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Kevin Silber

on 26 February 2014

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Transcript of Amnesia

We have looked at the various forms of memory that can be seen to be impaired through amnesia

We used this to analyse the cognitive deficits associated with a few of the more interesting forms of amnesia

We have also looked at the anatomical damage that is believed to be associated with these forms of amnesia.
There are a number of different types of amnesia, mostly as a result of damage to different parts of the brain.
In order to make comparisons between these various forms we need to consider the variety of ways in which memory can be assessed

There are a number of different types of memory and little agreement as to how we should carve memory up
- anterograde and retrograde memory
- long and short term memory
- episodic and semantic and procedural memory
- implicit and explicit memory

In addition, a number of non-memory problems that often accompany the amnesia can be present. These include frontal lobe symptoms, confabulation and perceptual deficits

Any way we decided to carve memory up would not be doing justice to the range of memory skills that could be either lost or retained.

Hence we need to categorise types of memory more discretely

The following slide shows the categories that have been adopted by neuropsychologists working in this area.
Temporal Lobe Amnesia
Korsakoff Syndrome
This is most commonly caused by chronic alcoholism
The currently accepted theory is that it arises due to a thiamine deficiency brought on by a poor diet. However, this must interact in some way with the effects of alcohol as people in famine situations with a thiamine deficiency do not tend to develop Korsakoff syndrome.

The brain damage occurs in the diencephalon but there is no real concensus as to whether there is a critical structure which must be damaged for amnesia to manifest itself.
Other Amnesias
There are many other forms of amnesia but we do not have the space to go through them in this lecture series

You should try to explore some of the other forms so that you knowledge is as broad as possible.
This presentation will cover:

Types of memory assessed
Korsakoff Amnesia
Temporal lobe amnesia
Herpes Simplex amnesia
Other amnesias
Lecture Outline
Let's take a closer look at these various divisions of memory
Anterograde and Retrograde Memory
Anterograde memory is the ability to learn new things after the point of injury

It is tested primarily using paired associate learning but is also measured by recall and recognition abilities
Retrograde memory is the ability to remember things from before the point of injury

It is tested in a number of different ways:
- the famous faces test
- autobiographical memory test
- tests of famous events

All of these tests have one thing in common, namely, that they are designed to detect temporal gradients in the amnesic pattern
Long term and Short Term Memory
We will briefly look at the tests used for each of the categories.

Immediate Memory
Memory span is used here.

Short-term Memory
The Brown-Peterson test is typically used here. One, two or three items are presented after which there is a distraction task of varying lengths of time. The patient is then asked to recall the items.

Long-term memory
A variety of tests are used here to examine
semantic memory
episodic memory
autobiographical memory
Implicit Memory
Implicit memory is what we learn and remember without being conscious of an effort to learn
A classical test is the Clapperade phenomenon
More often tests deal with emotional or perceptual learning

Explicit Memory
Most often this deals with tests of semantic priming as a way of testing lexical memory
However, tests can be used to test post-morbid semantic learning
Long-term Memory
Semantic Memory
Semantic refers to knowledge
Semantic memory is the remembering of general information and is often tested by way of general knowledge tests
There are many tests of semantic memory and we will see some elements of these in a future lecture

Episodic Memory
As the name suggests, this is the ability to remember specific things that have happened and the time frame in which they happened
These can be personal events like what you had for breakfast
They can be public events like remembering the first time Andy Murray won a grand slam title

Autobiographical Memory
This is your the memory of personal information
It would include current personal information like your address
It would also include past personal information like where you went to primary school
These are assessed using the Wisconsin Card Sorting Test (WCST) and release from Proactive Interference (PI)

Wisconsin Card Sorting Test
Involves changing the ways in which cards are sorted

Release from Proactive Interference
Release from PI involves presenting series of lists from the same categories
Successive recalls from successive lists contains intrusions from previous lists
A final list is from a different category and you normally see no intrusions in its recall.
Frontal Symptoms
This is the making up of material (usually experiences) which is untrue
It may or may not be feasible

Perceptual Deficits
These are typically tested by the digit-symbol task which requires the subject to pair numbers with abstract symbols.
Other Corollary Symptoms
Some researchers (Malamud and Skillicorn, 1956) suggest the mamillary bodies, others (Victor et al., 1989) the dorsomedial thalamic nucleus (DMTN), and still others (Mayes et al., 1988) both.
Mayes et al. (1987) have also implicated the hippocampus.
The majority of research tends to suggest that damage to the mamillary bodies or DMTN alone is insufficient but the research data are not at all clear.
We can now look at the pattern of the deficit seen in Korsakoff patients. However, only a brief coverage of the research is possible here.
All WKS patients show normal digit span (immediate memory).
STM results are less clear using the Brown-Peterson task with Kopelman (1985) showing normal performance and Mayes et al (1988) showing impaired performance

Amnesic patients do poorly on paired associate learning (anterograde amnesia). However, Lhermitte and Signoret (1972) showed normal retention when cued recall was used.
Methodology may be important here as Kopelman (1985) showed that memory is relatively normal if the same level of acquisition as controls is achieved by providing longer exposure times for the material to be learned.

