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

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Presentation on theme: "Lecture 7 Visual Perception (Dr Roger Newport) Hemianopia/Visual Field Cuts Blindsight u Akinetopsia u Achromatopsia u Agnosia Prosopagnosia Split Brain."— Presentation transcript:

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

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

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

5 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

6 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

7 Finger-pointing performance by D.B. (From Weiskrantz et al., 1974) Blindsight - Famous Case DB

8 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 Retina - SC - Th - Cortex Retina - Pulvinar - Extrastriate cortex Retina - LGN - V2/V4/V5/ TEOV2/V4/V5/

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

10 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)

11 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 o /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

12 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 Akinetopsia (motion blindness)

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

14 Ishyhara plates Cerebral Achromatopsia

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

16 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." Cerebral Achromatopsia - Famous Case

17 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?

18 V1 V4

19 Wechslers 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 (Zeki) vs MS (Heywood and Cowey) Awareness vs. constancy Cerebral Achromatopsia - dissociations

20 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

21 MS Dont know Dont know, but same as above No activation of V4 in PB suggests V4 = colour constancy Wavelength info = V1/V2 Colour awareness - V4 or more anterior (IT)?

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

23 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).) Associative Agnosia

24 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

25 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 DFControls Perceptual matching Posting Posting task

26 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 - Cant 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.

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28 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 - Famous case Dr. P

29 Prosopagnosia 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) Brain region involved

30 Are faces just very difficult objects Or 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?

31 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 Cant recognise faces Less impaired at cows. If faces just more difficult then shouldnt have patients more impaired at other objects (i.e. cows). Prosopagnosia

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

33 Face and Greeble areas overlap Face and Greeble areas dont overlap Novices Experts Prosopagnosia Suggests faces special due to expertise

34 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?

35 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

36 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

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

38 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 specialised for language

39 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.

40 Next Week Attention


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