lecture 7 visual perception (dr roger newport) hemianopia/visual field cuts blindsight u akinetopsia...
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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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