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Memory Flashcards

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1
Q

Epileptic seizures involve two concurrent processes. What are they?

A
  1. EXCITATION in groups of neurones

2. loss of INHIBITory potential

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2
Q

Of GABA and glutamate, which is inhibitory?

A

GABA

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3
Q

What form of epilepsy is responsible for informing us the most about the operation of memory?

A

Temporal lobe epilepsy (TLE)

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4
Q

What is distinctive about ‘simple partial seizures’, as distinct from ‘complex partial seizures’

A

In the former case, the patent does NOT lose awareness

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5
Q

What is the most common form/location of Temporal Lobe Epilepsy (TLE)?

A

Hippocampal sclerosis (HS)

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6
Q

What is gliosis?

A

Excessive growth in glial cells after neuronal loss occurs)

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7
Q

What is occurring in hippocampal sclerosis?

A
  1. Neuronal loss

2. Gliosis

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8
Q

Does Temporal Lobe Epilepsy (TLE) typically occur early or late in life?

A

EARLY

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9
Q

What three aetiologies were mentioend for Temporal Lobe Epilepsy (TLE)?

I T V

A
  1. Infections
  2. Tumours
  3. Vascular malformations
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10
Q

In the case of Temporal Lobe Epilepsy (TLE), what steps can be taken to cure or reduce seizure?

A

Surgical removal of the lesioned hippocampus

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11
Q

What is the name of the operation that Henry Molaison (HM) underwent?

A

Bilateral resection (of medial temporal tissue)

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12
Q

Which parts of brain were removed when Henry Molaison (HM) underwent his bilateral resection?

A
  1. Amygdala
  2. (most of) hippcampi
  3. (part of) parahippocampal gyrus
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13
Q

After his bilateral resection, what was the state of Henry Molaison’s (HM) attention span?

A

Normal

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14
Q

After his bilateral resection, what was the state of Henry Molaison’s (HM) intelligence?

A

Normal

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15
Q

After his bilateral resection, what was the state of Henry Molaison’s (HM) retrograde memory?

A

Recovered over time

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16
Q

Amnesia can be retrograde and/or anterograde. Which one relates to impairment in the formation of new memories?

A

Anterograde

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17
Q

What type of amnesia did Henry Molaison (HM) have after his bilateral resection?

A

Anterograde amnesia

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18
Q

What is declarative memory?

A

Access to information

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19
Q

What is procedural memory?

A

Remembering how to ‘do’ things (ie playing piano)

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20
Q

After Henry Molaison’s (HM) bilateral resection, which type of memory was impaired, declarative or procedural?

A

Declarative

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21
Q

Based on the case of Henry Molaison (HM), which brain lobe is essential for memory function?

A

Medial temporal lobe

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22
Q

Based on the case of Henry Molaison (HM), which from of memory is the medial temporal lobe essential for? (two terms)

A

Declarative, anterograde

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23
Q

Taking into account what we learned from the case of Henry Molaison (HM) and everything we’ve learned since…

do we now assume that memory relies on a specific module in the brain, or a wider network of regions?

A

A wider network

neuroanatomical network

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24
Q

Taking into account what we learned from the case of Henry Molaison (HM) and everything we’ve learned since…

are memory functions anatomically symmetric or asymmetric?

A

Asymmetric

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25
Q

Which region of the brain was described in lectures as the ‘engine’ of memory?

A

Temporal lobes

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26
Q

What does it mean for someone to have ‘material specific’ memory impairments?

A

The impairment only affects some types/forms of memory (like verbal or visual)

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27
Q

What form of ‘material specific’ memory impairment results from legions in the LEFT of the medial temporal lobe (MTL)?

A

Verbal memory

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28
Q

What form of ‘material specific’ memory impairment results from legions in the RIGHT of the medial temporal lobe (MTL)?

A

Visual/non-verbal memory

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29
Q

In which brain region (lobe) is the hippocampus located?

A

Medial temporal lobe (MTL)

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30
Q

What is the other name for the hippocampus?

A

Cornu ammonis

Ammon’s horn

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31
Q

What are the code letters or the hippocampus/Cornu ammonis

A

CA1 to CA3

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32
Q

What are the three bits of the hippocampal formation?

