Module 37 - Memory Flashcards
1
Q
What are the categories of human memory?
A
- Qualitative categories
- Declarative vs non-declarative/procedural
- Temporal categories
- Immediate vs working vs long-term
2
Q
What are the different qualitative categories of memory?
A
Declarative vs non-declarative/procedural
3
Q
What are the different temporal categories of memory?
A
Immediate vs working vs long-term
4
Q
What is the general concept of qualitative categories - “types” - of memory (the hierarchy)?
A
- Declarative = available to consciousness = you can say it out loud → often can be learned in a single exposure (one trial learning)
- Nondeclarative = generally not available to consciousness → usually requires many repetitions (gradual learning)
5
Q
What is the general concept of temporal categories - “stages” - of memory (the hierarchy)?
A
- Immediate memory
- Working memory
- Long-term memory
6
Q
What is the timeframe of each of the temporal categories - “stages” - of memory?
A
- Immediate memory
- Fractions of a second-seconds
- Working memory
- Seconds to minutes
- Long-term memory
- Days-years
7
Q
What are the different anatomical structures that are involved at different times in the storage of explicit memories? (important question)
A
- Less than 1 second (“attention” or “registration”)
- Brainstem - diencephalic activating systems, frontoparietal association networks, specific unimodal and heteromodal cortices
- Seconds to minutes (“working memory”)
- Frontal association cortex; specific unimodal and heteromodal cortices
- Minutes to years (“consolidation”)
- Medial temporal structures; medial diencephalic structures; specific unimodal and heteromodal cortices
- Years
- Specific unimodal and heteromodal cortices
8
Q
True or false: you can forget things at any moment of the continuum of stages of memory.
A
True
9
Q
Which memory is implicit and which memory is explicit?
A
Declarative memory is explicit and nondeclarative memory is implicit
10
Q
What are some of the characteristics of declarative memory?
A
- Explicit memory
- Easily verbalized
- Conscious
- Often can be learned in a single exposure (one trial learning)
11
Q
Which structure(s) of the brain is responsible for forming new declarative memories? (important question)
A
Hippocampus and the diencephalon (which is composed of the thalamus and the hypothalamus)
12
Q
Which structure(s) of the brain is responsible for storing declarative memories?
A
Occurs in diffuse cortical areas
13
Q
What is the case of H.M. (1926-2008)
A
- He has a bilateral medial temporal lobe resection (1953)
- Removed hippocampus, amygdala, temporal cortex
- He then could not form new memories: problem with consolidation
- No problem with old memories → long term memory
- Some measures of memory were not affected
- WHAT WAS IMPACTED WAS THE TRANSFER FROM THE IMMEDIATE MEMORY TO LONG-TERM MEMORY = HIS WORKING MEMORY WAS IMPACTED
14
Q
What happens 2 years post-operation in the case of H.M. (1926 - 2008)
A
- Intelligence scores similar to pre-operation
- No deficits in perception, abstract thinking, or reasoning
- Could form non-declarative memories
- BUT he could not form DECLARATIVE memories
15
Q
How were we able to determine that H.M was able to form non-declarative memories?
A
- The number of errors to form the task of drawing between the lines in a mirror = # of errors decreased
16
Q
What was everyday life like for H.M?
A
- Obvious inability to recall events n his daily life
- Memory deficiency was “permanent”
- “Every day is alone… whatever enjoyment I’ve had and whatever sorrow I’ve had.” -H.M
17
Q
What is the difference between retrograde amnesia and anterograde amnesia? (important question)
A
- Retrograde amnesia (RA) is a loss of memory-access to events that occurred or information that was learned in the past. It is caused by an injury or the onset of a disease.
- Anterograde amnesia is a loss of the ability to create new memories after the event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact.
18
Q
There is another case called patient N.A. He was in a fencing foil accident and damaged his thalamus and mammillary bodies in the brain (without damage to other parts in the brain). What type of deficits did the patient have? What are the structures that this patient damaged known for?
A
- Similar amnesia to H.M. case
- The thalamus and mammillary bodies are particularly sensitive to alcoholism → they degenerate.
