4X Where/How What motion shapes colours objects and faces M-ganglion cellsP-ganglion cellsMagnoLGNParvoV1V2V3V4MTV5ITcortexParietalWhere/HowWhatmotionXshapescoloursobjects andfaces
5BlindsightClinical 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) damageDiagnosis • forced choice reporting of ‘unseen’ stimuli
6Blindsight - Famous Case DB 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 exception was in a small region in the upper left quadrant where he had 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
7Blindsight - Famous Case DB Finger-pointing performance by D.B. (From Weiskrantz et al., 1974)
8Neuropathology • striatal cortex (V1) damage BlindsightClinical 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) damageDiagnosis • forced choice reporting of ‘unseen’ stimuliTheories • stray light • islands of vision • primitive visual pathwaysstray light, but no blindsight at optic discislands of vision: Friedrich patient, but GYprimitive visual pathways - sparse, but widespreadStray light. Some light from visual stimulus strays into areas that can see. But if stimulus displayed in natural optic disc blindspot, no blindsight shown so suggests light not straying into other visual areas.Islands of visual cortex: Friedrich patient: found island of vision well away from macular sparing surrounded by functionally dead area that displayed blindsight whereas dead area did not. But GY shows blindsight across hemianopia. Able to track moving objects etc. Would require multiple ‘islands’ but MRI suggests this isn’t so.Even in the absence of Vl in the monkey, visualinformation can reach a large constellation of visual‘association’ areas in the brain. Some of these paths arisethrough parallel projections from the retina to the superiorcolliculus, with further relays via the thalamus to thecortex , or by direct projections to the pulvinar andthence to the extrastriate cortex [l]. It is known thatintralaminar neurons in the LGN survive removal of Vl,and project to V2, V4, V5 and TEO [ Recently,a projection from the LGN to the inferotemporal cortexhas been demonstrated [2Zoo]. The LGN projections thatsurvive Vl removal are relatively sparse in density, butare nevertheless widespread and probably encompass allextrastriate visual areas.Retina - SC - Th - CortexRetina - Pulvinar - Extrastriate cortexRetina - LGN - V2/V4/V5/ TEO
9X X Where/How What motion shapes colours objects and faces M-ganglion cellsP-ganglion cellsMagnoLGNParvoV1V2V3V4MTV5ITcortexParietalWhere/HowWhatmotionXshapescoloursobjects andfacesX
10Akinetopsia (motion blindness) Clinical features • inability to detect moving objects • defective smooth pursuit/reaching for moving objectsNeuropathology • bilateral damage to area MT (V5; T-O-P junction)
11Akinetopsia (motion blindness) - Famous case LM Case LM - akinetopsia43 yr old. Sinus vein thrombosisV5 damaged bilaterally - V1 sparedCould not see movement of objects but could see still objects. People would suddenly appearDiagnosed as agoraphobicCan see movements/reach for/catch very slow moving objects (< 10o/s)LM could not speech read, but could tell forms of words from picturesContrast HJA (ventral stream damage) who could speech read, but not tell forms of words from pictures
12Akinetopsia (motion blindness) The consequences of inactivating areas V1 and V5 on visual motion perceptionG Beckers and S Zeki Brain , 49-60TMS study - Stimulated V1 and V5Motion perception disrupted most with V5 stimulation up to 30ms after visual stimulation onsetV1 stimulation also partially disrupts motion perception, but later (60-70ms after VS onset).Takes 30-50ms for signals to go from V1 to V5Disruption of V5 causes motion blindness more than V1Direct fast route from retina to V5 via pulvinar bypassing V1Slower route to V5 through V1
13X Where/How What motion shapes colours objects and faces M-ganglion cellsP-ganglion cellsMagnoLGNParvoV1V2V3V4MTV5ITcortexParietalWhere/HowWhatmotionXshapescoloursobjects andfaces
15Cerebral Achromatopsia Usually caused by bilateral damage to V4(lingual and fusiform gyri (occipitotemporal junction))characterized by an inability to identify or discriminate colourUsually full field deficit but hemiachromatopsia possible if damage is unilateralStill able to perceive form and motion - dissociation with akinetopsia and visual form agnosiasAchromatopsia is not:due to peripheral damage (e.g. retina)due to primary visual area damagec) colour agnosia: disorder of colour categorizationd) colour anomia: disorder of colour naming
16Cerebral Achromatopsia - Famous Case The case of the colorblind painter by Oliver SacksFacts: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."
17Damasio et al., (1989b) in Heilman and Rothi (1993) 42 patients. Which part of V4?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 gyrusCalcarine sulcusLingual GyrusFusiform Gyrus
19Cerebral Achromatopsia - dissociations Wechsler’s Patient (1933) - colour and form dissociationAnoxia from house fire - left virtually blindincapable of recognizing objects and could not navigate surroundingscolour 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: Coma from electric shock. Blind, but can discriminate colours consciously1. is patient’s ability to discriminate colour wavelength based or2. are colour constancy mechanisms partly intact.If 1, then expect the processing to be confined to areas V1/Vwhere there are many wavelength selective cells,If 2. Then expect a participation of area V4 .PB (Zeki) vs MS (Heywood and Cowey)Awareness vs. constancy
20Zeki et al., 1999. Colour processing in a blind patient Age-matched ControlPBV1 onlyComa from electric shock.Blind, but can discriminate colours consciously
21No activation of V4 in PB suggests V4 = colour constancy Wavelength info = V1/V2Colour awareness - V4 or more anterior (IT)?MSDon’tknowDon’tknow, but same as aboveFig. 1. Color constancy. Zeki et al. (1) illuminated an array of colors with varying amounts of long, medium, and short wavelength light. Each color patch reflectsa constant proportion of the incident lights at any wavelength. (a) The green patch reflects 70% of the medium wavelength light. Normal observers report thisas green when it is presented surrounded by other colors but as white when it is presented in isolation. Patient PB would report this patch as green or whitedepending on the intensity of the medium wavelength light. (b) How constancy was tested. Here the green patch is now illuminated by much more longwavelength light. The proportions of available light reflected from each surface remain unchanged but the absolute levels of reflected intensity are greatlychanged, the long wavelengths now dominate. Normal observers still report the patch to be green when viewed in the presence of other colors. Patient PB,however, no longer perceives the patch to be green and now reports it to be red or white, depending on the intensity of the light. All units are arbitrary.
