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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
What is synaptic plasticity?
Where learning occurs because biochemistry of synapses has changed, altering effect on post-synaptic neuron
25
What is long-term potentiation?
Long term increase in excitability of neuron due to particular synaptic input caused by repeated high frequency activity of that input.
26
What is Hebb's rule?
Strengthening of a synapse that is repeatedly active when the post-synaptic cell fires
27
What is glutamate?
Excitatory neurotransmitter
28
What does LTP do to synapse?
Increases sensitivity of receptors to glutamate Increases amount of glutamate Synthesises protein in post-synaptic dendrite
29
In what parts of brain does LTP occur?
- hippocampus (entorhinal cortex) esp. Dentate gyrus and CA1 | - pre-frontal cortex, thalamus, motor cortex, visual cortex, amygdala
30
What does long term depression do?
Reverses effect of LTP | Low frequency input at synapse which decreases synaptic strength
31
What is habituation & what does habituation do?
Long term repeated stimulation of neuron, reduces synaptic strength (loses impact)
32
What is sensitization?
noxious stimuli causes exaggerated response in post synaptic neuron when noxious stimuli repeated
33
What are some mechanisms of synaptic plasticity?
long term potentiation Long term depression Habituation Sensitization
34
What is memory?
Mental process for acquiring and retaining information for retrieval at later time
35
What is explicit memory?
Memory that can be consciously recalled
36
What is implicit memory?
Memory for which no specific learning event can be remembered
37
What is procedural memory?
Memory of skills and procedures Motor skills Independent of hippocampus (does involve cerebellum and basal ganglia)
38
What is declarative memory?
Accumulation of facts/data from experiences Primarily processed through hippocampus Is relational, and can be accessed independent of environment
39
What are the serial models of processing memory?
Atkinson-shiffrin Tulving's Levels of processing model
40
What is Atkinson-Shiffrin model of memory?
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
What is working memory?
Items from short term memory and recalled items from long term memory 7+/-2 memories
42
How is long term memory created?
Long term potentiation
43
What are the two parallel processes of learning?
Repetition (shallow) | Elaborate (deeper - relies on making meaning)
44
What is tulving's model of parallel distributed processing?
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
What is episodic memory?
a 're-experiencing' of events
46
What are elements of tulving's model of episodic memory?
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
What are components of Tulving's model of semantic memory?
Not linked to verbal or visual Knowledge based No autonoetic awareness Makes possible retention, acquisition and retrieval of factual knowledge
48
What do squire and Zola say about episodic and semantic memory?
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
What does Tulving say about episodic and semantic memory?
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
What did Varga-khadem study show?
Support for tulving's model. Episodic memory relies on semantic memory; semantic operates independently Episodic memory relies on hippocampal circuit.
51
What types of memory processing does declarative memory mark possible?
Recall Recognition Manipulation of information internally
52
What do learning tests test?
Ability to encode episodic memories
53
What do recall tasks test?
Ability to consolidate, retain and retrieve information
54
What are limitations of free recall tests?
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
How do you test for retrieval?
Recognition tests - Prompt brain where to find it ('remember when we discussed the list before')
56
Testing visual semantic memory
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
What are types of verbal semantic memory impairment
Wernicke - syntax w/out vocab | Broca - telegrammatic, vocab w/out syntax
58
What is semantic dementia?
Progressive disintegration/atrophy of inferolateral and anterior temporal lobe Independent of MTL early spread to ventromedial frontal lobes
59
Strengths of semantic dementia
``` Preserved working memory Strong anterograde memory Weaker retrograde memory (reverse temporal gradient) No spatial weakness No phoneme or syntax issue Good organisational memory ```
60
Deficits in semantic dementia?
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
Describe modality dissociation in semantic dementia
Can happen in one modality (eg verbal, not visual) | Categorisation is independent of modality
62
What does semantic dementia indicate about declarative memory?
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
What are the focal symptoms of alzheimers?
Dysphrasia, acalculia, dyspraxia, agnosia
64
What is required for diagnosis of alzheimers?
Deficit in two cognitive areas - Amnestic (memory loss - most common) Non-amnestic: language, visuo-spatial, executive function
65
What is pathology of alzheimers?
``` Atrophied brain (esp FT lobes) Neurofibral tangles (essential) Excess glial cells Neural degeneration Excess senile plaque ```
66
What is spread of alzheimers?
Hippocampus/MTL to P cortex to FL | symptoms mirror pathology
67
What are initial clinical presentations of alzheimers?
``` Anterograde amnesia Impairment in learning, delayed recall and recognition tests (MTL) Long term (retrograde) memory OK ```
68
What are second stage clinical presentations of alzheimers
Wernicke's aphasia (loss of words) (posterior temporal lobe) Visuospatial and topographical (parietal lobes) Dyspraxia, acalculia, agnosia
69
What are third stage clinical presentations of alzheimers?
Change of personality - Apathy or aggression (frontal lobe) | General impairment of all functions
70
How is alzheimers diagnosed?
Tests measured against peers Unrelated word pairings (indicative of MTL functioning) Free recall and recognition impaired (indicates problem w encoding, not frontal lobe)
71
What is parietal lobe responsible for?
Visuospatial memory

Bio psych (14 decks)

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