- Can present with anterograde and retrograde amnesia
19
Q
What is Korsakoff’s syndrome?
A
- Alcoholism, thiamine (B1) deficiency
- Thalamus and mammillary bodies degeneration
- Anterograde and retrograde amnesia
20
Q
What did these cases teach us? What are the important structures for declarative memory? (important question)
A
- Midline diencephalic structures
- Left diencephalic lesions: verbal memory deficits
- Right diencephalic lesions: visual-spatial memory deficits
- Medial temporal lobe structures (hippocampus)
- Establishes new declarative memories (inability = anterograde amnesia)
21
Q
What happens with a left diencephalic lesion? (important question)
A
Verbal memory deficits
22
Q
What happens with a right diencephalic lesion? (important question)
A
Visual-spatial memory deficits
23
Q
What did the study with the taxi drivers in London demonstrate?
A
- The number of months spent as a taxi driver (months) correlated with the size of the hippocampus
- The time spent learning the roads of London = meant a larger hippocampus volume
- This tells us that the hippocampus has a very important role in establishing new declarative memories.
24
Q
What is retrograde amnesia is typically more indicative of what?
A
Retrograde amnesia (loss of events preceding injury) more indicative of generalized lesions associated with head trauma &/or degenerative disorders
25
Anterograde amnesia is typically indicative of damage to which structures?
* Midline diencephalic structures
* Medial temporal lobe structures (hippocampus)
26
Immediately after a TBI injury, what can we expect to see in a patient?
* Immediately after the injury, when the patient cannot form any new memories and suffers from anterograde amnesia, typically associated with:
* Restlessness
* Increased agitation
* Disruption of the sleep/wake cycle
* But they also have preserved memories from long ago
* Typically know who their family is
* Typically know where they work
* Etc.
* But they also have a small retrograde amnesia period.
27
What is the goal standard measurement for objective tests after a TBI?
* GOAT = The Galveston orientation and amnesia test
* A clinically useful tool for monitoring post-traumatic amnesia
28
What type of question does the GOAT assessment ask?
* Ask questions about long term memory
* When were you born and what is your name
* Ask questions about immediate memory
* Where are you now and how did you get here
* Ask questions surrounding the accident → the time around the injury to the head
* When were you admitted to the hospital
29
What is a normal score on the GOAT?
Normal = 76 - 100
30
What is a borderline score on the GOAT?
Borderline = 66 - 75
31
What is an impaired score on the GOAT?
Impaired \< 66
32
True or false: The GOAT is used to determine when a patient is ready to move on from the acute care site to the rehab site.
* True, we want to use the GOAT to have a good idea if the patient is able to remember and retain new information.
* Rehab center you will need to start remembering and retaining new info, therefore it would not be appropriate to transfer the patient when they are in a state of post-traumatic amnesia
33
What type of scoring would a patient have on the GOAT in the post-traumatic amnesia phase after the TBI?
GOAT \< 75 but it will diminish over time
34
What is the interpretation of the GOAT?
The duration of post-traumatic amnesia (PTA) is defined as the period following a coma in which the GOAT score is \< 75. PTA is considered to have ended if a score \> 75 (sign should be greater than) is achieved on three consecutive administrations (3 different days for example)
35
What is the prognostics of the GOAT?
* Duration of PTA after a TBI provides one of the earliest and best predictors of long-term outcome
* The longer someone remains in this PTA will have a worse prognosis, compared to someone who remains in this PTA state for a shorter period of time.
36
Fill in the blanks !!! (important question)
IMAGE
37
Which structures are necessary for forming new memories?
The hippocampus and the medial diencephalic structures
38
Damage to either the hippocampus and the medial diencephalic structures causes what?
Anterograde amnesia
39
We know how (kind of) new memories are formed, meaning that we know what brain structures are important for forming new memories. BUT, where are the long-term declarative memories stored?
