L3 - Memory Loss, Amnesia and the Hippocampus

Question 1

What is an engram?

Answer 1

A memory trace - a hypothetical, permanent change in the brain as a result of a memory.

Question 2

How does patient HM provide evidence for a localised memory engram?

Answer 2

Surgeons removed patient HM’s hippocampus, and its associated, surrounding structures to treat their epilepsy. Although the epilepsy was treated, patient HM’s ability to form new memories, and remember old ones, were significantly impaired - anterograde and retrograde amnesia respectively.

Demonstrates that there could be some localised structures that are pivotal in the formation of new memories and recall of old ones.

Question 3

What cognitive functions were intact in patient HM?

Answer 3

• IQ (118)
• Digit span
• Spatial working memory
• Procedural memory

Question 4

What was impaired in patient HM?

Answer 4

Declarative memory - episodic and semantic memory impairments.

Question 5

What was the reason for Clive Wearing’s memory deficits?

Answer 5

Virus in the brain which affected the hippocampus - herpes simplex infection at 46.

Question 6

What were Clive Wearing’s memory deficits?

Answer 6

Lost his episodic memory

Question 7

What is retrograde amnesia?

Answer 7

Loss of access to events that happened in the past, prior to a trauma

Question 8

What is anterograde amnesia?

Answer 8

A deficit encoding, storing or retrieving new events occurring after a trauma.

Question 9

What was Ribot’s law?

Answer 9

For retrograde amnesia, memory impairments are more pronounced for events occurring briefly before the traumatic event.

Question 10

What is post-traumatic amnesia (PTA)?

Answer 10

The loss of ability to form new memories, typically following some form of concussive head injury. Gradually improves over time.

Question 11

What is Transient Global Amnesia (TGA)?

Answer 11

A sudden impairment in forming and retrieving new memories in normal, otherwise healthy individuals. Tends to resolve rapidly.

Question 12

Define etiology

Answer 12

Cause, or set of causes, of a disease or condition.

Question 13

What are the 4 most common causes/etiologies of anterograde amnesia?

Answer 13

• Bilateral damage to the temporal lobes and hippocampus
• Alcoholic Korsakoff syndrome
• Prolonged anoxia
• Herpes

Question 14

What is the key deficit in anterograde amnesia?

Answer 14

Episodic learning - this is regardless of the domain of information (visual or verbal) and the type of test (recall or recognition).

Question 15

What are the preserved abilities in those with anterograde amnesia?

Answer 15

• intellect and language
• non-declarative memory (priming, procedural memory, etc)
• digit span
• recency effect in free recall tasks
• Brown-Peterson short term forgetting task

Question 16

Describe the Brown-Peterson short term forgetting task.

Answer 16

A 3-word, or 3-letter phrase is read out, and followed by a 3-digit number which participants have to count down from, for example in 2s.

Ex: farm, mouse, car. 124 –> 122, 120, 118, etc.

Then a cue appears which instructs participants to recall the 3 earlier words.

This is one trial, so this procedure repeats
many times.

Question 17

Why do neurotypical participants have difficulties remembering items on the Brown-Peterson task?

Answer 17

Proactive interference. As trials progress, the accumulation of more and more 3-word combinations in short term memory interferes with learning of novel 3 word combinations, decreasing recall ability.

Question 18

Why might people with anterograde amnesia have an intact ability to perform the Brown-Peterson task?

Answer 18

Short term memory is unaffected, but when items enter long term memory, recall becomes difficult. Therefore, 3-word phrases do not build up in memory, causing less interference for learning of current 3-word phrases.

Question 19

What was initially suggested to be the reason for amnesia?

Answer 19

Cognitive deficits in the ability to process information at a deep enough level. However, the lack of deep enough processing was later found to result from frontal deficits, and when these were accounted for, memory impairments remained.

Question 20

What other reasons were later suggested as the cause of amnesia?

Answer 20

• quicker forgetting; perhaps long term memory traces decay more rapidly in amnesiacs. This was proven wrong, however - when the initial rate of learning was equated, the rate of forgetting was equivalent between subtypes of amnesiacs Koppelman (1985).
• retrieval interference; perhaps there is a build up of cues, triggering the activation of many interfering memories, blocking the retrieval of the correct memory. This was also proven wrong, it was found that explicit instructions did not benefit amnesiacs in accessing the relevant item (explicit cue should link to the relevant memory and induce recall of the correct memory trace.

Question 21

What is the contextual processing theory of amnesia?

Answer 21

The hippocampus requires what and where (contextual) information about an object or event. It’s deficits in the hippocampal integration of this information which causes an impairment in forming episodic memories

Question 22

What is the animal evidence for the contextual processing theory of amnesia?

Answer 22

Animals with hippocampal regions are poor at using environmental context in spatial learning tasks (Winocur & Mills, 1970).

