Memory Flashcards
(130 cards)
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
2
Q
when was papez’s circuit founded?
A
1937?
3
Q
what did papez propose?
A
that a specific circuit was devoted to emotional experience and expression
4
Q
what does the limbic system comprise of?
A
amygdala and Papez’s circuit
5
Q
what does the amygdala do?
A
supports memory for emotionally arousing experiences
6
Q
what part of the brain is typically involved in classical fear conditioning?
A
amygdala
7
Q
where are stress hormones released from?
A
adrenal glands
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
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
10
Q
what does papez’s circuit comprise of?
A
mamillary bodies, fornix, anterior thalamic nuclei, cingulate gyrus and hippocampus
11
Q
what are the mamillary bodies apart of?
A
the hypothalamus
12
Q
what is an efferent pathway?
A
pathway that is outgoing
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
14
Q
what happens when lesions occur to parts of Papez’s circuit?
A
declarative memory impairment
15
Q
how does damage to papez’s circuit often happen?
A
strokes and tumours
16
Q
what is the only part of papz’s circuit that resides in the mesial temporal lobes?
A
the hippocampus
17
Q
if any part of papez’s circuit is damaged, what sort of impairment is this similar to?
A
mesial temporal lobe damage
18
Q
where does the primary somatosensory cortex sit on the brain?
A
the most anterior part of the parietal lobe
19
Q
the prefrontal cortex is responsible for what sort of processes?
A
cog. control processes eg problem solving, planning, monitoring and self correction
20
Q
where does the prefrontal cortex sit on the brain?
A
anterior in the frontal lobes
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
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 `
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
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
25
what it the Diencephalon? where is it found in the brain? what does it comprise of?
it is the "interbrain"
found right in the middle of the brain
comprises of thalamus and hypothalamus
26
the dorsal medial parts of the thalamus primarily are related to what part of the brain?
prefrontal cortex
27
damage to the thalamus often results in...?
damage to the corresponding part of the brain
28
why does damage to the thalamus sometimes lead to memory impairment?
because parts of the thalamus directly correspond to areas of the brain that are involved in memory function
29
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?
anterior medial parts
30
if you damage the mammillo-thlamic tract or the anterior thalamus, which type of memory deficit are you more likely to experience?
mesial temporal type
31
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?
more frontal type impairment.
| difficulties in encoding memories in an organised way or the retrieval of the memories
32
what are Schwann cells? where is it found? what do they offer
myelin sheath, it is found around the axon and it encourages conduction of the electrical charge
33
what is an action potential?
a electrical process that propogates a neural message
34
what is the resting membrane potential of a cell body?
negative 70 mV
| this is the electrical charge that the cell sits at
35
at what voltage does an action potential occur?
negative 55 mV
36
what does the successful firing of a cell result in?
allows for NT's to be released across the synaptic clef
37
does one particular axon contain the one type of neurotransmitter?
yes
38
how are NT's released into the synaptic clef?
a certain electrical charge voltage opens the gated Ca2+ channel (calcium) which releases NT's
39
NT's crossing the synaptic clef attach to what?
receptors in the dendrite
40
an inhibitory post synaptic potential does what?
reduces the voltage in the post synaptic cell
41
what is long term potentiation?
changes to the biochemistry of synapses the alter the effect on post synaptic neuron
42
what does long term potentiation involve?
a long term increase in the excitability of cell due to input from cell a
43
who described LTP? when?
Hebb, 1949
44
what is the result of LTP?
cell b undergoes some change where it responds more strongly to cell A
45
at a synaptic level, what 3 things are happening during LTP ?
