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PS1080 > introduction to cognitive neuropsychology > Flashcards

introduction to cognitive neuropsychology Flashcards

1
Q

what is cognitive neuropsychology?

A

the study of the structure and function of the brain as it related to perception, reasoning, remembering, and all other forms of knowing and awareness

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2
Q

what is amnesia?

A

a general term that describes memory loss

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3
Q

causes of amnesia

A

organic
- acute damage to the brain
- degenerative disease
psychogenic (purely psychological)

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4
Q

forms of amnesia

A

retrograde & anterograde

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5
Q

what is pronounced anterograde amnesia?

A

inability to encode/retrieve memories for events encountered for after the onset amnesia

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6
Q

what is variable retrograde amnesia?

A

inability to retrieve memories acquired before the onset of amnesia

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7
Q

main features of the amnesic syndrome

6 features

A
  1. pronounced anterograde amnesia
  2. variable retrograde amnesia
  3. intact short-term memory
  4. preserved general intelligence (IQ)
  5. skills such as driving and playing music unaffected
  6. some residual learning capacity
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8
Q

what parts of the brain are important for memory

5 parts

A
  1. amygdala
  2. basal ganglia
  3. cerebellum
  4. frontal lobes
  5. occipital lobes
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9
Q

function of amygdala

A

emotional content of episodic memories

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10
Q

function of basal ganglia

A

important for learning motor skills

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11
Q

function of cerebellum

A

memory for automatised skills

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12
Q

function of the frontal lobes

A

working memory; source montoring; prospective memory

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13
Q

function of the occipital lobes

A

visual perceptual representation memory

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14
Q

effects of damage to the hippocampus

4 effects

A
  • Henry Molaison had his medial temporal lobes (2/3 of the hippocampus)
  • his epilepsy improved, personality unchanged, IQ increased
    However:
  • unable to encode/retrieve new episodic memories
  • developed severe anterograde amnesia
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15
Q

other aspects of Henry Molaison’s memory

3 aspects

A
  • developed retrograde amnesia for the period 10-15 years prior to the operation
    still normal:
  • STM
  • learning of new procedural memories
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16
Q

what is Korsakoff’s syndrome caused by?

A

thiamine deficiency (usually due to alcoholism)

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17
Q

what is Korsakoff’s syndrome?

A

damage to the diencephalon
- patients often appear to be drunk, uncoordinated, confused

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18
Q

amnesia in Korsakoff’s

3 points

A
  • STM normal
  • encoding/retrieval of new episodic long-term memories impaired (anterograde amnesia)
  • temporal gradient of retrograde amnesia
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19
Q

temporal gradient of retrograde amnesia:

A

Recall for events in the time immediately leading up to its onset very poor, but earlier memories relatively intact

20
Q

what is viral encephalitis?

2 points

A
  • sudden onset of acut fever, headache, nausea
  • usually extensive bilateral temporal lobe damage
21
Q

how is viral encephalitis caused?

A
  • caused by herpes crossing blood-brain barrier
22
Q

amnesia due to viral encephalitis:

3 points

A
  • particularly severe amnesic disorder
  • similar to Korsakoff’s, but better insight, and flatter temporal gradient
  • often deficits of spatial and semantic memory, e.g., surface dyslexia; problems with face recognition
23
Q

common types of dementia

4 types

A
  • alzhermer’s
  • vascular
  • mixed alzheimer’s & vascular
  • lewy body dementia
24
Q

amnesia due to dementia

3 points

A
  • progressive neural disease
  • general degeneration of the brain; atrophy due to growth of neural plagues & tangles
  • pattern of impairment involves ‘information-processing’ deficits superimposed upon an amnesic syndrome
25
Q

what is transient global amnesia?

A

sudden onset of anterograde amnesia and retrograde amnesia for recent events preceding attack

26
Q

features of transient global amnesia

6 features

A
  1. no loss of personal identity; recognition of family
  2. anxious, agitated
  3. resolves within 12 hours
  4. rare
  5. mostly over 50s - often men
  6. triggers emotional upset
27
Q

what is transient global amnesia caused by?

