr old. Sinus vein thrombosis V5 damaged bilaterally - V1 spared Could not see movement of objects but could see still objects. People

would suddenly appear Diagnosed as agoraphobic Can see movements/reach for/catch very slow moving objects (< 10°/s)

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V5 timecourse

Beckers & Zeki (1995) examined brief V5 disruption using TMS.

Motion perception disrupted most with V5 stimulation up to 30ms after visual stimulation onset

V1 stimulation also partially disrupts motion perception, but later (60-70ms after VS onset).

Takes 30-50ms for signals to go from V1 to V5– Direct route to V5?– Reafference to V1?– May explain motion performance in blindsight?

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Agnosias

Three reasons why people might fail to recognize objects:– Perceptual Deficit: e.g. acuity, field cut, loss

of color vision– Apperceptive agnosia: unable to perceive

full shape of object despite intact low level processing.

– Associative agnosia: ability to perceive shape, but unable to recognize it.

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Apperceptive agnosia

Intact low-level perception– acuity– brightness discrimination– color vision

Unable to recognize objectsUnable to extract global

structure.

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Associative agnosia

Able to see whole form of shapes

No problem copying figures

However, unable to recognize the objects

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Associative agnosia

Theoretical explanations:

– Disconnection between visual representation and language?

– Damage to visual memory representation?

– Slightly impaired perception?

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Anatomical considerations

Apperceptive agnosia:– right inferior parietal lobe

(Middle Cerebral Artery)

Associative agnosia:– left occipitotemporal

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Prosopagnosia

Wigan (1844), Quaglino & Borelli (1867), Hughlings Jackson (1872), Charcot & Bernard (1883), Wilbrand (1892)

Inability to visually recognize facesEven a spouse’s face does not seem

familiar

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Prosopagnosia - specificity

Seems specific to faces. Patients can still recognize others by:– Silhouette– Voice– Clothing

Note: not like amnesia

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Prosopagnosia

Is face processing special?Or, are faces simply the most difficult

objects we discriminate?Most people withprosopagnosia have

difficulty recognizing differences within categories:– types of car– porcelain fixtures– breed of dog

Also, often suffer achromatopsia

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Faces are difficult

Most objects are identified by unique components

However, faces have the same basic components:nose, eyes,ears, hair

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Are faces special?

Farah tried to find objects as difficult as faces:– Spectacle frames– Undergrads recognized 87% of faces, 67%

of eyeglass frames (faces easier)– LH recognized only 64%

of faces, and 63% of eyeglass frames

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Are faces special?

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Are faces special?

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Are faces special?

Farah examined inversion effect Sequential matching task Undergrads:

– Upright: 94% correct– Inverted: 82% correct

Prosopagnosic LH– Upright: 58%– Inverted: 72%

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Double dissociations

Assal, Faure & Anderes (1984) report zooagnosic farmer MX– Lost ability to recognise cows– Still recognises faces

Bruyer et al (1983) report reverse– Fails to recognise faces– Intact perception of cows

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Double Dissociation

If faces are simply difficult, we should not find patients with spared face recognition who are impaired on other tasks.M

X

Faces Cows

Acc

ura

cy

MX

RB

RB

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Prosopagnosia

Selective to faces in a few patients Unable to recognize faces Able to discriminate equally difficult objects:

– cows– office furniture– spectacle frames

Why are ‘pure’ prosopagnosics so rare?– Lesions tend to be large?– Overlap in processing in most patients?

Functional imaging can resolve this question

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Anatomical considerations

Fusiform gyrus. Usually bilateral,

occasionally right hemisphere only (Landis et al. 1986)

Near V4 (color vision) Functional imaging

gives convergent evidence (Sergent & Signoret 1992)

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Vision in split brain patients

Commissurotomy is neurosurgical treatment for intractable epilepsy where the Corpus callosum is completely divided.

Allows systematic investigation of hemispheric specialization and integration

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Split brain patients

By using rapid (tachistoscopic) stimuli we can avoid eye movements.

Using chimeric faces, Sperry projected different images to each hemisphere.

Most able to return to work within 2 years of surgery.

Typically, appear healthy

Language‘man’

Left handwoman

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Split brain patients

Picture presented in RVF (i.e. to LH)

– Patient could name or reach for the object correctly with right hand.

Picture presented in LVF (i.e. to RH)

– Patients could not name/describe the object

– Subjects could reach for the correct

– object with their left hand Likewise, unable to find a

object felt with one hand by using the other hand.

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Split brain patients

Left hemisphere clearly specialized in language. Right hemisphere appears better at copying designs,

reading facial expressions, fitting forms in molds Similar effects can be seen in healthy people, e.g.

most think A and C look more similar than A and B

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Cortical visual processing

M-ganglion cells

P-ganglion cells

MagnoLGN

ParvoLGN

V1

V1

V2

V2

V3

V4

MTV5

ITcortex

ParietalDorsal system is fast, but color blind.Helps with motor control (Where/How).

Ventral system is slow, but detailed.Helps with object identification (What).

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Visual Form Agnosia

DF has ventral damage– Profound agnosia :: can not even tell orientation of object– Motor control accurate :: motor system functions accurately.

Patient DF ControlsPosting task

Perceptual matching

Posting

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Ventral vs Dorsal damage (Goodale et al. [1994] Curr Biol. 4:604-610)

When shown two shapes (left), DF was poor at saying if the shapes were same or different, RV was good at this task.

DF RV

chance

100%

0%

DFControl RVF

req

uen

cy

25%

0%

Distance from centre (mm)0 15 0 15 0 15 30

When asked to grasp an object, DF grasped near the centre (like healthy people), RV was poor at this task.