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Learning and Memory > (4) Memory Disorders > Flashcards

(4) Memory Disorders Flashcards

1
Q

What is organic amnesia?

A

Organic: acute damage to the brain or degenerative disease (e.g. Alzheimer’s)

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2
Q

What is functional amnesia?

A

Functional: purely psychological

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3
Q

What is retrograde amnesia?

A

Retrograde: losing memories before the onset

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4
Q

What is Anterograde amnesia?

A

Anterograde: inability to make new memories

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5
Q

Main features of the amnesic syndrome (relatively ‘pure’ amnesia)?

A
  1. Pronounced anterograde amnesia (inability to form memories for events encountered after the onset of amnesia)
  2. Variable retrograde amnesia (inability to retrieve memories acquired before the onset of amnesia).
  3. Intact short-term memory (STM), e.g., digit span task
  4. Preserved general intelligence (IQ)
  5. Skills such as driving and playing music unaffected, procedural skills
  6. Some residual learning capacity
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6
Q

How does the occipital lobes work in amnesia?

A

-Occipital lobes (Visual Perceptual representation memory)

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7
Q

How does the frontal lobes work in amnesia?

A

-Frontal lobes [working memory (central executive); source monitoring; prospective memory]

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8
Q

How does the cerebellum work in amnesia?

A

-Cerebellum (Memory for automatised skills, where the memory is stored)

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9
Q

How does the basal ganglia work in amnesia?

A

-Basal ganglia (Important for learning motor skills)

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10
Q

How does the amygdala work in amnesia?

A

-Amygdala (Emotional content of episodic memories)

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11
Q

What can happen if the hippocampus is damaged? (Henry Molasion case study)

A

HM: operated on in 1950s to bilaterally remove the medial temporal lobes (about 2/3 of the hippocampus)

  • Following surgery, his epilepsy was greatly improved
  • Personality unchanged
  • IQ went up
  • Unable to form new episodic memories
  • HM had developed severe anterograde amnesia
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12
Q

What remained normal in the Henry Molasion case study?

A
  • But still normal:
  • STM
  • Learning of new procedural memories
  • Note that memory loss due to psychosurgery is rare however…
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13
Q

What is Korsakoff’s syndrome?

A
  • Caused by thiamine deficiency (usually due to alcoholism)
  • Damage to diencephalon in particular
  • Patients often appear to be drunk – uncoordinated, confused
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14
Q

What happens with Korsakoff’s syndrome?

A
  • STM normal
  • Formation of new long-term memories impaired (anterograde)
  • Retrograde amnesia stretching back years or decades
  • Temporal gradient of retrograde amnesia: Recall for events in the time immediately leading up to its onset very poor, but earlier memories relatively intact
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15
Q

What is Viral encephalitis?

A
  • Caused by herpes virus crossing blood-brain barrier
  • Sudden onset of acute fever, headache, nausea
  • Usually extensive bilateral temporal lobe damage
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16
Q

What happens with Viral encephalitis?

A
  • Particularly severe amnesic disorder (e.g., Clive Wearing)
  • Similar to Korsakoff’s, but better insight, and flatter temporal gradient (early memories may be lost also)
  • Often deficits of spatial and semantic memory, e.g., surface dyslexia; problems with face recognition
17
Q

What is dementia?

A
  • Effects of Alzheimer’s disease
  • Progressive disease
  • Caused by a general degeneration of the brain resulting in atrophy and growth of plaques
  • Pattern of impairments involves ‘information processing’ deficits superimposed upon an amnesic syndrome (Morris & Kopelman, 1986)
18
Q

What is Transient global amnesia?

A
  • Sudden onset of anterograde amnesia as well as retrograde amnesia for recent events preceding attack
  • No loss of personal identity; recognise family members
  • Anxious, agitated, repetitive questioning
  • Resolves within 12 hrs; mean of 4 h
  • Fairly rare
  • Mostly over 50s, more often men
  • Triggers include emotional upset, vigorous exercise
  • Caused by disruption of blood flow to thalamic/medial temporal cortex?
19
Q

What is Psychogenic amnesia?

A
  • Amnesia that is not due to organic factors (much less common than organic amnesia).
  • Two noteworthy types: fugue states and dissociative amnesia
  • Fugue states: Amnesia including loss of identity.
  • This type of amnesia is the one most commonly depicted in TV/movies (e.g., Memento).
20
Q

What is a fugue state?

A
  • Sufferer typically found wandering, often a long way from home.
  • Triggers include severe stress, depressed mood, history of transient organic amnesia (Kihlstrom & Schacter, 1995).
  • Lasts a few hours or days (can be longer).
  • After recovery, memories from the fugue state are lost.
  • Very rare
21
Q

What is Psychogenic amnesia: Dissociative type?