D C S

A

D C C S

  1. Dentate gyrus
  2. CA3 - CA1
  3. Subiculum
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33
Q

Where would you find the ‘subiculum’?

A

In the hippocampal formation

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34
Q

What does the ‘subiculum’ do?

A

Nobody knows

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35
Q

When it comes to memory function, information is integrated in which systems, and sent to which formation for long term storage?

A

Sensory … and … hippocampal

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36
Q

Memory is access via reciprocal connections between which two brain formations/regions?

A

Hippocampal formation and temporal neocortex

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37
Q

Surgical case studies show that hippocampal formation is not necessary for consolidation of over information, T/F

A

FALSE!

Hippocampal formation and surrounding structures are essential for learning and consolidating novel information

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38
Q

Who is associated with ‘Consolidation Theory’, and what is it?

A

Squire (2004)

After a period of consolidation, information can be retrieved independently of hippocampal formation

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39
Q

Who is associated with Multiple Trace Theory (MTT), and what is it?

A

Moscovitch (2005)

Retrieval of episodic memory ALWAYS involved hippocampal formation

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40
Q

What type of memory task is the hippocampal formation particularly necessary for?

A

Paired/relational learning

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41
Q

What neurological condition is particularly useful for studying memory?

A

Temporal Lobe Epilepsy (TLE)

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42
Q

What are the 3 regions outside the temporal lobe (the ‘extra temporal brain’) that our particularly involved in memory?

P F D

A

P F D

  1. Papez’s circuit
  2. Frontal lobes
  3. Diencephalon

P F D

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43
Q

What constitutes the limbic system? (2)

A

Papez circuit + amygdala

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44
Q

Together, what do the amygdala and paper’s circuit constitute?

A

The limbic system

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45
Q

The slides mention two ways in which the amygdala supports memory of emotionally arousing experiences. Name them

A
  1. Classical fear conditioning

2. Rich representations of emotional experiences

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46
Q

What can lesions in the amygdala result in? (2)

A
  1. Loss of fear conditioning and fear learning

2. Reduced memory for emotionally laden events

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47
Q

What are the 5 things comprising Papez’s circuit?

M F A C H

A

M F A C H

  1. Mamillary bodies
  2. Fornix
  3. Anterior thalamic nuclei (ATN)
  4. Cingulate gyrus
  5. Hippcampus

M F A C H

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48
Q

What type of memory is impaired by lesions on Papez circuit?

A

Declarative memory

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49
Q

If you’re going to have legions anywhere on the Papez circuit, where would you want them if you wanted to retain as much declarative memory as possible?

A

Hippocampus or Anterior thalamic nuclei (ATN)

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50
Q

How are the frontal lobes involved in memory?

A

Developing strategies for encoding and retrieval

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51
Q

What brain bits comprise the Diencephalon?

A

Thalamus and hypothalamus

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52
Q

What brain bit is comprised by the thalamus and the hypothalamus

A

The Diencephalon

the ‘interbrain’

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53
Q

Is the thalamus contain mini bits of brain that are connected to all the other bits of the brain?

A

Yes, actually it does

54
Q

Having legions in which regions of the thalamus is more likely to cause memory deficits? (2)

A M

A

A M

Anterior and medial

A M

55
Q

If you have legions in the posterior region of the thalamus, are you more or less likely to have memory deficits than if the lesion was in the medial region?

A

Less

Anterior and medial lesions more likely to cause memory deficits than posterior or lateral lesions.

56
Q

Dense amnesic syndrome is associated with damage to which tract?

A

Mammillo-thalamic tract (MTT)

57
Q

Which two brain regions does the mammillo-thalamic tract (MTT) connect?

AT & H

A

AT & H

Anterior thalamus and hippocampus

AT & H

58
Q

If you have damage to the Medio Dorsal Nucleus (MDN) and/or the Internal Medullary Lamina (IML)…

but your Mammillo-thalamic tract (MTT) is okay

are you likely to have difficulties with memory retrieval?

A

Yes!

But… not recognition

amazing

59
Q

Of the following brain bits, which appears most associated with recognition (as opposed to retrieval)?

  • Medio Dorsal Nucleus (MDN)
  • Mammillo-thalamic tract (MTT)
  • Internal Medullary Lamina (IML)
A

Mammillo-thalamic tract (MTT)

60
Q

If you have damage to the dorsal medial nuclei (DMN) region of the thalamus, what type of memory is likely to be impaired?

