Emotion & Cognition Flashcards
1
Q
What is double dissociation
A
-Method of study where both brain damage and non-brain damage data is used to analyse how areas of the brain work
2
Q
Describe three features of object recognition
A
- Modular – the object recognition system is built of specialised functional modules
- Constructive – it builds representations from sensory input and contextual information
- Semantic – higher level information about e.g. objects’ functions are built into the representation
3
Q
How was the visual system originally divided?
A
- Dorsal pathway or ‘where’ system
- Ventral pathway ‘what’ system
4
Q
Describe how the visual systems have different representation in the eye
A
- Temporal cortex (ventral pathway) has all receptive fields in the fovea this lends itself to fine dsircrimination
- Parietal cortex (dorsal pathway) has 60% of receptive fields outside fovea this lends itself to spatial recognition
- Receptive field = area where an object will cause neuron to fire
- Observed in lesion studies with monkeys (lesion to inferotemporal area = poor identification/ lesion to parietal area = poor spatial recognition
5
Q
what neuropsychological evidence in humans has shown different pathways in object recognition?
A
-Temporal cortex lesions (ventral) ->
visual agnosia
-> Deficit in recognizing objects
-Parietal cortex lesions (dorsal) ->
Deficits of spatial awareness
-> hemispatial neglect ->
Optic ataxia
-Object tasks activate ventral system (fusiform gyrus)/ Spatial task dorsal activation (parietal cortex) in fMRI studies
6
Q
What evidence shows the what vs where divide in object recognition is more fine grained is not as broad as originally hypothesised?
A
- Lesions to ventral system were seen to only effect perception but not vision for action (letter box study) suggesting these may be a better theory rather than just simply “what”
- Ventral system made up of different systems itself including systems for object constancy (recognising object from different angles)/ integrating features into whole object/ recognising functions of the object
7
Q
Describe the different types of agnosia and what system they effect
A
- Affect temporal cortex, thus the ventral pathway
- Apperceptive agnosia= deficit in object constancy, caused by lesions to left fusiform cortex
- integrative agnosia= deficit in integration (can’t identify overlapping object but can when same objects are not overlapping/ can not integrate objects into one whole object ) caused by lesions to lateral occiptal complex
- Associative agnosia= unable to associate objects with their function (normally end up picking those that look most alike) caused by lesion to medial temproal lobe
- Prosopagnosia= deficit in face recognition caused by lesion to fusifrom face area (FFA)
- Overall tells us object recognition is a constructive process involving many modules and has a semantic element (meaning is automatically processed) not merely a retinal input but is made up of what we are aware of
8
Q
How are faces processed?
A
- Holistically (whole face processed before individual features) which is different to other object recognition
- Faces encoded by spatial relations between features while objects may be coded on individual features themselves
- Possibly evidence for anatomical modularity
9
Q
What is the expertise hypothesis?
A
- Face recognition may be as a result of expertise rather than FFA (evidenced inconsistently with experts in different fields such as bird experts)
- No other objects has selective pattern of activation like FFA, except other biological identification processes, showing a dedicated module and contradicts expertise hypo
10
Q
Explain evidence against anatomical modularity
A
-Advancements fMRI have lead to multivariate analysis of patterns rather than univariate. Face recognition done across various brain regions not isolated to FFA
11
Q
What is inattentional blindness?
A
-Seeing something but not being aware of it as it is not given attention
12
Q
Define two types of selective attention
A
- Overt attention= purposely moving head or eyes towards stimulus
- Covert attention= paying attention to something while appearing to pay attention to another stimulus
13
Q
What is the cocktail party effect?
A
- An example of covert attention where you can focus on the person you are speaking with as well as well as give attention to neighbouring conversations
- Evidenced with the dichostic listening experiment where participants would remember psychical aspects of speaker but not the content of the unattended channels
14
Q
What does early selection refer to in terms of attention
A
- Early selection states that stimuli are processed based on psychical attributes and then are selected by attention
- Cueing effects were used to help evidnece this (arrow that indicated stim gave a quicker reaction time than arrow that indicated opposite location of stim)
- However this theory does not explain how information can still pass through filter (such as hearing ones name in a convo is often picked up upon). Dichotic tasks could also be biased by certain words in unattended stream so were not being filtered out at an early process on a semantic level
15
Q
What is the spotlight model of attention?
