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Lecture 3: Memory Disorders Flashcards

1
Q

What is Memory?

A

The retention (storage) of information that can be revealed at a later time

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2
Q

How was knowledge preserved from the 5th - 10th century AD?

A

Through oral tradition teaching

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3
Q

How was knowledge preserved in the 15th century?

A

The printing press

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4
Q

Why does it make sense to want to fix dementia?

A

Because dementia is a major cause of memory loss and costs a lot of money

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5
Q

What did Hermann Ebbinghaus do?

A

Used himself and developed the first methods for assessing learning and memory of a controlled experience

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6
Q

Who developed the first methods for assessing learning and memory of a controlled experience?

A

Hermann Ebbinghaus

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7
Q

What constituted Ebbinghaus’s method for assessing memory?

A

He made himself remember nonsense syllables and found that he could recall less and less nonsense syllable as time passed

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8
Q

What are the characteristics of STM?

A

They have rapid decay and they are vulnerable to disruption

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9
Q

What are the characteristics of LTM?

A

They have a slow decay and are less vulnerable to disruption

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10
Q

What causes the consolidation of STM?

A

Rehearsal and practice

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11
Q

What is Reconsolidation?

A

When LTM can be can be retrieved to be updated

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12
Q

What happens to LTM once it enters Reconsolidation?

A

It enters the volatile short term state before going back to LTM

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13
Q

What is the state of LTM?

A

It is in an inactive state

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14
Q

What are the two reasons memory can be disrupted?

A
  • Storage failure

* Retrieval failure

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15
Q

What is the amnesia like in Storage Failure?

A

The amnesia is permanent

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16
Q

What is the amnesia like in Retrieval Failure?

A

The amnesia is temporary

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17
Q

What occurs in Retrieval failure?

A

The memory is there its just that the brain mechanisms in pulling out that memory are impaired

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18
Q

What do the Seven Sins of Memory highlight?

A

The fragility and plasticity of the brains memory systems

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19
Q

What are the Seven Sins of Memory?

A
  • Transience
  • Absent-mindedness
  • Blocking
  • Misattribution
  • Suggestibility
  • Bias
  • Persistence
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20
Q

What is Transience?

A

The weakening of memory over time

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21
Q

What is Absent-mindedness?

A

Deficient interface between attention and memory (when we don’t pay enough attention to a certain task or event so we don’t remember the event)

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22
Q

What is Blocking?

A

Failed search for info (tip of the tongue)

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23
Q

What is an example of blocking?

A

Proper name anomia

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24
Q

What is Misattribution?

