Distorted Worlds Revision Notes PDF

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LECTURE 1: CAN YOU BELIEVE WHAT YOU SEE?1: Understand the reasons behind our perception of visual illusions Charles Bonnet Syndrome —occurs when central visual field degenerates—can sometimes result in rich visual hallucinations - Evidence shows spontaneous nervous activity in brain associated w/fa...

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LECTURE 1: CAN YOU BELIEVE WHAT YOU SEE? 1.1: Understand the reasons behind our perception of visual illusions

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Charles Bonnet Syndrome—occurs when central visual field degenerates—can sometimes result in rich visual hallucinations - Evidence shows spontaneous nervous activity in brain associated w/facial processing which causes perception/hallucination Common misconceptions about vision: - Automatic + effortless process - Vision sends exact copy of what is in front of you to brain - We perceive a rich + continuous visual environment—we only see things in detail and in colour that we fixate upon evidence from this comes from retina (photoreceptors: rods and cones)—  RODS: Work in low light conditions—vision in dark is B+W + unable to process colour info  CONES (found primarily in fovea): Sensitive to colour—enable powerful acuity and only work when we have lots of light

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Graph shows acuity across the visual field—there is no acuity at blind spot bcos there are no rods and cones (light receptor cells)—i.e. we only get rich colour info based on what we fixate upon

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Evidence saccades (quick simultaneous movement of both eyes between two or more phases of fixations in same direction) help build up a picture Transsaccadic memory buffer enables us to take forward visual info from one saccade to the next saccade however would take up large cognitive demand as we would be building up picture through many individual fixations - Evidence for this comes from change blindness— eyes fixate parts of interest (people, sphinx) if distracted by flicker miss change then evident that eyes are not building up a veridical (i.e. true representation) image of a scene through saccades

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How does vision work

Vision= hierarchical (i.e. low lvls/aspects of visual input is dealt with separately to high lvls/aspects of visual input) and modular (i.e. different modular structures of brain deal w/different aspects of visual processing) But processing is in parallel + projections feedback as well as feedforward

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V1/Primary visual cortex (striate cortex) = cortical area of brain where most input is directed - Vision= retinatiopically mapped—i.e. damage to V1 associated with damage to sight in associated field - Loss of V1= cortical blindness - Damage to part of V1= blindness for corresponding part of visual field (hemianopia)

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V4= Evidence suggests area is involved in colour perception Damage to both V4s (rare) can lead to loss of colour vision + inability to identify/discriminate colour—however still preserved processing of form + motion - Rich et al (2006)— -

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Group of synaestheses perceived a colour when saw particular letter e.g. saw blue letter even if it wasn’t blue – there was cross between colour + form info Investigating whether perception of seeing colour implicated neural processing for both coloured and greyscale letters Findings showed synaestheses and non synaestheses activated V4 (blue) for coloured letters and (red) grey letters—shows ppts perceive colour THEN brain area activated

V5= Deals w/motion info Damage to V5s motion blindness (perceive things as static images) TMS studies on V5 also reveal its role (e.g. Beckers and Zeki, 1995)

Visual pathways beyond early visual cortex:  VENTRAL (‘What) STREAM— - Where object info occurs human face recognition (fusiform) + colour recognition - Damage to ventral stream can result in visual agnosia  -

DORSAL (‘Where) STREAM— Process spatial info (i.e. where are things in relation to each other) Damage to dorsal stream can lead to visual spatial neglect or optic ataxia= can be seen when ppl attempt to reach for object but cannot even though they are aware of object

1.2: Describe and define visual agnosia

1.3: Understand evidence suggesting that ‘normal’ visual perception is not an accurate representation of the world around us

VISUAL AGNOSIA= ‘Failure to know’ visual info—i.e. can no longer identify by sight - Visual agnosia can only be detected if patient has no problem w/memory or lang skills needed to produce words but unable to detect info purely through sight Challenges for visual perception: - Input often insufficient (i.e. things can often be excluded from vision), ambiguous + overwhelming (i.e. vast amount of visual input) - ‘The Blind Spot’—demonstrates brains ability to ‘fill in’ which leads to over interpretation of incoming stimuli using laws of occlusion even if this is not true representation of what we actually see - Illusory contours— 

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1.4: Describe the progression of visual input from the eye to complete conscious perception and understand how this process might differ from common misconceptions of vision

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Ambiguous input: Binding the correct parts together—visual system binds together different aspects of objects to help differentiate things ambiguous input demonstrate that this is v. cognitively demanding task - Cannot see both percepts at same time— visual system designed to only see one at a time e.g.