A
- Attention enhances sensory processing of objects in the spatial location attention is directed
- However study has posed a object selection rather than spatial, objects cued in same object as target were reacted to faster than objects outside of object but same distance away
- Inhibition of return has also shown object selection where if the delay between cue and target becomes longer the uncued condition becomes faster
16
Q
What does the late selection model of attention refer to?
A
-All stimuli receive semantic analysis before attentional selection filters what enters into awareness
17
Q
How does load theory incorporate both early and late selection
A
- Low perceptual load evidences late selection as main task did not use up all attention so distractor had greater influence as it was also processed increasing rt’s
- High perceptual load evidences early selection as task used all attention so distractor was filtered out reducing rt’s
- fMRI shows high load increases activation in visual cortex in main task but low in non-main task (early selection) and low condition increased activity in task that appeared between main task trials as left over attention increased spotlight (late selection)
18
Q
What are contralesional stimulus and ipsilesional stimulus?
A
- contra= things occurring on opposite side to lesion
- Ipsil= things occurring on the same side as the lesion
19
Q
How can hemisphere neglect be tested?
A
- Cancellation tests (crossing lines out on page and see what lines are neglected)
- Most common area to cause neglect is damage to tempoparietal junction
20
Q
Is neglect the same as being blind?
A
- No, stimuli on each side can often be detected but when presented together the contralesional side will often be missed and the ipsilesional stim being recognised
- This is known as visual extinction
- fMRI still shows activation of damaged hemisphere even though the subject reports no awareness
- Therefore, neglect is a product of a lack of attention, the person is not consciously aware of contra stim but is processing it unconsciously
21
Q
What has hemisphere neglect contributed in terms of understanding attention?
A
- Fear stims in neglected field reduced visual extinction, it appears that if a stim is sufficiently meaningful or important it can break through the attention filter despite not being aware of it. Similar to the cocktail party effect
- Also shown objects being similar increase extinction but when processed at a semantic level, words with similar meaning less likely to be neglected compared to presentation of words with different meanings
- Pre-attentive info can affect processing, perceptual load studies that reduce targets also reduced preservation showing unperceived stimulus still influence our behaviour (evidence for late stage processing!)
- Attention operates on internal representations as well as external!, people with neglect report ipsilateral stimulus of memories (Italians and Florence landmark)
- Inhibits spatial memory, those with neglect revisited previously crossed out stimulus more often if the mark was invisible showing issues with internal as well as external attention
- attention operates within objects rather than spatial frame (will draw out right side of images rather than just images on the right side of a space) even if the object rotates attention neglects the original contralesional side again showing object based neglect
- Cueing increases reaction time in ipsilesional field compared to contralesional showing a difficulty in engaging from ipsilesional side
22
Q
What is the difference between top-down and bottom-up attention?
A
- bottom-up= stimulus driven, features of objects can determine what we give attention to (these features compete especially if similar) such as a bright light drawing your attention
- top-down= personal relevance (cocktail party), emotional significance, goal relevance, semantic relevance are all examples of top-down approach as these are relevant to the person persons relationship with the object
23
Q
How is attention competition resolved?
A
- Bottom-up not sufficient requires top-down measures indicating that a attentional template is required
- Neurons respond selectively to different stimulus’s (some prefer squares, others triangles etc) activity remaining high wins competition for the stimulus associated with the neuron. However, if the stimulus is negative neuron firing is suppressed meaning it will not win the “competition”
- This competition occurs in brain regions which process visual features (inferior temporal cortex) not in a separate specialised region. Neurons in visual region are co-opted to process stimuli and resolve attention competition
- Cueing can prime certain areas to direct attention before person is consciously aware of it
24
Q
How has EEG evidenced neuron activation in attention
A
- Cueing can prime certain areas to direct attention before person is consciously aware of it, cue and target being congruent increases activation
- Inhibition of return reflected in firing rates in cueing tasks (higher for valid cue in short delay, higher for invalid cue in longer delay)
25
How has fMRI evidenced neuron activation in attention
- Cueing tasks have shown locations of stimulus's are modulated by the brain in V1 (create map of locations on brain) at very early stage
- Competitive interactions happen at multiple points in processing, V4 (involved in feature integration and object representation) activation is lower when items present simultaneously compared to cued (bottom-up) but when asked to focus on just one object this effect disappeared (top-down)
- Activation increased in FFA on face recognition compared to houses depsite both being in visual field. Therefore, attention modulates higher processing regions through activation
26
What is the biased competition model of attention?