* Storage occurs in the cortex
* Storage site related to the modality in question (e.g. visual cortical areas appear to be involved in storing visual memories)
* Degradation in long-term memory proportional the amount of cortex damaged (mass action principle)
* If a lot of your cortex is damaged, you are probably going to lose a lot of memory.
40
What is the mass action principle?
* Degradation in long-term memory proportional the amount of cortex damaged
* If a lot of your cortex is damaged, you are probably going to lose a lot of memory.
41
Where is the acquisition and storage of declarative information for short-term memory storage?
Hippocampus and related structures
42
Where is the acquisition and storage of declarative information for long-term memory storage?
A variety of cortical sites: Wernicke’s area for the meanings of words, temporal cortex for the memories of objects and faces, etc.
43
What happens when you aks a patient to recall one of the images you have shown to them on a screen after a series of pictures, for example, a chair?
* The same areas of the brain light up when you are perceiving an object as when you are recalling/ imagining it.
* In this case, imagery is remembering = considered as memory
* You can see that the blue spaces light up = the chair
* This concludes a theory that memories are stored in the cortex or part of the cortex that is responsible for the modality
* For example, if you remember how someone’s voice sounds like = it would be stored in the auditory cortex.
44
What factors help with forming long term memories? (How do we remember things better?)
* Association is important for storage
* The capacity of working memory depends upon meaning to the person and amount of associated information that has already been stored
* For example, let’s say someone really likes pizza, they can tell you all the good pizza shops in Halifax. If you add a new pizza shop that opened, it will be easy to remember since you associate with the rest.
* But if you compare it to someone who does not like pizza, the names of the pizza shops will be so random to the person that they won’t remember them → so if you add the name of the new pizza place, it is going to be difficult to remember
* Motivation and interest also influence memory
* Adult learning principles
* For example, this neuroscience might be difficult to learn since you have not done much neuroscience but you are motivated to pass this class, therefore you will learn it
* \*\*\*We know that a lot of storage happens by association
* \*\*\*The normal human capacity for meaningless information ~ 7- 9 digits
45
What is the normal human capacity for meaningless information?
~7 to 9 digits
46
Why are we better at remembering an image of food when we are hungry?
Motivation → better at remembering things about food when we are hungry
47
How do we retrieve long-term memories? We (kind of) know how we form and store memories, but how do we retrieve them later?
* Retrieving memories appears to involve frontal lobes
* Damage to frontal lobes = difficulty with recall, sometimes accompanied by confabulation → (Confabulation is a symptom of various memory disorders in which made-up stories fill in any gaps in memory. German psychiatrist Karl Bonhoeffer coined the term “confabulation” in 1900. He used it to describe when a person gives false answers or answers that sound fantastical or made up.)
48
What happens to damage to the frontal lobe in terms of memory?
Damage to frontal lobes = difficulty with recall, sometimes accompanied by confabulation → (Confabulation is a symptom of various memory disorders in which made-up stories fill in any gaps in memory. German psychiatrist Karl Bonhoeffer coined the term “confabulation” in 1900. He used it to describe when a person gives false answers or answers that sound fantastical or made up.)
49
What is confabulation?
It is when people make stuff up to make up for the fact that they don’t remember → (Confabulation is a symptom of various memory disorders in which made-up stories fill in any gaps in memory. German psychiatrist Karl Bonhoeffer coined the term “confabulation” in 1900. He used it to describe when a person gives false answers or answers that sound fantastical or made up.)
50
What are some of the characteristics of non-declarative?
* “Implicit” memory
* Difficult to verbalize
* More unconscious
* Usually require many repetitions (gradual learning)
* Example = learning how to play a sport
51
Which structures in the brain are responsible for nondeclarative memory?
* Premotor cortex
* Basal ganglia
* Amygdala
* Cerebellum
52
What are the four different types of nondeclarative memory?
* Procedural motor learning
* Classical conditioning
* Priming
* Operant conditioning
53
What is procedural motor learning?
* Example → HM star diagram
* Skiing
* Shooting a basketball
* Riding a bike
* Dancing
* Playing the guitar
* It is motor learning → therefore all the brain structures that ADAM talked about for motor learning are also important for procedural motor learning.
