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Brain, Biology and Behaviour > Week 11 - Memory + language > Flashcards

Week 11 - Memory + language Flashcards

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1
Q

What’s the difference between STM and LTM?

A

They differ in their capacity. STM = 7 items. LTM = vast.

STM requires rehearsal. LTM can be reconstructed after years, although maybe not accurate.

Once forgtetting STM, it is lost. LTM, a trigger may help you reconstruct a forgotten memory.

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2
Q

What is a reverberating circuit?

A

Hebb’s idea regarding STM storage = A circuit in which neuron A excites neuron B, which excites neuron C, which then re-excites neuron A.

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3
Q

What happens when storing something in short-term memory for a sufficient period of time?

A

It makes it possible for the brain to consolidate STM in to LTM (presumably build new synapses).

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4
Q

What’s wrong with Hebb’s theories regarding STM and LTM?

A

Holding onto a memory for a long enough time does not automaticlaly turn it into a permanent memory.

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5
Q

What was wrong with Hebb’s theory of consolidation?

A

The time needed for consolidation varies enormously, not just for the time it takes to synthesise proteins for establishing a long-term memory.

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6
Q

What is a flashbulb memory and how are they formed?

A

Emotionally significant events are quickly rememebred. They arouse the locus coeruleus, which increases norepinephrine release throughout the cortex and dopamine release in the hippocampus. Emotional experiences also increase the secretion of epinephrine and cortisol that activate the amygdala and hippocampus.

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7
Q

What is working memory?

A

Baddeley replaced the concept of STM. Working memory has to do with how we store information while we are working with it.

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8
Q

What are the three (four actually) components of working memory?

A

Visuo-spatial sketchpad - visual information
Phonological loop - auditory info dependent of modality
Episodic buffer - access LTM to make sense of STM.

Central executive - directs attention toward one stimulus or another so allows active manipulation

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9
Q

Damage to which area of the brain results in amnesia?

A

The Hippocampus.

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10
Q

What is the difference between retrograde and anterograde amenisa?

A

Retrograde - memory loss before injury

Anterograde - memory loss after injury

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11
Q

What parts of the brain did HM have removed?

A

Hippocampus, amygdala and nearby structures bilaterally removed to relieve epilepsy.

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12
Q

What did these removed brain bits result in for HM?

A

Moderate retrograde amnesia, SEVERE ANTEROGRADE AMNESIA.

  • could not learn hospital
  • could not remember telling story
  • Can learn new facts (semantic memory)
  • STM span remained in tact but poor episodic memory (events)
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13
Q

What does HM’s characteristics suggest?

A

Hippocampus is vital for formation of new long-term memories.

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14
Q

Was HM’s procedural memory affected?

A

No, procedural memory was in tact. Could draw something seen in a mirror, could remember and learn how to do things.

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15
Q

What type of memory is episodic memory a part of?

A

Declarative memory - memory you can articulate to others.

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16
Q

What other type of memory is there apart from declarative?

A

Procedural memory - allows you to do things - motor memory that allows body to perform a skill - don’t have conscious access to it, not stored as language.

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17
Q

Which type of memory was affected for HM? Explicit or implicit? And which is typical of amnesia?

A

EXPLICIT. He couldn’t remember seeing people the day before, but had a clear preference for those who were friendly toward him.

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18
Q

What is Korsakoff’s syndrome?

A

Memory disorder resulting from brain damage caused by longterm deficiency of B1 (thiamine).

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19
Q

In whom is Korsakoff’s syndrome most prominent?

A

Alcoholics. Diet suffers.

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20
Q

What does this B1 deficiency result in ?

A

The brain has trouble using glucose for energy.

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21
Q

What happens when glucose can’t be used for energy in the brain?

A

Death and shrinkage of neurons, particularly in mamillary bodies, dorsomedial thalamus, axons to prefrontal cortex.

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22
Q

What are symptoms of Korsakoff’s?

A

Apathy, confusion, amnesia.

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23
Q

Do Korsakoff sufferers have better implicit or explicit memory?

A

Better implicit. Also difficulty reasoning about their memory, difficulty ordering past events, “confabulate” - remember “guesses” as true memory.

24
Q

Do Korsakoff sufferers have retrograde or anterograde amnesia?

A

Both.

25
Q

What symptoms characterise Alzheimer’s disease?

A
  • Severe anterograde amnesia, as it continues will get retrograde amneisa also.
  • better procedural than declarative memory
26
Q

What are the genetic components of Alzheimer’s?

A

Person with Down syndrome end up with AD in mid-life.
Genes on chromasome 14 and 1 related to early onset (10% of cases of AD)
Genes on chromosome 10 and 19 related to late onset (90% of cases) but these are not strongly associated.