A

Assigning a memory to an incorrect source

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25
What is suggestibility?
When memories are implanted (a memory is false but they believe it to be true)
26
What is Bias?
When personal beliefs influence memories
27
What is Persistence?
Repeated recall of specific memories ex. PTSD
28
What is Psychogenic Amnesia?
Amnesia with no physical cause
29
What is Retrograde Amnesia?
Memory loss for events occurring prior to the trauma (very old memories are intact)
30
What is Anterograde Amnesia?
Inability to form new memories
31
What is amnesia like in the real world?
A mix of anterograde and retrograde
32
What are some physical causes of Amnesia?
* Stroke * Viral infection * Tumours * Closed head injury * Thiamine deficiency * Age-related neurodegeneration
33
Why can a stroke cause amnesia?
Because in a stroke temporal lobes are highly susceptible to cerebrovascular injury
34
Where in the brain are tumours common?
In the brain ventricles
35
How can a closed head injury cause amnesia?
The skull is intact but the brain twists on its axis
36
What is the cause of Korsakoff's syndrome?
Thiamine deficiency
37
What is the first task when treating dementia?
Establishing whether amnesia is organic (due to injury of the brain) or psychogenic (psychological basis)
38
How do clinicians determine whether amnesia is organic or psychogenic?
By looking at the patient's medical record and assessing behavior
39
How do clinicians assess neurophysical status?
By using batteries of tests for disorders of attention, perception, emotions, and sensorimotor processing
40
What is the ultimate goal of the batteries of test when diagnosing amnesia?
To determine how extensive, or specific the memory deficits are
41
Why is it difficult to assess retrograde amneis?
Because patients memories of past personal events are being screened
42
What law is used in Retrograde amnesia?
Ribot's law
43
What is Ribot's law?
Recent memories are lost first and older memories are the most resilient
44
What two tests are used to assess Retrograde Amnesia (RA)?
* Boston Remote Memory Test | * Dead or Alive Test
45
What happens in the Boston remote memory test?
They ask about memories of public events like the challenger explosion
46
What occurs in the Dead or Alive test?
They ask the patient whether a famous person is still living
47
What test is used to asses Anterograde Amnesia?
David Wechsler's memory scale revised
48
Why is the Wechsler Scale more objective?
Because it doesn't depend on the recall of personal experience
49
What kind of questions does the Wechsler Scale ask?
Age, DOB, draw a figure from memory, count backwards from memory, read a story then recall what happens.
50
What did Korsakoff observe before coming up with Korsakoff's Syndrome?
He observed that alcoholics were incapable of new learning
51
What is Korsakoff's syndrome caused by?
Deficiency of thiamine (B1)
52
What occurs in Korsakoff's Syndrome?
Alcohol inhibits gut absorption of B1 and alcohol also causes chronic liver disease and the liver is then unable to store B1
53
What is B1 important for?
Brain glucose metabolism, transmitter synthesis (ACTh, GABA)
54
What is Korsakoff's syndrome alleviated by?
High doses of B1
55
Which parts of the brain is affected by Korsakoff's Syndrome?
* Mamillary bodies * Mediodorsal thalamic nuclei * Temporal lobes (sometimes)
56
What do the Mammillary bodies connect to?
They connect to the hippocampus
57
What does the Mediodorsal thalamic nuclei connect to?
They connect the the prefrontal cortex to the thalamus
58
What does damage to the mammillary bodies cause?
Anterograde amnesia
59
What does damage to the Mediodorsal thalamic nuclei do?
Leads to amnesia for autobiographical amnesia
60
What are the characteristics of Amnesic Syndrome?
* Intact short term and semantic (general facts about the world) memory * General intellect is intact * Intact procedural and perceptual learning * Severe anterograde amnesia * Variable degree of retrograde amnesia * Selective failure of episodic memory (personal events)
61
What are the two explanation for Amnesic Syndrome?
1. Failure to store contextual information needed to distinguish different memories 2. Deficit in memory consolidation (temporal lobe amnesia)
62
What are the symptoms of frontal lobe damage?
1. Confabulation 2. Source amnesia 3. Unable to specify memories in detail 4. Impaired STM
63
What is Confabulation?
Production of false memories
64
What is source amnesia?
Forgetting knowledge source (but memory is accurate)
65
What is the key structure within the mediotemporal lobe required for memory consolodation?
The hippocampus
66
What does the hippocampus mediate?
The formation of new declarative memories
67
What is declarative memory?
Memory of facts, events and data
68
What is Procedural memory?
How to do things
69
What are the two types of Long Term Memory?
* Declarative memory | * Procedural memory
70
What are the two types of Declarative memory?
* Episodic memory | * Semantic memory
71
What is Episodic Memory?
Personal experiences
72
What is Semantic Memory?
General factual info (ottawa is the capital)
73
What did patient H.M. who had his hippocampus removed uncover?
The memory systems
74
What did patient H.M. have done to him?
He had hippocampus removed
75
What kind of amnesia did patient H.M. after having his hippocampus removed?
Anterograde amnesia
76
What symptoms did H.M. have after having his hippocampus removed?
* No recall of past learning trials | * No ability to make new declarative memories
77
What is the theory about how the Mediotemporal hippocampal system affects new memories?
When a new memory is formed it has certain elements (auditory, visual, olfactory) in the cortical lobes and the MTH binds together the elements and a new memory is formed. Overtime the MTH is no longer needed because the connections between the elements are strengthened
78
Why can't patient H.M. form new memories?
Because he has no MTH
79
What does destruction of CA1 of the hippocampus cause?
Anterograde amnesia
80
What is the pathway
81
What is the pathway from disease to lab bench to clinic?
Genetically modified mice are created that either over express or knock out a gene that encodes proteins that are believed to be linked to a brain disorder and scientists basically try to treat these mice and if they are successful it goes to clinic
82
What did Eric Kandel do?
* Linked synaptic plasticity to learning | * Showed CREB is critical for LTM
83
What is synaptic plasticity linked to?
Learning
84
What is critical for LTM?
CREB
85
What did Bliss and LeDoux discover?
Synaptic strengthening in the hippocampus
86
How does CREB help with LTM?
NMDA allows calcium into the cell which activates kinases. The kinases phosphorylates proteins like CREB. CREB is a transcription factor which can activate transcription of genes into MRNA which create proteins
87
What is crucial for memory storage?
Synaptic plasticity
88
What are the three "memory enhancer" drugs?
* AMPAkines * PDE Inhibitors * Activators of nAChRs/Cholinesterase Inhibitors
89
What are AMPAkines?
Drugs that enhance ion flow through AMPA receptor channels (ex. Racetams). Which allows more calcium into the cell to activate cAMP and kinases to be activated
90
What does cAMP do?
Binds to PKA and activates it
91
How do PDE Inhibitors work?
They increase cAMP levels by inhibition of breakdown ex. Rolipram, mesembrine
92
How do Activators of nAChRs or Cholinesterase inhibitors work?
They increase activation of nAChRs or increase levels of ACh at the synapse
93
What does cAMP do?
Binds to PKA and activates it so it can activate CREB

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