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Neuro > Lecture 3: Memory Disorders > Flashcards

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
Q

What is suggestibility?

A

When memories are implanted (a memory is false but they believe it to be true)

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26
Q

What is Bias?

A

When personal beliefs influence memories

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27
Q

What is Persistence?

A

Repeated recall of specific memories ex. PTSD

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28
Q

What is Psychogenic Amnesia?

A

Amnesia with no physical cause

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29
Q

What is Retrograde Amnesia?

A

Memory loss for events occurring prior to the trauma (very old memories are intact)

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30
Q

What is Anterograde Amnesia?

A

Inability to form new memories

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31
Q

What is amnesia like in the real world?

A

A mix of anterograde and retrograde

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32
Q

What are some physical causes of Amnesia?

A
  • Stroke
  • Viral infection
  • Tumours
  • Closed head injury
  • Thiamine deficiency
  • Age-related neurodegeneration
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33
Q

Why can a stroke cause amnesia?

A

Because in a stroke temporal lobes are highly susceptible to cerebrovascular injury

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34
Q

Where in the brain are tumours common?

A

In the brain ventricles

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35
Q

How can a closed head injury cause amnesia?

A

The skull is intact but the brain twists on its axis

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36
Q

What is the cause of Korsakoff’s syndrome?

A

Thiamine deficiency

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37
Q

What is the first task when treating dementia?

A

Establishing whether amnesia is organic (due to injury of the brain) or psychogenic (psychological basis)

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38
Q

How do clinicians determine whether amnesia is organic or psychogenic?

A

By looking at the patient’s medical record and assessing behavior

39
Q

How do clinicians assess neurophysical status?

A

By using batteries of tests for disorders of attention, perception, emotions, and sensorimotor processing

40
Q

What is the ultimate goal of the batteries of test when diagnosing amnesia?

A

To determine how extensive, or specific the memory deficits are

41
Q

Why is it difficult to assess retrograde amneis?

A

Because patients memories of past personal events are being screened

42
Q

What law is used in Retrograde amnesia?

A

Ribot’s law

43
Q

What is Ribot’s law?

A

Recent memories are lost first and older memories are the most resilient

44
Q

What two tests are used to assess Retrograde Amnesia (RA)?

A
  • Boston Remote Memory Test

* Dead or Alive Test

45
Q

What happens in the Boston remote memory test?

A

They ask about memories of public events like the challenger explosion

46
Q

What occurs in the Dead or Alive test?

A

They ask the patient whether a famous person is still living

47
Q

What test is used to asses Anterograde Amnesia?

A

David Wechsler’s memory scale revised

48
Q

Why is the Wechsler Scale more objective?

A

Because it doesn’t depend on the recall of personal experience

49
Q

What kind of questions does the Wechsler Scale ask?

A

Age, DOB, draw a figure from memory, count backwards from memory, read a story then recall what happens.

50
Q

What did Korsakoff observe before coming up with Korsakoff’s Syndrome?

A

He observed that alcoholics were incapable of new learning

51
Q

What is Korsakoff’s syndrome caused by?

A

Deficiency of thiamine (B1)

52
Q

What occurs in Korsakoff’s Syndrome?

A

Alcohol inhibits gut absorption of B1 and alcohol also causes chronic liver disease and the liver is then unable to store B1

53
Q

What is B1 important for?

A

Brain glucose metabolism, transmitter synthesis (ACTh, GABA)

54
Q

What is Korsakoff’s syndrome alleviated by?

A

High doses of B1

55
Q

Which parts of the brain is affected by Korsakoff’s Syndrome?

A
  • Mamillary bodies
  • Mediodorsal thalamic nuclei
  • Temporal lobes (sometimes)
56
Q

What do the Mammillary bodies connect to?

A

They connect to the hippocampus

57
Q

What does the Mediodorsal thalamic nuclei connect to?

A

They connect the the prefrontal cortex to the thalamus

58
Q

What does damage to the mammillary bodies cause?

A

Anterograde amnesia

59
Q

What does damage to the Mediodorsal thalamic nuclei do?

A

Leads to amnesia for autobiographical amnesia

60
Q

What are the characteristics of Amnesic Syndrome?

A
  • 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
Q

What are the two explanation for Amnesic Syndrome?

A
  1. Failure to store contextual information needed to distinguish different memories
  2. Deficit in memory consolidation (temporal lobe amnesia)
62
Q

What are the symptoms of frontal lobe damage?

A
  1. Confabulation
  2. Source amnesia
  3. Unable to specify memories in detail
  4. Impaired STM
63
Q

What is Confabulation?

A

Production of false memories

64
Q

What is source amnesia?

A

Forgetting knowledge source (but memory is accurate)

65
Q

What is the key structure within the mediotemporal lobe required for memory consolodation?

A

The hippocampus

66
Q

What does the hippocampus mediate?

A

The formation of new declarative memories

67
Q

What is declarative memory?

A

Memory of facts, events and data

68
Q

What is Procedural memory?

A

How to do things

69
Q

What are the two types of Long Term Memory?

A
  • Declarative memory

* Procedural memory

70
Q

What are the two types of Declarative memory?

A
  • Episodic memory

* Semantic memory

71
Q

What is Episodic Memory?

A

Personal experiences

72
Q

What is Semantic Memory?

A

General factual info (ottawa is the capital)

73
Q

What did patient H.M. who had his hippocampus removed uncover?

A

The memory systems

74
Q

What did patient H.M. have done to him?

A

He had hippocampus removed

75
Q

What kind of amnesia did patient H.M. after having his hippocampus removed?

A

Anterograde amnesia

76
Q

What symptoms did H.M. have after having his hippocampus removed?

A
  • No recall of past learning trials

* No ability to make new declarative memories

77
Q

What is the theory about how the Mediotemporal hippocampal system affects new memories?

A

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
Q

Why can’t patient H.M. form new memories?

A

Because he has no MTH

79
Q

What does destruction of CA1 of the hippocampus cause?

A

Anterograde amnesia

80
Q

What is the pathway

A
81
Q

What is the pathway from disease to lab bench to clinic?

A

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
Q

What did Eric Kandel do?

A
  • Linked synaptic plasticity to learning

* Showed CREB is critical for LTM

83
Q

What is synaptic plasticity linked to?

A

Learning

84
Q

What is critical for LTM?

A

CREB

85
Q

What did Bliss and LeDoux discover?

A

Synaptic strengthening in the hippocampus

86
Q

How does CREB help with LTM?

A

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
Q

What is crucial for memory storage?

A

Synaptic plasticity

88
Q

What are the three “memory enhancer” drugs?

A
  • AMPAkines
  • PDE Inhibitors
  • Activators of nAChRs/Cholinesterase Inhibitors
89
Q

What are AMPAkines?

A

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
Q

What does cAMP do?

A

Binds to PKA and activates it

91
Q

How do PDE Inhibitors work?

A

They increase cAMP levels by inhibition of breakdown ex. Rolipram, mesembrine

92
Q

How do Activators of nAChRs or Cholinesterase inhibitors work?

A

They increase activation of nAChRs or increase levels of ACh at the synapse

93
Q

What does cAMP do?

A

Binds to PKA and activates it so it can activate CREB

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