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L&M Flashcards

0
Q

Epilepsy: What happens in neurons?

A

Glutamate (excitatory neurotransmitter) and GABA (inhibitory neurotransmitter) are in trade-off all the time. In seizure, lack of GABA leads to overwhelming excitation.

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1
Q

What is epilepsy?

A

Sudden excitation in groups of neurons with loss of inhibitory potential
(All neurons fire at same time; brain can’t process it)

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2
Q

What is TLE?

A

Sudden, unprovoked seizures emerging from medial or lateral temporal lobe. Can be simple partial or complex partial

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3
Q

Cause of TLE

A

Most common hippocampal sclerosis - loss of neurons, growth of glial cells

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4
Q

What is declarative memory

A

Conscious access to previously learned information. Memory that can be articulated

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5
Q

What is procedural memory?

A

‘How to’ memory (eg riding a bike)

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6
Q

HM’s memory loss?

A

Lack of declarative memory; anterograde amnesia; procedural memory intact (can learn new skills, can’t remember having learnt them)

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7
Q

Are medial temporal lobes more important for anterograde or retrograde; declarative or procedural memories?

A

Anterograde and declarative

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8
Q

What is result of left MTL lesion?

A

Verbal episodic memory impairment

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9
Q

What is result of right MTL lesion?

A

Visual / spatial memory impairment

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10
Q

What role do temporal lobes play in memory?

A

Engine room of memory

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11
Q

What are the pathways memory takes?

A

Sensory input (unimodal and polymodal associations) from FTP (frontal, temporal, parietal); info into (or out of) perirhinal and para hippocampal cortices; into (or out of) entorhinal cortex, into (or out of) hippocampus (process goes both ways)

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12
Q

What is role of hippocampus?

A

In association w surrounding structures, hippocampus essential for learning and consolidating. Two views: retrieval can happen independent of hippocampus (squire - consolidation theory); retrieval dependent on hippocampus (Moscovitch - multiple trace theory)

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13
Q

What are relational memory tasks?

A

Association of two things: eg table as word and table as object. Hippocampus essential.

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14
Q

What are the 3 extra temporal zones related to processing of memory?

A

Papez’s circuit
Diencephalon
Frontal lobes

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15
Q

What is Papez’s circuit responsible for?

A

Amygdala + Papez’s circuit = limbic region (emotional expression and experience)
Declarative memory

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16
Q

What does Papez’s circuit comprise of?

A

Mammillary bodies, anterior thalamic nuclei, fornix, cingulate gyrus, hippocampus. Circuit starts and ends with hippocampus

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17
Q

What do lesions in Papez’s circuit result in?

A

Declarative and relational memory impairment

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18
Q

What role do frontal lobes play in memory?

A 
Motor programming (posterior of frontal lobe - just before central sulcus)
Problem solving and higher level cognitive functioning (anterior of frontal lobe [pre-frontal cortex]). This separates us from all other animals
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19
Q

Where are strategies developed and implemented for storing and retrieving memories?

A

Frontal lobes

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20
Q

What do lesions in frontal lobe result in?

A

Lack of context for memories (eg don’t remember source for memory/information), confabulation and distortion of memories,

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21
Q

What is the diencephalon?

A

Thalamus and hypothalamus

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22
Q

What does damage to dorso-medial nuclei in thalamus result in?

A

deficit in selecting appropriate information

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23
Q

What does damage to intralaminar/midline nuclei of thalamus do?

A

Damage to semantic memory and memory retrieval (reduced mental flexibility)

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24
Q

What is synaptic plasticity?

A

Where learning occurs because biochemistry of synapses has changed, altering effect on post-synaptic neuron

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25
Q

What is long-term potentiation?

A

Long term increase in excitability of neuron due to particular synaptic input caused by repeated high frequency activity of that input.

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26
Q

What is Hebb’s rule?

A

Strengthening of a synapse that is repeatedly active when the post-synaptic cell fires

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27
Q

What is glutamate?

A

Excitatory neurotransmitter

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28
Q

What does LTP do to synapse?

A

Increases sensitivity of receptors to glutamate
Increases amount of glutamate
Synthesises protein in post-synaptic dendrite

29
Q

In what parts of brain does LTP occur?

A
  • hippocampus (entorhinal cortex) esp. Dentate gyrus and CA1

- pre-frontal cortex, thalamus, motor cortex, visual cortex, amygdala

30
Q

What does long term depression do?

A

Reverses effect of LTP

Low frequency input at synapse which decreases synaptic strength

31
Q

What is habituation & what does habituation do?

A

Long term repeated stimulation of neuron, reduces synaptic strength (loses impact)

32
Q

What is sensitization?

A

noxious stimuli causes exaggerated response in post synaptic neuron when noxious stimuli repeated

33
Q

What are some mechanisms of synaptic plasticity?

A

long term potentiation
Long term depression
Habituation
Sensitization

34
Q

What is memory?

A

Mental process for acquiring and retaining information for retrieval at later time

35
Q

What is explicit memory?

A

Memory that can be consciously recalled

36
Q

What is implicit memory?

A

Memory for which no specific learning event can be remembered

37
Q

What is procedural memory?

A

Memory of skills and procedures
Motor skills
Independent of hippocampus (does involve cerebellum and basal ganglia)

38
Q

What is declarative memory?

A

Accumulation of facts/data from experiences
Primarily processed through hippocampus
Is relational, and can be accessed independent of environment

39
Q

What are the serial models of processing memory?

