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Neuro 210 > Memory Disorders (amnesias) > Flashcards

Memory Disorders (amnesias) Flashcards

1
Q

What is the definition of memory?

A

memory is the retention/storage of information that can be revealed at a later time

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2
Q

What is the difference between neural memory and external memory?

A

neural memory is the memory we store in our brains and it can be suseptible to damage and amnesia/dementia etc…

external memory is like books, libraries, the internet..etc.. any external device besides our brains that store information that can be retrieved at a later time

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3
Q

What was Ebbinghaus’s experiment on memory and how did it contribute to the understanding of memory storage?

A

he did an experiment to show that retention of nonsense syllables fades over time
- he drew a ‘forgetting curve’ that had time as the x-axis and percent recited in the y-axis and studied a set of non-sense syllables and tested himself over a period of time from 1min after rehersal to 30 days after rehersal to see how much her can remember

results: number of syllables he could retain, faded over time

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4
Q

What are the properties of STM?

A

active state (while things are shifting around), rapid decay due to not rehersing, and vulnerable to disruption

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5
Q

What are the properties of LTM?

A

inactive state, slow decay and less vulnerable to disruption because its been rehersed

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6
Q

What is consolidation and reconsolidation?

A

consolidation is the process of storing information from short term memory into long term memory (first time)

reconsolidation is the process of retaking the memory out of LTM and bringing back into STM and then changing it/working with it and putting it BACK into LTM

they have similar but not identical mechanisms for protein synthesis in the brain

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7
Q

What are 2 reasons memories can be disrupted and what can they result in?

A

the two reasons are not mutually exclusive (one event does not cause or influence the other)

  1. storage failure (inability to store STM to LTM) –> results in permanent amnesia
  2. retrieval failure (inability to bring whats in LTM to STM)–> results in temporary amnesia
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8
Q

What are the seven sins of memory by definition?

A

these are “sins” that can be experienced by anyone

  • they are not always serious in a way that they need to be treated
  • they just highlight the fragility and plasticity of the brains memory systems
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9
Q

List and describe the 7 sins of memory?

A
  1. Transience: weakening of memory over time (i.e. ebbinghause forgetting curve experiment)
  2. Absent-mindedness: deficit interface between attention and memory (forgetting where u put something becuse u were doing another thing)
  3. Blocking: failed search for info… i.e. tip of the tongue or aka proper name anomia (you know the name but cant say it)
  4. Misattribution: assigning a memory to incorrect source
  5. suggestibility: when memories are implanted i.e. through advertisements
  6. Bias: current beliefs influence memories (i.e. religion..etc.)
  7. persistence: repeated recall of specific memories like flashbacks or even PTSD
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10
Q

What is Amnesia?

A

amnesia is memory loss

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11
Q

What is psychogenic amnesia

A

amnesia with no physical cause

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12
Q

what is retrograde amnesia?

A

failure to remember what happened for events occuring prior to the trauma but can remember childhood memories and has ability to form new memories

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13
Q

What is anterograde amnesia?

A

failure to form new memories (i.e. problem with consolidation)

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14
Q

What are 6 physical causes of amnesia?

A
  1. stroke (temporal lobes are highly suceptible to cerebrovascular injury)
  2. viral infection: herpes, simplex encephalitis of temporal lobes
  3. Tumours: common in brain ventricles around temporal area
  4. closed head injury: skull is intact but brain twists on axis (i.e. whiplash, concussions..etc..)
  5. thiamine deficiency: Korsakoff’s syndrome
  6. Age-related neurodegeneration: senile dementia/alzheimers
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15
Q

What is a clinicans first task in dealing with individuals who may have memory problems?

A

their first task is to establish whether amnesia is organic (due to injury in the brain) or psychogenic (psychological basis)
- checking to see patients medical records for any history of brain injurt (psychogenic amnesia is suspected if no brain injury occured)

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16
Q

What tests are done to test for other psychological deficits besides memory loss?

A

Most patients will show psychological deficits besides memory loss
- clinicans assess behavior and behavior is influenced by multiple types of neural processing

  • need to assess: neuropsychological status by using batteries of tests for disorders of attention, perception, motivation, emotions and sensorimotor processing
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17
Q

What is the ultimate goal of clinican’s assessment?