A
  • Refers to loss of memory for specific events due to trauma (no anterograde amnesia)
  • 25-45% of homicide suspects claim amnesia for 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)
22
Q

How do amnesia patients cope with different types of memory?

A
  • Amnesia provides evidence for a dissociation between STM and LTM
  • Amnesics have poor episodic memory, and often (though not always) have poor semantic memory, but:
  • show normal sized priming effects, pre activation in memory, brain respond quicker to certain events
  • 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
  • This illustrates the dissociation between explicit memory and implicit memory
23
Q

Life with anterograde amnesia

A
  • Ability to lead an independent life depends on severity of amnesia
  • Wilson and Hughes (1997) describe an anterograde amnesic with some spared memory abilities.
  • Was able to retrain as a professional furniture refinisher
  • Developed a system based on post-it notes, a colour-coded filofax, and a watch with multiple alarms
  • Was able to start a new relationship
  • Cases like this provided the real-life inspiration for Guy Pearce’s character in the film Memento.
24
Q

-Why can’t amnesics form new episodic memories?

A
  • Several theories have been considered, including:
    1) Faulty encoding, can be encoded normally but forgotten quicker
    2) Accelerated forgetting
    3) Faulty retrieval (perceive in context)
    4) Faulty encoding/storage of contextual information
25
Q

Problem with initial encoding?

A
  • Cermak (1979): amnesic deficit due to lack of deep encoding, e.g., bad at learning word pairs like hungry-thin (cf. Levels of processing theory)
  • However, Meudell, Mayes, and Neary (1980) found similar levels of-processing effect in amnesics and normal
26
Q

What has been said about patients with hippocampal lesions?

A
  • Some studies show that patients with hippocampal lesions forget faster than controls, even after material has been adequately learned (Huppert & Piercy, 1979; Squire, 1981).
  • In other studies various different types of amnesics forget at the same rate as controls, provided initial learning is adequate (Huppert & Piercy, 1978; Squire,1981; Kopelman,1985).
27
Q

Retrieval deficit?

A
  • Transient amnesia shows that retrieval deficits can cause amnesia – once amnesia resolves, memories that were unavailable can be retrieved normally (Kritchevsky, 1992)
  • But what kind of retrieval deficit are we talking about?
  • Clue is offered by difference between recognition and recall. Recognition is sometimes unimpaired in amnesics (Aggleton & Shaw, 1996), but recall is always impaired.
  • 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.
  • Meudell et al. (1978): amnesics made four times as many intrusion errors as controls (interference from previous list)
  • Stopping/blocking to get to correct memory
28
Q

Could retrieval difficulties be related to absence of contextual information?

A
  • Contextual information allows us to distinguish between otherwise similar memories
  • Encoding specificity principle: LTM is generally better when context at retrieval and encoding match.
  • Huppert and Piercy (1976): Amnesia due to inability to encode and retrieve contextual information…
29
Q

What did Huppet and Piercy (1976) do with amnesic patients?

A
  • METHOD Two groups: Amnesic (Korsakoff patients) and Normal controls.
  • Presented a set of pictures on Day 1 and a set of pictures on Day 2.
  • Recognition test after Day 2 pictures.
  • Both groups asked to do 2 tasks:
    1. ‘Day 2 recognition’: Say ‘yes’ only if the pics had been seen on Day 2
    2. ‘Ever seen recognition’: Say ‘yes’ if the pics had been seen at all (i.e., regardless of which day)
30
Q

What did Huppet and Piercy (1976) find?

A
  • Normal: extremely good and saying yes to pictures which they’ve seen on day 2
  • Amnesic: high false alarm rate, picture presented on day 1, thought it was only presented on day 2
  • Asked if they recognised picture on any day: no difference in recognition
31
Q

Contextual deficit theory: problems?

A
  1. Semantic memories are also impaired, but these are not contextual.
  2. Definition of context is vague
  3. Why remember information, but not its context?
  4. Context processing deficits vary substantially across patient groups (e.g., Parkin & Hunkin, 1997; Squire, 1982).
    - Contextual deficit unlikely to be the whole story
32
Q

Consolidation theory?

A
  • Patients like HM have retrograde amnesia stretching back 10-15 years. Could this reflect the time of consolidation processes?
  • Standard Consolidation Theory
  • Squire (1992); Dudai (2004)
  • Episodic memories are initially encoded and stored in hippocampus, and retrieving these memories requires reactivating the hippocampus
  • Over time, the hippocampal memory trace becomes less important, and the cortex can retrieve the memory without the hippocampus
  • Consequently, older memories are spared in retrograde amnesia
33
Q

What is Temporal gradient ?

A
  • Ribot’s (1881) law of retrograde amnesia: recent memories are more likely to be lost (opposite of forgetting).
  • Temporal gradient may be due to slow scale consolidation processes => earlier memories have had longer to be consolidated

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