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Memory Flashcards

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1
Q

what are the 3 regions of the extra temporal brain that are particularly involved in memory?

A
  • papez’s circuit
  • frontal lobes
  • diencephalon
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2
Q

when was papez’s circuit founded?

A

1937?

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3
Q

what did papez propose?

A

that a specific circuit was devoted to emotional experience and expression

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4
Q

what does the limbic system comprise of?

A

amygdala and Papez’s circuit

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5
Q

what does the amygdala do?

A

supports memory for emotionally arousing experiences

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6
Q

what part of the brain is typically involved in classical fear conditioning?

A

amygdala

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7
Q

where are stress hormones released from?

A

adrenal glands

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8
Q

release of NT’s accentuates what? where does this happen?

A

the laying down of the memory so it is a stronger memory

in the amygdala

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9
Q

lesioned amygdala can lead to what?

A

loss of conditioned fear, and impairment of new fear learning as well as reduced capacity for formation of emotionally laden events

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10
Q

what does papez’s circuit comprise of?

A

mamillary bodies, fornix, anterior thalamic nuclei, cingulate gyrus and hippocampus

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11
Q

what are the mamillary bodies apart of?

A

the hypothalamus

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12
Q

what is an efferent pathway?

A

pathway that is outgoing

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13
Q

what is the order of the closed circuit of papez’s circuit?

A

hippocampus to the mamillary bodies to the anterior thalamic nuclei, to the mid section of the cingulate cortex

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14
Q

what happens when lesions occur to parts of Papez’s circuit?

A

declarative memory impairment

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15
Q

how does damage to papez’s circuit often happen?

A

strokes and tumours

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16
Q

what is the only part of papz’s circuit that resides in the mesial temporal lobes?

A

the hippocampus

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17
Q

if any part of papez’s circuit is damaged, what sort of impairment is this similar to?

A

mesial temporal lobe damage

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18
Q

where does the primary somatosensory cortex sit on the brain?

A

the most anterior part of the parietal lobe

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19
Q

the prefrontal cortex is responsible for what sort of processes?

A

cog. control processes eg problem solving, planning, monitoring and self correction

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20
Q

where does the prefrontal cortex sit on the brain?

A

anterior in the frontal lobes

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21
Q

what role do the frontal lobes play in memory formation?

A

they play a large role in the organisational aspect of it (the executive side of it)
now how the memories are made, but where they are laid down and how easily you can access them

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22
Q

how can damage to the frontal lobes affect memory?

A

it can damage the mem ories regarding the context in which they are made `

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23
Q

what is confabulation? what does it result in?

A

damage to the prefrontal cortex, which results in the individual making statements of facts involving bizarre distortions of memory

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24
Q

what does DLPF stand for? what does it refer to?

A

dorsal, lateral, pre frontal

the area in which damage is most likely to result in impairment to chronological orders of memories

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25
Q

what it the Diencephalon? where is it found in the brain? what does it comprise of?

A

it is the “interbrain”
found right in the middle of the brain
comprises of thalamus and hypothalamus

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26
Q

the dorsal medial parts of the thalamus primarily are related to what part of the brain?

A

prefrontal cortex

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27
Q

damage to the thalamus often results in…?

A

damage to the corresponding part of the brain

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28
Q

why does damage to the thalamus sometimes lead to memory impairment?

A

because parts of the thalamus directly correspond to areas of the brain that are involved in memory function

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29
Q

which are more likely to cause memory deficits?

damage to the anterior medial parts of the thalamus or damage to the posterior lateral sections of the thalamus?

A

anterior medial parts

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30
Q

if you damage the mammillo-thlamic tract or the anterior thalamus, which type of memory deficit are you more likely to experience?

A

mesial temporal type

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31
Q

if you damage the medio dorsal nucleus and/or the internal medullary lamina, you are more likely to suffer from what type of memory impairment? which leads to issues of what?