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
46
where does LTP most commonly take place?
parts of the brain most associated with memory eg hippocampus, Entorhinal cortex, thalamus, amygdala, and the visual, prefrontal and motor cortices
47
what is Long term depression in regards to synapses
decrease of synaptic strength due to low frequency stimulation at synapse
48
what is habituation in regards to synapses?
repeated stimulus reduces strength of synaptic response due to reduced NT release
49
what is sensitisation in regards to synapses?
single noxious stimulus causes exaggerated synaptic response to repeat presentation of noxious stimulus
50
Matlin's definition of memory?
maintaining information overtime
51
Ashcroft's definition of memory
mental processes of acquiring and retaining info for later retrieval
52
what is the main difference between terminology of implicit/explicit vs procedural/declarative?
procedural/declarative stemmed from trying to understand amnesia's and place more emphasis on cog theories.
53
procedural memory is supported by what systems?
memory systems independent of hippocampal function including
54
in what sort of way is declarative memory encoded and activated/retrieved?
in a systematic way where relevant information is grouped together
55
why can declarative memories be activated independently of the environment?
because information is being put into an existing semantic framework
56
what are the 4 models of memory?
atkinson - shiffrin, levels of processing, tulvig's model
| parallell distributed processing model
57
how many types of serial models are there? what are they?
3. atkinson - shiffrin, levels of processing, tulvig's model
58
how many types of parallel models are there? what are they?
1. parallell distributed processing model
59
what makes a 'serial' model?
things happen sequentially
60
what are the 3 steps of memory in the atkinson shiffrin model?
sensory memory, working memory, long term memory
61
what are iconic and echoic memory? where are they placed in what model?
they sit in the sensory memory in the atkinson shiffrin model, iconic is images, echoic is audible
62
who proposed the levels of processing memory model?
Craik and Lockhart
63
what did craik and lockhart take an interest to?
how well people remember things, the "depth" to which people process memories
64
how do you get shallow or deep understanding?
maintenance v elaborative rehearsal
65
does maintenance rehearsal lead to shallow or deep processing?
shallow
66
What did Tulvig focus on in his model of memory ?
separating out LTM
67
what did Tulvig separate LTM into?
procedural, episodic and semantic memory
68
what is different about the foundations of tulvig's model?
it was born out of studying abnormalities as opposed to normative memory functioning
69
what does the parallel distribution processing model emphasise that is different to the others?
it places emphasis not on the elements, but rather the connections between elements and the strengths of those
70
what does the PDP primarily argue?
that memory consists of simultaneous activation of connections in different areas
71
what type of model is most useful for the study of amnesia?
serial models
72
what is the proposed structure of LTM?
declarative + procedural
| episodic + semantic
73
how did Tulvig describe episodic memory?
a memory system that makes 'time travel' through subjective time possible
74
what is autonoetic awareness
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
does episodic memory develop late in childhood?
yes
76
episodic memories depend on what memory systems?
the semantic memory system, but additionally served by other unique memory systems
77
what is semantic memory?
"knowledge memory"
| - things that are facts
78
what is unique about semantic memory?
you cannot distinctly remember when you learned that memory, you cannot travel back to the moment when you learned it
79
does semantic memory have any link to autonoetic awareness ?
no
80
what do squire and zola argue about semantic and episodic memory systems?
that these systems are entirely parallel, and they run side by side using the same structures
81
what 2 things tulvig argue about the relationship between semantic and episodic memory systems?
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
squire and zole argue that the declarative memory system is dependent on what ? and that damage to this system will result in what?
hippocampal system
| damage to hippocampal system will result in equal amounts of impairment in the episodic and semantic memory functions
83
who argues that the semantic and episodic memories are not dissociable
squire and zola
84
what is the serial parallel independent hypothesis and who introduced it?
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
if something is a parallel system, what does this mean?
they they operate using the same neural structures
86
tulvig argues that the encoding of both episodic and semantic memories rely on what?
the semantic memory system
87
what does tulvig argue in regards to the retrieval of episodic and semantic memory?
that this can happen independently, and that the two systems do not need the other to retrieve info
88
what is a no dissociation system?
damage to X or Y equally affects A and B
89
what is a single dissociation system? example?
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
what is a double dissociation system? example?
damage to X affects A and not B, and damage to Y affects B and not A
91
what sort of dissociation is assumed in Tulvigs SPI model of encoding? why?
a single dissociation, because both episodic and semantic memory rely on semantic memory system, but episodic only relies on episodic memory system
92
what sort of dissociation is assumed in Tulvigs SPI model of retrieval? why?
double dissociation, they are both independent on each other.