A

Active retrieval

Petrides 1996

61
Q

If you have damage to the intralaminar/midline nuclei region of the thalamus, what type of memory is likely to be impaired?

A

Semantic memory + memory retrieval

62
Q

You see a patient who can remember past experiences but cannot remember which year Obama was elected. In which brain region is he likely to have damage?

A

In the intralaminar/midline region of the thalamus

63
Q

What type of memory impairment is associated with lesions on Papez’s circuit?

A

Impaired relational memory/encoding (hippocampal type of amnesia)

64
Q

What type of memory impairment is associated with lesions on frontal lobes?

A

Impaired ability to organise the encoding, retrieval and maintenance of memories

65
Q

What type of memory impairment is associated with lesions on dorsal medial nuclei (DMN), intralaminar nuclei or the midline nuclei regions of the thalamus?

A

Retrieval

Mental flexibility

66
Q

Long term potentiation (LTP) is an example of what?

A

Synaptic plasticity

67
Q

What is the name for the following process:

‘A long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high frequency activity of that input’

A

Long term potentiation

68
Q

What is the name given to the following process?

“When an axon of cell A…excites cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells so that A’s efficiency as one of the cell’s firing B is increased”

A

Hebb’s rule

69
Q

What’s the name of the rule associated with long term potentiation?

A

Hebb’s rule

70
Q

During long term potentiation (LTP), what is happening to the membrane of the post-synaptic neutron?

A

New receptors are getting inserted…

71
Q

Of the Glutamates and GABA, which was inhibitory and which is listed in the slides alongside the discussion of long term potentiation?

A

GABA is inhibitory

but it is Glutamate that is listed on that slide

72
Q

What are the three synaptic changes that LTP causes?

A
  1. Increased SENSITIVITY of receptors to glutamate
  2. increased AMOUNT of glutamate released by pre-synaptic terminal
  3. Protein synthesis in post-synaptic dendrites
73
Q

What are the sit4s of long term potentiation (LTP) that are mentioned in the slides? (7)

H E P M T A V

A

H E P M T A V

  1. Hippocampus
  2. Entorhinal cortex
  3. Prefrontal cortex
  4. Motor cortex
  5. Thalamus
  6. Amygdala
  7. Visual cortex

H E P M T A V

74
Q

The slides mentioned three other forms of synaptic plasticity, beyond long term potentiation (LTP). What were they?

LTD H S

A

LTD H S

  1. Long term depression
  2. Habituation
  3. Sensitisation

LTD H S

75
Q

What type of thing is Long term depression, and what actually is it?

A

It’s an example of synaptic plasticity

It is actually..

Low frequency stimulation at synapse can decrease synaptic strength

76
Q

What type of thing is Habituation, and what actually is it?

A

It’s an example of synaptic plasticity

It is actually..

Repeated stimulation reduces strength of synaptic response (reduced
neurotransmitter release)

77
Q

What type of thing is Sensitization, and what actually is it?

A

It’s an example of synaptic plasticity

It is actually..

Single noxious stimulus causes exaggerated synaptic response to repeat presentation of noxious stimulus

78
Q

If we were to say that learning in memory is caused by main a specific thing at the level of neurons, what would that thing be?

A

Long term potentiation

79
Q

What was Matlin’s (1998) definition of memory?

A

‘Maintaining information over time’

80
Q

What was Ashcroft’s (1994) definition of memory?

A

‘The mental processes of acquiring and retaining information for later retrieval’

81
Q

We learned about two different ways of thinking about memory:

  • the implicit/explicit way, and
  • the procedural/declarative way

They can be related, but do not completely map onto each other.

Which one was derived from dissociable cognitive theories?

A

The procedural/declarative one

82
Q

The hippocampal formation is essential for PROCEDURAL memory formation, T/F

A

FALSE!

Procedural memory formation is supported by memory systems that are independent of the hippocampal formation

83
Q

Is declarative memory relational?

A

Yup

84
Q

We learned about 4 models of memory. What were they?

