Amnesia

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Amnesia
Students' amnesia?
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Amnesia
THE ADVANTAGE OF HAVING BAD MEMORY IS THAT YOU
CAN ENJOY GOOD THINGS FOR THE FIRST TIME SEVERAL
TIMES.-FRIEDRICH NIETZSCHE
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Categories of Amnesia

• There exist various criteria for categorizing
  amnesia which are used in combination
• Time based which temporal part of LTM is lost?
  retrograde, anterograde
• Disease based which disease caused it?
• Brain localization where in the brain is the
  lesion?
• Functionally based which memory function is
  affected WM, LTM (semantic, episodic, implicit)
• The purest case of amnesia is the 'amnesic
  syndrome' which has no other cognitive deficits

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1. Time-based

• Retrograde Amnesia Memory loss of events before
  the amnesia began
• Anterograde Amnesia impairment/inability to
  build up novel memories from experiences.
  Prominent in almost all memory deficits

web.lemoyne.edu/.../psy340/graphics/amnesia.jpg
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2. Disease-based

• Closed head injury caused by blow on the head,
  road traffic accidents
• Results in
• Post-traumatic amnesia (PTA) unconsciousness for
  some time, confusion about time/space/ persons
• Retrograde amnesia, which gradually shrinks.
  However, time immediately before the onset of
  amnesia, is typically not remembered
• Anterograde amnesia, almost always present

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2. Disease-based, cont.

• All of the following diseases can cause the
  'Amnesic syndrome', a pure form of amnesia
• Encephalitis Herpes simplex encephalitis (HSE),
  a viral infection causing lesions in the limbic
  regions in the temporal lobe, hippocampus,
  entorhinal, perirhinal, parahippocampal crtices,
  amygdala, and polar limbic cortices (O'Connor
  Verfaille, 2004)

http//homepage.psy.utexas.edu/homepage/class/Psy3
01/Salinas/sec2/Brain/11.GIF
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2. Disease-based, cont.

• Anoxia oxygen deficit due to decreased vascular
  perfusion or reduced oxygen content in the blood,
  caused by e.g., cardiac arrest or respiratory
  distress. Most likely, hippocampal damage is
  involved, but also basal ganglia, thalamus, white
  matter projections and diffuse cortical areas.
  (O'Connor Verfaille, 2004)

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2. Disease-based, cont.

• Wernicke-Korsakoff Syndrome (WKS), short
  Korsakoff-Syndrome, caused by alcohol abuse
• Diagnostic criteria
• dietary deficiencies (thiamine deficit)
• occulomotor abnormalites
• cerebellar dysfunction
• altered mental state
• anterograde amnesia
• Wernicke, because
• Wernicke's encephalopathy
• is also involved.

nawrot.psych.ndsu.nodak.edu/.../image002.jpg
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Korsakoff-Syndrome
Thiamine (vitamin B1) is necessary for memory and
other brain functions. People who drink a lot of
alcohol often replace food with alcohol. As a
result, they take in fewer vitamins, leading to
vitamin deficiencies. In addition, alcohol
increases the body's need for B vitamins while
interfering with its ability to absorb, store,
and use thiamine.
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Brain areas implicated in the Korsakoff syndrome

• The limbic system (hippocampus, amygdale), parts
  of the diencephalons (mammillary bodies of the
  hypothalamus and dorsomedial nucleus within the
  thalamus), and parts of the basal forebrain
  (nucleus basalis of Meynert) are all implicated.

www.u.arizona.edu/.../amnesia_files/carls417.jpg
http//www.benbest.com/science/anatmind/FigVII23.g
if
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Serial position curve in Korsakoff-patients
www.mtsu.edu/.../Cognitive/sts/separate.html
Cermak, Naus, Reale (1976)

• In general Extremely poor STM, as evidenced by
  serial recall.
• No primacy effect
• Overall poor performanc
• very strong recency effect

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2. Disease-based, cont.

• Dietary deficiencies, as happened with British
  soldiers in war captivity in Japan, due to lack
  of thiamine, same effect as in Korsakoff
• Poisoning
• From attempted suicide
• Accidents, intrusion of objects into the brain

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2. Disease-based, cont.