22The AgnosiasBauer (1993) In Hielman and Rothi 1993A failure of recognition that cannot be attributed to:primary sensory defectsmental deteriorationattentional disturbancesaphasic misnamingunfamiliarity with sensorially presented stimuliOriginally classified as having two types Lissauer (1889) :Apperceptive and Associative
23Associative Agnosiacan perceive, but not recognise objectsGood acuity etcCan see global structure (full shape)Can match to sample*Can copy (see right)But still cannot recognise objectsCannot recognise own copyUsually occurs followingleft 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).)
24Apperceptive AgnosiaCan seeCan do obstacle avoidance etcGood acuity etc, butCannot recognise objectsCannot see global structure (full shape)Cannot match to sampleCannot copyRare. Usually occurs following gross damage to lateral parts of occipital lobes feeding ventral streamDeficit in form perceptionCopying example
25Apperceptive Agnosia - Famous Case DF Posting task• Anoxia from carbon monoxide poisoning• MRI shows damage in ventrolateral occipital region, sparing V1• Normal colour/light discrimination etc.• No blind spots• Smooth pursuit okCannot recognize many objects, particularly drawings or letters when presented visuallyCannot copy line drawings or pictures, but can draw from memoryCan do spatial tasksPatient DFControlsPerceptualmatchingPosting
26Other AgnosiaAlexia - left fusiform/lingual areasInability to form coherent lexical representations from lettersTopographagnosia or topographical agnosia - right lingual gyrusInability to navigate routes using familiar landmarks - deficit in familiar scene perceptionProsopagnosia - 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 recognitionGSR picks up when when familiar vs. unfamiliar faces shown.Recognition not lost, awareness of recognition lost.
28Prosopagnosia - Famous case Dr. P Sacks, The Man Who Mistook His Wife for a HatDr. P. well educated musician and teacherpossible degenerative disease or large tumorcouldn't recognize facesHe recognised people on the basis of their "body music"-their voices and the manner in which they movedWould talk to people-shaped objects expecting a replyAlso had agnosia for objects - at times unable to tell the difference between his feet and his slippers Could recognise geometric objects by touch
29ProsopagnosiaBrain region involvedGeorge 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)
30ProsopagnosiaIs prosopagnosia special (i.e. is there a special face processing area in the brain) or just another type of agnosia?Are faces a separate (special) class of objects or are faces just very difficult objects?Are faces just very difficult objectsOr are they special because of our level of expertise?
31ProsopagnosiaProsopagnosia 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 facesBruyer 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).
32ProsopagnosiaAre faces special objects, or are we face experts?Activation of the middle fusiform 'face area' increases with expertise Gauthier et al., 1999Sequential matching taskInverted and upright. Expertise specific to upright
33ProsopagnosiaExpertsNovicesFace and Greeble areas overlapFace and Greeble areas don’t overlapSuggests faces special due to expertise
34IS FACE RECOGNITION NOT SO UNIQUE AFTER ALL? ProsopagnosiaConclusions?IS FACE RECOGNITION NOT SO UNIQUE AFTER ALL?Gauthier & Logothetis (2000)COGNITIVE NEUROPSYCHOLOGY, 17 (1/2/3), 125–142Faces are not “special”They are the “default special”in the primate recognition systemthe 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
35ProsopagnosiaButGauthier et al. 2004: Greebles not treated like facesCW profound object agnosia. OK on faces, poor on greeblesGrill-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)
36Split Brain PatientsThe Corpus CallosumThe two cerebral corticesare interconnected by thelargest fiber system in thebrain, the corpus callosumHuman CommissurotomyA neurosurgical treatmentfor intractable epilepsyCorpus callosum iscompletely dividedAllows systematicInvestigation of hemisphericspecialization and integration
37Split Brain PatientsVisual Recognition StudiesPicture presented in RVF (i.e. to LH)Patient could name or reach for the object correctly with right handPicture presented in LVF (i.e. to RH)Patients could not name/describe the objectSubjects could reach for the correctobject with their left handSplit brains can perform independent incompatible motor commandsSay manpoint to womanHead-stone/sky-scrapersprared (VP) v full (JW)
38Left hemisphere specialised for language Split Brain PatientsLeft hemisphere specialised for languagecup‘cup’S can report ‘cup’RH can select cupLH cannotspoonS report nothingLH can select spoon(RH cannot), but S cannot say what it isPatient NGSpringer & Deutsch (1998)
39Split Brain PatientsLeft hemisphere as an ‘interpreter’70/30Shovel to clean out the chicken shed (PS)80/20Birds and chimps 75% (optimisation)Humans 63% (frequency matching)Left Brain - 63%Right Brain 75%VP athlete ex.