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Title: Amnesia

Students' amnesia?
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
  • 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

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
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

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)

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)

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.
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.
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.
Serial position curve in Korsakoff-patients
Cermak, Naus, Reale (1976)
  • In general Extremely poor STM, as evidenced by
    serial recall.
  • No primacy effect
  • Overall poor performanc
  • very strong recency effect

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

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
The Amnesic Syndrome Pure 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)

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 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
  • 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

Clinical cases of anterograde Amnesia
  • The infamous Patient H.M. (Bilateral Temporal
  • 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
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//

  • 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)

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

The Amnesic Syndrome, cont. Memory systems and
consciousness (Tulving, E. 1985 Memory and
Consciousness. Canadian Psychologist, 26, 1-12.)
Memory system
Explaining the Amnesic Syndrome
  • Where is the deficit to be located in the course
    of learning?
  • 1. Input
  • 2. Storage
  • 3. Retrieval

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

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.

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
  • 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
  • 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

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

Degraded stimuli

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
  • STO ___ store
  • Instruction Subjects are explicitly told that
    the words stem from the list they had learned

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
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

Explaining the Amnesic Syndrome, cont.
  • 4. Context Deficit Theory Evidence
  • Amnesics and normal subjects had to learn
  • 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

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
    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)

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.

Medial temporal lobe
Figure 7. Axial CT brain scan of a patient with
Alzheimer's disease. http//
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.

  • 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.

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.
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.