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Investigating Psychology > Chapter 2 > Flashcards

Chapter 2 Flashcards

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1
Q

What is the three step model psychologists often use to represent memory?

A

Encoding, storage, retrieval

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2
Q

What did Tulving say were the three types of declarative memory?

A

Semantic, spatial, episodic

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3
Q

What is non-declarative memory?

A

How to do something.

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4
Q

Where is the hippocampus located?

A

The medial temporal lobe.

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5
Q

Which brain structure is associated with episodic memory?

A

The hippocampus

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6
Q

What is episodic memory?

A

Refers to specific events in one’s life.

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7
Q

What is converging evidence?

A

Evidence from different kinds of studies.

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8
Q

Using cognitive neuropsychology to study amnesiacs can help us understand what?

A

Normal memory.

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9
Q

What kind of memories can’t/couldn’t CW and HM form?

A

New episodic memories.

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10
Q

How does CW feel most of the time?

A

In an eternal present, as if he has just woken up.

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11
Q

What disease did CW contract?

A

Encephalitis

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12
Q

What can CW remember?

A

Some events before the encephalitis and skills such as music.

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13
Q

Amnesiacs often have what kind of amnesia?

A

Anterograde and varying retrograde.

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14
Q

Why did HM have surgery?

A

For epilepsy.

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15
Q

In amnesic syndrome, what are the implications of amnesiacs having a normal performance on STM tasks?

A

That there is a separation between STM and LTM in the brain.

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16
Q

In amnesic syndrome, what are the implications of semantic memory being unaffected?

A

That there is a separation in the brain between episodic and semantic memory.

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17
Q

In amnesic syndrome, what often happens to procedural memory?

A

Nothing

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18
Q

What is the difference between explicit and implicit recall abilities in anterograde amnesiacs?

A

Implicit is still possible (man who hid pin when shaking hands) but explicit isn’t.

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19
Q

Because amnesic syndrome patients are not a homogenous group, what are needed?

A

Sub-classifications e.g. Korsakoff or fugue

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20
Q

To what extent are single case studies like HM useful?

A

Yes, very useful but not possible to generalize.

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21
Q

What did Milner and colleagues believe about the role of the hippocampus in LTM and STM?

A

That it is responsible for converting STM to LTM.

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22
Q

How did Milner and colleagues know that LTM memories are not stored in the hippocampus?

A

Because HM did not have retrograde amnesia.

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23
Q

What does evidence from NA show?

A

That other brain areas can be involved in anterograde amnesia.

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24
Q

Which brain areas were affected with NA?

A

The mammillary body (part of the diencephalon), which receives input from the hippocampus and relays it to the thalamus.

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25
Q

Which area of the brain is affected in Korsakoff’s syndrome?

A

The mammillary body, same as NA

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26
Q

Korsakoff’s syndrome is due to a deficiency of which vitamin?

A

Thiamine (B1)

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27
Q

Converging evidence of the role of the hippocampus in LTM shows what about birds?

A

Larger hippocampus, better at remembering where they stored food.

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28
Q

What happens to place cells (individual neurons) in the hippocampus of a rat in a specific locations in its environment?

A

Specific neurons fire suggesting that the rat has built a cognitive map of its environment to encode locations of important items in its environment.

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29
Q

What is the difference between the brains of black-taxi drivers and bus drivers in London?

A

Taxi drivers have higher volume (and higher for more time/expertise) of right hippocampus because a lot of spatial information versus bus drivers only specific routes.

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30
Q

What does converging evidence help you be more confident about?

A

Causality

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31
Q

What is a quasi-experiment?

A

Using groups which already exist and not assigning participants randomly.

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32
Q

What was Huppert and Piercy’s experiment on Korsakoff’s patients?

A

Show sets of photos on day one and different set on day two. After ten minute delay on day two, show photos and ask which seen on day two. Easy for controls versus Korsakoff’s.

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33
Q

In the Huppert and Piercy, how did Korsakoff’s patients do for item based information versus context based information?