93
what was common across the 3 children in Vargha-Khadem 1997 study?
they all had abnormally small bilateral hippocampi, and the lesions were discrete
they all had significant memory impairment relative to intellectual capacity
94
what everyday memory deficits did the children incur?
spatial, temporal and episodic memory
95
what were the overall findings of the Vargha-Khadem 1997 study? what does this tell us?
that the 3 children had intact semantic memory and impaired episodic memory. that these two systems must be functionally dissociable
96
how do episodic and semantic memory functions interact?
episodic memory function relies on semantic memory, but semantic memory function does not rely on intact episodic memory
97
what is a primary dementing illness?
where the disease directly affects the neural tissue
98
what is the most common primary dementing illness?
Alzheimer's disease
99
what is the prevalence of alzeimer's disease in different age groups?
~ 2% in 65-70 year olds
| ~ 20$ in 80+ year olds
100
definitive diagnoses of AD can only be made when?
when part of the brain is actually looked at under microscope?
101
during life, what can only be diagnose?
Dementia of the Alzheimer Type (DAT)
102
what is classified as late onset of AD?
after 60 + years of age
103
the ApoE allele can lead to what?
late onset AD, but there is not a 1 to 1 association for this
104
amyloid peptides are what?
a principal component of senile plaques
105
which 3 genes are involved with the creation of amyloid beta peptides? mutations of these genes can lead to?
amyloid precursor protein, presinilin 1, and presinilin 2
| abnormal production of amyloid beta peptides
106
people with Down's Syndrome are unusually prone to developing AD, what age does this typically occur at for these individuals?
around 40 years old
107
what is insidious onset?
it is not a sudden onset, unlike an acute event like a stroke
108
DAT has what sort of onset?
insidious onset
109
how long does death occur on average after onset of DAT?
8.5 years
110
how many main phases are there in DAT ?
3
111
how long does phase 1 of DAT typically last?
| what happens?
2-3 years
- failing memory
- some spatial disorientation
- some mood disturbance
112
what commonly happens in phase 2 of DAT?
```
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
what is anomia?
loss of common nouns in speech, it is a type of dysphasia
114
what is dyspraxia? example?
individual experiences trouble with sequencing a series of motor movements
making a cup of tea
115
what is agnosia?
person cannot identify what they are looking at.
| they can draw it but cannot say what it is
116
what is acalculia?
loss of ability to do arithmetical function
117
what is phase 3 of DAT? what commonly happens?
the terminal stage
become very apathetic
lose neurobiological function
do not eat very much and often become quite thing
118
what is operational criteria for diagnosis of AD?
probable AD
possible AD
definite AD
119
to be diagnosed with probable AD, a patient must have what?
deficits in 2 or more areas of cognition
120
in probable AD, what are 3 Non-amnestic presentations
language, visuospatial, executive dysfunction
121
what are some other key criterion for probable AD
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
definite AD diagnosis needs
histopathological evidence of AD obtained from biopsy or autopsy
123
what is an atrophied brain? why does this happen?
a shrunken brain
| because of the death of many neurons
124
which lobes of the brain tend to be affected first in this AD atrophied brain?
frontal and temporal lobes before parieto-occipital regions
125
what other things have to be identified of the brain to diagnose AD?
proliferation of glial cells
| intensity of neuropathological features correlate with severity of dementia
126
what are the two necessary features you need to see to diagnose AD
- large amounts senile plaques
| - large amounts of neurofibrillary tangles (NFTs)
127
what is found in the centre of a senile plaque?
lots of amyloid
128
where do neuropathological changes in AD typically begin?
hippocampus/medial temporal lobes
129
where do neuropathological changes in AD typically spread to from it's first stages?
spread posteriorly to parietal cortex
130
where do neuropathological changes in AD typically spread to from the parietal cortex?
frontal cortex