A L T P

A

A L T P

  1. Atkinson-Shiffrin (1968)
  2. Levels of processing
  3. Tulvings
  4. Parallel distributed processing model

A L T P

85
Q

Of the models of memory we learned, three were serial models and one was parallel. Which one was parallel

A

The Parallel Distributed Processing Model

86
Q

Tell me all about the Atkinson-Shiffrin model of memory

A

> > SENSORY MEMORY&raquo_space; attention&raquo_space; WORKING MEMORY&raquo_space; encoding/retrieval&raquo_space; LONG TERM MEMORY

87
Q

Who came up with this model of memory?

> > SENSORY MEMORY&raquo_space; attention&raquo_space; WORKING MEMORY&raquo_space; encoding/retrieval&raquo_space; LONG TERM MEMORY

A

Atkinson-Shiffrin (1968)

88
Q

Tell me all about the Levels of Processing model of memory

A

Information is retained according to the depth of processing it has undergone…

leading to

  • Shallow to deep continuum, and
  • Maintenance vs elaborative rehearsal distinction
89
Q

Who do we associate with the Levels of Processing mode of memory?

A

Craik & Lockhart (1972)

90
Q

If I told you about a model of memory that focused on depth of processing, and levels of rehearsal, what type of model might it be… and who would we associated with it?

A

Levels of processing model

Craik & Lockhart (1972)

91
Q

What was same same and what was special about Tulving’s model of memory (1972, 1983, 2001)

A

The pathway from STM to LTM was same same like the Atkinson-Shifrrin model

I think the new bit was that he divvied LTM up into procedural/episodic/semantic

92
Q

Tell me all about the Parallel Distributed Processing model of memory

A

Well, basically…

Memory = activation of a whole network of distributed areas

Knowledge is basically the pattern of activation

Learning, therefore, becomes about strengthening connections between relevant locations

93
Q

Of the two types of models of memory, which is mot useful for studying amnesia

A

Serial

94
Q

Which form of memory is autonoetic awareness related to?

A

Episodic memory

95
Q

WTF is autonoetic awareness?

A

Highly personalized feeling of (re)experiencing oneself in the autobiographical past or present

96
Q

According to Tulving’s model, episodic memory was entirely independent of semantic memory, T/F

A

FALSE!

Tulving believed episodic memory depended on semantic and other forms of memory

97
Q

Some people argue that episodic and declarative memory are entirely parallel. Name a couple of them

A

Squire and Zola

These guys made the case that

98
Q

What is Tulving’s view on whether episodic and semantic memory are parallel systems?

A

He recons they are not parallel

99
Q

Tulving recoded one memory system (of episodic and semantic) was dependent on the other? Which way around was it?

A

He believed that episodic relied on semantic

That is, if you damaged your episodic memory you can keep your semantic memory. But if you damage your semantic memory, both your semantic and episodic memory are fucked

100
Q

What is Vargha-Khadem et al (1997) associated with?

A

The study of the kids that showed semantic memory could be encoded without episodic memory

101
Q

Who is associated with the (1997) study that showed semantic memory could be encoded without episodic memory

A

Vargha-Khadem (1997)

102
Q

In Vargha-Khadem’s (1997) study, what did neuroimaging work reveal about the brains of the three subjects? (2 things)

A

All three had:

  1. abnormally small bilateral hippocampi

2 relatively intact extra-hippocampal temporal lobes

103
Q

So after the Vargha-Khadem’s (1997), what might we conclude about the dissociability of episodic and semantic memory?

A

They must be functionality dissociable… but there is still much to learn

104
Q

Declarative memory allows 3 types of memory processing. What are they?`

A
  1. recall
  2. recognition
  3. manipulate memory internally
105
Q

Of all dementing illnesses, how common is Alzheimer’s?

A

The most common of them all…

Probably 50% of all dementias are AD

106
Q

If you live to 80, what are the chances of you getting Alzheimer’s

A

1 in 5, buddy

107
Q

Can you diagnose a living person with Alzheimer’s?

A

No

108
Q

In relation to Alzheimer’s, What is the fancy name for the only diagnosis you can actually give a living person

A

Demential of the Alzheimer Type

109
Q

What is the most common aetiology of AD?

A

Sporadic

110
Q

What is going on with the early onset autosomal dominant cases?