27
Q

What are amyloid deposits and what role do they play?

A

several types of proteins fold abnormaly and form problems

Amyloid plaques end up between neurons which interfere with firing (damage from axons, dendrites, which decreases plasticity)- apolipoprotein causes cell loss and prevents removal of amyloid protein.

Tau proteins produce unsual foldings (tangles) INSIDE cell bodies - associated with death of neurons.

28
Q

Which parts of brain are particularly susceptible to amyloid plaques?

A

Cortex (basal forebrain) and hippocampus.

29
Q

On which types of questions do Korsakoff sufferers confabulate?

A

Mainly events/about their own lives. The answer may have been true at some stage, but not necessarily now, but sometimes the answer is fanciful and implausible. Occasionally patients attempt to act on confabulations.

30
Q

Which way do patients with Korsakoff’s learn better? Completing sentences forcing more active role in remembering, or simply reading a list over and over?

A

Reading a list; when they complete sentences, they confabulate.

31
Q

Are any drugs effective for Alzheimer’s?

A

Not at this point.

32
Q

What else does not meet up with LTM and STM?

A

Some memories are neither LTM nor STM.

ECT can disrupt LTM - why if altering activity in brain briefly, can secure memories be disrupted?

Often STM doesn’t get transferred into LTM.

33
Q

What is semantic memory?

A

Facts.

34
Q

What is Episodic memory?

A

What happened, where & when.

35
Q

What is procedural memory?

A

Motor task/performance knowledge.

36
Q

What does a time gradient refer to regarding retrograde amensia?

A

Memory gets better the longer back in time memory is reached/worsened up to point of operation/damage.

37
Q

What does damage to basal ganglia effect?

A

Using patterns, statistics, motor movement.

38
Q

What brain bit is involved in spatial memory? (hint: london taxi drivers have big ones, rats with damage here can’t make mental maps).

A

Hippocampus.

39
Q

Hippocampus is important for…

A
  • Consolidation of a memory
  • NOT involved in “establishing” a memory but bind pieces together (makes a map of where the memory is - ie. different parts of the brain)
40
Q

What brain bit is semantic dementia associated with?

A

Temporal lobe - loss of semantic knowledge - implicate posterior regions also.

41
Q

What is anaphasia?

A

Loss of language ability.

  • unable to speak or unable to comprehend speech
  • unable to write
42
Q

What is Brocca’s aphasia (also non-fluent aphasia)?

A

Deficit mainly in speech production.
Speech is halting, telegraphic.
Similar difficulty with writing and sign language.

43
Q

Which type of words are usually still present in Brocca’s aphasia?

A

verbs, but kept simple. Changing tenses, prepositions, pronouns etc. typically lost.

44
Q

What type of comprehension problems come with Brocca’s aphasia?

A

Relatively simple sentences are well understood.

If grammar becomes complex, it becomes more difficult.

45
Q

What is Brocca’s aphasia actually a problem with? Muscles? Coordination? Language?

A

Language. Regardless of whether or not you are speaking or signing or comprehending, it is the language itself that is challenging.

46
Q

Do people with Brocca’s aphasia have insight into their problem?

A

Yes. People usually know what’s up.

47
Q

Where is damage in people with Brocca’s aphasia?

A

LEFT FRONTAL LOBE, thalamus and basal ganglia.

48
Q

What is Wernicke’s aphasia?

A

Seriously impaired language comprehension. Speech is effortless, melodic and produced at a normal rate. Content unintelligible: errors in choice of words and phonemes.

49
Q

Do people with Wernicke’s aphasia have insight into their problem?

A

No. They are generally unaware there is a problem, despite not really understanding what’s being said, or what they’re saying.

50
Q

What’s up with Wernicke’s aphasia (fluent aphasia)?

A

Phonemic paraphasia - shift order of individual phonemes and phoneme clusters

Anomia - difficulty selecting words that convey the intended meaning

Poor language comprehension

51
Q

What damage causes Wernicke’s aphasia?

A

Wernicke’s area, near auditory cortex - Left temporal lobe

52
Q

What is Conduction aphasia?

A

Inabilitiy of Brocca’s and Wernicke’s area to communicate via the ARCURATE FASCICULUS.

53
Q

What does conduction aphasia look like?

A

People have trouble repeating what they hear.

Can have some aspects of aphasia also.

54
Q

What is the bundle of axons between Brocca’s and Wernicke’s area that allows them to communicate?

A

ARCURATE FASCICULUS.

55
Q

What is anomia?

A

Form of aphasia in which there is an inability to recall the names of everyday objects.

Brain, Biology and Behaviour (11 decks)

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