A

more frontal type impairment.

difficulties in encoding memories in an organised way or the retrieval of the memories

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32
Q

what are Schwann cells? where is it found? what do they offer

A

myelin sheath, it is found around the axon and it encourages conduction of the electrical charge

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33
Q

what is an action potential?

A

a electrical process that propogates a neural message

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34
Q

what is the resting membrane potential of a cell body?

A

negative 70 mV

this is the electrical charge that the cell sits at

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35
Q

at what voltage does an action potential occur?

A

negative 55 mV

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36
Q

what does the successful firing of a cell result in?

A

allows for NT’s to be released across the synaptic clef

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37
Q

does one particular axon contain the one type of neurotransmitter?

A

yes

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38
Q

how are NT’s released into the synaptic clef?

A

a certain electrical charge voltage opens the gated Ca2+ channel (calcium) which releases NT’s

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39
Q

NT’s crossing the synaptic clef attach to what?

A

receptors in the dendrite

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40
Q

an inhibitory post synaptic potential does what?

A

reduces the voltage in the post synaptic cell

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41
Q

what is long term potentiation?

A

changes to the biochemistry of synapses the alter the effect on post synaptic neuron

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42
Q

what does long term potentiation involve?

A

a long term increase in the excitability of cell due to input from cell a

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43
Q

who described LTP? when?

A

Hebb, 1949

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44
Q

what is the result of LTP?

A

cell b undergoes some change where it responds more strongly to cell A

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45
Q

at a synaptic level, what 3 things are happening during LTP ?

A
  1. new receptors are inserted in the post synaptic membrane
  2. the receptors are more sensitive
  3. Cell a (pre synaptic membrane) releases more NTs
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46
Q

where does LTP most commonly take place?

A

parts of the brain most associated with memory eg hippocampus, Entorhinal cortex, thalamus, amygdala, and the visual, prefrontal and motor cortices

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47
Q

what is Long term depression in regards to synapses

A

decrease of synaptic strength due to low frequency stimulation at synapse

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48
Q

what is habituation in regards to synapses?

A

repeated stimulus reduces strength of synaptic response due to reduced NT release

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49
Q

what is sensitisation in regards to synapses?

A

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

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50
Q

Matlin’s definition of memory?

A

maintaining information overtime

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51
Q

Ashcroft’s definition of memory

A

mental processes of acquiring and retaining info for later retrieval

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52
Q

what is the main difference between terminology of implicit/explicit vs procedural/declarative?

A

procedural/declarative stemmed from trying to understand amnesia’s and place more emphasis on cog theories.

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53
Q

procedural memory is supported by what systems?

A

memory systems independent of hippocampal function including

54
Q

in what sort of way is declarative memory encoded and activated/retrieved?

A

in a systematic way where relevant information is grouped together

55
Q

why can declarative memories be activated independently of the environment?

A

because information is being put into an existing semantic framework

56
Q

what are the 4 models of memory?

A

atkinson - shiffrin, levels of processing, tulvig’s model

parallell distributed processing model

57
Q

how many types of serial models are there? what are they?

A
  1. atkinson - shiffrin, levels of processing, tulvig’s model
58
Q

how many types of parallel models are there? what are they?

A
  1. parallell distributed processing model
59
Q

what makes a ‘serial’ model?

A

things happen sequentially

60
Q

what are the 3 steps of memory in the atkinson shiffrin model?

A

sensory memory, working memory, long term memory

61
Q

what are iconic and echoic memory? where are they placed in what model?

A

they sit in the sensory memory in the atkinson shiffrin model, iconic is images, echoic is audible

62
Q

who proposed the levels of processing memory model?

A

Craik and Lockhart

63
Q

what did craik and lockhart take an interest to?

A

how well people remember things, the “depth” to which people process memories

64
Q

how do you get shallow or deep understanding?

A

maintenance v elaborative rehearsal

65
Q

does maintenance rehearsal lead to shallow or deep processing?

A

shallow

66
Q

What did Tulvig focus on in his model of memory ?