A

to determine how extensive or specific the memory deficits are

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18
Q

What is the assessment of retrograde amnesia (RA)? What is the Law used to design tests?

A

difficult to assess bc its testing on memories of past events that arent the person’s childhood

  • Uses ribot’s law (1882) to design tests –> states that the older the memory, the more resistant it is to disruption (older memories are more resilient)
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19
Q

What are the 2 tests given in RA assessment?

A
  1. Boston Remove Memory Test (BRMT)
    - assesses distant memories of public events and famous people (test is based on how old the person is and what era they were born in)
  2. Dead or Alive test
    - tests recognition of whether a famous person is still living
    (a flaw in this is that the person might not even be familiar with the famous people from their era in the first place)
20
Q

What is the goal of the tests in RA assessment?

A

to target specific decades to assess temporal extent of retrograde amnesia (aka how long ago the memory loss before the trauma goes on for)

21
Q

What is the procedure for the assessment of Anterograde Amnesia (AA)?

A

the David Weschler’s Memory scale-revised is commonly used along with a range of tests

  • each index has a mean of 100 in a normal population for the WMS-R
  • involves a balanced assessment of verbal and non-verbal memory (explicit vs. implicit memory)
22
Q

What are 7 tests included in the WMS-R for assessing AA?

A
  1. personal and current information
  2. mental control (counting backwards from 20, reciting the alphabet)
  3. logical memory (reading a story and recalling as much of it as possible)
  4. visual paired associates (learn and recall pairs of pictures)
  5. Verbal paired associates (learn and recall pairs of words)
  6. Visual reproduction (shown a figure, then asked to draw it from memory)
  7. Digit span (read a sequence of numbers and then repeat them back in correct order)
23
Q

What is Korsakoff’s Syndrome and the Amnesic Syndrome?

A

Korsakoff’s syndrome is observed in alcoholics that were incapable of learning new memory (had AA)
- caused by deficiency of thiamine aka vitamin b1
- not directly caused by alcohol consumption
its just that alcohol causes no gut absorption of b1 and that leads to chronic liver disease and then leads to no liver storage of b1

  • vitamin b1 causes brain glucose metabolism and transmitter synthesis
24
Q

What is the treatment of korsakoff’s syndrome?

A

high doses of vitamin b1 injections

25
Q

What is the neuroanatomy of Korsakoff’s syndrome? where is the damage in the brain that causes memory loss?

A

damage to the mammillary bodies and mediodorsal thalamic nuclei and significant damage to medial temporal lobes is associated with korsakoff’s syndrome

26
Q

What happens when the mammillary bodies are damaged?

A

connected to hippocampus therefore damages elicit anterograde amnesia

27
Q

What happens if you damage the mediodorsal thalamic nuclei?

A

this area connects the preforntal cortex to thalamus therefore the damage leads to amnesia for autobiographical information like info about yourself and recalling celeb names

28
Q

What kind of disorder is korsakoff’s syndrome?

A

organic

29
Q

What are the 3 normal characteristics/brain functioning in amenesic syndrome?

A
  1. intact short term and semantic memory
  2. general intellect is intact (normal IQ)
  3. intact procedural and perceptual learning
30
Q

what are 3 deficits (severe) in people with amnesic syndrome in terms of brain functioning?

A
  1. severe AA
  2. variable degree of RA
  3. selective failure of episodic memory (memory of personal events)
31
Q

What are 2 explanations for amnesic syndrome?

A
  1. failure to store contextual infromation needed to distinguish different memories (failure to encode for context of situation to form distinct memory of an event)
  2. deficit in memory consolidation (temporal lobe amnesia) —> difficulty in storing memory to LTM from STM
32
Q

What are 4 symptoms of frontal lobe damage and its effect on memory?

A
  1. confabulation: production of false memories
  2. source amnesia: forgetting knowledge of sources and where things come from
  3. unable to specify memories in great detail
  4. impaired working memory (STM)

frontal lobes guide in memory retrieval

33
Q

Which area of the brain has been shown to be critical for memory consolidation

A

the hippocampus

  • receives input from all neocortical areas
  • it processes information and sends output back to same areas that provided the input
34
Q

What areas of the brain are associated highly with explicit Long term memory?

