Amnesia Flashcards

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1
Q

Retrograde amnesia

A

Retrograde amnesia is inability to remember information that was learned before the brain damage occurred

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2
Q

Anterograde Amnesia

A

Anterograde amnesia is the inability to learn new information after brain damage.

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3
Q

Define amnesia

A

Amnesia is a selective memory impairment following brain damage that can affect the ability to learn new things or remember past events, or both. Amnesia can be the result of differentially effected short term memory, working memory and long term memory

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4
Q

Tulving 1972- structure of memory

A

suggested that memory is separated into short term memory (STM) and long term memory (LTM) and that LTM is further divided into episodic (personal events), semantic (knowledge about objects and the world) and procedural memory (cognitive and motor skills).Cohen and Squire (1980) made the distinction that episodic and semantic memory are declarative (i.e. people are exlplicitly aware of these memories) whereas procedural memory is non-declarative (people not explicitly aware of this memory)

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5
Q

Smith et al (2013)

A

assessed levels of anterograde and retrograde amnesia in eleven memory impaired patients with medial temporal lobe damage. The results showed that retrograde amnesia was only observed once anterograde amnesia reached a substantial level of severity, after which anterograde and retrograde were associated. Note that retrograde amnesia tend to be mild in comparison to anterograde when the two are observed together.
This suggests that there are possibly common mechanisms or anatomical overlap between anterograde and retrograde amnesia and also suggests these mechanisms only overlap once anterograde amnesia becomes severe. However, the modular nature of memory is evident in that anterograde and retrograde amnesia often double-dissociate, supporting that amnesia is due to selectively impaired aspects of memory.

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6
Q

Ribbots Law

A

The finding that retrograde amnesia is often mild and the most recent memories are the most ‘forgotten’ is known as Ribbots law

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7
Q

Example double dissociation between anterograde and retrograde amnesia

A

HM was a patients with severe epilepsy who had parts of the medial temporal lobe removed, including a significant portion of the hippocampi. HM showed mild retrograde amnesia (unable to recall revents from up to about three years before the brain damage) and intact STM/ However, HM had severe anterograde amnesia i.e. he was unable to learn new information. The opposite has been observed by Goldberg et al.’s (1981) who described 36 year old patient who sustained an open head injury and initially showed retrograde and anterograde amnesia, but at a follow-up 2 years later revealed a full recovery of learning ability and thus retrograde amnesia was present on the absence of anterograde. This supports that anterograde and retrograde amnesia are due to deficits in independent or dissociable mechanisms

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8
Q

Older theories of amnesia

A

It has historically been suggested amnesia is due to rapid forgetting i.e. a problem with the LTM store, which would explain both anterograde and retrograde symptom i.e. neither old memories nor new memories are stored well. This is logical when considering the correlation between anterograde and retrograde observed by Squire and Alvarez (1995) and other aspects of the associations between retrograde and anterograde amnesia which have been observed in more recent studies. But anterograde and retrograde often double dissociate

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9
Q

How are anterograde and retrograde generakky explained by modern concepts of memory and amnesia

A

The processes of consolidation and retrieval map directly on to anterograde and retrograde amnesia, whereby anterograde amnesia is theorised to be due to inability to consolidate memory and retrograde amnesia and theorised to be due to an inability to retrieve memories from LTM. It is suggested that the hippocampal formation is especially linked to anterograde amnesia due to its role in the consolidation process.

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10
Q

Regions in the Hippocampal formation

A

hippocampus, dentate gyrus, parahippocampal gyrus and entorhinal cortex. This is the area which was severely damaged in patient HM who had severe anterograde amnesia

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11
Q

Who suggested the role of hippocampi in anterograde and retrograde amnesia and what is this role

A

Meeter and Murre (2004) suggested that when new information is first acquired, the hippocampi is important in the consolidation of the information. Once information is consolidated, it is then stored in the neocortex (which is separate from the hippocampi) and becomes independent of the hippocampi. It is suggested that it takes longer periods of time for information to be consolidated into the neocortex i.e. from months to years.

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12
Q

What does the theory about the role of hippocampi in memory consolidation suggest about anterograde and retrograde amnesia

A

This process explains why anterograde amnesia is more largely associated with hippocampal damage. Specifically, this is because consolidation processessing which place in the hippocampi is jeopardised and so new memories cannot be stored. This theory also explains why mild retrograde amnesia is also often observed in association with hippocampal damage and anterograde amnesia (i.e. in the case of HM). This is because as consolidation to the neocortex takes months to years, information that has been learned recently before the brain damage has not completed the consolidation process and therefore is still dependent on the himppocampi. This also explains ribbots law i.e. the most recent memories will be the most affected by retrograde amnesia, because they are the most dependent on the hippocampi.

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13
Q

What is anatomical basis of memory consolidation in the hippocampi

A

A process called long term potentiation (LTP) refers to a persistent strengthening of synapses based on recent patterns of activity in the brain. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. This is suggested to be the anatomical basis of a memory trace, thus supporting that the hippocampus is involved in the consolidation of memories

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14
Q

Who is indexing thoery by and what does it state

A

Shallice and Cooper 2011: It has further been suggested that the hippocampus not only gradually transfers memories to the neocortex, but also keeps an ‘index’ of neocortical areas where the memory is stored, through the memory traces formed via LTP. This is known as ‘indexing theory’ (Teyler and DiScenna, 1986).

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15
Q

Limitations of the hippocampal explanation of amnesia

A

it should be noted that there a few cases of severe retrograde amnesia that have been observed following hippocampal damage. For example, Rosenbaum et al (2008) describe a patient named SJ who had severe retrograde amnesia, especially for old memories following bilateral lesions of the hippocampi. There are reconciliations that can be made between these findings and the indexing theory, such that it is plausible that a damaged index can lead to an impairment in retrieving memories.

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16
Q

Alternative to indexing theory

A

Multiple trace theory
Older memories are still dependent on hippocampi, but It is suggested that older memories have more traces to the hippocampi and therefore are more resistant to this effect, but they are not entirely resistant and specific damage could jeopardise these traces.

17
Q

Conclusion

A

In conclusion, older models of amnesia which propose that the main mechanism of the disorder is ‘forgetting’ would expect to find an association between anterograde and retrograde amnesia. Although this association is often observed, it is found that when patients suffer from both forms, anterograde tends to be much more severe than retrograde. Additionally, there tends to be an increased deficit for more recent past events in retrograde amnesia. Anterograde and retrograde are also dissociable, which overall demonstrates that there may be some overlap in the mechanisms contributing to the two forms, but these mechanisms can be understood as separate at least to the point where they can be selectively impaired. The theory put forward by Meeter and Murr (2004) which suggests that memories are encoded initially in the hippocampi via LTP and gradually become stored independently in the neocortex, comprehensively accounts for these observations. Occasional observations of severe retrograde amnesia following hippocampal damage challenge this theory somewhat, although this can be reconciled when considering that the hippocampus may serve as an index for memories stored in the neocortex and so specific damage could jeopardise the recall of even very old memories.