A

separating out LTM

67
Q

what did Tulvig separate LTM into?

A

procedural, episodic and semantic memory

68
Q

what is different about the foundations of tulvig’s model?

A

it was born out of studying abnormalities as opposed to normative memory functioning

69
Q

what does the parallel distribution processing model emphasise that is different to the others?

A

it places emphasis not on the elements, but rather the connections between elements and the strengths of those

70
Q

what does the PDP primarily argue?

A

that memory consists of simultaneous activation of connections in different areas

71
Q

what type of model is most useful for the study of amnesia?

A

serial models

72
Q

what is the proposed structure of LTM?

A

declarative + procedural

episodic + semantic

73
Q

how did Tulvig describe episodic memory?

A

a memory system that makes ‘time travel’ through subjective time possible

74
Q

what is autonoetic awareness

A

James’ notion that there is a personal experience in this sort of memory, that it is a memory of something that has happened to you, and is not just a memory of something you have heard etc

75
Q

does episodic memory develop late in childhood?

A

yes

76
Q

episodic memories depend on what memory systems?

A

the semantic memory system, but additionally served by other unique memory systems

77
Q

what is semantic memory?

A

“knowledge memory”

- things that are facts

78
Q

what is unique about semantic memory?

A

you cannot distinctly remember when you learned that memory, you cannot travel back to the moment when you learned it

79
Q

does semantic memory have any link to autonoetic awareness ?

A

no

80
Q

what do squire and zola argue about semantic and episodic memory systems?

A

that these systems are entirely parallel, and they run side by side using the same structures

81
Q

what 2 things tulvig argue about the relationship between semantic and episodic memory systems?

A

that they use many of the same structural features but are not parallel, and that the episodic memory is a unique extension of semantic memory

82
Q

squire and zole argue that the declarative memory system is dependent on what ? and that damage to this system will result in what?

A

hippocampal system

damage to hippocampal system will result in equal amounts of impairment in the episodic and semantic memory functions

83
Q

who argues that the semantic and episodic memories are not dissociable

A

squire and zola

84
Q

what is the serial parallel independent hypothesis and who introduced it?

A

Tulvig, argues that you need to separate the encoding and retrieval of info, and that when you do this, the semantic and episodic memory system are not parallel systems

85
Q

if something is a parallel system, what does this mean?

A

they they operate using the same neural structures

86
Q

tulvig argues that the encoding of both episodic and semantic memories rely on what?

A

the semantic memory system

87
Q

what does tulvig argue in regards to the retrieval of episodic and semantic memory?

A

that this can happen independently, and that the two systems do not need the other to retrieve info

88
Q

what is a no dissociation system?

A

damage to X or Y equally affects A and B

89
Q

what is a single dissociation system? example?

A

damage to X affects A and not B, but damage to Y affects both A and B
analog TVs could get with sound but no picture, but could never get picture with no sound

90
Q

what is a double dissociation system? example?

A

damage to X affects A and not B, and damage to Y affects B and not A

91
Q

what sort of dissociation is assumed in Tulvigs SPI model of encoding? why?

A

a single dissociation, because both episodic and semantic memory rely on semantic memory system, but episodic only relies on episodic memory system

92
Q

what sort of dissociation is assumed in Tulvigs SPI model of retrieval? why?

A

double dissociation, they are both independent on each other.

93
Q

what was common across the 3 children in Vargha-Khadem 1997 study?

A

they all had abnormally small bilateral hippocampi, and the lesions were discrete
they all had significant memory impairment relative to intellectual capacity

94
Q

what everyday memory deficits did the children incur?

A

spatial, temporal and episodic memory

95
Q

what were the overall findings of the Vargha-Khadem 1997 study? what does this tell us?

A

that the 3 children had intact semantic memory and impaired episodic memory. that these two systems must be functionally dissociable

96
Q

how do episodic and semantic memory functions interact?

A

episodic memory function relies on semantic memory, but semantic memory function does not rely on intact episodic memory

97
Q

what is a primary dementing illness?