-Competition occurs at the level of object properties and whole objects - as we have seen, monkey neurophysiology and human neuroimaging studies demonstrate attentional modulation of neuronal signals throughout visual cortex (ventral visual stream – the ‘what’ pathway)
27
How does evidence for the frontoparietal cortex being the source of attentional signals affect the BCMA?
- The BCMA may occur as the result of attentional signals arriving from elsewhere
- Frontopareietal regions activated in preparation for target stimulus (top-down bias signals) not activated when passively attending cue
- Activation of targets were in posterior areas showing a network between the two
28
How does frequency oscillation (coherence) explain how attention selection is communciated?
-This provides a mechanistic explanation for the two different types of attentional selection – top down, (search task) voluntary attention depends on frequency synchronisation between parietal and prefrontal cortex in the middle frequency band (beta band) whilst bottom-up, (pop out task) reflexive attention depends on frequency synchronisation between these regions in the upper frequency band (gamma band).
29
How has long and short term shown to be separate
-Double dissociation of lesions studies (K.F preserved long term mem loss of short term mem, H.M opposite)
30
What is the modal model of memory and evidence against aspects of it?
- Input-> sensory mem-> STM-> LTM
- STM-> LTM through rehearsal, LTM-> STM thorugh retrieval (rehearsal loop)
- Info at each level can be lost through decay
- STM defined as unitary store but has been seen to have multiple seperate stores such as visualspatial and phonological (again shown through double dissociation)
31
What comprises the WMM?
-Visual-spatial sketchpad/ Central executive/ phonological loop/ episodic buffer
32
What is the 'g' factor and its link to WMM?
- 'g' factor defined as either GF= fluid intelligence (reasoning/problem solving) or CF= crystallised intelligence (general knowledge)
- GF was shown to be indicator of WMM (WMM not linked to CF) and specifically linked to executive attention
- Later research showed executive intention was correlated to ability to implement rules and not necessarily a component of fluid intelligence
33
What is chunking?
- GF indicates ability to build mental program to manage tasks. This is done by chunking, breaking a problem down into more manageable tasks
- WM involves maintenance and manipulation of information and construction/implication of rules to apply to chunking
34
What is goal neglect?
- Failure to use rules and chunking despite being aware of them is called goal neglect. Lower IQ increases goal neglect
- However more complex rules were seen to increase goal neglect. This suggests the overall complexity of mental program required to complete a task is important when considering link between WM and GF
35
What is the standard model of the role of the PFC in WMM?
- Info stored in PFC and hold representation to-be-remembered stimuli or template of them. Evidenced through identification direction (of stim) based neuron firing, a temporary representation of the spatial location of the cue. Lesions to PFC showed deficit in this to be remembered info hypothesis showing impaired WM
- PFC organised according to type of information stored
- WMM memory has separate systems for objects and locations like the ventral and dorsal pathways in visual processing, evidenced by higher activation in ventral PFC for patterns/objects and higher activation in dorsal PFC in spatial cues
36
What evidence is there against the standard model for PFC involvement in WMM?
- Confounds for lesion studies which studied representation as multiple mechanisms used in processing tasks such as attention and strategy
- Chunking uses the PFC so fMRI study of activation in dorsal PFC could of been as a result of manipulating info rather than the PFC being a store of it
- Further animal study showed neurons in PFC can encode both location and identity of an object (not seperate stores) therefore, PFC neurons can adapt to the different info presented
- These neurons were also labelled as for attention or memory and majority were selective for attention. Thus, counters the idea PFC stores representation and is not important for WM but is in fact used for selective attention
- Dorsal vs Ventral argument also may be more to do with what is done with the info rather than what it is. Dorsal= manipulation and Ventral = maintence, PFC is organised thus on type of processing not the type of stimulus
37
Where is info for representations in WM held and what is now seen as the role of the PFC in WM?
- Multivoxel analysis has visual processing regions also store representations. This means the same regions that are activated in categorising stimulus's also hold representations of them
- PFC shown to be involved in coding/processing of what attention should be focused on (what is the rule, e.g. is it speed or direction of an object we are looking for?) also this role may involve enhancing attention to internal representations of task relevant stimuli in working memory and manipulating such information by biasing specific sensory regions with signals during working memory (same as what is does to attention)
38
How is the PFC related to inhibition in learning?
