Updated for 1999
Lecture Notes - Week 12
RELATIONAL LEARNING-Chapter 15
ANTEROGRADE AMNESIA
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trouble learning new information
RETROGRADE AMNESIA
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trouble remembering old information that preceded the brain injury
KORSAKOFF’S SYNDROME
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thiamine deficiency, caused by alcoholism
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deterioration of mammillary bodies
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profound anterograde amnesia
BILATERAL REMOVAL OF MEDIAL TEMPORAL LOBE – H.M.
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intact intellect
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old learning generally OK, although some retrograde amnesia
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immediate verbal memory OK, but verbal learning is impaired (e.g., new
slang)
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no personality change (unlike Phineas Gage)
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socially appropriate
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not easily bored
Preserved Areas of Functioning in H.M.:
Pre-illness memory
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intact basic knowledge (intellectual, social, linguistic)
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motor/cognitive skills
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personal preferences
New Learning Capacities
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Motor learning - mirror-drawing task
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Repetition priming
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word-stems
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stimulus fragments
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Psychophysiological responses
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electrodermal response
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classical conditioning
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Operant conditioning
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Evaluative responses
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emotional responses preserved as implicit learning (e.g., pin in doctor’s
hand)
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"liking" ratings
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staff member association with "generosity"
CONCLUSIONS DRAWN BY MILNER:
1) hippocampus is not the site of long-term memory storage, nor is it
needed to access long-term memories
2) hippocampus is not the site of immediate (short-term) memory storage
3) hippocampus is involved in converting short-term memories to long-term
DECLARATIVE MEMORIES
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can be consciously recalled as facts, events, or stimuli (explicit)
NON-DECLARATIVE MEMORIES
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not conscious, operate automatically, don’t include facts, but they control
behaviors (implicit)
PRIMING TASK
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showed list of words
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then asked for recall (explicit) or showed first few letters and asked
to say the first word that came to mind (implicit)
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amnesic subjects’ explicit memory was <50% of controls’, but they performed
equally on the implicit task
CA1 OF HIPPOCAMPUS
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can be damaged by anoxia (lack of oxygen)
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contains many NMDA receptors
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various metabolic disturbances cause excessive release of glutamate, resulting
in too much calcium in the cells
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this begins to destroy the neurons
WORKING MEMORY – information about things that have just happened
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radial maze tasks
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rats with lesions of the hippocampus can’t remember which arms they had
already visited
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these rats COULD learn to avoid certain arms that never contained food
(this is what type of learning?)
SPATIAL PERCEPTION AND LEARNING
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Morris milk maze
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rats with hippocampal lesions perform poorly when having to use visual
cues
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these rats will swim directly for the platform, however, if it is in view
(this is what type of learning?)
PLACE CELLS
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recorded from individual pyramidal cells in the hippocampus
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found different neurons had different spatial receptive fields – responding
to visual cues/relationships
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information is provided by pattern of cell responding, neural networks
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even deaf, blind rats can navigate the maze, but not when they’re dizzy!
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study with normal rats in 8-arm radial maze, let them learn the maze, then
had them in the dark
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their "place cells" no longer could provide the mental map, but if light
turned on briefly and then back off, the rats knew their way around
ROLE OF SENSORY STIMULATION
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excitability of hippocampal formation neurons increased by exposure to
enriched environment (long-term potentiation)
HIPPOCAMPUS AND PATTERN COMPLETION
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Carlson’s breakfast example
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asking what he had for breakfast stimulates language association area
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which then triggers hippocampus to "complete the pattern" by pulling the
other bits of information which are stored in various parts of association
cortex
Human Communication - Chapter 16
Broca’s aphasia
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inability to speak due to damage to the inferior left frontal lobe and
underlying subcortical white matter
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speech is slow, non-fluent
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hard time with "function" words (e.g., a, the, in)
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can say "content" words (e.g., nouns, verbs, adjectives)
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3 types of speech deficits produced by damage to Broca’s area:
1. agrammatism - difficulty in using grammatical constructions (e.g.,
-ed, have)
2. anomia - word-finding difficulty
3. articulation problems - mispronunciations
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can comprehend speech much better than they can speak, but still have deficits
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deficits parallel production problems
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understanding grammar, sequence of commands
Wernicke’s aphasia
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inability to understand due to damage to middle and posterior portions
of the superior temporal gyrus of the left hemisphere
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poor speech comprehension; can’t repeat
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production of meaningless speech which is fluent and unlabored
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uses function words but few content words
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they seem unaware of their deficit (unlike Broca’s) Why?
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3 types of speech deficits associated with Wernicke’s aphasia:
1. Recognition of spoken words - "pure word deafness"
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can recognize other sounds (doorbell, etc.)
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can read and write or read people’s lips
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can speak sensibly
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auditory system of left hemisphere specialized for recognition of short
sounds and right hemisphere for long sounds. How do we know that?
2. Comprehension of word meaning - damage to posterior language
area
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damage to this area alone produces "transcortical sensory aphasia"
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people with this disorder can repeat - they can recognize words
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they cannot comprehend the meaning of what they hear and repeat
3. Ability to convert thoughts into words
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people with Wernicke’s aphasia and those with transcortical sensory aphasia
cannot speak sensibly
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Wernicke’s aphasia essentially is the combination of pure word deafness
and transcortical sensory aphasia
Meaning of words is stored in appropriate association cortex
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damage to particular areas creates specific kinds of aphasias
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inability to identify body parts, spatial relationships (e.g., "down"),
etc.
Conduction Aphasia
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damage to arcuate fasciculus, which connects Broca’s and Wernicke’s areas
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meaningful, fluent speech
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relatively good comprehension - but can they repeat?
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very poor repetition
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arcuate fasciculus is pathway to repeat unfamiliar words
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another pathway exists to frontal area from association areas, based on
the meaning of the word, not the sounds
Anomic Aphasia
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generally occur from damage to left temporal/parietal lobes, without involving
Wernicke’s area
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may be considered a partial amnesia for words
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can have specific anomias resulting from damage to particular cortical
areas
Table 16.1 is a VERY nice summary of the above information!
Pure Alexia
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alexia without agraphia;
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lesions that prevent visual information from reaching the visual association
cortex of the left hemisphere
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can recognize words if spelled aloud to them
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it is a perceptual disorder, like pure word deafness
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not the same as visual agnosia - people with visual agnosia can still read,
people with pure alexia can identify objects
Reading
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whole-word reading - direct recognition of the word as a whole
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phonetic reading - sounding word out
Dyslexia - faulty reading
1. surface dyslexia
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deficit in whole-word reading
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make errors based on "surface" of word - how it looks, rather than its
"deeper" meaning
2. phonological dyslexia
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can read by whole-word method, but can’t sound out words
3. spelling dyslexia
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have deficits in both whole-word and phonetic reading
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but still recognize letters and can read words if they say each letter
aloud
4. direct dyslexia
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like transcortical sensory aphasia, except with written words
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can read aloud, but cannot understand what they are reading
5. comprehension without reading
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cannot read
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but can pick correct answer from among choices of labels for a picture
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even though cannot name picture or read aloud the choices
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opposite of direct dyslexia
Writing deficits may involve:
1. problems with motor control
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e.g., can write numbers but not letters, consonants but not vowels, etc.
2. problems with spelling - involves deficits in either:
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audition (sounding things out in your head)
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phonological dysgraphia - can’t write unfamiliar words or pronounceable
nonwords
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visual image (picturing the word in your head)
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orthographic dysgraphia - can only sound out words, not picture
them - trouble writing irregular words
Table 16.2 is a VERY nice summary of the above information!