WKS patients have an extensive, temporally graded, retrograde amnesia. The nearer to the injury the harder it is for them to remember (Albert et al., 1979).

The Claparede (1911) phenomenon shows that WKS patients have some implicit memory. They also show intact classical conditioning (Talland, 1965).
Several studies have confirmed the view that semantic memory remains intact (Talland, 1965; Butters et al., 1986). However, some caution is needed here as these tests most often examine semantic memory that is formed early in life.

Given that amnesics show a temporal gradient in retrograde amnesia then such tests might give a falsely optimistic picture

When tests are carried out that tap into more recently acquired semantic memories then some deficit is often seen (e.g.. Butters, 1985).
Frontal syndromes are very prominent in WKS patients. They typically show perseveration on the WCST (e.g. Hunkin, 1991).
They also show poor release from PI (Squire, 1982).
WKS patients often confabulate (Kopelman, 1987) but their confabulations are rarely fantastic and are likely to decline in frequency as the patient comes to adapt to the amnesic situation.
WKS patients also show perceptual deficits on tasks such as the Embedded Figures Test and reversing the Necker cube (Talland, 1965).
The most famous and well tested case of temporal lobe amnesia is Scoville and Milner’s (1957) patient H.M. who was given a temporal lobectomy to relieve severe epileptic seizures.
The research points to two potentially critical structures, the hippocampus and the amygdala, but as with WKS whether damage to one or both is required for amnesia to occur is unclear.
Temporal lobe damage can be caused by a number of things including, ischaemia, anoxia, metabolic abnormalities, viral infections and dementia. The pattern of amnesia is not always the same.
Digit span is usually found to be normal although Corkin et al. (1985) report reduced digit span in anoxia cases.
Most cases also show normal performance on STM tests.
A large number of studies (e.g. Corkin, 1984) have shown H.M. to be impaired on tests of anterograde learning. However, performance may be task specific as Freed et al. (1987) have shown normal rates of forgetting in a number of paradigms.
Other temporal lobe patients tend to show impaired anterograde learning (e.g. Zola-Morgan et al., 1986).
Temporal lobe patients do not show frontal syndromes nor do they show confabulation.
However, some studies report some perceptual deficits such as poor odour discrimination (H.M.) and visual impairments (Mohr et al., 1971).
The retrograde amnesia in temporal lobe patients is very varied. H.M., T.J (Parkin and Hunkin, 1991) and R.B. (Zola-Morgan et al., 1986) all showed a temporal gradient similar to that seen in WKS patients. However, the range of retrograde amnesia has been reported to extend for 10 years (Trillet et al., 1980) or for as little as 3 months (Milner, 1959).
Most temporal lobe patients show implicit memory suggestive that the residual learning capability remains intact. Similarly, semantic memory appears to remain relatively intact but their can be selective deficits as in M.R.L. (Beatty et al., 1987).
Herpes Simplex Encephalitis
This comes about when the Herpes Simplex virus attacks brain tissue. The cases of this memory disorder are very rare.
HSE produces consistent brain damage across patients. The damage is to the lateral and medial temporal cortex with some damage to the frontal and parietal lobes.
The acute phase of the disease includes confusion and severe amnesia. The confusion is reduced over time and the amnesia lessens, although both anterograde and retrograde amnesia persist.
There is no impairment of digit span and show normal STM as measured by the Brown-Peterson task (Butters and Cermak, 1980).
Anterograde amnesia is severe and there is very rapid forgetting of learned material (Lhermitte and Signoret, 1972). Their forgetting is far more rapid than is seen with WKS.
There is also severe retrograde amnesia for both personal knowledge (Warrington and McCarthy, 1988; Cermak and O’Connor, 1983) and for knowledge of the current time (Conrad, 1953).
There is variability as to how far back this retrograde amnesia extends - from 3 months to 20 years (Foletti et al., 1980).
Some patient’s (e.g. Hanley et al.’s (1989) B.D.) have particular problems remembering faces.
As far as semantic memory is concerned, many patients have severe language difficulties (Gordon et al., 1990). Category naming tasks tend to be performed poorly although some studies have not considered word frequency in their tests (see Stewart et al., 1992).
Generally, implicit memory is intact in HSE patients (Kapur, 1988) but there are some anomalies. For example, although classical conditioning was found to be normal in Warrington and Weiskrantz’s (1982) patient, he had no recollection of the conditioning procedure.
HSE patients do suffer frontal damage but their frontal performance on the WCST is far less impaired than it is for WKS patients (Leng and Parkin, 1988).
Confabulation, another frontal syndrome, is also extremely rare in such patients.
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