Lecture 16 - Memory and Perception Flashcards

1
Q

How is memory not a single function?

A
  • Memory is not a single function
  • Episodic – memory of specific events e.g. where you were during 9/11
  • Semantic – memory for facts e.g. dopamine hypothesis
  • Working – short term, rehearsal e.g. phone numbers (briefly)
  • Procedural – motor memory e.g. riding a bike/playing piano
  • These types of memory can be dissociated from each other and disrupted independently
  • (E.g. by different types of lesion)
  • Damage to memory is often referred to as amnesia
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2
Q

Describe the neurology of memory

A
  • Hippocampus, amygdala and related structures in the medial temporal lobe (MTL)
  • Medial = inside
  • Fornix = major output of the hippocampus
  • Mammillary body = further output ~ pushing towards thalamus (information relay station)
  • Amygdala = emotion processing
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3
Q

What is anterograde amnesia?

A
  • Poor ability to acquire new information
  • Information acquired before damage is relatively spared, especially further back in time
  • Also, information in working memory (ongoing rehearsal) is spared
  • Specifically:
  • Impaired declarative (explicit) memory: episodic and semantic
  • Relative preservation of non-declarative (implicit) memory:
  • perceptual (familiarity with stimuli)
  • procedural (motor skills & habits)
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4
Q

What causes anterograde amnesia?

A

Disorders e.g. Korsakoff’s syndrome
- Thiamine (vitamin B1) deficiency
- Due to alcoholism: poor diet and impaired absorption of thiamine from intestine
- Produces bilateral degeneration of mamillary bodies
Temporal lobectomy (1950s)
- E.g. for patients with intractable seizures
- Bilateral removal of temporal lobes

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5
Q

Who was HM?

A
  • Henry Molaison (1926-2008)
  • Major seizures (epilepsy) since 16 years of age
  • Drugs failed to contain seizures
  • Surgical bilateral removal of anterior hippocampal regions at age 27 (1953)
  • Important case in neuropsychology of memory:
  • Circumscribed lesion (surgical)
  • Surgery successful in combating epilepsy
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6
Q

What were some of HM’s deficits?

A
  • Pure deficits: IQ unaffected by surgery, no personality change or other deficits outside memory
  • Even within memory, deficits are specific to the formation of new memories
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7
Q

What happened to HM’s working memory?

A
  • Intact working memory:
  • Normal digit span (e.g. repeat the sequence: 5 3 8 2 9 1 6)
  • Unless interrupted (constant rehearsal)
  • Rate of forgetting within normal range
  • Can hold a conversation, but later that day will not remember having held it
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8
Q

What happened to HM’s semantic and episodic memory?

A
  • Semantic memory disrupted, absence of new episodic memory:
  • Language essentially frozen in 50’s
  • Reported date and age as prior to operation
  • Could not remember events or people met post-operation
  • Could not learn location of new home
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9
Q

What happened to HM’s ability to learn new motor skills?

A
  • Could learn new motor tasks
  • E.g. typical improvement on mirror tracing task (Milner 1962, 1965)
  • Improvements in short term. Lost when pushed to LTM
  • Deficits specific to semantic & episodic memory
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10
Q

What are dissociations (experimental design)?

A
  • Some tasks impaired, while others spared
  • Suggests these tasks use different resources or regions
  • E.g. semantic dementia patients: impaired semantic, spared episodic
  • Problem: maybe one task is more difficult, so it will always fail first
  • “Solution”: Double Dissociations
  • One patient group: Task A spared, Task B impaired
  • Other patient group: Task A impaired, Task B spared
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11
Q

What is the difference between anterograde and retrograde amnesia?

A
  • Anterograde = since lesion
  • Retrograde = prior to legion
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12
Q

Describe the neurology of retrograde amnesia

A
  • Hippocampus, amygdala and related structures in the medial temporal lobe (MTL)
  • More amygdala-driven than hippocampus-driven
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13
Q

How was HM affected by retrograde amnesia?

