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Theories of Amnesia

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Kevin Silber

on 18 March 2014

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Transcript of Theories of Amnesia

They showed subjects 80 pictures on day 1 and a different 80 pictures on day 2.
Of the 80 pictures on each day, 40 were presented once and 40 were presented three times (160 trials per day.
Ten minutes after the presentations on day 2 subjects were shown pictures and had to say whether they were shown on day 1 or day 2.
Amnesics scored well on day 1 1x pictures and on day 2 3x. However, unlike controls they confused day 1 3x and day 2 1x items.

If amnesics consolidate normally but do not encode correctly then what is it that they fail to encode?
There are at least two methods by which a piece of information can be retrieved. One does not require context information but can be achieved via familiarity alone. The other does require context.
Huppert and Piercy (1978) demonstrated the use of familiarity by WKS amnesics.
However, there is now good reason for having less confidence in this theory.
Several researchers (e.g. Kopelman, 1985) have shown that such rapid forgetting was a consequence of methodology rather than a lack of consolidation.
When amnesics and controls are presented items at the same rate then one does, indeed, see more rapid forgetting.
However, if amnesics are given longer presentation times then the rate of forgetting for amnesics and controls is identical. This suggests a failure to properly encode rather than to properly consolidate.
Three possibilities exist for the amnesic’s inability to remember. Information could be inadequately encoded, consolidated, or retrieved.
A retrieval deficit was popular in the 1970s (see Warrington and Weiskrantz) but has now been disregarded.
The consolidation hypothesis suggests that amnesics are unable to form permanent memory traces.
Early evidence for this theory came from the fact that amnesics tend to forget extremely quickly. This suggests that they encode material but fail to consolidate it.

However, for other memories temporal information would have to be stored explicitly along with the content of the information. In this case such information might be inadequately processed.

Evidence suggests that structures in the mid-line diencephalon might be responsible for the encoding of such temporal information and this would account for its loss in some amnesics.

In considering why such a temporal deficit might be present we need to examine how such temporal information might be encoded under normal circumstances.
It seems likely that temporal information can sometimes be derived from logical problem solving. For example drinking a cup of coffee would have to be preceded by making it.
Frontal patients perform badly only on the discrimination task and such poor temporal discrimination has also been found in some, but not all, amnesics.
The suggestion from such data is that on top of the memory impairment due to limbic damage, some patients may also suffer a frontal memory component to their total deficit profile.
However, this argument is subject to debate as some amnesic patients show such temporal discrimination problems without having damage to the frontal lobe.
The degree of frontal lobe damage that accompanies the main source(s) of amnesia is critical in determining the pattern of deficits seen.
In an unpublished paper, Corsi got subjects to read pairs of words presented sequentially. On some trials the subject was required to state which of two words had been presented most recently.
On some trials both had been presented and on others only one had been presented.
This allowed for the distinction between temporal discrimination (former task) and recognition (latter task).

Whilst motor memory is a form of implicit procedural memory which is uniformly preserved in all amnesics, verbal priming tasks differ in the degree to which they can be learned.
Schacter et al. (1990) suggest that the degree of preservation depends on how intact the left temporal lobe language centres remain. If this is the case then it would account for the variability in performance among temporal lobe amnesics.
Despite this confusion, it may be the case that the episodic/semantic distinction serves some useful clinical purpose.
The alternative of lumping together these categories into declarative memory does not seem fruitful, at least not from a diagnostic point of view.
The third category of procedural memory might mark the distinction between explicit and implict memory.
However, the evidence for implicit procedures is not so clear here either.

The data on IQ is also equally open to debate.
Good performance on tests like the WAIS requires the recollection of early acquired knowledge. Yet the pattern of retrograde amnesia seen in many amnesics is one of a temporal gradient with earlier memories being better recalled.
There is evidence to suggest that vocabulary and other general intellectual knowledge acquired later in life does show some impairment.