- Damage to PFC seems to stop the ability to surpress information in rule based learning (no negative feedback loop). Those with damage appear to to be unable to surpress a previously learnt rule and carry out a new rule, continuing to apply the original (Wisconsin card sorting task)
- However, performance of these tasks has been seen to be unaffected by those with similar frontal lobe injuries showing the PFC may not affect universal WM. Participants struggle with more realistic tasks though
- Six elements task showed that PFC could be a supervisory system (SAS model), used to facilitate task solving that is not automatic and requires more cognitive resources explaining this deficit with real life scenarios. SAS model is what supervises when new rules have to be learnt (a controller)
39
What is the criticism of the SAS model?
- Homunculus criticism= If PFC is a controller what is controlling the controller and then what is controlling that controller
- Does not explain how control is carried out just states what is controlled. This lead to fractionating of the PFC to break it down into different components to explain how these systems work together to coordinate functions
40
What are the subdivisions of the PFC and their function?
- DLPFC/ APFC/ VLPFC = cold cogntion= analytical cognition
- OFC= hot cognition= emotion and value cognition
- All systems communicate with one another
41
How has the PFC been fractionated into different executive function?
- Shifting = attention shifting
- Updating = update contents of working memory
- Inhibition= inhibiting previously learnt rules and processes
42
How have fractionated PFC executive functions been mapped onto the brain?
- Right lateral PFC damage inhibits monitoring, quality control and adjusting for tasks = UPDATING
- Left lateral PFC damage problems with setting a stimulus response relationship =SHIFTING
- Left medial PFC (ACC) damage problems with initiating and sustaining response, seen to monitor conflict and associates effort with choice (is it worth it etc)
- No evidence for inhibition in PFC
43
How has further study contradicted or supported brain mapping of PFC executive functions?
- Left lateral PFC is involved in task setting but is part of a larger network in the frontal and parietal regions
- Right lateral PFC linked to inhibition which was not observed originally but may be as a result of playing a attentional role, overall goes beyond monitoring function first observed
- Overall neuropsychological vs imaging contradiction
44
What is the multiple demand hypothesis of PFC?
- PFC is not fractionated but same regions are involved differently in different tasks
- It constructs attentional episodes which refers to neurons in the network being able to adapt to the info currently being attended to and can vary their coding as a result
45
What is the gateway hypothesis of BA10 (frontopolar cortex)?
- Distinguishes between stimulus orientated and stimulus independent (internal mental processes and thought) which we switch between
- Idea is that their are two gates and if both are in position B (open) sensory input and output (muscles) is allowed giving rise to stimulus orientated attention. If both gates are in position A (closed) there is a focus on internal representations
- Evidenced through lesions and 6 elements task (couldn't remember to do other tasks i.e switching from stimulus task to a task you internally have to remember)
- Neuroimaging studies have also evidenced this through double dissociation with medial BA10 correlated to internal processing and Lateral BA10 when switching from internal and external processing
- Schizophrenia seen with having abnormal BA10 as they struggle to distinguish between external and internal processing (voices in head vs actual voices etc)
46
Whats the OFC's role in cognitive control?
- Impairment to OFC increases risky decision making and shows a impaired ability to learn about response-reward contingencies
- Lack of anticipation of reward or punishment in lesion patients potentially showing a poor feedback system to learn from (no value markers) i.e the somatic marker hypothesis
- Some evidence shows OFC possibly not used for learning contingencies but rather unlearning them
- Overall OFC facilitates effective decision making based on knowledge of the value of different actions
47
How has the OFC been fractionated by cognitive control
- Medial OFC = preference for reward outcomes
- Lateral OFC = preference for punishment
- Activation of these areas then changes learning
48
How is the OFC involved in counterfactual thinking?
- Idea OFC may be involved in complex emotions such as regret
- OFC lesions resulted in people not being modulated by satisfaction (counterfactual thinking) shows a inability to able experience consequences and integrate this info into future choices. Do not appear to experience "regret" similairy to controls
49
What are corticostriatal loops?
-Loops in the brain that run parallel to each other such as to the the PFC and basal ganglia. These loops play different roles such as the reward processing loop between the ventral striatum and OFC
50
What is the role of the basal ganglia in cognitive control?
- Loss of dopamine neurons in basal ganglia (striatum) and is linked to Parkinson's disease so shows a link to motor control
- Other deficits in impairment have been seen in planning, WM, stroop task (also seen in PD)
- Overal PD suffers shows mental and psychical flexibility (mirror each other) and that dopamine loss in striatum is linked to loss of WM
- Ritalin which increases dopamine in these areas helped to mediate cognitive flexibility (task switching)
51
What is PFC's interaction with dopamine?
