Chapter 16 Flashcards

1
Q

Describe why assessment is important in memory problems

A

Involves combining test results with info from other professionals + neuroimaging techniques.

B) Standardized test results allow the patient’s performance to be compared to healthy people using standardized norms
C) Contributes to the diagnosis of the clinical problem underlying the memory deficit
D) Important in communicating info about the patient to other professionals in a standardized way + patterns of strengths/weaknesses–>important in planning the treatment program.
E) The specification of the patient is essential for any publication + new discoveries can influence clinical practice.

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2
Q

Compare anterograde amnesia with retrograde amnesia

A

Anterograde–>problem in encoding, storing or retrieving ongoing information that can be used in the future (case of HM, CW & KI)
Retrograde–>refers to the loss of access to events that happened in the past, typically before the onset of the disease.

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3
Q

Describe amnesic syndrome + how it occurs

A

In its pure form, the amnesic syndrome involves grossly impaired episodic memory + with preserved working memory, semantic memory, implicit memory + intelligence.

Episodic memory allows individual, specific memories to be retrieved–> episodes are linked to the specific time + place of the experience

This associative link provides a way of specifying that particular experience + subsequently retrieving that memory

Loss of the capacity to link experiences to their spatial/temporal context would grossly disrupt subsequent recollection.

The same thing happens to rats with hippocampal lesions–> bad at making use of environmental context in a spatial learning task

Amnesic patients may have difficulty in imagining future activities but able to imagine the component experiences, but could not integrate them into a whole,

although the hippocampus plays a role in both episodic memory and the use of imagination to predict the future, these are best seen as separate functions.

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4
Q

Describe Huppert + Piercy study that compares amnesiacs to a control group on picture recognition

A

the performance of amnesic + control patients can be roughly equated by giving the amnesic patients longer to encode the pictures than the controls.

The study involved presenting pictures either once or twice on each of two successive days.

After the second day’s presentation, participants were shown a sequence of pictures + asked to say if they’d seen each picture.

If they recognized–>decide on which day that picture had been shown.

Amnesiac patients: more likely to say that items presented twice on day 1 had in fact been presented on day 2–> b/c the degree of familiarity was greater.

Control group: opposite pattern. More accurate in assigning items to day 1 if they had been presented twice–> 2 presentations = 2 chances of linking that picture to the day 1 context.

In the absence of episodic memory’s ability to link to context, amnesic patients had to rely on a general feeling of familiarity.

The same thing happened to answers to trivial pursuit questions e.g. what the favourite food of the comedian and film star was, Bob Hope.

Patients are able to recall the “fact,” but bad at recalling that they had just been given this info–>confused recency with the degree of familiarity.

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5
Q

Define source amnesia

A

Applied to the characteristic difficulty that amnesic patients experience in recollecting the source of a given memory.

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6
Q

Describe the Modal model of amnesia by Baddley (That was proven far too simple)

A

Model consistent with a contextual hypothesis

1) Assumes that the essence of episodic memory is the capacity to “glue” experiences to a specific context, which provides a contextual tag–>allows individual experiences to be retrieved.
2) Assumes that recall + recognition involves the same underlying storage processes with different constraints on subsequent retrieval.
3) Assumes that semantic memory represents the residue of many episodes + could be retrieved through a separate mechanism.

Testing Jon (Fargha-Khadem’s patient) convinced Baddeley that the modal model of amnesia was wrong, or far too simple.

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7
Q

Describe the case of Jon and how it goes against the modal model of amnesia

A
  • Born prematurely–> anoxia + substantial damage to his hippocampus.
  • Above-average intelligence
  • Good semantic memory skills–> Jon’s knowledge of the world is excellent but takes longer than controls to acquire new facts
  • Recognition was so well preserved and recall so impaired

Doors and People Test–>Separate measure for visual + verbal recall and recognition. Each of these components is assessed separately, then combined to give overall visual scores, overall verbal scores + combined recall versus recognition.

a) If episodic memory is impaired, semantic memory should have been impaired too since it is based on an accumulation of episodes; this was not the case
b) crystallized intelligence based on prior learning should have been impaired e.g. reduced vocabulary; this was not the case.
c) If recall and recognition involve essentially the same storage process, they both should have been impaired; this was not the case.

