L3 - Memory Loss, Amnesia and the Hippocampus Flashcards
What is an engram?
A memory trace - a hypothetical, permanent change in the brain as a result of a memory.
How does patient HM provide evidence for a localised memory engram?
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.
What cognitive functions were intact in patient HM?
- IQ (118)
- Digit span
- Spatial working memory
- Procedural memory
What was impaired in patient HM?
Declarative memory - episodic and semantic memory impairments.
What was the reason for Clive Wearing’s memory deficits?
Virus in the brain which affected the hippocampus - herpes simplex infection at 46.
What were Clive Wearing’s memory deficits?
Lost his episodic memory
What is retrograde amnesia?
Loss of access to events that happened in the past, prior to a trauma
What is anterograde amnesia?
A deficit encoding, storing or retrieving new events occurring after a trauma.
What was Ribot’s law?
For retrograde amnesia, memory impairments are more pronounced for events occurring briefly before the traumatic event.
What is post-traumatic amnesia (PTA)?
The loss of ability to form new memories, typically following some form of concussive head injury. Gradually improves over time.
What is Transient Global Amnesia (TGA)?
A sudden impairment in forming and retrieving new memories in normal, otherwise healthy individuals. Tends to resolve rapidly.
Define etiology
Cause, or set of causes, of a disease or condition.
What are the 4 most common causes/etiologies of anterograde amnesia?
- Bilateral damage to the temporal lobes and hippocampus
- Alcoholic Korsakoff syndrome
- Prolonged anoxia
- Herpes
What is the key deficit in anterograde amnesia?
Episodic learning - this is regardless of the domain of information (visual or verbal) and the type of test (recall or recognition).
What are the preserved abilities in those with anterograde amnesia?
- intellect and language
- non-declarative memory (priming, procedural memory, etc)
- digit span
- recency effect in free recall tasks
- Brown-Peterson short term forgetting task
Describe the Brown-Peterson short term forgetting task.
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.
Why do neurotypical participants have difficulties remembering items on the Brown-Peterson task?
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.
Why might people with anterograde amnesia have an intact ability to perform the Brown-Peterson task?
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.
What was initially suggested to be the reason for amnesia?
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.
What other reasons were later suggested as the cause of amnesia?
- 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.
What is the contextual processing theory of amnesia?
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
What is the animal evidence for the contextual processing theory of amnesia?
Animals with hippocampal regions are poor at using environmental context in spatial learning tasks (Winocur & Mills, 1970).
What is the human evidence for the contextual processing theory of amnesia?
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.
What is the modal model of amnesia (Baddeley, 1998)?
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.
What evidence was used to criticise the modal model?
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)
Spatial information about an object or event arrives at the hippocampus from where?
The where pathway, originating in parietal regions
Spatial information about an object or event arrives at which part of the hippocampus?
Parahippocampal gyrus
“what” information about an object or event arrives at the hippocampus from where?
What pathway, visual/sensory processing areas
“what” information about an object or event arrives at which part of the hippocampus?
Perirhinal cortex
Information from the perirhinal cortex and parahippocampal gyrus is binded where?
Entorhinal cortex
If your ability to recognise and know is intact, which area of the hippocampal regions would also be intact?
The perirhinal cortex, the what pathway.
What is the severity of memory loss dependent on?
The extent of hippocampal damage and surrounding structures.
If your ability to recall is intact, which area of the hippocampal regions would also be intact?
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.
What is the alternative explanation to retrograde amnesia, for difficulties in recall of the past?
Suppressing of past events to avoid emotional turmoil/trauma.
What were the initial methods of assessment of retrograde amnesia and what were the associated issues with these methods?
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.
What was Koppelman, Wilson and Baddeley’s (1990) probe method for assessing retrograde amnesia?
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.
What is the standard model of system consolidation (Squire, Cohen & Nadel, 1984)?
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.
What is the model detailing the independence of the neocortex in recalling memories once they are in long term memory stores?
The standard model of system consolidation (Squire, Cohen & Nadel, 1984).
How can the standard model of system consolidation explain retrograde amnesia, and support Ribot’s law?
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.
What is the alternative, competing theory to the standard model of system consolidation, and what does it argue?
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.
Describe the effect of 1) partial and 2) full, hippocampal loss on the recall of distant memories, and the relevant theories supporting each.
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.
