(4) Memory Disorders Flashcards
1
Q
What is organic amnesia?
A
Organic: acute damage to the brain or degenerative disease (e.g. Alzheimer’s)
2
Q
What is functional amnesia?
A
Functional: purely psychological
3
Q
What is retrograde amnesia?
A
Retrograde: losing memories before the onset
4
Q
What is Anterograde amnesia?
A
Anterograde: inability to make new memories
5
Q
Main features of the amnesic syndrome (relatively ‘pure’ amnesia)?
A
- Pronounced anterograde amnesia (inability to form memories for events encountered after the onset of amnesia)
- Variable retrograde amnesia (inability to retrieve memories acquired before the onset of amnesia).
- Intact short-term memory (STM), e.g., digit span task
- Preserved general intelligence (IQ)
- Skills such as driving and playing music unaffected, procedural skills
- Some residual learning capacity
6
Q
How does the occipital lobes work in amnesia?
A
-Occipital lobes (Visual Perceptual representation memory)
7
Q
How does the frontal lobes work in amnesia?
A
-Frontal lobes [working memory (central executive); source monitoring; prospective memory]
8
Q
How does the cerebellum work in amnesia?
A
-Cerebellum (Memory for automatised skills, where the memory is stored)
9
Q
How does the basal ganglia work in amnesia?
A
-Basal ganglia (Important for learning motor skills)
10
Q
How does the amygdala work in amnesia?
A
-Amygdala (Emotional content of episodic memories)
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
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…
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
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
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
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
- Semantic memories are also impaired, but these are not contextual.
- Definition of context is vague
- Why remember information, but not its context?
- 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