A

where the disease directly affects the neural tissue

98
Q

what is the most common primary dementing illness?

A

Alzheimer’s disease

99
Q

what is the prevalence of alzeimer’s disease in different age groups?

A

~ 2% in 65-70 year olds

~ 20$ in 80+ year olds

100
Q

definitive diagnoses of AD can only be made when?

A

when part of the brain is actually looked at under microscope?

101
Q

during life, what can only be diagnose?

A

Dementia of the Alzheimer Type (DAT)

102
Q

what is classified as late onset of AD?

A

after 60 + years of age

103
Q

the ApoE allele can lead to what?

A

late onset AD, but there is not a 1 to 1 association for this

104
Q

amyloid peptides are what?

A

a principal component of senile plaques

105
Q

which 3 genes are involved with the creation of amyloid beta peptides? mutations of these genes can lead to?

A

amyloid precursor protein, presinilin 1, and presinilin 2

abnormal production of amyloid beta peptides

106
Q

people with Down’s Syndrome are unusually prone to developing AD, what age does this typically occur at for these individuals?

A

around 40 years old

107
Q

what is insidious onset?

A

it is not a sudden onset, unlike an acute event like a stroke

108
Q

DAT has what sort of onset?

A

insidious onset

109
Q

how long does death occur on average after onset of DAT?

A

8.5 years

110
Q

how many main phases are there in DAT ?

A

3

111
Q

how long does phase 1 of DAT typically last?

what happens?

A

2-3 years

  • failing memory
  • some spatial disorientation
  • some mood disturbance
112
Q

what commonly happens in phase 2 of DAT?

A 
intellect and personality deteriorate 
dysphasia 
dyspraxia 
agnosia 
acalculia 
disturbance of posture and gait 
increased muscle tone leading to tenseness of muscles 
delusions can occur
113
Q

what is anomia?

A

loss of common nouns in speech, it is a type of dysphasia

114
Q

what is dyspraxia? example?

A

individual experiences trouble with sequencing a series of motor movements
making a cup of tea

115
Q

what is agnosia?

A

person cannot identify what they are looking at.

they can draw it but cannot say what it is

116
Q

what is acalculia?

A

loss of ability to do arithmetical function

117
Q

what is phase 3 of DAT? what commonly happens?

A

the terminal stage
become very apathetic
lose neurobiological function
do not eat very much and often become quite thing

118
Q

what is operational criteria for diagnosis of AD?

A

probable AD
possible AD
definite AD

119
Q

to be diagnosed with probable AD, a patient must have what?

A

deficits in 2 or more areas of cognition

120
Q

in probable AD, what are 3 Non-amnestic presentations

A

language, visuospatial, executive dysfunction

121
Q

what are some other key criterion for probable AD

A

onset takes place between 40 and 90
there is a progressive deterioration of memory and/or cog functions
no disturbance of consciousness
can’t be other causes

122
Q

definite AD diagnosis needs

A

histopathological evidence of AD obtained from biopsy or autopsy

123
Q

what is an atrophied brain? why does this happen?

A

a shrunken brain

because of the death of many neurons

124
Q

which lobes of the brain tend to be affected first in this AD atrophied brain?

A

frontal and temporal lobes before parieto-occipital regions

125
Q

what other things have to be identified of the brain to diagnose AD?

A

proliferation of glial cells

intensity of neuropathological features correlate with severity of dementia

126
Q

what are the two necessary features you need to see to diagnose AD

A
  • large amounts senile plaques

- large amounts of neurofibrillary tangles (NFTs)

127
Q

what is found in the centre of a senile plaque?

A

lots of amyloid

128
Q

where do neuropathological changes in AD typically begin?

A

hippocampus/medial temporal lobes

129
Q

where do neuropathological changes in AD typically spread to from it’s first stages?

A

spread posteriorly to parietal cortex

130
Q

where do neuropathological changes in AD typically spread to from the parietal cortex?

A

frontal cortex

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