54
What is the basal ganglia’s involvement in procedural motor learning?
* We know that the Basal Ganglia is extremely important for motor learning and motor skill acquisition.
* A study has been done → different doors and where a reward was behind one of the doors; patients with Parkinson’s disease that did not have their dopamine medication → did not do very well with this task = to notice that the reward was behind a specific door/ then when on medication patients did better and controls = not with PD = did great.
* This just serves as a bit of support to know that dopamine and the basal ganglia re important for procedural motor learning.
55
Where is the acquisition and storage of nondeclarative information for short-term memory storage?
Sites unknown but presumably widespread
56
Where is the acquisition and storage of declarative information for long-term memory storage?
* Cerebellum
* Basal ganglia
* Premotor cortex
* And other sites related to motor behavior
57
What is classical conditioning?
* Learn to associated two sensory stimuli (classical conditioning)
* Pavlov and his dogs E.g. food (unconditioned stimulus) → salivation (unconditioned response)
* Present bell just before food, the animal learns association and begins salivating when the bell is sounded (now a conditioned response to a conditioned stimulus)
58
What is priming?
* Priming is “change in the processing of a stimulus due to a previous encounter with the same or related stimulus… with or without conscious awareness of the original encounter” - P. p. 698
* Resistant to brain damage, aging, and dementia → meaning that these individuals still respond to priming quite well.
59
Explain the study to show how priming works.
* Participants are shown “primed” list under false pretenses (for example, within a paragraph)
* Later asked to complete word stem list (task 2) - contains stems of words and both primed and unprimed list.
* In task 2, participants complete stems of primed words to form primed words themselves more often than chance would predict.
* What this means is that because the individual had seen the primed words before, the patient was much quicker to fill in words like “element” or “technical” because these words where primed.
60
What is operant conditioning/instrumental conditioning?
* Learn to associate a stimulus with a response
* For example, when a certain behavior is followed by a reinforcing stimulus the likelihood of that behavior changes.
* Positive reinforcement (reward) leads to increase in that behavior.
* Negative reinforcement (punishment) leads to decrease in that behavior.
* Basal Ganglia!
61
What type(s) of nondeclarative learning are the basal ganglia important for?
Operant conditioning
Procedural motor learning
62
Why do we know that the basal ganglia, cerebellum, and pre-frontal cortex are important structures for memory storage?
Because damage to these structures interferes with the ability to learn new motor skills
63
In general, where would visual information/memories be stored?
In the visual association cortices
64
In general, where would auditory information/memories be stored?
Auditor association cortices
65
True or false: Memories are not primarily stored within brain regions originally involved in processing each kind of information.
False = they are !!!
66
Are declarative and non-declarative memories both primarily stored within brain regions originally involved in processing each kind of information?
YES, non-declarative memories are similar to declarative memories.
67
We know that retrieving DECLARATIVE memories appears to involve the frontal lobes. BUT, what about NON-DECLARATIVE?
Likely very similar regions for RETRIEVING … (this is distinct for learning and storage)
68
Is there an evolutionary pressure on neural connections for some “memory”? How do we know?
* Yes, some “memory” appears to come from evolutionary pressure on neural connections.
* From birth (i.e. before they could have learned this association), baby birds are scared of shadows that look like predators, but not other shadows… proves that it is learned before they are born.
69
Making a change in synaptic plasticity lasting more than a few hours requires ___________ and \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. These take at least several hours,i.e. Considerably longer than any short-term plasticity.
Making a change in synaptic plasticity last more than a few hours requires gene transcription and protein synthesis. These take at least several hours,i.e. Considerably longer than any short-term plasticity.
70
True or false: As our memory moves into long term memory we likely need changes in gene transcriptions. There are likely structural changes.
TRUE
71
What are the different memory cellular mechanisms involved at different times in memory storage?