A

– Mutations in 3 genes: amyloid precursor protein (APP), presinilin 1 (PSEN1), presenilin 2 (PSEN2)
– All alter production of amyloid β (Aβ) peptide – principal component of senile plaques

111
Q

What is the mean number of years to death after onset?

A
  1. 5 years

range: 2-20 years

112
Q

How many phases doesAD have?

A

3

113
Q

What happens in phase 1 of AD, and how long does it last?

A
  1. Failing memory (amnestic presentation)
  2. Muddled inefficiency in Activities of Daily Living (ADL)s
  3. Spatial disorientation
  4. Mood disturbance can
    occur (agitated or apathetic)

(lasts 2-3 years)

114
Q

What happens in phase 2 of AD?

A
  1. Intellect and personality deteriorate
  2. Focal symptoms appear (dysphasia, dyspraxia, agnosia and acalculia)
  3. Disturbance of posture and gait, increased muscle tone
  4. Delusions/hallucinations can occur
115
Q

What happens in phase 3 of AD

A
  1. Profound apathy, become bed ridden
  2. Eventually lose neurological function
  3. Bodily wasting occurs
116
Q

What are the three diagnoses relevant to AD (McKhann)

A
  1. Probable AD
  2. Possible AD
  3. Definite AD
117
Q

What are the diagnostic criteria for PROBABLE AD

A
  1. Deficits in 2 or more areas of cognition
    – Amnestic presentation: most common
    – Nonamnestic presentations: Language, Visuospatial, Executive dysfunction
  2. Progressive worsening of memory and/or other cog. functions
  3. No disturbance of consciousness
  4. Onset between 40 and 90
  5. In the absence of other causes
  6. Biomarkers
118
Q

What are the diagnostic criteria for POSSIBLE AD

A
  1. Made on the basis of dementia syndrome if have variations in onset, presentation or clinical course
  2. Can be made in the presence of another disorder, which is not considered to be the cause of the dementia
119
Q

What is the diagnostic criteria for DEFINITE AD

A
  1. Histopathological evidence of AD obtained from biopsy or autopsy
120
Q

In AD, what is occurring at a pathology level?

A
  1. Grossly atrophied brain
    – Affects frontal and temporal lobes > parieto- occipital regions
  2. Extensive degeneration of neurons
  3. Accompanying glial cell proliferation
  4. Extensive amounts of senile plaques
  5. Extensive amounts of neurofibrillary tangles
  6. Intensity of neuropathological features correlates closely with severity of dementia
121
Q

One of the diseases we learned about is associated with senile plaque. What is it?

A

Alzheimer’s Disease (AD)

122
Q

One of the diseases we learned about is associated with excessive neurofibrillary tangles. What is it?

A

Alzheimer’s Disease (AD)

123
Q

In terms of brain regions, where does Alzheimer’s Disease (AD) start?

A

Hippocampus / MTL

124
Q

In terms of brain regions, to where does Alzheimer’s Disease (AD) spread after it starts in the hippocampus?

A
  1. Posteriorly to the parietal cortex

1. Also the frontal cortex

125
Q

What are the first markers of cognitive impairment in the progression of Alzheimer’s Disease (AD)?

A

MTL type impairment

  1. Anterograde memory deficits
    - can’t learn
  2. Retrograde memory deficits
    - recent memories for first
126
Q

What are the second markers of cognitive impairment in the progression of Alzheimer’s Disease (AD)?

A
  1. Wernicke-type aphasia (spread into posterior temporal lobe)
    - word finding difficulties
    - fluent
  2. Visuospatial deficits/topographical disorientation (spread into parietal lobes)
    - Dyspraxia (movement/coordination), agnosia (can’t process sensory info), acalculia
127
Q

What are the third markers of cognitive impairment in the progression of Alzheimer’s Disease (AD)?

A
  1. Behaviour change (into fontal lobes)
    - Apathy (more common)
    - Agitation
  2. Generalised impairment (into neocortex)
128
Q

What is the brain chemical that is out of balance during Alzheimer’s Disease (AD)?

A

Acetylcholine

129
Q

Acetylcholine imbalance is associated with what disease?

A

Alzheimer’s Disease (AD)

130
Q

What prevents Alzheimer’s Disease (AD)?

A

So far, nothing… - not diet, physical cognitive or social activity

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