Lecture 7 Visual Perception (Dr Roger Newport)

Hemianopia/Visual Field Cuts

Blindsight

Akinetopsia

Achromatopsia

Agnosia

Prosopagnosia

Split Brain

Macular sparing

Hemianopia (and other visual field cuts)

QuadrantanopiaHomonymousHemianopia

Bitemporal

M-ganglion cells

P-ganglion cells

MagnoLGN

ParvoLGN

V1

V1

V2

V2

V3

V4

MTV5

ITcortex

Parietal

Where/How

What

Xshapescolours

objects and faces

motion

Blindsight

Clinical features • loss of half of the field of vision • can detect and discriminate visual stimuli in blind field without awareness (e.g. colour, luminance, motion, orientation)

Neuropathology • striatal cortex (V1) damage

Diagnosis • forced choice reporting of ‘unseen’ stimuli

Visual field maps for the left (L) and right (R) eyes of a patient with Visual field maps for the left (L) and right (R) eyes of a patient with blindsight. Patient D. B. could see almost nothing in his LVF. The only blindsight. Patient D. B. could see almost nothing in his LVF. The only exception was in a small region in the upper left quadrant where he had exception was in a small region in the upper left quadrant where he had unclear visual experiences. (From Weiskrantz et al., 1974)unclear visual experiences. (From Weiskrantz et al., 1974)

DB: surgical removal of right striate cortexunaware of visual stimuli in left field but above chance at :Presence v absence of visual stimulus; Direction of visual stimulus ; Horizontal vs. Vertical

Blindsight - Famous Case DB

Finger-pointing performance by D.B. (From Weiskrantz Finger-pointing performance by D.B. (From Weiskrantz et al., 1974)et al., 1974)

Blindsight - Famous Case DB

Blindsight

Clinical features • loss of half of the field of vision • can detect and discriminate visual stimuli in blind field without awareness (e.g. colour, luminance, motion, orientation)

Neuropathology • striatal cortex (V1) damage

Diagnosis • forced choice reporting of ‘unseen’ stimuli

Theories • stray light • islands of vision • primitive visual pathways

stray light, but no blindsight at optic discislands of vision: Friedrich patient, but GYprimitive visual pathways - sparse, but widespread

Retina - SC - Th - CortexRetina - Pulvinar - Extrastriate cortexRetina - LGN - V2/V4/V5/ TEO

M-ganglion cells

P-ganglion cells

MagnoLGN

ParvoLGN

V1

V1

V2

V2

V3

V4

MTV5

ITcortex

Parietal

Where/How

What

Xshapes

colours

objects and faces

motion

X

Akinetopsia (motion blindness)

Clinical features • inability to detect moving objects • defective smooth pursuit/reaching for moving objects

Neuropathology • bilateral damage to area MT (V5; T-O-P junction)

Case LM - akinetopsia

43 yr old. Sinus vein thrombosisV5 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 (< 10o/s)

LM could not speech read, but could tell forms of words from pictures

Contrast HJA (ventral stream damage) who could speech read, but not tell forms of words from pictures

Akinetopsia (motion blindness) - Famous case LM

The consequences of inactivating areas V1 and V5 on visual motion perceptionG Beckers and S Zeki Brain 1995 118, 49-60

TMS study - Stimulated V1 and V5

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

Disruption of V5 causes motion blindness more than V1Direct fast route from retina to V5 via pulvinar bypassing V1Slower route to V5 through V1

Akinetopsia (motion blindness)

M-ganglion cells

P-ganglion cells

MagnoLGN

ParvoLGN

V1

V1

V2

V2

V3

V4

MTV5

ITcortex

Parietal

Where/How

What

Xshapescolours

objects and faces

motion

Ishyhara plates

Cerebral Achromatopsia

Achromatopsia is not:

a) due to peripheral damage (e.g. retina) b) due to primary visual area damagec) colour agnosia: disorder of colour categorizationd) colour anomia: disorder of colour naming

Cerebral Achromatopsia

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

Usually full field deficit but hemiachromatopsia possible if damage is unilateral

Still able to perceive form and motion - dissociation with akinetopsia and visual form agnosias

The case of the colorblind painter by Oliver Sacks

Facts:Auto accidentNo clear damage (no bleeding)No recollection of accidentAlexia for five days."Driving in a fog"His studio was "..now utterly gray and void of colour. His canvases, the abstract colour paintings he was known for, were now grayish or black and white. At this point the magnitude of his loss overwhelmed him."

Over time he adapted. "I am completely divorced from colour."

Cerebral Achromatopsia - Famous Case

Damasio et al., (1989b) in Heilman and Rothi (1993)42 patients.achromatopsia associated with lesions below calcarine sulcus that damaged middle third of lingual gyrus, but not fusiform gyrus

Calcarine sulcus

Lingual Gyrus

Fusiform Gyrus

Which part of V4?

V1

V4

Wechsler’s Patient (1933) - colour and form dissociationAnoxia from house fire - left virtually blind incapable of recognizing objects and could not navigate surroundings

colour vision sufficiently preserved to distinguish shades of colours.

‘‘He knew at once the colours of small objects which he couldneither name nor tell the form of. He picked out colours on command’’

PB (Zeki) vs MS (Heywood and Cowey)Awareness vs. constancy

Cerebral Achromatopsia - dissociations

Zeki et al., 1999. Colour processing in a blind patient

PBAge-matched Control

Coma from electric shock. Blind, but can discriminate colours

consciously

V1 only

MS

Don’tknow

Don’tknow, but same as above

No activation of V4 in PB suggests V4 = colour constancyWavelength info = V1/V2Colour awareness - V4 or more anterior (IT)?