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8
Q

Describe what neuroimaging & testing results discovered about Jon’s memory

A
  • Considerable difficulty teaching Jon the distinction between remembering and knowing.
  • When control participants made a remember judgment–> could describe their recollection
  • Jon however, tried to form a visual image of the cards + if his image of the word was clear and bright–> categorized this as remembering.
  • Jon was using a strength rather than a recollective criterion.
  • The “remember” judgments are accompanied by a specific activation pattern that differs from that evoked by “know” responses. Jon proved to lack the remember component.
  • Jon does have the capacity to recollect but has great difficulty in laying down their episodic memory traces
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9
Q

How is Jon different from other amnesiacs?

A
  • Got his hippocampal damage at a very early age
  • Damage is limited to the hippocampus but perirhinal and entorhinal cortices are entirely spared.
  • The hippocampus is important for episodic memory, but familiarity-based recognition judgments are based on the adjacent perirhinal regions that are preserved
  • Later studies on amnesiacs show that hippocampal volume had a minimal effect on memory for items, but a clear impact on context memory
  • The greater the volume of the hippocampus, the better the memory of which word went with which scene
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10
Q

Define Consolidation + how it affects amnesia

A
  • Memory traces are initially fragile + become more resistant to forgetting as time progresses
  • It depends crucially on the hippocampus + related areas–>damage to this area interferes with the consolidation process.
  • When learning is followed by a period of sleep, long-term retention is better than when remaining awake during that time
  • The retention of information by amnesic patients was greatly enhanced if learning is immediately followed by their removal to a quiet, dim interference-free room.
  • 4 densely amnesic patients + 6 controls attempted to remember a story 1 hour later.
  • When the hour was spent in a darkened room, patients performed almost as well as controls.
  • However, when the hour was filled with cognitive tasks, the patients remembered virtually nothing
  • Amnesic patients are particularly susceptible to the disruption of the process of consolidation, particularly during the early stages.
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11
Q

Describe Dewar’s study with Mild cognitive impaired (MCI) patients

A

MCI patients and controls learned a list of words + were tested after a delay of 9 minutes (divided into 3), with interfering material presented during either the first, 2nd or 3rd part of the retention period.

Interference during the first stage caused more forgetting than in the later phases–>b/c the initial stages of consolidation are particularly vulnerable.

The process of hippocampal consolidation over this initial period –>operates at the cellular + subcellular level–> based on the mechanism of long-term potentiation (LTP)

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12
Q

What is retrograde amnesia?

A

Patients often suffer from both, however, the severity of anterograde is not highly correlated with the degree of retrograde amnesia, suggesting different origins

Problem with measuring retrograde amnesia–>the tester typically does not have control over the learning of the material to be recalled (learned many years ago)

Ribot’s law–>earlier memories are better preserved in those with retrograde amnesia + are more durable than those acquired more recently

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13
Q

What are some methods of testing retrograde amnesia + what are issues with them?

A

1) Scales testing degree of knowledge of news events or horse races is likely to vary substantially across patients + is continually ageing so needs constant revising and revalidating.
2) Requesting autobiographical recollections to probe the patient’s memory of their earlier life + cross-check with kin–> not very practical for lab studies + is time-consuming

Retrograde amnesia generally leads to impairment in autobiographical memory on both the personal + the semantic scales.

Personal semantic memory–> Factual knowledge about one’s own past.

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14
Q

Describe Autobiographical Memory Interview (AMI) by Kopelman, Wilson, and Baddeley

A

Involved asking people to remember factual questions that could be regarded as probing a form of personal semantic memory.
Some were remote (name of first school). Intermediate (first job), recent (last Christmas)
For each life period, had to recollect a specific personal event (winning a race at school)
Episodic recollections were rated in terms of amount + specificity of info retrieved.
The test was validated + found to be sensitive and reliable.

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15
Q

What is Alcoholic Korsakoff syndrome?

A

Patients have difficulty learning new information, although events from the past are recalled.

A tendency to invent material to fill memory blanks.

The most common cause is alcoholism, especially when this has resulted in a deficiency of vitamin B1.

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16
Q

What is confabulation?

A

This occurs when the reported autobiographical information is false but not intentionally misleading.

Typically found in patients with a dysexecutive syndrome (disruption to the operation of the central executive component of working memory)–>resulting from damage, typically, to both frontal lobes.

Provoked confabulation–>can occur as a result of an amnesic patient’s attempt to fill in a gap in knowledge, so as to avoid embarrassment.
Spontaneous confabulation–>tends to be much more florid, is less common + tends to be linked to frontal-lobe damage.