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Automatic computation of occluders—Sometimes occluders are added to create meaningful shape occuluders show how visual formation forms conscious perception

Bind visual input together to form meaningful object

Gestalt principles:

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Wertheimer (1923) wanted to look @ rules of vision that help us bind elements of visual input together e.g. using rules of similarity, proximity, continuity and closure to bind visual elements to understandable whole

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Ambiguous input: The importance of context - We have evolved mechanism to use context to help resolve ambiguities associated w/ visual input - Context can help resolve illusions such as ebbinghaus illusion—i.e. where both orange circles are same size but harder to identify with surrounding blue circles (dorsally we know size of circles but ventrally w/context we don’t know)

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However, we now use fMRI to look @ visual processing within brain

e.g. Ponzo illusion—knowing that the lines are the same size does not change how we perceive them visually (top line looks longer)

Overwhelming input: - Sometimes vast amount of visual info may not allow us to process all visual input—therefore important selection mechanism= attention

LECTURE 2: 2.1: Define and describe episodic memory, including understanding how it can be assessed.

Examples of memory distortions:  E.P.—Larry Squire: demonstrated repetition of forgetting context of different situations + failed memory test about animals.  Hyperthymesia: highly superior autobiographical memory - Whilst this form of memory may appear advantageous, this can become frustrating for the patient

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Episodic memory= personally experienced events Use episodic memory to form autobiographical memories Episodic memory should contain 3 W’s: - What? contains allocentric (i.e. how things are spatially related to each other) and egocentric (i.e. spatial relationship you have w/particular memory) visuospatial info - Where?  - When?  i.e. ‘temporal tag’ of memory Tulving suggested episodic memory= unique to humans - Clayton & Dickinson, 1998; Clayton et al, 2003 argued against true episodic memory in animals—suggested that animals have instead learnt through associative learning (therefore lack context needed to form episodic memory) or basing memory on familiarity - Provided two different types of food (worms +peanuts) to birds experimenters wanted to see if birds remembered what, where and when they stored food if they had short delay (4h) they would retrieve worms where as if they had long delay (124hr) they would retrieve peanuts - The experimenters then devised set of behavioural criteria for episodic-like memory in animals: - Content: recollecting what happened, where + when on basis of specific past event - Structure: forming integrated ‘what-where-when’ representation - Flexibility: episodic memory is set within declarative framework—involves flexible deployment of info

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Burns, Russell & Russell (2015)—

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Children were shown what handles to turn in specific order on music order  had to remember what-where and when Findings showed that only 16 of 2yr olds ppts had integrated memory of whole event (i.e. could remember what-when-where specifics) vs. higher no. of 3yr olds (59) AUTONOETIC CONSCIOUSNESS (Tulving 2002)—relating to/characterized by capacity to be aware of one’s own existence as an entity in time -- enables us to have vivid memories - However, we cannot be sure if children or animals are using autonoetic

2.2: Understand and evaluate the evidence for inaccuracies in episodic memory.

consciousness w/episodic memory Dissociation of episodic and semantic memory  Vargha-Khadem et al (1997)— wanted to show that episodic + semantic memory dissociates - Assessed 3 patients w/early hippocampal damage who were unable to form episodic memory—researcher wanted to establish if they could form semantic memories - Found picture recall was significantly worse for patients vs. healthy controls (i.e. severe episodic memory difficulties) however demonstrated perfectly good semantic knowledge shows there are two separate systems 

Schmolck et al (2002) wanted to assess if there would be semantic as well as episodic impairments in relation to brain damage - Do patients w/anterograde amnesia show deficits in semantic memory? - 3 groups: control ppts, amnesia patients w/damage confined to hippocampus, HM + others w/extended brain damage (i.e. bigger lesions) - Conducted series of 18 semantic tests e.g. Pointing to picture task (name cue), pointing to picture (description cue) + semantic feature task (Y/N Qs)