• Cerebrovascular Accident, CVA ( Stroke) through
• Bilateral posterior cerebral artery (PCA)
  infarction. Since the left and right PCA have a
  common source, a stroke in this artery often
  results in a bilateral damage of the temporal
  lobes including hippocampus
• Aneurysm Rupture of the Anterior Communicating
  Artery (AcoA) affects the basal forebrain,
  anterior cingulate, anterior hypothalamus
• (O'Connor Verfaille, 2004)

An occlusion in an artery in the brain may
cause a CVA
www.neurosurgery.ufl.edu/Images/ischemia.jpg
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The Amnesic SyndromePure form of amnesia without
any other cognitive deficiencies

• CharacteristicsWhat remains intact?
• WM usually intact, Memory span OK, also same
  qualitative characteristics, i.e., recency effect
• LTM semantic memory (vocabulary score,
  generating category members) and other general
  intellectual functions, generally intact
• LTM autobiographic memory also intact, but
  amnesic for recent events before onset of amnesia
• LTM procedural, implicit memory also spared
  (motor tasks, perceptual tasks, artificial
  grammar learning)

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The Amnesic Syndrome, cont.Pure form of amnesia
without any other cognitive deficiencies

• Characteristics What is affected?
• LTM anterograde amnesia, episodic memory
  dramatic inability to learn s.th. new after the
  onset of amnesia due to inability to build up new
  episodes, i.e., memories in various modalities,
  sequences of events linked together in a coherent
  whole
• LTM Retrograde amnesia, an inability to retrieve
  information that was learned prior to the onset
  of amnesia if it was not purely semantic or
  implicit memory
• Contingent upon RA impaired temporal
  localization of past experience, as, e.g. in
  Korsakoff, which leads to confabulation

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Clinical cases of anterograde Amnesia

• The infamous Patient H.M. (Bilateral Temporal
  Lobectomy)
• Oliver Sacks Lost Mariner Jimmie G.
  (Korsakoffs Type)
• Oliver Sacks William Thompson (Korsakoffs Type
  with much confabulation)
• Oliver Sacks Stephen R. (Korsakoffs Type)

From PPt on the web, by Ellie Moradi Colin
Schwartz Chris Yco Melissa Bergh
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Amnesic syndrome The patient H.M.

• The Anatomy of Amnesia
• In 1957 W. B. Scoville, a neurosurgeon, reported
  that one of his patients had suffered a dramatic
  loss of memory following surgery for the removal
  of the diseased areas of his brain that were
  causing continuous, prolonged epileptic seizures
  (Scoville Milner, 1957). In the first (and
  nearly the last) operation of its kind, Scoville
  removed the medial portions of both temporal
  lobes, including the hippocampi and amygdalas.
  The patient, H.M., obtained considerable relief
  from the seizures but only at the cost of
  forgetting everything that happened to him only
  minutes after experiencing it. If you were to
  walk into his room, introduce yourself and leave,
  he would have no recollection of your name or
  face when you returned 5 minutes later. H.M.
  shows a little retrograde amnesia, but his major
  symptom is a pervasive anterograde loss. He has
  little trouble recalling the events of his life
  up to the time of his surgery, but from then on
  he has no sense of time passing. Each moment of
  each day exists as an island of experience with
  no idea of what has gone before and no memory of
  what should happen next.
• http//core.ecu.edu/psyc/grahamr/DW_3311Site/Lectu
  reF/Lect3.2.html

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• H.M. has been cared for all this time by his
  mother, who usually accompanies him wherever he
  goes. It so happened, however, that in 1966 the
  mother was in Hartford Hospital, recovering from
  a minor operation, just when H.M. was about to
  leave for Boston. It was his father, therefore,
  who packed H.M.'s clothes for him and brought him
  to meet us at Dr. Scoville's office prior to the
  journey. The father had also taken the patient to
  visit his mother in the hospital that very
  morning, the third such visit within a week. Yet
  when we questioned H.M., he seemed not to
  remember any of these visits, although he
  expressed a vague idea that something might have
  happened to his mother. On the journey to Boston,
  he kept saying that he felt a little uneasy and
  wondered if something might be wrong with one of
  his parents, though he could not be sure which
  one. On being asked who had packed his bag for
  the trip, he said "Seems like it was my mother.
  But then that's what I'm not sure about. If there
  is something wrong with my mother, then it could
  have been my father." Despite our explaining the
  situation to him repeatedly during the journey,
  H.M. was never able to give a clear account of
  what had happened, and was still feeling "uneasy"
  when he reached Boston, wondering if something
  was "wrong" with one of his parents. Gradually,
  this uneasiness wore off, and although he was
  told repeatedly that he could telephone home any
  time he wished, he no longer seemed to know why
  he should do so. Next day he appeared completely
  unaware that there had been any question of
  illness in his family. (Milner et al., 1968)