A

ok at item-based information (ever seen) and not good at context-based information (when seen).

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34
Q

What is it called when you can remember what seen but not when seen?

A

Source amnesia.

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35
Q

What is confabulation?

A

Invent things but really believe what saying because not good at source monitoring. Disruption to the retrieval systems and memory reconstructed inaccurately.

36
Q

What is source monitoring?

A

Knowing when and where etc. ( context-based information) something happened. E.g see science fiction film, not remember seen and then confabulate actually happened to you.

37
Q

What pattern does retrograde amnesia usually follow?

A

A temporal gradient (earlier memories better than later ones).

38
Q

What is consolidation theory?

A

Memories are ‘rehearsed’ in the hippocampus before being consolidated in the neocortex.

39
Q

What did Takashima et al. discover about the activation of the hippocampus when recalling recently learned information versus recalling information after a participant had slept?

A

Hippocampus is activated with recently learned information but not otherwise.

40
Q

Is the neocortex or the hippocampus more active when recalling after a participant has slept?

A

Neocortex

41
Q

What is the reason for the temporal gradient in retrograde amnesic patients?

A

The hippocampus is responsible for more recent memories while the neocortex for older memories. Therefore a hippocampus lesion explains the temporal gradient.

42
Q

What is the reminiscence bump?

A

Better recall for teens and twenties than later.

43
Q

What is a possible reason for the reminiscence bump?

A

The teens and twenties are the period when one is trying to consolidate one’s identity.

44
Q

What are is a problem with testing autobiographical memory?

A

Difficult to verify, other people’s details can be incorporated into the memory.

45
Q

What was Hupbach’s experiment and what did it show?

A

Participants shown set of items, later shown empty basket or not before learning second set. Reminder group more likely to confuse the two groups when later tested on set one. Shows that bringing to mind set one while learning set two changes memory representation of set one.

46
Q

What is implicit/procedural memory?

A

Stored without conscious awareness.

47
Q

How is implicit memory tested in experiments?

A

Show something to participants but don’t tell them going to test them later.

48
Q

What was HM able to learn using implicit memory?

A

Mirror tracing

49
Q

What is the double dissociation between Huntingdon’s/Parkinson’s disease patients and amnesiacs? What does this show?

A

Amnesiacs have problems with explicit memory but not implicit and Huntingdon’s etc. is vice-versa. Shows that explicit and implicit memory are different systems in the brain.

50
Q

Declarative memory should be on a continuum between what and what?

A

Recollection to familiarity.

51
Q

What three kinds of information does an episodic memory contain?

A

What, where, when information.

52
Q

What are we usually given when we are asked to recall information?

A

Some sort of cue or forced choice (choose between different options).

53
Q

What are the three types of memory test used?

A

Free recall, cued recall and recognition. Recognition is the easiest.

54
Q

Although recognition tests are easiest, what can researchers manipulate?

A

When the picture was shown so the participant needs to find the correct temporal information.

55
Q

What kind of links are affected for amnesiacs?

A

What, where, when links (source memory).

56
Q

Why is free recall harder than recognition (especially for amnesiacs)?

A

Because what, where, when links are largely absent, incorrect familiar items get mixed up with correct ones. Difficult to determine context (source memory)

57
Q

Which structure is implicated in source memory?

A

Hippocampus

58
Q

The fact that Alzheimer’s patients are better at serial recall than free recall (unlike normal adults) shows what?

A

That we cannot generalize from clinical populations to normal populations.

59
Q

Are older adults better or worse at source-based information than younger adults? Why is is?

A

Worse, less good at binding where/when info with what info (fractionation of episodic memory).

60
Q

Fractionation of episodic memory in older adults suggests what?

A

That, perhaps, different areas of the brain are associated with the difference between recollection and familiarity.

61
Q

What is Aggleton and Brown’s neural model of episodic memory?

A

System one includes hippocampus, mammillary bodies and anterior thalamic regions and is responsible for recall. Damage here and recognition still OK. System two is the perirhinal cortex and is responsible for recognition (without context).