A

Atkinson-shiffrin
Tulving’s
Levels of processing model

40
Q

What is Atkinson-Shiffrin model of memory?

A

Serial model
Sensory memory –> working memory –> long term memory
Movement from 1–> 2 relies in attention; 2–> 3 encoding; 3–>2 retrieval
(Loss from 1- lack of attention; loss of 2&3 - forgetting)

41
Q

What is working memory?

A

Items from short term memory and recalled items from long term memory
7+/-2 memories

42
Q

How is long term memory created?

A

Long term potentiation

43
Q

What are the two parallel processes of learning?

A

Repetition (shallow)

Elaborate (deeper - relies on making meaning)

44
Q

What is tulving’s model of parallel distributed processing?

A

Memory occurs in a number of places (distributed). Memory happens in connections between nodes, therefore sparking off one memory will spark off the other memories connected to that node.

45
Q

What is episodic memory?

A

a ‘re-experiencing’ of events

46
Q

What are elements of tulving’s model of episodic memory?

A

Allows person to re-experience through autonoetic awareness, previous experiences, and to project them to future
Develops late in childhood
Conscious recollection of past events
Depends on semantic memory
Not discrete (shares neural processes) but also has distinct (unshared) components

47
Q

What are components of Tulving’s model of semantic memory?

A

Not linked to verbal or visual
Knowledge based
No autonoetic awareness
Makes possible retention, acquisition and retrieval of factual knowledge

48
Q

What do squire and Zola say about episodic and semantic memory?

A

Entirely independent and parallel (separate). Damage to hippocampus results in equal impairment to both, therefore systems aren’t dissociable (dissociable = can have impairment to one w/out affecting other

49
Q

What does Tulving say about episodic and semantic memory?

A

Encoding to episodic relies on semantic. Retrieval from both is independent.
Share some components. Single dissociation (can have semantic w/out episodic; can’t have episodic w/out semantic

50
Q

What did Varga-khadem study show?

A

Support for tulving’s model. Episodic memory relies on semantic memory; semantic operates independently

Episodic memory relies on hippocampal circuit.

51
Q

What types of memory processing does declarative memory mark possible?

A

Recall
Recognition
Manipulation of information internally

52
Q

What do learning tests test?

A

Ability to encode episodic memories

53
Q

What do recall tasks test?

A

Ability to consolidate, retain and retrieve information

54
Q

What are limitations of free recall tests?

A

Don’t distinguish between retention (MTL) and retrieval impairment (FL)
If test shows impairment in retention, but not in retrieval = MTL
(Can’t test for retrieval w/out retention)

55
Q

How do you test for retrieval?

A

Recognition tests - Prompt brain where to find it (‘remember when we discussed the list before’)

56
Q

Testing visual semantic memory

A

Hard. Can have impairment in visual semantic memory while having intact perceptual memory.
Can draw teapot but not know what it is (associative agnosia)

57
Q

What are types of verbal semantic memory impairment

A

Wernicke - syntax w/out vocab

Broca - telegrammatic, vocab w/out syntax

58
Q

What is semantic dementia?

A

Progressive disintegration/atrophy of inferolateral and anterior temporal lobe
Independent of MTL
early spread to ventromedial frontal lobes

59
Q

Strengths of semantic dementia

A 
Preserved working memory
Strong anterograde memory
Weaker retrograde memory (reverse temporal gradient)
No spatial weakness
No phoneme or syntax issue
Good organisational memory
60
Q

Deficits in semantic dementia?

A

Unable to remember correct word
Impaired word associations
Applies to objects (teapot mistakenly identified as teabag)
Loss occurs within particular categories (eg colour, number, faces)
Not related to abstract or concrete, or degree of difficulty

61
Q

Describe modality dissociation in semantic dementia

A

Can happen in one modality (eg verbal, not visual)

Categorisation is independent of modality

62
Q

What does semantic dementia indicate about declarative memory?

A

That episodic memory can operate with impaired semantic memory (graham). Episodic memory only affected if it relies on semantic memory (perceptually different objects (recognising 2 different types of telephone) rather than perceptually identical)

63
Q

What are the focal symptoms of alzheimers?

A

Dysphrasia, acalculia, dyspraxia, agnosia

64
Q

What is required for diagnosis of alzheimers?

A

Deficit in two cognitive areas -
Amnestic (memory loss - most common)
Non-amnestic: language, visuo-spatial, executive function

65
Q

What is pathology of alzheimers?

A 
Atrophied brain (esp FT lobes)
Neurofibral tangles (essential)
Excess glial cells
Neural degeneration
Excess senile plaque
66
Q

What is spread of alzheimers?

A

Hippocampus/MTL to P cortex to FL

symptoms mirror pathology

67
Q

What are initial clinical presentations of alzheimers?

A 
Anterograde amnesia
Impairment in learning, delayed recall and recognition tests (MTL)
Long term (retrograde) memory OK
68
Q

What are second stage clinical presentations of alzheimers

A

Wernicke’s aphasia (loss of words) (posterior temporal lobe)
Visuospatial and topographical (parietal lobes)
Dyspraxia, acalculia, agnosia

69
Q

What are third stage clinical presentations of alzheimers?

A

Change of personality - Apathy or aggression (frontal lobe)

General impairment of all functions

70
Q

How is alzheimers diagnosed?

A

Tests measured against peers
Unrelated word pairings (indicative of MTL functioning)
Free recall and recognition impaired (indicates problem w encoding, not frontal lobe)

71
Q

What is parietal lobe responsible for?

A

Visuospatial memory

Bio psych (14 decks)

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