* Seconds to minutes
* The ongoing electrical activity of neurons
* Changes in intracellular Ca2+ and other ions
* Changes in second messenger systems
* Minutes to hours
* Protein phosphorylation and other covalent modifications \
* Expression of immediate early genes
* Hours to years
* Additional changes in gene transcription
* Translation resulting in structural changes of proteins and neurons
72
What are the memory cellular mechanisms involved in memory storage within seconds to minutes of the memory?
* The ongoing electrical activity of neurons
* Changes in intracellular Ca2+ and other ions
* Changes in second messenger systems
73
What are the memory cellular mechanisms involved in memory storage within minutes to hours of the memory?
* Protein phosphorylation and other covalent modifications
* Expression of immediate early genes
74
What are the memory cellular mechanisms involved in memory storage within hours to years of the memory?
Additional changes in gene transcription
Translation resulting in structural changes of proteins and neurons
75
What are the different anatomical structures involved at different times in the storage of explicit memories?
* Less than 1 second (“attention” or “registration”)
* Brainstem-diencephalic activating systems
* Frontoparietal association networks
* Specific unimodal and heteromodal cortices
* Seconds to minutes (“working memory”)
* Frontal association cortex
* Specific unimodal and heteromodal cortices
* The ongoing electrical activity of neurons
* Minutes to years (“consolidation”)
* Medial temporal structures
* Medial diencephalic structures
* Specific unimodal and heteromodal cortices
* Years
* Specific unimodal and heteromodal cortices
76
What are the different anatomical structures involved at less than 1 second in the storage of explicit memories? (important question)
* Less than 1 second (“attention” or “registration”)
* Brainstem-diencephalic activating systems
* Frontoparietal association networks
* Specific unimodal and heteromodal cortices
77
What are the different anatomical structures involved at seconds to minutes in the storage of explicit memories? (important question)
* Seconds to minutes (“working memory”)
* Frontal association cortex
* Specific unimodal and heteromodal cortices
* The ongoing electrical activity of neurons
78
What are the different anatomical structures involved at minutes to years in the storage of explicit memories? (important question)
* Minutes to years (“consolidation”)
* Medial temporal structures
* Medial diencephalic structures
* Specific unimodal and heteromodal cortices
79
What are the different anatomical structures involved at years in the storage of explicit memories? (important question)
* Years
* Specific unimodal and heteromodal cortices
80
Can we observe physical changes associated with memory storage/performance?
* There is structural changes that occur with learning and memory
* For example, the hippocampal volume (related to remembering spatial information) correlated with time as taxi driver (a job which depends on skill in this area)
* Hippocampal = responsible for spatial information
81
True or false: The hypothalamus is responsible for remembering spatial information.
FALSE → the hippocampus
82
How is memory affected by brain damage?... gives examples of possible causes to create memory loss.
* Hemorrhages (little blood-brain bleeds)→ they can be multifocal (DAI = diffuse axonal injury) or unifocal (in one spot) = usually multifocal for memory loss.
* Contusions (bruise to the brain) → anteromedial temporal lobes (because we know that it is where the hippocampus and diencephalon are located)
* Concussions infarcts or ischemia
* Global cerebral ischemia - memory often prominent
* Top or basilar artery or PCA - medial temporal lobes, medial thalami
* Hippocampus particularly vulnerable to anoxic injury
* ACA aneurysm - damage to basal forebrain - memory loss as well as deficits seen with frontal lobe lesions.
83
Name a degenerative disease that could cause memory loss.
Alzheimer’s - selective disease process to bilateral hippocampal, temporal, and basal forebrain structures.
84
Name a few examples of multifocal lesions that could cause memory loss.
* Multiple sclerosis
* Tumor
* ICH → Intracerebral hemorrhage
* CNS infection
* Toxicity/metabolic encephalopathies
* Vasculitis
* Hydrocephalus
* Etc.
85
What is psychogenic amnesia?
* NO damage to temporal lobes
* It is a potential cause for memory loss
* It can cause symptoms like
* Dissociation
* Repression
* Conversion
* Malingering
86
True or false: We can have deficits in forming new declarative memories, while (mostly) sparing existing memories and procedural memory.
True → the example is patient H.M.