A

the medial temporal lobe; diencephalon

–> with memories associated with facts and events (concious memory)

35
Q

What was noted about H.M and his declarative (explicit) and non declarative (implict) memory types?

A

H.M had anterograde amensia with barely any spared memories for events and facts (declarative memory)
- his non declarative implict memories for H.M are intact because the brain structures responsible for underlying motor memory like cerebellum and striatum are still intact in HM

36
Q

What is the process by which the hippocampus binds together elements of a memory trace in the neocortex and what are the details?

A
  • called consolidation
  • all the areas of the brain like somatosensory, smell, taste, motor..etc.. of an event get connected to the medial temporal hippocampus (MTH) system into ONE cluster of neurons (therefore, a bunch of clusters get turned into one) and new memories will rely primarily on the neocortical activity for retrieval and old memories will become independent of the MTH systems and just form connections in the neocortex to be retrieved instead of having to be linked together to form a memory for retrieval in the MTH
  • primary role of the hippocampus is to bind together the individual elements of a memory trace like sensation and sounds (the contex)
37
Q

How does the hippocampus aid in reconsolidation of memory? (from LTM to STM and then back to LTM)

A
  • the hippocampus normally sotres an index to neocortical patterns that is used to retrieve memories
    i. e. if it gets presented with the same 2 types of neurons involved in a previous event u tried to encode, then it will “fill in the blanks” and associate the rest of the neurons involved in that event to create the memory and bring it to STM this is called “pattern completion”
38
Q

What is priming and how is it used in reconsolidation?

A

priming task is showing a full picture, and then a week later they are shown 3 different pictures: one that has a part of the initial pic, one that looks nothing like it and one that is mushed up.. people will remember the one that has the part of the first pic they saw a week ago due to priming

39
Q

How did HM preform in priming task

A

he preformed well but still needed more hints than normal

40
Q

What occurs when theres a lesion localized to area CA1 of the hippocampus?

A

poor recall of lists, stories, diagrams … i.e. anterograde amnesia

  • normal retrograde memory and intact cognitive functions other than memory
41
Q

What is the CA1 area and what do we know about it?

A

we know its a region that has to do with plasticity and LTP (learning) in the hippocampus that is 1/10000 the size of what H.M had lesioned off which produced the same amount of deficits as H.M had

42
Q

What are the 8 steps to put a drug out in the market for people to use legally (relating to neurological disorder treatment)?

A
  1. examine the neurological disorder
  2. Identify the gene responsible for the disorder
  3. implant the gene into a animal model and alter it to see the animal model of the disease
  4. track the pathogensis of the disease in the animal (the symptoms, the deficits, the behaviors)
  5. Basic neurobiology of the disorder based on animal model (what occurs at the synapses..what NT’s are released or not released..etc.)
  6. Therapeutic interventions (seeing what proteins are involved/linked to the disorder and coming up with a drug to target the proteins)
  7. Preclinical trial —> assessing effectiveness in experiment (double blind)
  8. Effectiveness in general population?
43
Q

what was eric kandel’s contribution to learning and memory and synaptic plasticity?

A

first to directly link synaptic plasticity to learning and showed that CREB activation is needed for long term memory (used fruitflies w tim tully)

44
Q

What was tim bliss and joe ledoux’s contribution to learning and memory and synaptic plasticity?

A

discovered synaptic strengthening in the hippocampus (bliss) and amygdala contribution to learning and memory (LeDoux)

45
Q

What is the main idea behind memory enhancers/ smart pills or Nootropics?

A

since synaptic plasticity is crucial for memory storage, boosting synaptic plasticity therefore should improve memory

46
Q

What are the 3 ways of boosting synaptic plasticity in the brain?

A
  1. AMPAkines: drugs that enhance ion flow through AMPA receptor channels (which indirectly increase cAMP levels –> PKA –> then active CREB)
  2. Activators of nACHR’s of cholinesterase inhibitors –> increases activation of NAChR’s or increase levels of aCh at synapse which also activates kinases and indirectly makes more cAMP and pKA and leads to more active CREB
  3. PDE Inhibitors –> increase cAMP levels by inhibiting phosphodiesterases which breakdown cAMP (increases active CREB)

Neuro 210 (12 decks)

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