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PSY 335
Memory and Amnesia
Memory Disorders
Influences on Memory
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Alcohol – Bits & Pieces
Stress -- Kolb & Whishaw Seg 32 (CD 2)
Diabetes – Kolb & Whishaw Ch 13 Seg 6
(CD 3)
Kinds of Memory Disorders
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Organic – having a physical cause
Functional – having a psychological
cause
Dys (as a prefix) means difficulty or
limited ability to perform.
A (as a prefix) means complete inability
or lack of a function.
Alcohol & Memory
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Alcoholic amnesia – alcohol prevents
consolidation so nothing is remembered and
no memory can be recovered.
Alcoholic blackout – state-dependent memory,
so recall is possible if one is back in the same
state.
Because many crimes are committed while
drunk, memory failure is frequently blamed on
alcohol.
Sleep & Memory

New sleep studies suggest a "memory lifecycle” with three stages - stabilization,
consolidation, and re-consolidation.
•
•
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Initial stabilization takes up to 6 hours.
Sleep needed for consolidation, deep non-REM
Alcohol disrupts consolidation
Sleep deprivation produces effects similar to
aging.
•
Procedural memory and recognition memory are most
strongly affected.
Sources of Organic Dysfunction

Accident
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Disease
• Car accidents and other injuries (e.g., N.A.)
• War
• Encephalitis (viral) – inflammation of the lining
•
•
•
of the brain, causing swelling.
Stroke
Alzheimer’s disease
Korsakov’s syndrome (prolonged alcoholism)
Alzheimer’s Disease

A fatal degenerative disease caused by
cell failure – neurofibrillary tangles and
plaques that interfere with cell function.
• All areas of the brain are eventually affected,
but frontal lobes and memory go first.

Confusions and memory problems do
not resemble normal aging, amnesia or
other memory problems.
Classification of Disorders
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
See Rivermead Behavioural Memory Test
(RBMT) pg 263, Table 11.1 and Wechsler
Memory Scale -- tests used to assess
memory problems.
Disorders classified by type of symptom:
• Generalizing – confusion, fuzziness, mental
•

slowing.
Localizing – few generalizing symptoms but
impairment of specific functions.
Clusters of symptoms are a syndrome.
• Concern about symptoms is a symptom itself.
Frontal Lobe Deficits
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Confabulation – production of a false
memory.
• Momentary confabulation – responses that
•
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could be correct.
Fantastic confabulation – responses clearly
fictional.
Source amnesia – fact is remembered
but not the source.
Memory of temporal order.
Frontal Lobe Deficits (Cont.)
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Impaired recall – more “ugly stepsisters,”
no categorization.
Metamemory is impaired, including FOK
(feeling of knowing) judgments and
monitoring of search.
False recognization:
• Increased false alarms
• Increased intrusions
Frontal Lobe Deficits (Cont.)
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Faulty encoding and poor representation
may be a cause of poorly focused
search.
• Information is needed to guide search.


The left frontal lobe guides encoding.
The right frontal lobe guides retrieval.
Frontal Lobe Deficits (Cont.)
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Emotional deficits:
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Impaired awareness of memory loss:
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If confabulations are believed by others,
there is no feedback on normalcy.
• Cognitive apathy, lack of motivation
• Flattened affect
• Inaccurate assessment of performance
• Lack of distress
Alien Hand (Anarchic Hand)
Syndrome – a Frontal Lobe Deficit
Peter Sellars in
“Dr. Strangelove:
or How I learned to
story worrying and
love the bomb”
Damage to the Parietal
Association Cortex

Confusion about directions, inability to use
words describing spatial relations:
•
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Under, up, down
Inability to name body parts or point to parts of
the body.
Capgras syndrome (rt. Posterior parietal)
inability to recognize close family members
•
•
Sometimes animals or even furniture
Invasion of the body snatchers
Reading & Writing Disorders
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Alexia – inability to read
Agraphia – inability to write
Caused by damage to the left angular
gyrus which integrates information from
the sensory modalities.
Pure Word Deafness
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A person can hear and speak, read and
write normally but cannot understand
speech.
Occurs with bilateral destruction of the
auditory cortex or disconnection from
Wernicke’s area.
Because Wernicke’s area is not
damaged, speech produced is OK.
Perceptual Deficits
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Aphasia – involves inability to name
something.
Agnosia – involves inability to recognize
something.
Visual agnosias – inability to combine
individual visual impressions into
complete patterns.
Types of Visual Agnosias
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Object agnosia – inability to recognize
common objects.
Prosopagnosia – inability to recognize
faces. Kolb & Wishaw Disc 3, segment 1
Color agnosias:
• Achromatopsia (cortical color blindness)
• Color anomia – inability to name colors.
• Color agnosia – inability to recognize colors
Other Agnosias
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Amusia – tone deafness, melody
deafness, disorders of rhythm, measure,
tempo.
Astereoagnosia – inability to recognize
the nature of an object by touch.
Asomatoagnosia – knowledge of one’s
own body.
• Indifference to illness, asymbolia for pain
Pure Anomia

Loss of memory of words (anomic
aphasia)
• Cannot name pictures of common objects
• Difficulty reading and writing
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
Produced by damage to either Broca’s or
Wernicke’s area (fluent anomia).
Use circumlocutions to get around
missing words.
Broca’s Aphasia
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Broca’s area may contain memories of the
movements needed to produce speech.
Produces three deficits:
•
•
•
Anomia – word-finding difficulty
Agrammatism – loss of grammatical construction
Difficulty with articulation
Slow, laborious, nonfluent speech without
function words with with content words.
Conduction Aphasia
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
Disruption of verbal short term memory
due to damage to the subcortical axons
that connect Broca & Wernicke’s areas.
Results in poor repetition – only
meaningful words can be repeated
(through other means).
• Non-words cannot be repeated (blaynge).
Amnesic Syndrome
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Short term memory is intact (unimpaired)
Anterograde amnesia present affecting
both recognition and recall tasks.
Retrograde amnesia present, but extent
varies.
Semantic memory largely intact but can
be affected by antero & retro amnesias.
Procedural memory is intact.
Causes of Amnesic Syndrome
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Damage to:

Herpes simplex encephalitis
Korsakoff’s syndrome (thiamine
deficiency plus chronic alcoholism)
Direct injury (H.M., N.A.)
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• Hippocampus
• Temporal cortex (adjacent to hippocampus)
• Diencephalon (especially mamillary bodies)
Anterograde Amnesia
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No new declarative information can be
added to long-term memory
Events from the present are quickly
forgotten
Usually accompanied by retrograde
amnesia.
Performance on IQ tests is unimpaired
because it relies on info learned in past.
Retrograde Amnesia
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
Declarative information from the past is
forgotten.
Information is forgotten in a temporal gradient
(based on time):
•
•
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Ribot’s law – newer information forgotten first.
Both semantic and episodic information show this
gradient.
Difficult to test due to differences in life
experiences, impairment varies.
Focal Retrograde Amnesia
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Loss of remote memory unaccompanied
by anterograde amnesia.
May occur when the temporal cortex is
damaged but not the hippocampus.
Cases reported without head injury and
with loss of procedural memory are
probably malingering (faking).
Evidence for Implicit Memory
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Alzheimer’s patients show impaired
priming.
Huntington’s Chorea patients show
normal priming but impaired procedural
memory.
Procedural memory and priming are
spared by amnesia.
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