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Healthy ppts + ppts w/hippocampal lesions had little differences during semantic tasks—shows that hippocampus is not involved in semantic memory Findings for HM + others who appeared to have semantic impairments replicated researchers then ranked ppts performance on all tests and found performance of MTL + patients correlate w/extent of lateral temporal damage  i.e. patients w/more damage further than medial temporal lobe displayed MORE semantic memory damage Bird & Burgess (2008)—

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Red lines= subcortical connections Black lines= cortical connections Shows links between hippocampus + other brain regions model demonstrates importance of connections between hippocampus + implications for episodic memory

What might distort episodic memories?  Schemata= i.e. mental shortcuts which enable us to know how to respond in particular situations (e.g. enter restaurant get menu choose what you want etc.) if events didn’t happen in particular order this would violate our schema and therefore might distort episodic memory - Research study involving asking undergrads what was in an office after sitting and waiting in office for 3 mins found ppts remembered non-salient items more and also listed typical salient items found in office even though they weren’t present during study i.e. office scheme activated in room and then after leaving room the schema was ‘reactivated’ so memory was distorted as they listed things typically found in office  DRM (Deese, Roediger & McDermott paradigm)— - Ppts learn lists of words grouped around theme (e.g. SLEEP: dream, snooze, bed, blanket) without actual theme being listed (sleep) findings have shown ppts likely to recall missing theme word as an actual target (i.e. sleep) and confidence as high for sleep as other words 

Patihis et al (2013)— Looked @ false memory in highly superior autobiographical memory (HSAM) - Used DRM + results showed these ppts were just as likely or even MORE likely than ppts from previous studies to recall missing theme word as actual target—i.e. recall false info - Found ppts w/more extreme superior autobiographical memory more likely to be tricked w/misinformation

 Implications for inaccuracies: - Eyewitness fallibility (Loftus & Palmer)—people report inaccuracies + are susceptible to misinformation - Tversky and Marsh (2000)—looked @biases in memory w/out awareness— found if ppts wrote nice letter supporting somebody to join fraternity, they remember more socially positive things vs. if ppts wrote negative letter about not sharing room w/someone, they remembered more annoying

2.3: Outline the neural systems involved in episodic memory and the effect(s) of selective damage to these regions.

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things Place cells= spatially encoding world around us - Seems to be link between episodic memory + spatial representation Maguire et al (2000) (and 2006: compared w/London bus drivers)—London taxi drivers study - Study shows strong correlation w/enhanced grey matter in hippocampal regions + amount of time spent as taxi drivers - Taxi drivers then compared to London bus drivers (given set routes rather than learning flexibility of different routes)—found bus drivers did not show same effect as taxi drivers - Woolett & Maguire (2011)—Longitudinal study of early taxi drivers and showed hippocampal grey matter changes only in those who qualified - Maguire et al (2006)—then looked @previous taxi driver who sustained hippocampal damage found that driver demonstrated inability to remember previous routes used to get from Bank to St Pauls shows hippocampal damage implications on episodic memory -

2.4: Appreciate the theories concerning the relationship between our episodic memory system, scene construction and imagination of future and fictitious events.

Place cells/Maguire studies—generally involve allocentric spatial memory + suggest this is key spatial memory in hippocampus—this is brought together w/egocentric info from other brain regions to produce complete mental visual image of event i.e. hippocampus able to put allocentric + egocentric info together to form spatial representation

Implanting false memories—Social Factors  Edelson et al (2011) - Attempted to experimentally implanted memories - Wanted to look at memory conformity (i.e. idea that memory can be manipulated through social interaction) -

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Results show evidence of memory conformity in Test 2 (i.e. when ppt told other 4 confederates gave incorrect answer they also gave same answer) When ppts are not having social manipulation—there is enhanced connectivity within amygdala regions during trials when ppts make persistent errors—i.e. suggests enhanced connectivity within amygdala regions is predictive of making LT persistent errors