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Theoretical implications

• 1. The Amnesic Syndrome had been one crucial
  piece of evidence for the separation of Short
  and Long Term Memory
• 2. The observation of spared implicit learning
  and memory in amnesics has led to a distinction
  between explicit and implicit processes in normal
  subjects, too
• 3. Further fractionation of LTM into semantic,
  episodic, and implicit/procedural memory

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The Amnesic Syndrome, cont.Memory systems and
consciousness(Tulving, E. 1985 Memory and
Consciousness. Canadian Psychologist, 26, 1-12.)
Memory system
Consciousness
Episodic
Autonoetic
Semantic
Noetic
Anoetic
Procedural
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Explaining the Amnesic Syndrome

• Where is the deficit to be located in the course
  of learning?
• 1. Input
• 2. Storage
• 3. Retrieval

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Explaining the Amnesic Syndrome, cont.

• 1. Input theories
• In the spirit of the 'levels of processing'
  hypothesis, it has been suggested that amnesics
  do not spontaneously encode material at the deep
  level of processing, e.g., in terms of semantics.
• Evidence
• Amnesics are good at detecting consecutive
  rhyming words in long lists of items but bad at
  detecting words from the same semantic category
• BUT presumably amnesics had already forgotten the
  previous word before they could realize a
  semantic similarity in the first place.
• --gt floor effect

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Explaining the Amnesic Syndrome, cont.

• 'Deep-level-of-encoding deficit'
• Counter-evidence
• When giving amnesics enough time/training to
  encode the items semantically they do show the
  standard levels of processing effect.

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Explaining the Amnesic Syndrome, cont.

• 2. Storage, Consolidation of Memory traces
• Maybe amnesics learn normally but forget faster
  due to inadequate consolidation of memory traces?
• Evidence
• They forget information after a short time
  interval
• BUT
• Their initial level of performance is based on
  WM, not LTM, so there was no LT learning in the
  first place, hence, there is no evidence for LTM
  forgetting.
• Counter-evidence
• If stimulus material is presented to the amnesics
  longer so that the level of initial learning is
  high, they show equal forgetting rates as normal
  subjects

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Explaining the Amnesic Syndrome, cont.

• 2. Storage, Consolidation of Memory traces
• Counter-evidence
• If learned words are tested by identifying
  degraded word forms, amnesics were as good as
  normal subjects

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Degraded stimuli

• BADGE
• BADGE

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Explaining the Amnesic Syndrome, cont.

• 3. Retrieval The interference hypothesis
  (Warrington, E.K. Weiskrantz, L. (1970).
  Amnesic syndrome Consolidation or retrieval?
  Nature, 228, 628-630.)
• Maybe amnesics suffer from interference (e.g.,
  proactive interference, PI)?
• Evidence
• Amnesics are good at tasks with partial cueing,
  presumably because partial cueing avoids
  interference between items. The cues rule out
  competing items fromearlier learning. If such
  cues had not been given, their performance would
  have been worse due to interference. They had to
  learn a list of words, including STORE. When cued
  with a part of the word, they can complement it
  easily
• STO ___ store
• Instruction Subjects are explicitly told that
  the words stem from the list they had learned
  immediately.

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Counter-evidence Letter cueing Amnesics and
normal subjects had to learn to respond to 1st
list cyc --gt cyclone 2nd list cyc --gt
cycle Amnesics showed equivalent performance on
the first transfer trial as normal subjects. The
interference hypothesis would have predicted
greater difficulty with the 2nd list since the
new pairing would interfere with the old
pairing. Priming Same procedure as cued recall
but instruction differs no mentioning of the
learning task and of the list, subject is just
asked to fill in the missing letters with words
that come to their mind immediately Their
memory defect shows only when they are making a
conscious effort to remember
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Explaining the Amnesic Syndrome, cont.