-Depletion of dopamine in PFC reduces WM specifically spatial working memory
52
How does gating apply to the basal ganglia?
-Allows or prevents new goal states entering PFC, for example changing the goals when more negative or positive consequences prefer (PFC would get stuck in one without it)
53
What is a feeling?
- Subjective experience of an emotion not the emotion itself
- Can have physiological responses (can be subjective)
- Can have a behavioural component (subjective)
54
What categories of emotion are there?
- Basic= unique characteristics, developed through evolution and reflected in facial expressions (instinctive, universal, predictable, measurable changes in sensory, perceptual, motor and physiological functions) blind Olympic athletes have further evidenced these emotions
- Complex= combinations of basic emotions that can be socially or culturally involved (jealousy, love and last longer even a lifetime and have no universal facial expressions)
55
What is James-Lange theory?
- Stimulus creates a physiological reaction which your body then recognises creating a autonomic emotional reaction
- However, physiological responses can be interpreted differently (sweating can be sign of anxiety or excitement)
- This as a hormonal process would be too slow to explain the fast onset of emotions (cortex seen to generate feeling as well - thus a dual system)
56
What are the two emotion systems?
-One for emotional responses (physiological) and one for generating conscious feeling of emotion (feeling itself) evolved together but physio system developed first
57
What neural structure is seen to play a crucial role in the two system theory of emotion?
- Amygdala (particularly in the emotion of fear)
- However, amygdala lesion does not remove feeling fear study has shown the internal response is actually increased or the same despite a lack of behavioural response. Amygdala thus plays role in translating internal threat into external response
- Plays a role in learning (fear conditioning) increases during training but drops off in extinction. Lesions prevent fear conditioning
- Greater activation more emotional info recalled
58
How is fear learning communicated in the amygdala?
- Low road= fast, crude information
| - High road= slower, higher detailed info including sensory info analysed in visual cortex
59
What is the interaction between the amygdala and hippocampus in fear learning?
- Amygdala responsible for impaired physio reaction, even in explicit learning where subjects are told what causes shock (fear stim) amygdala activates when fear stim doesn't occur
- Hippocampus responsible for learning factual learning of fear stim (what signals it)
- These were double dissociated and shows amygdala acts to modulate hippocampal consolidation for arousing emotional events
60
Is the amygdala unconsciously a mediator for learning?
-No, even in explicit learning where subjects are told what causes shock (fear stim) amygdala activates when fear stim doesn't occur
61
What is the influence of emotion on attention?
- Emotion seen to increase attention
- Activation in visual cortex driven by activation in the amygdala (only for fearful faces) therefore, amygdala tunes sensory attention
- Amygdala plays a key role in getting an unattended but emotional stimulus into conscious awareness by providing feedback to primary sensory cortex.
62
What is the insular cortex's role in the experience of emotion and interoception (awareness of bodily states)?
-Insular cortex showed greater activation in response to heart rate (auditory) trails compared to general note trials, was also correlated with anxiety (greater activation in more anxious people)
63
What is the insular's role in disgust?
-Insular regions lead to an inability to detect faces of disgust
64
What is the OFC's role in emotion?
-Reward, inhibition of previously learned associations, using subjective states as outcomes of decisions to guide future responding
65
What does grapheme-phoneme rules and direct dictionary look up refer to?
- Grapheme= pronunciation of a word using letter/sound correspondence rules
- Dictionary= taken from store of information (normally used for words which are not consistent with a rule like "have" compared to "cave")
66
What are the two routes of reading?
- Lexical route = looking up words in long-term memory to retrieve knowledge about their meaning and pronunciation
- Non-lexical route = uses rules relating to orthography (how it is written) and phonology (how it sound)
- Both happen at same time, system is not gated
67
Describe the features of the lexical route and how it works
- model refer to handout
- Lexical route allows activation of words meaning (semantics) from either the orthographic form or its retrieved sound
- Does not work for novel words (not part of lexicon), only words which have previously been learnt and also works for irregular words
68
Describe the features of the non-lexical route and how it works
- Refer to handout
- Uses grapheme to phoneme rules to drive pronunciation, rules come from knowledge of reading/speaking
- Does not work for irregular words as rules do not apply to these
69
How are non-words processed by lexical system?