Such patients have difficulty in setting up appropriate retrieval cues.

Information that would clearly be implausible to most normal or indeed most brain-damaged people are accepted + elaborated.

17
Q

Describe the hippocampal and systems model of consolidation

A

The hippocampus and surrounding regions play a crucial role in memory consolidation. They typically assume two types of consolidation.

The first, hippocampal consolidation–>relatively rapid process, operates at the cellular and subcellular level and involves the initial encoding of new information within the hippocampus.

Systems consolidation–>involved in gradually transferring information from the hippocampus to other brain regions for more long-term storage.

These two are not mutually exclusive.

The above models differ in detail but all assume that the hippocampus + associated regions act as an intermediary

They detect + store novel information at a relatively rapid rate, then hold it while it is gradually transferred to more cortical areas.

18
Q

Describe the standard model of consolidation

A

Links within the cortex are assumed to take longer to set up but are more durable.

This consolidation process continues to progress within the neocortex after traces have been lost from the hippocampus

memory traces that have been in the brain for many years will be particularly robust (Ribot’s law)

19
Q

Describe the Multiple Trace Hypothesis, proposed by Nadel and Moscovitch:

A

They argue for the role of the hippocampus in retrieval + encoding.

LT consolidation sets up recorded traces of experience within the hippocampus–> multiple replicas of earlier experiences.

Partial damage to the hippocampus removes some of the available traces–> causes the temporal gradient in retrograde amnesia with older traces being more likely to survive b/c they’re numerous

However, complete damage to the hippocampus should lead to total retrograde amnesia.

20
Q

Describe Traumatic brain injury (TBI)

A

This occurs when the head receives a sharp blow or is subject to a sudden acceleration or deceleration.

The brain swirls around + damage from the bony protuberances within the skull + from the twisting and shearing of fibres within the brain.

Other causes of TBI include falls, sports injuries and blast, with an estimated 10–20% of returnees suffering from TBI.

If the brain injury was severe–>expected to be in a coma, sometimes for many weeks. Or persistent vegetative state in which physical functions continue to perform but mental functions do not.

On recovering consciousness, the patient is likely to move into a state of post-traumatic amnesia (PTA)–>Patients have difficulty forming new memories, attention can be disturbed + capacity for new learning grossly impaired. Tends to improve with time.

The Wessex Head Injury Matrix Scale (WHIM)–>picks up the tiny changes that occur in behaviour as the brain slowly recovers from major trauma.

Overall, it is estimated that some 5.3 million Americans are currently living with some degree of TBI

Out of 513 retired NFL players aged 50 or older–>preliminary evidence that some 35% showed signs of mild cognitive impairment (MCI)–>predictive of dementia.

21
Q

Describe the study by High who monitored comatose brain injury patients

A

Monitored the progress through PTA of 84 patients whose brain injury was sufficient to lead to a coma.

They typically first recovered personal knowledge, followed by place + finally temporal orientation.

The estimated current date was typically displaced backwards, especially in more severe cases–>error of up to 5 years, then error rate reduced due to shrinkage of their retrograde amnesia.

Length of time in PTA can vary considerably–>patient is likely to be left with a degree of retrograde amnesia.

The shrinkage in the degree of retrograde amnesia is variable but the dense period of continuing amnesia immediately preceding the TBI is very characteristic.

22
Q

Describe Gina Geffen’s study of the Australian football player

A

Tested football player + collogues using a test of speed of semantic processing involving the patient in reading brief sentences that are either obviously true or obviously false (e.g Nuns are bought in pairs)

Patient + all his teammates were somewhat slowed on this sensitive speed test of semantic processing.

23
Q

Describe Alzheimer’s disease

A

Discovered by Alois Alzheimer
Disease of the elderly with symptoms that vary but always include an increasingly severe deficit in episodic memory–>most prominent cause of senile dementia (50% of cases of dementia) + occurs in about 10% of the population

Early stages of AD can be difficult to diagnose
Diagnosis requires that there is a memory impairment + at least two other deficits (problems of language, action control, perception, or executive function)

Two cardinal signs of AD: amyloid plaques + neurofibrillary tangles.
Faulty protein division–>production of beta-amyloid, which is toxic to neurons–>formation of the clumps of amyloid that form the plaques.
Neurofibrillary tangles–>occur within the neurons–>based on the microtubules that structure + nourish the cell.
Abnormal proteins form, resulting in the twisting and collapse of the microtubules–>ultimately in cell death

The disease typically develops through a series of stages
Begins in the medial temporal lobes + hippocampus–>creating the initial memory problems,
Progresses to the temporal + parietal lobes and to other brain regions.

