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PSYC3914 > PSYC3914 > Flashcards

PSYC3914 Flashcards

1
Q

How does fMRI work?

A

Activation of brain area means oxygen to that area increases. Oxygen is not subjected to transverse relaxation since it’s not magnetic, where as deoxygenated blood is. Therefore can differentiate between areas activated, and those not activated.

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2
Q

Describe the Information theory of the brain

A
  • the brain as a compressor of information (minimal representations)
  • brain as communication from different areas
  • the bit
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3
Q

Describe Marrs levels of explanation

A
  1. Computational theory - goal, logic, object recognition, emotion perception.
  2. representation and algorithm - how can this computation be implemented, representation for input, algorithm for transformation.
  3. hardware implementation - how can it be realised physically
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4
Q

Describe evidence to suggest that the SCN is the master clock

A
  • activity in the SCN correlates with circadian rhythms
  • lesion of SCN abolish free-running rhythms
  • isolated SCN continues to cycle
  • transplanted SCN imparts rhythm of donor
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5
Q

identify the stages of sleep

A
  1. relaxed wakefulness - non-rem, resting
  2. stage N1 (non-rem) - theta waves
  3. N2 (non-rem) - slow waves intermingle with bursts of activity
  4. N3&4 (non-rem) - deep sleep, large slow delta waves
  5. dreaming/REM sleep-active brain in paralyzed body.
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6
Q

In the Maze Rat task, they identified multiple memory systems. What were they?

A

Fornix - place strategy (all –> need to remember which one have been in)
Caudate - Response strategy (every 2nd one)
amygdala - conditioned cue preference (associate light with food)

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7
Q

Describe the pathway in the brain for US-UR association for eyeblink conditioning.

A

Eye –> trigeminal nerve –> trigmeninal motor nucleus and cranial motor nucleus –> abducens nerve

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8
Q

Describe the pathway in the brain for CS-CR association for eyeblink conditioning.

A

Ear –> pons –> cb –> red nucleus –> cranial motor nucleus

Also input from trigeminal nucleus –> inferior olive –> cb

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9
Q

What impact does inactivation of these structures have on eyeblink conditioning:

  • red nucleus
  • pontine nucleus
  • inferior olive
  • cerebellum
A
  • red nucleus - impairs expression of CR, but once inactivation is reversed, CR spontaneously appears. Critical for expression fo CR
  • pontine nuclei - damage prevents learning, part of pathway conveying CS input
  • inferior olive - leision prevents learning but no effect on previously learned CR
  • cerebellum - lesion prevents learning and blocks expression of previously leanred CR
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10
Q

Where, in regards to the cerebellum, does learning occur & how.

A
  • climbing fibres in cb from inferior olive –> this is the US input.
  • synapse between Purkinje cell in the cb cortex and parallel fibres –> this is the Cs input
  • synapse between parallel fibres and Purkinje cells is where learning occurs
  • learning reduces inhibitory effect of parallel fibres on Purkinje cells
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11
Q

Describe the 3 steps of LTP

A
  1. weak stimulation of pre-synaptic input causes little or no activity in post synaptic neurons
    2 .strong, high-frequency stimulation fo presynaptic input causes long-lasting increase in sensitivity in post synaptic neuron
  2. weak stimulation of presynaptic input now produces APs in post synaptic cells
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12
Q

What 3 properties does LTP have that make it a good model for learning?

A
  1. persistence - potentiation is enduring.
  2. synaptic specificity - only stimulated pre-synaptic inputs show potentiation.
  3. associativity of LTP - can get LTP transferring to another synapse as long as your delivering some stimulation at that pathway and strong stimulation at another.
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13
Q

What two mechanisms does LTP and learning share in common?

A

saturation and neurochemistry

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14
Q

Describe the neurochemistry of LTP

A
  • Glutamate binds to AMPA, depolarising it.
  • Glutamate binds to NMDA with calcium channel on it –> calcium enters causing production of new AMPA receptors.
  • increases sensitivity of receptor
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15
Q

What are the requirements for NMDA calcium channels to open?

A

ligand-gated - requires glutamate to bind

voltage-gated - post-synaptic neuron must be depolarised

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16
Q

What two properties of LTP are a result of the nature of the NMDA Receptor?