This is a pertinent place to introduce a conceptual problem.
The distinction between episodic and semantic memory and recollection is by no means clear. Many of the retrograde amnesia tests are tests of general knowledge rather than episodic recall.
Even autobiographical recollections are suspect as they are difficult to verify and may be comprise semantic knowledge about oneself rather than the memories of specific episodes.
The investigations moved on in the 1980s to consider the distinction between semantic and episodic memory.
Deficits in episodic memory were frequently seen in the absence of semantic deficits and/or deficits in language and IQ.
However, the picture is not so clear if we look to anterograde amnesia as patients mostly have difficulty acquiring new language (Gabrielli et al., 1988).
Much of the early research on amnesia supported the idea that STS and LTS were distinct. That immediate memory span was almost invariably intact in amnesic patients was seen as evidence for Atkinson and Shiffrin’s (1968) modal model of memory.
That model has subsequently been challenged from ordinary memory research (e.g. Baddeley, 1986). Furthermore, the amnesia evidence only supports a single dissociation as no cases are reported where immediate memory is the only deficit.
It seems that this difference might be accounted for by frontal damage differences as performance on the BP task correlates well with the degree of frontal damage and diencephalics are more likely to have frontal lesions (Leng and Parkin, 1989).
Analysis of the context deficit hypothesis (described shortly) may shed light on this as only WKS amnesics have a loss of memory for temporal context. It seems that if we compare recognition memory with discrimination memory then both groups are poor. However, for WKS amnesics there is no correlation between the two whereas for HSE patients there is.
Do different functional deficits result from different aetiologies?
This question has typically been pursued by contrasting diencephalic and temporal lobe amnesia.
Here we need to consider qualitative rather than quantitative differences. Evidence has centred around differences observed in performance on the Brown-Peterson (BP) task. Here diencephalics perform poorly whereas temporal lobe patients fair better (sometimes even at a normal level).
Is this indicative of a functional difference?
Mishkin (1982) has argued that there are two distinct circuits, a hippocampal one and an amygdaloid one. His data suggest that destruction to either alone is insufficient to produce memory loss. This is consistent with the data from H.M., the WKS patients of Victor et al. (1989) and many HSE patients.
However, other cases (e.g. R.B.) had a discrete lesion of region CA1 of the hippocampus and yet he had a severe anterograde amnesia despite having no sign of retrograde amnesia.
We have looked at a number of aetiologies of amnesia and so it is pertinent to ask whether there is a structure (or set of structures) that must be damaged in order for any form of amnesia to occur.
On the one hand the large variation in causes suggests that there is not a critical single structure. However, most patients present with large diffuse lesions so the data are not clear.
Perhaps more likely is the idea that a set of structures are critical. The obvious candidate for such a view would be the limbic system.
In today’s lecture we will cover:
Is there a critical lesion?
Different kinds of amnesia?
Theories concerning STS and LTS
The role of the frontal lobes
The consolidation hypothesis
The context deficit hypothesis

There does not appear to be a single place that can be regarded as the seat of memory

Memory is more of a distributed function

This leads to the various types of amnesia that are seen

It is not clear whether the cognitive deficit is encoding, storage or retrieval, or some combination of these
Huppert and Piercy explained the results by suggesting that amnesics were basing their judgements on familiarity and not context.
Those items presented three times on day 1 were as familiar as those presented once on day 2. This makes sense if you plot the forgetting curves of all four types of item.
This result, and other similar findings, have prompted Mayes et al (1988, 1991) to propose the context deficit hypothesis. They suggest that context information fails to be encoded which makes recognition difficult and recall virtually impossible.
Parkin suggests this explanation.
The hippocampus is involved in forming the context in which a target stimulus is stored. Maybe WKS damages the input to this hippocampal system whereas HSE damages the efficiency of this system.
If HSE affects the consolidation of memories in general whereas WKS affects only the input of context then this would explain the difference in recognition-temporal context found between the two groups.
Most of the early data is consistent with this view apart from one problem. It seemed that no deficit could be found from fornix lesions alone ( the fornix connects the hippocampus to the mammillary bodies).
However, Gaffan and Gaffan (1991) suggested that the most reliable data from the literature suggests memory loss in patients with damage solely to the fornix. Indeed, Hodges and Carpenter (1991) report two fornix lesion patients with WMS scores which are comparable to other amnesics (although their Recognition Memory Test scores were better than one would expect).
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