AD is basically characterized by a single overall feature–> that of defective episodic memory

24
Q

Describe the case study of Oxford philosopher Iris Murdoch

A

They compared the sentence content + structure of one of Murdoch’s early novels, with a middle novel + her final novel

Her last novel used considerably shorter sentences + more high-frequency words–>was adapting to her growing language constraints.

As the disease progressed she had linguistic problems such as:
Word-finding + defining difficulties, bad spelling, low capacity to name pictures or to generate items from a given semantic category

Appeared to maintain a very amiable disposition

25
Q

Describe how Alzheimer affects episodic memory

A

There is evidence that as the disease progresses even recency tends to decline

Despite the difficulty AD patients have in acquiring new information, once learned it appears to be forgotten no more rapidly than occurs in normal elderly people

Equivalent performance across the groups of normal, AD, and elderly participants when tested after 5 minutes on picture recognition with varying exposure times

26
Q

Describe how semantic memory is affected by Alzheimer’s

A

A clear semantic deficit would be reflected in:
A) Difficulties in naming pictures of objects or animals
B) Picking the appropriate picture given its name
C) Describing the characteristic of a named or pictured object
D) Answering general questions such as whether an elephant has pricked up or floppy ears

A steady decline in semantic memory in AD patients was associated with the degree of temporal lobe atrophy

Semantic dementia–> a disease in which episodic memory is relatively well preserved, with atrophy occurring principally in the left temporal lobe rather than the more medial found in AD

27
Q

Patients with AD perform/don’t perform well in which tasks?

A

Patients with AD perform well in:

a) Reading mirror-reversed words.
b) Lexical decision task involving the speed of deciding whether a sequence of letters comprised a real word or not.
c) Priming on relatively automatic tasks
d) Pursuit rotor (requires keeping a stylus in contact with a moving target)–>The patients performed less well initially but improved at the same rate as an elderly control group.
e) Maintain small amounts of material over an unfilled delay
f) Capacity for sustained attention or vigilance

Patients with AD don’t perform well in:

A) Implicit memory tasks tested by stem completion (patients were shown a word (stamp) and later ask to “guess” a word beginning with st).
B) Priming on more complex tasks (recall is primed by presenting associatively related cue words)
C) Maintain small amounts of material over a delay filled with articulatory suppression
D) Dual-task performance deficit even when each of the combined tasks are very easy
E) Clear impairment in the capacity to bind features such as colour + shape into remembered objects

28
Q

Describe Bradley’s study on AD patient’s dual-task performance

A

Series of tasks that combined auditory digit recall e.g. repeating a telephone number + concurrent nonverbal task.

One study:
-Memory span task (Number of digits) + secondary tracking task (keeping the stylus in contact with moving light)
adjusted to the same level for elderly, young + AD patients

-Then required to perform the memory span + tracking tasks simultaneously.

  • Young + elderly = equivalent, normal small decrement
  • AD patient= significant decline which increased as the disease progressed
29
Q

Describe Mario Parra’s discovery of familial AD

A

Found a rare genetic form of familial AD found in Colombia–> any family member with the specific gene suffers early-onset AD, typically beginning in their forties.

30
Q

What drugs/methods slow down AD?

A

Donepezil, rivastigmine, and galantamine.
(Done being pleasant, risk vast stigma, galavant)

Operate as inhibitors of cholinesterase–>a substance that breaks down the neurotransmitter acetylcholine.

Acetylcholine tends to be depleted in AD–>drugs resist further depletion.

31
Q

What treatment methods exist for AD

A

The problem of maintaining a sense of personal identity is a prominent disturbing feature of AD.

The problem for patients who need to move to a care home–>surrounded by new + unfamiliar people.

Patients can be taught to use simple memory aids (message boards or calendars) + modify the environment in simple but useful ways.

Reality orientation training (ROT)–>helping patients in the latter stages of dementia maintain orientation in time/place

Reminiscence therapy–>Helps dementia patients cope with their growing amnesia by maintaining a sense of personal identity by recollecting their past by constructing a personal life-story book (photographs + other mementoes)