A

disruption of blood flow to thalamic/medial temporal cortex

28
Q

what does amnesia provide evidence for?

A

amnesia provides evidence for a dissociation between STM and LTM

29
Q

What traits to amnesics have but poor episodic and semantic memory?

3 traits

A

– show normal sized priming effects
– still have motor memory (skills), such as making a telephone call or making coffee (procedural memory)
– can learn new procedural skills such as
tracking a moving target in the pursuit
rotor task

30
Q

what do the amnesic traits show

A

it shows the dissociation between explicit memory and implicit memory

31
Q

theories of anterograde amnesia: why can’t amnesics encode/store/retrieve new episodic memories?

4 points

A
  1. faulty encoding
  2. accelerated forgetting
  3. faulty retrieval
  4. faulty encoding/storage of contextual information
32
Q

accelerated forgetting

2 points

A
  • Some studies show that patients with hippocampal lesions forget faster than controls, even after material has been adequately learned
  • In other studies various different types of amnesics forget at the same rate as controls, provided initial learning is adequate
33
Q

transient amnesia and retrieval deficit

A

Transient amnesia shows that retrieval deficits can cause amnesia – once amnesia resolves, memories that were unavailable can be retrieved normally

34
Q

what did Warrington and Weiskrantz 1970 suggest?

A

Warrington and Weiskrantz 1970 suggested that retrieval deficit is due to response competition. partial information (e.g. 1st letter of studied word) helps overcome competition

35
Q

Could retrieval difficulties be related to absence of contextual information?

A

contextual information allows us to distinguish between otherwise similar memories

36
Q

encoding specifity principle:

A

LTM is generally better when context at retrieval and encoding match

37
Q

deficit in encoding/retrieving context: Hupper and Piercy

A

Huppert and Piercy (1976): suggested that amnesia is due to the inability to encode and retrieve contextual information

38
Q

conextual deficit theory: problems

4 problems

A
  1. semantic memories can also be impaired, but these are not contextual
  2. definition of context is vague
  3. why remember a stimulus but not its context?
  4. context-processing deficits vary substantially across patient groups
39
Q

what is a temporal gradient in retrograde amnesia?

A

a pattern of retrograde amnesia characterized by greater loss of memory for events from the recent past

40
Q

temporal gradient in retrograde amnesia (patient PZ)

A

Patient PZ’s retrograde amnesia gradient for information from his published autobiography. The earlier the information the better it is recalled

41
Q

Ribot’s (1881) law of retrograde amnesia

A

recent memories are more likely to be lost (opposite of normal forgetting)

42
Q

what may a temporal gradient be due to?

A

temporal gradient may be due to slow-scale consolidation process -> earlier memories have had longer to be consolidated

43
Q

Standard Consolidation Theory (Dudai, 2004; Squire, 1992)

3 points

A
  1. Episodic memories are initially encoded and stored in hippocampus, and retrieving these memories requires reactivating the hippocampus
  2. Over time, the hippocampal memory trace becomes less important, and the cortex can retrieve the memory without the hippocampus
  3. Consequently, older memories are spared in retrograde amnesia
44
Q

what what are the two types of psychogenic amnesia?

2 types

A
  • fugue states
  • dissociative amnesia
45
Q

Psychogenic amnesia: Fugue states

5 effects

A
  • Sufferer typically found wandering, often a long way from home.
  • Triggers include severe stress, depressed mood, history of transient organic amnesia
  • Lasts a few hours or days (can be longer).
  • After recovery, memories from the fugue state are lost.
  • Very rare.
46
Q

Psychogenic amnesia: Dissociative type

3 points

A
  • Refers to loss of memory for specific events due to trauma (no anterograde amnesia).
  • 25-45% of homicide suspects claim amnesia for the crime!
  • No cases reported before 1800: “dissociative amnesia is not a natural neuropsychological
    phenomenon, but instead a culture-bound syndrome, dating from the 19th century” (Pope et al., 2007).
47
Q

Amnesia summary

A

PS1080 (9 decks)

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