Question 23

What is the human evidence for the contextual processing theory of amnesia?

Answer 23

Amnesiacs were worse at stating which day they saw particular stimuli on, compared to controls. However, amnesiacs were more likely to report seeing the stimulus more recently than another if they saw it twice, and only saw the other stimulus once. This was interpreted as a reliance on familiarity in the absence of contextual information, by amnesiacs (Huppert & Piercey, 1978).

They confuse recency with familiarity.

Question 24

What is the modal model of amnesia (Baddeley, 1998)?

Answer 24

Assumes:

• an episodic memory is consolidated when ‘mnemonic glue’ binds items together with their contexts.
• recall and recognition involve he same underlying processes (we now know this is flawed).
• semantic memory is a consequence of episodic information over time.

Question 25

What evidence was used to criticise the modal model?

Answer 25

Case study on Jon:

Jon had intact recognition, but impaired recall compared to healthy & normal individuals (when the modal model assumes that recall and recognition shares underlying mechanisms).

Jon could not form episodic memories, but his semantic memories were intact (M.Model assumes that semantic memories rely on many episodic memories)

Jon had normal intelligence and average linguistic capabilities (crystallised intelligence from prior learning should be impaired)

Question 26

Spatial information about an object or event arrives at the hippocampus from where?

Answer 26

The where pathway, originating in parietal regions

Question 27

Spatial information about an object or event arrives at which part of the hippocampus?

Answer 27

Parahippocampal gyrus

Question 28

“what” information about an object or event arrives at the hippocampus from where?

Answer 28

What pathway, visual/sensory processing areas

Question 29

“what” information about an object or event arrives at which part of the hippocampus?

Answer 29

Perirhinal cortex

Question 30

Information from the perirhinal cortex and parahippocampal gyrus is binded where?

Answer 30

Entorhinal cortex

Question 31

If your ability to recognise and know is intact, which area of the hippocampal regions would also be intact?

Answer 31

The perirhinal cortex, the what pathway.

Question 32

What is the severity of memory loss dependent on?

Answer 32

The extent of hippocampal damage and surrounding structures.

Question 33

If your ability to recall is intact, which area of the hippocampal regions would also be intact?

Answer 33

All of them - both perirhinal and parahippocampal regions would be required to provide what and where information respectively. The entorhinal cortex would be needed to bind this information and pass it to the hippocampus, and the hippocampus itself would be required to use this information to form an episodic memory.

Question 34

What is the alternative explanation to retrograde amnesia, for difficulties in recall of the past?

Answer 34

Suppressing of past events to avoid emotional turmoil/trauma.

Question 35

What were the initial methods of assessment of retrograde amnesia and what were the associated issues with these methods?

Answer 35

To test memory for photos of historically famous individuals, for news events, horse races and TV shows aired for a single season.

Issues:

• knowledge for such events and individuals is likely to vary between participants.
• continuous updating to add new, relevant events is required due to the nature of the material.

Question 36

What was Koppelman, Wilson and Baddeley’s (1990) probe method for assessing retrograde amnesia?

Answer 36

The autobiographical memory interview (AMI):

Semantic scale: subjects were asked to remember specific, factual information from certain time periods (where did you typically spend Christmas during your childhood?)

Personal scale: asked to recollect a specific event from each time period (winning a race at school)

Responses were rated for amount and specificity.

Question 37

What is the standard model of system consolidation (Squire, Cohen & Nadel, 1984)?

Answer 37

Over time, as memory traces are transferred from short to long term memory, the hippocampus is no longer required for memory recall - this process can be completed independently by the neocortex.

Question 38

What is the model detailing the independence of the neocortex in recalling memories once they are in long term memory stores?

Answer 38

The standard model of system consolidation (Squire, Cohen & Nadel, 1984).

Question 39

How can the standard model of system consolidation explain retrograde amnesia, and support Ribot’s law?

Answer 39

Robust memories are easier to remember than recent memories, because they are not as consolidated in the neocortex. Therefore, recall is poorer for more recent events.

Question 40

What is the alternative, competing theory to the standard model of system consolidation, and what does it argue?

Answer 40

Multiple trace theory (Nadel & Moscovitch, 1997; 1998) - argues the hippocampus is necessary for access to, and recall of, distant memories.

Hippocampus acts as a bookmark to the relevant trace in the neocortex; without the hippocampus, distant memories within the neocortex cannot be found/accessed.

Question 41

Describe the effect of 1) partial and 2) full, hippocampal loss on the recall of distant memories, and the relevant theories supporting each.

Answer 41

Partial hippocampal loss may still result in recall of distant memories, as some indexes/bookmarks for memories may still be intact - fits with multiple trace theory.

Full hippocampal loss/global damage can still result in recall of distant memories, in accordance with standard model of systems consolidation, as neocortical access to the memories are independent of the hippocampus.