- While they cannot be read correctly they do evoke some lexical and meaning activation based on words in the lexicon they look similar to (SARE may activate CARE)
- The word they look similar to being a regular or irregular word will also effect pronunciation (FINT closer PINT than MINT so pronounced irregularly)
70
What effects have been found in the dual cascade model and why do they occur?
- Words read faster than non-words (both systems support words)
- H freq words read faster than L freq words (more practice)
- Reg words read faster and more accurately than irregular words, especially L freq ones (lexical and non-lexical paths conflict for irregular words and less practice for L freq)
- Larger orthographic neighbourhood or a nonword the faster it is read aloud (more template words)
- Non-words that sound like words read faster aloud than those than do not (practice of existing pronunciation)
- More letters in a nonword the slower it is read but this has no effect on real words (nonwords need to be segmented which slows processing, real words can be processed in one fixation via lexical route)
71
Where are words processed in the brain?
- contralateral hemisphere in visual area 4, occipital pole)
- Then is transferred to the visual word from area located in the ventral area of the left occipital lobe. This can swap to right hemisphere due to a lesion at a young age
72
What has fMRI studies shown about word processing in terms of effort and engagement
- BOLD signal increases with engagement (capacity of stim to evoke knowledge in that region) non-word does not engage while real word will
- BOLD signal increases with effort or amount of resources needed to process a stimulus. Real word L freq requires more effort than H freq word
73
How do pseudo words, high frequency words, low frequency words, regular words and irregular words interact with effort and engagement?
-Refer to handout
74
How the elements of the DRC map onto the brain
-Refer to photos
75
What is alexia?
- pure alexia= "pure verbal blindness" inability to recognise orthagraphic strings as a result from damage which disconnects visual areas and occipital area
-
76
What are the two main classifications of dyslexia?
- Peripheral = any reading disorder in which visual word form fails to be achieved (fail to recognise linguistic significance)
- Central= any reading disorder in which impairment occurs after the stage of visual word form (reading system)
77
Where do different dyslexia's occur in the DRC?
-Refer to handout
78
What are the different peripheral dyslexia's?
- Pure alexia
- Attentional dyslexia
- Neglect dyslexia
79
What are the different central dyslexia's?
- Phonological dyslexia
- Deep dyslexia
- Semantic dyslexia
- Surface dyslexia
80
What is the saffran effect?
-Knowing the meaning of or a category of the the word despite not being able to conceptualise it
81
Outline what pure alexia is and how it occurs?
- Word identification impossible, except via explicit sequential identification of individual letters, subject to length effect (longer word longer to read)
- Contextual info does not help (rest of letters in word) one letter at a time processing
- Saffran effect
- Result of damage to the visual word form area (VWFA) or disconnection from it
- Can be hemisphere related (hemi-alexia)
82
Outline what attentional dyslexia is and how it occurs?
- Attention span is to wide difficulty in identifying letters or words when flanked by other items of the same category (letters from letters/ words from words/ numbers from numbers), naming of a letter or a word in isolation preserved and less interference when categories differ
- Also migrate letters to analogous (same position) in neighbouring words (left hem = left lem)
- Associated with left parietal lesion
83
Outline what neglect dyslexia is and how it occurs?
- Failure to identify the initial or final letter(s) of a word or group of words, resulting in omissions, substitutions or additions. These errors often occur where a large string or characters proceeds or appear prior to the neglected character
- Tied to retinal field but orientation and location can both be independent of this
- Associated with parietal lesion
84
Outline what phonological dyslexia is and how it occurs
- Impaired ability to read new or made up word (or nonwords), and to sound out individual graphemes (loss or impairment of non-lexical route).
- Reading of words intact slight preference to concrete words
- Non-words better if contain simple graphemes and homophoneous to real words (BRANE)
- Lesion temporal lobe of dominant hemisphere
85
Outline what deep dyslexia is and how it occurs
- Cannot read non-words
- Semantic errors (ill=sick)
- Visual errors (sword=word)
- Derivation errors/ changing suffix (card=cards, beg=beggar etc)
- effects of syntactical class where less concrete words are impeded more as require more of semantic system (nouns concrete, verbs less so)
- Damage to dominant (left) hemisphere
- Loss or impairment of non-lexical route and non-semantic part of lexical route (semantic errors occur because patient only has semantic info)
86
What is semantic dyslexia and how does it occur?