Implanting false memories—Visual evidence

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Wade et al (2002)— - Recruited approx. 20 ppts and experimenters used doctored photographs + guided imagery (e.g. ask ppts how it would feel to be hot air balloon) of ppts when they were aged between 4-8yrs and superimposed images of them onto hot air balloon ride - Ppts were then shown superimposed image and asked if they could remember this memory - Over series of 3 interviews, experimenters tried to get ppts to remember false event (i.e. hot air balloon ride) - Found significantly large increase of false memory recalled from Interview 1 to Interview 2 Lavilleon et al (2015)—demonstrated ability to physically implant memories into mice by stimulating place cells

Episodic memory is reconstructive process:  Leads to phenomena— ‘imagination inflation’  First evidence comes from Garry et al (1996) - Ppts were given list of events that could happen to them as child + then asked to rate which ones were likely to happen—then asked to imagine what would happen if these events happened - Findings show forming images for imagined events led to shift belief of event ACTUALLY occurring Episodic memory arguably can be used in other ways i.e. imaginary or future events:  Hassabis et al (2007) compared imagination in patients w/ hippocampal lesions vs healthy ppts—given cues w/sensory details - Damage to hippocampus seems to not only affect memory of something that did happen but also to imaginary events  Addis et al (2007) looked @episodic memory for future events compared recall of past events vs. imagining future events (e.g. imagine your graduation or marriage)

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Found common brain networks are used when imagining things in future and remembering things from past

LECTURE 3: Does emotion distort cognition?

3.1: Critically evaluate the role of emotion in cognitive functions

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Plato would argue humans are made from 3 separate non-interactive elements: their intellect, will + emotions More recent cognitive revolution uses computer metaphors which do not integrate emotions LT memory can be distorted by emotional impact—e.g. 9/11 many ppl report seeing film of both planes hitting WTC even though this footage doesn’t exist ST attention can be cued exogenously to salient negative event e.g. car accident

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Hard to remove emotional saliency in particular situations—i.e. decision making largely influenced by emotions Perception/sensory experience also modulated by emotion—i.e. cognition not independent—influenced by emotional experiences

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What are emotions?  Can we objectively measure emotions? - Whilst we can use biological/physiological measurements such as GSR + heart rates etc.—these are not subjective  EMOTIONS= Mental + physical outcomes of subjective experiences—leads to bodily responses (e.g. facial expressions, peripheral NS arousal, speeded reaction times, particular pattern of neural activity…) - Subjective experience come from the appraisals + evaluations made cognitively OR automatically 

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3.2: Describe evidence for differences in the way that certain emotions are processed and the result of this on normal and pathological perception

Charles Darwin (1872) set out to identify evolutionary purpose of emotions—i.e. attempt to quantify universal emotions that lead to evolutionary success - Identified physical characteristics associated with a series of particular emotions (irrespective of age etc.) Paul Ekman (1971) suggested there are six primary basic universal emotions: happiness, sadness, surprise, disgust, anger + fear - Expressions appear to be innate—i.e. young infants show same range - Expressions appear to be universal—similar across all societies even in cultures w/little contact w/others (e.g. in rainforests of Papua New Guinea) - Expressions also equivalent in ppl blind from birth—however psychologists have also found slight differences - However, weakness= pictures used actors which can be argued to not display real emotion

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Neuroanatomy of emotion—James Papez (1937) attempted to quantify parts of brain involved in emotional processing - Proposed the Papez circuit suggested the cingulate gyrus integrates cortical +subcortical emotional processing

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Limbic system—certain elements of limbic system grouped together i.e. Consistent evidence implicates some structures of these structures in emotional processes

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Meta-analysis—83 studies to determine whether there is consistent activation of particular brain region Found clear neurological evidence for amygdala being implicated in fear SM= patient w/genetic disorder which bilaterally destroyed amygdala (UrbachWiethe disease) - Feinstein et al (2011) conducted systematic assessment of whether fear could be provoked in SM - Demonstrated ‘excessive approach’ response in pet shop—i.e. drawn towards the ‘scary animals’ rather than showing fear - Additionally, showed lack of fear response to horror films in compar...