A

NMDA channels are ligand-gated and voltage-gated. As a result you get:

  1. Specificity - the NMDA receptor requires the neuron to be depolarised, so will only get LTP in that synapse if other input pathways are not stimulated
  2. associability - The NMDA receptor requires a ligand, so if you apply weak simlation to a second input pathway, will get LTP at that second synapse.
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17
Q

Describe the changes in the synapse and memory traces from STM to LTM

A
  1. Generating synaptic change –> calcium activates protein kinases, which increase trafficking of the AMPA receptors back into the synapse. However since there hasn’t been the generation of MAP receptors, it’s unstable. Calcium also triggers enzyme to disassemble actin that obstruct AMPA trafficking.
  2. stabilizing the synaptic change –> rebuild actin, create double-stranded neural cadherins
  3. consolidate synaptic change –> translational processes (dendiritic spines contain machinery for local synthesis of proteins but new mRNA must be transcribed in the nucleus to supplement mRNA lost in dendrites; calcium triggers this). Spine growth –> enlarged dendritic spines
  4. maintaining memory trace –> reconsolidation
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18
Q

Describe the direct loop in the BG

A

Cortex sends excitatory input to striatum, which inhibits GPi, which reduces its inhibition on the thalamus, resulting in excitatory input to the cortex.

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19
Q

Describe the indirect loop in the BG

A

Cortex sends excitatory input to striatum, which inhibits GPe, which then reduces inhibition of the GPe on the GPi and STN, allowing the GPi to inhibit the thalamus, and the STN to excite the GPi, in turn inhibiting the thalamus, resulting in inhibitory effect on the cortex.

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20
Q

Describe the 3 models of the BG function

A
  1. modulate motor programs originating in the cortex - +ve feedback helps initiate movement, -ve feedback helps stop movement
  2. focusing/filtering of movement. Boost appropriate motor behavior, filter inappropriate
  3. error correction - anticipate errors and model to help correct.
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21
Q

Describe the influence of dopamine on the BG.

A

Dopamine acts on D1 in the striatum to increase inhibition from striatum to GPi. Dopamine acts on D2 in the striatum to decrease inhibition from striatum to Gpe. So increase direct pathway and inhibit indirect pathway, therefore results in net positive feedback from the thalamus to the cortex.

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22
Q

Describe the role of the BG in Huntington’s disease

A

death of GABAnergic cells in striatum = reduced inhibition on GPe = overall increased input to cortex = unwanted movements

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23
Q

Describe the role of the BG in parkinsons disease

A

death of dopaminergic neurons in SN = decreased input to cortex = block motor signals.

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24
Q

What is the neuropathology that underlies:

  • parkinsons
  • alzighmers
  • FTD
  • CJD
A
  • parkinsons - lewy bodies
  • alzighmers - amyloid plaques + neurofibrillary tangles
  • FTD - pick bodies
  • CJD - prions
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25
Q

Identify the 3 important parts of the definition of dementia

A
  1. change from previous level of function
  2. multiple cognitive domains and behavioural domains affected
  3. Impact on persons daily activities
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26
Q

Describe the change in the DSM 4 to 5 for dementia

A

re-termed “dementia” to “major neurocognitive disorder” + diagnosis does not require mememory imaprument if evidence of genetic mutation

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27
Q

Describe the 3 variants of FTD

A
  1. behavioural - personality/behavioural change, executive dysfunction
  2. semantic - loss of semantic knowledge
  3. progressive non-fluent aphasia - non-fluent speech + aggramatic
28
Q

What are the differences between Ungerleider and Mishkin VS Goodale and Milner’s theories of the dorsal and ventral streams.

A

U&M –> dorsal is where, and ventral is what. Function characterization in terms of information content.
G&M –> dorsal is how (vision guides action) and ventral is what + contributes to conscious perception and awareness. Functional characterization in terms of process.

29
Q

How can we reconcile Ungerleider and Mishkin VS Goodale and Milner’s theories

A

3 dorsal streams continue beyond parietal lobe:

  1. PFC - spatial WM, where
  2. PMC - action, how
  3. MTL - navigation
30
Q

What is the role of the LOC and its divitions?

A

Object recognition.
LO - changes in location, size (2D)
VOT - changes in 3D shape

31
Q

Describe three theories of the functional organisation fo the ventral stream

A
  1. Domain specificity hypothesis: anatomical models in the brain responsible for different categories. biologically innate.
  2. processing requirements hypothesis: organizational principle is process and modules - shaped by experience. FFA is not a face area, but related to expertise.
  3. Processing requirements - neural network model: Brain areas specialized for certain types of information by virtue of other areas they are connected to.
32
Q

Describe the role of the perirhinal cortex and parahippocampal cortex in episodic memory.

A

PRC - familiarity-based item recognition learning associations between objects, object perception
PHC - recollection of contextual information, autobiographical memory, spatial memory, navigation.

33
Q

Describe the standard consolidation theory of LTM for episodic memory.

A
  • Information initially represented in different parts of neocortex bound together into memory trace in MTL.
  • Short period of synaptic consolidation followed by prolonged period of consolidation. It is during this long period of consolidation that memories might be disrupted by lesions of the MTL.
  • eventually, memory trace is consolidated in cortex and becomes independent of MTL.
34
Q

Describe the multiple trace theory of LTM for episodic memory.