- Ability of patients to read fast and fluently (even irregular words in some patients), but inability to comprehend what they are reading (associated with Alzheimer's)
- Can read non-words/ irregular words and match spoken and written words and pseudo words
- Cannot match word to picture
- Loss of semantic part of lexical route
87
What is surface dyslexia and how does it occur?
- Regularisation (read irregular words with regular rules)
- Stress shift (guiTAR= GUItar)
- Comprehension based on pronunciation (bear= an alcoholic drink)
- Failure to apply contextual rules (guest=just)
- Incomplete decoding of digram vowels (niece=nice)
- Can read words and non words
- Reliance on non-lexical route and impairment to any part (5) of non-semantic elements of lexical route
88
What are the two types of memory consolidation?
- Cellular (synaptic)
| - System level (whole brain)
89
What generally happens to memories overtime?
- Initial memories are fragile and most forgetting happens here, overtime less if forgotten as what is remembered is consolidated (less resistance to interference)
- Allowing time for consolidation before more learning aids consolidation
90
Describe the shape of forgetting
- Memories become more resistant overtime
- Forgetting is not a constant rate, we forget less as time goes (sign of consolidation)
- If two memories have equal strength the older one will decay more slowly
91
Describe cellular consolidation
- Takes place in first few hours after initial memory forming hippocampus (trace hardening)
- Long term potential= synaptic efficacy induced by a tetanus (short burst of high-frequency stimulation) to the presynaptic neuron.
- Drinking/drug use can prevent interference helping consolidation
92
What is retrograde facilitation?
- subsequent encoding (mental exertion) interferes with memory consolidation, then factors (e.g. alcohol) blocking new encoding should promote memory stabilization.
- Resulting anterograde amnesia Inability to form new declarative memories) is accompanied by a retrograde facilitation: memories formed prior to drug intake/sleep are forgotten to a lesser degree than memories formed prior to placebo/wake.
93
What evidence is there for system consolidation?
- Patient HM showed retrograde anterograde amnesia where impairment of memories was greater for new than old
- Showed declarative memories become independent from hippocampus and more dependant on neocortex (wider system)
94
Outline the role of the hippocampus in consolidation and forgetting
- Damage to hippocampus impairs ability to remember more recently formed memories, older memories can be unaffected
- Hippocampus relays memories from different sensory areas to form overall essence of a memory, continuous activation to these traces causes the, to become independent of hippocampus
95
How are the hippocampus and neocortex an example of a complementary learning system?
- Hippocampus is a fast learning, temporary store of info
- Neocortex is a slow learning system which serves as a long-term store
- Both systems thus communicate and work together to achieve learning (sparring partners)
- As both systems encode integration occurs offline (sleep)
96
How does sleep effect declarative (semantic/episodic) and non-declarative (procedural skill) memories?
- REM sleep promotes motor skills (ND)
- Slow wave sleep promotes (D) memories
- Therefore sleep early in night aids (D) mem as it is slower and sleep late at night (after 3am) aids (ND) mem as REM sleep occurs here
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What is the sleep first effect?
- Sleeping after learning prevents crowding/interference so memories consolidated better than learning and then delaying sleep
- Hippocampus and neocortex communicate during slow wave sleep
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What does neural replay refer to?
- In moments of low encoding (sleep etc) brain replays recently acquired information to itself
- Happens primarily in slow wave sleep (hippocampus and neocortex can communicate) as when awake hippocampus is busy encoding info and not sending it to neocortex
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What does cuing refer to?
- Hippocampus can be directed during sleep
- Rash et. al. (2007) used aromas to reactivate areas used in learn task by secreting aroma while participants slept. This enhanced memory performance. Effectively it biases neural replays
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Other than stabilising memories what else can sleep do?
-Can make memories more accessible
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What is the role of sleep in false memory formation?
-Sleep increases creation of false information, it strengthens associations between individual memory and elements and fills gaps (false info) especially for semantic info
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How does sleep integrate new info with long-consolidated info
-Sleep helps develop this integration. Those who have slept will perform worse on word vs non-word recognition as the non-words are integrated into knowledge and require more processing than those who "wake" as they have not processed these connections
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Outline the interact of memory consolidation and emotions
- Emotional stimulus recall is boosted by REM sleep especially if emotion is negative. Therefore, negative emotional stim and late night sleep (where REM sleep occurs) will increase text recall
- Also enhances visual memory of emotional components of scene but also increases decay of non-emotional components, neutral cues which occur with a threat are better remembered
