Lecture 7 Visual Perception (Dr Roger Newport)  Hemianopia/Visual Field Cuts  Blindsight Akinetopsia Achromatopsia Agnosia  Prosopagnosia  Split Brain

Hemianopia (and other visual field cuts) Bitemporal Homonymous Hemianopia Quadrantanopia Macular sparing

X Where/How What motion shapes colours objects and faces M-ganglion cells P-ganglion cells Magno LGN Parvo V1 V2 V3 V4 MT V5 IT cortex Parietal Where/How What motion X shapes colours objects and faces

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

Blindsight - 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 cortex unaware 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 et al., 1974)

Neuropathology • striatal cortex (V1) damage 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 disc islands of vision: Friedrich patient, but GY primitive visual pathways - sparse, but widespread Stray 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, visual information can reach a large constellation of visual ‘association’ areas in the brain. Some of these paths arise through parallel projections from the retina to the superior colliculus, with further relays via the thalamus to the cortex [16], or by direct projections to the pulvinar and thence to the extrastriate cortex [l]. It is known that intralaminar neurons in the LGN survive removal of Vl, and project to V2, V4, V5 and TEO [17-211. Recently, a projection from the LGN to the inferotemporal cortex has been demonstrated [2Zoo]. The LGN projections that survive Vl removal are relatively sparse in density, but are nevertheless widespread and probably encompass all extrastriate visual areas. Retina - SC - Th - Cortex Retina - Pulvinar - Extrastriate cortex Retina - LGN - V2/V4/V5/ TEO

X X Where/How What motion shapes colours objects and faces M-ganglion cells P-ganglion cells Magno LGN Parvo V1 V2 V3 V4 MT V5 IT cortex Parietal Where/How What motion X shapes colours objects and faces 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)

Akinetopsia (motion blindness) - Famous case LM 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 (< 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) The consequences of inactivating areas V1 and V5 on visual motion perception G 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 V1 Direct fast route from retina to V5 via pulvinar bypassing V1 Slower route to V5 through V1

X Where/How What motion shapes colours objects and faces M-ganglion cells P-ganglion cells Magno LGN Parvo V1 V2 V3 V4 MT V5 IT cortex Parietal Where/How What motion X shapes colours objects and faces

Cerebral Achromatopsia Ishyhara plates

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 Achromatopsia is not: due to peripheral damage (e.g. retina) due to primary visual area damage c) colour agnosia: disorder of colour categorization d) colour anomia: disorder of colour naming

Cerebral Achromatopsia - Famous Case The case of the colorblind painter by Oliver Sacks Facts: Auto accident No clear damage (no bleeding) No recollection of accident Alexia 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."

Damasio 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 gyrus Calcarine sulcus Lingual Gyrus Fusiform Gyrus

V1 V4

Cerebral Achromatopsia - dissociations Wechsler’s Patient (1933) - colour and form dissociation Anoxia 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 could neither name nor tell the form of. He picked out colours on command’’ PB: Coma from electric shock. Blind, but can discriminate colours consciously 1. is patient’s ability to discriminate colour wavelength based or 2. are colour constancy mechanisms partly intact. If 1, then expect the processing to be confined to areas V1/V where 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

Zeki et al., 1999. Colour processing in a blind patient Age-matched Control PB V1 only Coma from electric shock. Blind, but can discriminate colours consciously

No activation of V4 in PB suggests V4 = colour constancy Wavelength info = V1/V2 Colour awareness - V4 or more anterior (IT)? MS Don’t know Don’t know, but same as above Fig. 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 reflects a constant proportion of the incident lights at any wavelength. (a) The green patch reflects 70% of the medium wavelength light. Normal observers report this as 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 white depending on the intensity of the medium wavelength light. (b) How constancy was tested. Here the green patch is now illuminated by much more long wavelength light. The proportions of available light reflected from each surface remain unchanged but the absolute levels of reflected intensity are greatly changed, 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.

The Agnosias Bauer (1993) In Hielman and Rothi 1993 A failure of recognition that cannot be attributed to: primary sensory defects mental deterioration attentional disturbances aphasic misnaming unfamiliarity with sensorially presented stimuli Originally classified as having two types Lissauer (1889) : Apperceptive and Associative

Associative Agnosia can perceive, but not recognise objects Good acuity etc Can see global structure (full shape) Can match to sample* Can copy (see right) But still cannot recognise objects Cannot recognise own copy Usually occurs following left occipitotemporal damage /anterior temporal lobe Disconnection 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).)

Apperceptive Agnosia Can see Can do obstacle avoidance etc Good acuity etc, but Cannot recognise objects Cannot see global structure (full shape) Cannot match to sample Cannot copy Rare. Usually occurs following gross damage to lateral parts of occipital lobes feeding ventral stream Deficit in form perception Copying example

Apperceptive 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 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 Patient DF Controls Perceptual matching Posting

Other Agnosia Alexia - left fusiform/lingual areas Inability to form coherent lexical representations from letters Topographagnosia or topographical agnosia - right lingual gyrus Inability 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 means And can recognise a face as being a face and Can 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.

Prosopagnosia - Famous case Dr. P Sacks, 1985 The Man Who Mistook His Wife for a Hat Dr. P. well educated musician and teacher possible degenerative disease or large tumor couldn'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 Brain region involved George et al. (1999). fMRI study of positive and reverse contrast faces. Bilateral fusiform gyri response to faces Right fusiform gyrus only when face became familiar (Note contrast to Alexia)

Prosopagnosia Is 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 objects Or are they special because of our level of expertise?

Prosopagnosia 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 MX Farmer lost ability to recognise cows Could recognise faces Bruyer et al., (1983) patient RB Can’t recognise faces Less impaired at cows. If faces just more difficult then shouldn’t have patients more impaired at other objects (i.e. cows).

Prosopagnosia Are faces special objects, or are we face experts? Activation of the middle fusiform 'face area' increases with expertise  Gauthier et al., 1999 Sequential matching task Inverted and upright. Expertise specific to upright

Prosopagnosia Experts Novices Face and Greeble areas overlap Face and Greeble areas don’t overlap Suggests faces special due to expertise

IS FACE RECOGNITION NOT SO UNIQUE AFTER ALL? Prosopagnosia Conclusions? 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 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.

Prosopagnosia But 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)

Split Brain Patients The Corpus Callosum The two cerebral cortices are interconnected by the largest fiber system in the brain, the corpus callosum Human Commissurotomy A neurosurgical treatment for intractable epilepsy Corpus callosum is completely divided Allows systematic Investigation of hemispheric specialization and integration

Split Brain Patients Visual Recognition Studies 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 Split brains can perform independent incompatible motor commands Say man point to woman Head-stone/sky-scraper sprared (VP) v full (JW)

Left hemisphere specialised for language Split Brain Patients Left hemisphere specialised for language cup ‘cup’ S can report ‘cup’ RH can select cup LH cannot spoon S report nothing LH can select spoon (RH cannot), but S cannot say what it is Patient NG Springer & Deutsch (1998)

Split Brain Patients Left hemisphere as an ‘interpreter’ 70/30 Shovel to clean out the chicken shed (PS) 80/20 Birds and chimps 75% (optimisation) Humans 63% (frequency matching) Left Brain - 63% Right Brain 75% VP athlete ex.

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