62
Q

How do researchers argue against Aggleton and Brown’s model? What are problems with these criticisms?

A

The entire MTL is responsible for recognition and recall. If they seem to not be working together, this is because the PFC is needed for recall. E.g PFC is damaged in Korsakoff’s and these patients are ok at recognition but not at recall. Problems are that the PFC is a large area and a lot of false positives on the recognition tests (therefore not that great recognition).

63
Q

What support is there for the 2-system proposal?

A

Patients with damage to the hippocampus but not the perirhinal cortex whose recognition is intact but not recall. Other evidence is not so clear.

64
Q

What evidence is there against the 2-system proposal?

A

Patients with damage to the hippocampus but with bad recall and recognition. But neuroatanomical data not necessarily complete so lesion could have extended beyond hippocampus.

65
Q

What doe fMRI studies show which is against the 2-system proposal?

A

That there is still some activation of the hippocampus in recognition tasks although it is much greater in recall tasks. Suggest that the hippocampus is always involved.

66
Q

Why is there contradictory evidence relating to the 2-system proposal? Who attempted to overcome these problems?

A

A) maybe don’t know the exact location of the lesion B) maybe the testing has not been thorough enough. Cipolotti.

67
Q

What were the results from Cipolotti and VC?

A

Definitely lesion only in the hippocampus in VC. Both recall and recognition (spatial and verbal) affected but face recognition was ok. Against the 2-system proposal. Hippocampus has a fundamental role in free recall and lesser role in recognition of verbal and spatial information and not at all for facial recognition.

68
Q

What is the recency effect?

A

Tendency to remember the later items when asked to remember a list of words.

69
Q

How is the recency effect in amnesiacs?

A

Usually a large effect.

70
Q

How was HM’s STM? What was he able to do?

A

STM ok and able to converse ok.

71
Q

In Atkinson and Shiffrin’s ‘modal model of memory’ where is incoming information first held?

A

In the limited capacity short-term store (STS).

72
Q

Where does information go after the STS?

A

To the permanent high capacity long-term store (LTS).

73
Q

As well as being the gateway to the LTS, what else is the STS?

A

Working memory/work space.

74
Q

What is a feature of the STS?

A

It is limited capacity and can be overloaded.

75
Q

How did Baddeley and Hitch show that the Atkinson and Shiffrin model needed to be modified?

A

PPS had to memorize numbers at the same time as doing verbal reasoning or learning different words (dual task paradigm). Little interference so different memory systems.

76
Q

What was Baddeley and Hitch’s initial model of working memory?

A

A ‘central executive’ and two slave systems or different limited capacity stores: Visuo-spatial sketch pad and the phonological loop.

77
Q

What is evidence for the phonological loop?

A

Phonological properties (e.g. How long a word is and similar words e.g. Rhyme) affect how well a word can be remembered and therefore longer word span

78
Q

Varying length of words suggests that how long can be held in the phonological loop?

A

2 seconds.

79
Q

What is articulatory suppression?

A

E.g. Saying the same word again and again

80
Q

Does disrupting the phonological loop by e.g. doing articulatory suppression affect the effects of short/rhyming words?

A

No effect when words presented visually but yes and effect when words read aloud.

81
Q

What did Baddeley and Hitch do because they determined that the modality of input to the phonological loop was important?

A

Split it into two parts

82
Q

Into what two parts did Baddeley and Hitch split the phonological loop?

A

Passive/auditory

Visual (converted to sound -based representations)

83
Q

What has since happened to the Visuo-spatial sketch pad?

A

Divided because showed double dissociation

84
Q

What is the central executive?

A

All about attention (dividing, switching, focusing)

85
Q

Digit span and visual tracking tests are very difficult to do simultaneously for whom? What does this show?

A

Alzheimer’s. Shows that divided attention is different to memory storage.

86
Q

What is the episodic buffer?

A

Third slave system which links grammar and meaning from LTM to STM and explains why we can remember longer sentences which are connected by grammar and meaning.

Investigating Psychology (9 decks)

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