• 4. Context Deficit Theory
• Maybe amnesics cannot learn the contextual cues
  that go along with the to-be-remembered stimulus
  which impedes memory
• intrinsic context features that are an integral
  part of the stimulus itself, e.g., its meaning
• extrinsic context features that are incidentally
  associated with the stimulus, e.g., time/place of
  learning. These cues are important for episodic
  memory

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Explaining the Amnesic Syndrome, cont.

• 4. Context Deficit Theory Evidence
• Amnesics and normal subjects had to learn
  pictures
• D1F1 (on Day 1, picture presented 1 time)
• D1F3 (on Day 1, picture presented 3 times)
• D2F1 (on Day 2, picture presented 1 time)
• D2F3 (on Day 2, picture presented 3 times)
• After learning on day 2, they were shown pictures
  from D1 and D2 and had to indicate if these
  picture were from D1 or D2
• All subjects were best for D2F3.
• Normal subjects discriminated all other pictures
  according to days.
• Amnesics, however, placed D1F3 as often on D2 as
  they did with D2F1, suggesting that their
  judgement was based on overall familiarity rather
  than distinct contextual cues, as is typical of
  episodic memory

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A modal model of amnesia (Baddeley, 1997)

• Warrington Weiskrantz as well as Baddeley
  suggest that amnesics have a deficit in relating
  two pieces of information
• 1. the content of learning. They can learn s.th.
  as in procedural/implicit learning but they
  cannot learn
• 2. cognitive links between previously separate
  events which are normally created in the process
  of episodic learning. These conscious links
  between novel experiences have to be stored, too.
  They include contextual links but are not
  restricted to them.
• Evidence Amnesics are good at learning
  high-association pairs (for which they have the
  links already) but poor on low-association pairs
  (for which the links still have to established
  and stored)

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Brain localization

• 1. Unitary, circuit view of amnesia All
  structures of the limbic system
• diencephalon
• medial temporal lobe
• mamillary bodies, mamillo-thalamic tract
• hippocampus, amygdaga
• play the same role in amnesia, damage to any of
  them causes the same kind of amnesia.

http//homepage.psy.utexas.edu/homepage/class/Psy3
01/Salinas/sec2/Brain/11.GIF
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Diencephalon
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Medial temporal lobe
Figure 7. Axial CT brain scan of a patient with
Alzheimer's disease. http//www.ipa-online.net/ip
aonlinev3/ipaprograms/guidetoaddiagnosis/section2.
asp
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Brain localization

• 2. Different components of the limbic system have
  different functions, hence, selective impairment
  leads to qualitatively different forms of amnesia
• Evidence
• temporal lobe TL damage (herpes simplex) vs.
  Diencephalic amnesia (Korsakoff) Patient H.M. Is
  the classical case of diencephalic A (although no
  Korsakoff-case). He had lost both hippocampi.
• TL patients learn less effectively and forget
  more rapidly than Kosakoffs.
• --gt no unitary view of amnesia
• Problem not only two different brain areas
  affected but also two different disease types.

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• Immediately after being struck, the player has
  complete recall of the play and the concussive
  impact, but a few minutes later the memory of
  both is lost (Newcombe, 1980). STM memory seems
  to be functioning, but there is apparently no
  consolidation to LTM.

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Posthypnotic amnesia
Consider, for example, posthypnotic amnesia the
phenomenon which gave hypnosis its very name.
After receiving appropriate suggestions, many
highly hypnotizable subjects come out of hypnosis
unable to remember the events and experiences
which transpired while they were hypnotized.
socrates.berkeley.edu/.../redis19.gif
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Posthypnotic amnesia
No conscious recall of stimuli under hypnosis
Normal priming effect
Normal recall after cancelling hypnosis
For example, subjects who have studied a list of
animal names while hypnotized will be unable to
remember them afterward. However, these
unremembered items will also give rise to priming
effects if asked to generate names of animals,
subjects will be more likely to give the names
they studied, compared to instances that they did
not encounter in hypnosis. Moreover, after the
amnesia suggestion has been canceled by a
prearranged reversibility cue, the subject will
regain perfect conscious memory for the studied
list. The reversibility of amnesia indicates
that, in contrast to the organic amnesias
associated with hippocampal damage, posthypnotic
amnesia reflects a deficit in retrieval rather
than encoding. But the preserved priming effects
show that the retrieval deficit affects explicit,
but spares implicit, expressions of memory.
socrates.berkeley.edu/.../redis19.gif