A failure of recognition that cannot be attributed to:primary sensory defectsmental deteriorationattentional disturbancesaphasic misnamingunfamiliarity with sensorially presented stimuli

Bauer (1993) In Hielman and Rothi 1993

Originally classified as having two types Lissauer (1889) :

Apperceptive and Associative

The Agnosias

can perceive, but not recognise objects

Good acuity etcCan see global structure (full shape)Can match to sample*Can copy (see right)But still cannot recognise objectsCannot recognise own copy

Usually occurs following left occipitotemporal damage/anterior temporal lobeDisconnection of areas associated with stored object knowledge

*but not nonmorphologically identical representations of the same object (e.g. matching a line drawing with the real object).)

Associative Agnosia

Can seeCan do obstacle avoidance etcGood acuity etc, butCannot recognise objectsCannot see global structure (full shape)Cannot match to sampleCannot copy

Rare. Usually occurs following gross damage to lateral parts of occipital lobes feeding ventral stream

Deficit in form perception Copying example

Apperceptive Agnosia

• Anoxia from carbon monoxide poisoning• MRI shows damage in ventrolateral occipital region, sparing V1• Normal colour/light discrimination etc.• No blind spots• Smooth pursuit ok

Cannot recognize many objects, particularly drawings or letters when presented visually

Cannot copy line drawings or pictures, but can draw from memory

Can do spatial tasks

Apperceptive Agnosia - Famous Case DF

Patient DF Controls

Perceptual matching

Posting

Posting task

Other Agnosia

Alexia - left fusiform/lingual areasInability to form coherent lexical representations from letters

Topographagnosia or topographical agnosia - right lingual gyrusInability to navigate routes using familiar landmarks - deficit in familiar scene perception

Prosopagnosia - Can’t identify faces - even extremely familiar ones (even themselves!)But can identify people by other meansAnd can recognise a face as being a face andCan discriminate between faces.

Some P patients (e.g. LF - Bauer) show covert recognition

GSR picks up when when familiar vs. unfamiliar faces shown.Recognition not lost, awareness of recognition lost.

Sacks, 1985 The Man Who Mistook His Wife for a Hat

Dr. P. well educated musician and teacher possible degenerative disease or large tumorcouldn't recognize faces He recognised people on the basis of their "body music"- their voices and the manner in which they moved

Would talk to people-shaped objects expecting a reply

Also had agnosia for objects - at times unable to tell the difference between his feet and his slippers 

Could recognise geometric objects by touch

Prosopagnosia - Famous case Dr. P

Prosopagnosia

George et al. (1999).fMRI study of positive and reverse contrast faces.

Bilateral fusiform gyri response to facesRight fusiform gyrus only when face became familiar(Note contrast to Alexia)

Brain region involved

Are faces just very difficult objectsOr are they special because of our level of expertise?

Prosopagnosia

Are faces a separate (special) class of objects or are faces just very difficult objects?

Is prosopagnosia special (i.e. is there a special face processing area in the brain) or just another type of agnosia?

Prosopagnosia often co-occurs with other types of agnosia (anatomical coincidence of separate areas or are faces just objects?)

Are faces just very difficult objects?

Assal et al.(1984) patient MXFarmer lost ability to recognise cowsCould recognise faces

Bruyer et al., (1983) patient RBCan’t recognise facesLess impaired at cows.

If faces just more difficult then shouldn’t have patients more impaired at other objects (i.e. cows).

Prosopagnosia

Activation of the middle fusiform 'face area' increases with expertise Gauthier et al., 1999

Sequential matching taskInverted and upright. Expertise specific to upright

Prosopagnosia Are faces special objects, or are we face experts?

Face and Greeble areas overlap

Face and Greeble areas don’t overlap

Novices Experts

Prosopagnosia

Suggests faces special due to expertise

the face-selective area in the middle fusiform gyrus may be most appropriately described as a general substrate for subordinate-level discrimination that can be fine-tuned by experience with any object category. Gauthier et al. 1999.

IS FACE RECOGNITION NOT SO UNIQUE AFTER ALL?Gauthier & Logothetis (2000)

COGNITIVE NEUROPSYCHOLOGY, 17 (1/2/3), 125–142

Faces are not “special”They are the “default special”

in the primate recognition system

Prosopagnosia

Conclusions?

Gauthier et al. 2004: Greebles not treated like faces CW profound object agnosia. OK on faces, poor on greebles

Grill-Spector et al. 2004:FFA is involved in detection and identification of faces, but it has little involvement in within-category identification of non-face objects (including objects of expertise e.g. birds, flowers, houses, guitars, cars etc)

Prosopagnosia

But

The Corpus CallosumThe two cerebral cortices are interconnected by the largest fiber system in the brain, the corpus callosum

Human CommissurotomyA neurosurgical treatment for intractable epilepsyCorpus callosum is completely dividedAllows systematicInvestigation of hemisphericspecialization and integration

Split Brain Patients

Say manpoint to woman

Visual Recognition StudiesPicture 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 objectSubjects could reach for the correctobject with their left hand

Split Brain Patients

Split brains can perform independent incompatible motor commands

Head-stone/sky-scraper sprared (VP) v full (JW)

cup

‘cup’

S can report ‘cup’RH can select cupLH cannot

spoon

spoonS report nothingLH can select spoon(RH cannot), but S cannot say what it is

Patient NGSpringer & Deutsch (1998)

Split Brain Patients Left hemisphere specialised for language

Left hemisphere as an ‘interpreter’

80/20

70/30

Birds and chimps 75% (optimisation)

Humans 63% (frequency matching)

Left Brain - 63%

Right Brain 75%

Shovel to clean out the chicken shed (PS)

Split Brain Patients

VP athlete ex.

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