A
  • Temporally graded retrograde amnesia:
  • Old memories (childhood) intact
  • Memories immediately before lesion lost e.g. forgot death of favourite uncle in 1950
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14
Q

What do patients like HM suggest about the neurology of memory?

A
  • Patients like HM suggest that the hippocampus does not store memories - old memories are preserved
  • Role of hippocampus in memory not yet completely understood
  • It may enable consolidation of new memories, which are stored elsewhere
  • This consolidation process must take time possibly decades
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15
Q

What is the consolidation timeline?

A
  • Testing retrograde amnesia:
  • HM: photos of celebrities suggest retrograde amnesia spans decades, with more distant memories relatively preserved (Marslen-Wilson & Teuber, 1975)
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16
Q

Describe the neurology of vision

A
  • Occipital lobes and surrounding temporal and parietal
  • Including PVC, ventral and dorsal streams
  • Damage to these systems can cause agnosia (damage to the ventral) or optic ataxia (damage to the dorsal)
  • Agnosia = the inability to recognize. A lack of knowing or perception
  • Optic ataxia = deficits in spatial perception, visuospatial processing and visual guidance of action
17
Q

What is visual agnosia?

A
  • Agnosia = the inability to recognise. A lack of knowing or perception
  • Agnosia can come in many flavours; visual, auditory, somatosensory etc.
  • Modality specific: individuals with visual agnosia would be able to name an object through touch
18
Q

What are the two types of visual agnosia?

A
  • Types of visual agnosia:
  • Apperceptive: unable to perceive full shape of object despite intact low-level processing
  • Associative: ability to perceive shape, but inability to recognize it, e.g. to name it
  • Visual agnosia not due to deficit in ‘early’ perception: e.g. acuity, field cut, loss of colour vision
19
Q

Describe apperceptive visual agnosia

A
  • Unable to perceive full shape of object despite intact low-level processing. Inability to extract global structure
  • Intact low-level perception
  • Acuity
  • Brightness discrimination
  • Color vision
  • Evidenced by impairments in drawing, copying and visual recognition, even of common objects
  • Can see parts, but not whole
  • Patient D.F – reason we know so much about dual stream visual processing
20
Q

Describe associative visual agnosia

A
  • Intact ability to recognise the whole form of shapes
  • No problem copying figures
  • However, inability to draw from verbal instruction or to recognize objects using vision.
  • E.g. a bike described as “a pole with two wheels” or a farmer observing a picture of a cow, which he couldn’t name, made “milking” movements with his hands. These movements signalled to him that he was looking at a cow
21
Q

What is prosopagnosia?

A
  • Can be characterized into two types: associative and apperceptive
  • Apperceptive prosopagnosia is defined as the inability to even perceive and cognitively process faces
  • Associative prosopagnosia is defined as inability to recognize or apply any meaning to the face, despite perceiving it (can still identify individuals through voice, hairstyle etc.)
  • Tends to involve damage to the fusiform gyrus in the lower part of the occipital and temporal lobe
  • Usually right-sided
  • ‘Fusiform face area’ (FFA) = renamed as a face area due to so many corroborating studies
22
Q

Are faces special? (experts)

A
  • We are experts at processing faces
  • Faces tend to include all the same features (eyes, nose, mouth), and very similar features are present in different individuals (e.g. family members), but we still recognize individuals well
  • The particular configuration of features is unique to an individual
  • Face-processing involves perception of the configuration as well as the features
  • A specialized face-processing system in the brain may process faces ‘holistically’ (as a whole), including configural information
23
Q

Are faces special? (difficult)

A
  • Faces are just difficult
  • Most ‘prosopagnosics’ have difficulty recognizing differences within other categories e.g. types of car, breed of dog, cows in a herd (when we see similar but different of)
  • The FFA is not only concerned with faces:
  • Also active when observing pictures of birds or cars (Gauthier et al., 1999, 2000)
  • If faces are special, why are ‘pure’ prosopagnosics so rare?
  • The idea that faces are ‘special’ (with dedicated neural & cognitive processing systems) is still controversial