A
  • Hippocampal cortex automatically encodes all aspects of experience, represented at different neuronal sites. Binds episode into memory trace.
  • reactivation of memory occurs in different neuronal and experiential context - results in new memory trace which shares some or all of the information with the initial episode.
  • multiple traces facilitate the extraction of factual information common to all, which becomes independent of semantic context = semantic memories. Not associated with hippocampus.
  • episodic memories still associated with hippocampus.
35
Q

What are the advantages of the multiple trace theory?

A
  • explains temporal gradient - older memories have more traces, so resistant to damage and have multiple retrieval cues.
  • explains why no temporal gradient for autobiographical episodic memories - because they never become independent of the temporal lobe, therefore a lesion here will effect all memories.
  • accounts of absence of temporal gradient for semantic memories - become independent of MTL, so lesion doesn’t effect.
36
Q

What is the role of the retrosplenial cortex in episodic memory?

A

may play a translational role between allocentric and egocentric spatial reference frames –> orient self in space, situate self in a recollected episodic.memory.

37
Q

What four types of pathology is semantic memory associated with?

A
  1. semantic dementia
  2. herpes simplex
  3. stroke
  4. alzighmers
38
Q

How is herpes simplex encephalitis caused and describe the deficits in semantic memory.

A
  • viral infection that effects the brain, particularly the temporal and frontal lobes, resulting in widespread necrosis.

Symptoms:

  • sometimes category-specific deficits. Typically patients have more impaired knowledge of living things than non-living things
  • deficits can be modality specific e.g. produce information in response to spoken names but not pictures.
  • confusion errors
39
Q

Describe the symptoms of semantic dementia.

A
  • severe degeneration of anterior and lateral temporal lobes
  • not category or modality specific
  • loss of word meanings
  • inability to recognize objects
  • generalsaition errors
40
Q

Describe the distributed organization model of semantic memory and explain how it accounts for the symptoms in herpes simplex encephalitis. What is a pitfall of this theory?

A

semantic memories are stored in areas involved in perception and action. different attributes are distributed around this network. The task determines which part of the representation is accessed.

Category and modality-specific impairments are caused by loss of part of the network for a concept, but not all the network.

Can’t explain findings with semantic dementia.

41
Q

Describe the distributed-plus-hub view and how this accounts for semantic memory.

A

In addition to distributed representation (as in the distributed organization model), there is this hub of neurons, in the anterior part of the temporal lobe. This model proposed that all of the connections between the different nodes of the semantic representation go via this hub. This hub houses neurons that are not modality specific.

This model can explain non-modality specific or category specific loss of knowledge and allows for generalsiation.

42
Q

Describe the PDP model and how it can be used to model semantic dementia and HSVE

A
  • Computational model where researchers attempt to model the architecture of the system to train different inputs and outputs by virtue of association strength between these inputs and outputs.
  • if there is degradation in the system, caused by loss of hidden units (e.g. loss of neurons in semantic hub), the network becomes impoverished.

model semantic dementia - damage stimulated by removing proportion of connections in the neural network = generalisation errors

model of HSVE - damage stimulated by introducing noise in the weights of connections = confusion errors

43
Q

What very general area of the brain do these arteries supply:

  • posterior cerebral artery
  • anterior cerebral artery
  • middle cerebral artery
A
  • posterior cerebral artery - medial and underside of temporal lobe, occipital lobe
  • anterior cerebral artery - medial part of the hemisphere
  • middle cerebral artery - lateral surface of the brain
44
Q

What impairments do strokes to the posterior cerebral artery lead to, and the middle cerebral artery.

A

posterior cerebral artery - strokes effect memory, vision, agnosia
middle cerebral artery - language impairments

45
Q

What does the internal carotid branch into

A

anterior cerebral artery and middle cerebral artery

46
Q

What are the Brodmann areas for brocha’s area and Wernicke’s area?

A

Brocha - 44/45

Wernike’s - 41/42 & 22

47
Q

Describe the characteristics of Brocha’s aphasia

A
  • non fluent
  • difficulty articulating - apraxia and dyspraxia of speech
  • anomia (word finding difficulties)
  • better comprehension, but not perfect
  • agrammatism
  • other neurological signs - right sided weakness, oro-facial apraxia (difficulty making skilled movements with mouth)
48
Q

Describe the characteristics of Wernike’s aphasia

A
  • severe anomia
  • fluent grammatical speech, but largely meaningless
  • paraphrasis (phonological approximations)
  • impaired reading
  • impaired comprehension
  • impaired repetition
49
Q

Describe the characteristics of conduction aphasia

A
  • impaired repetition, with relatively good spontaneous speech and comprehension
  • phenomic parapraxis in spontaneous speech
  • thought to be caused by damage to arcuate fasciculus
50
Q

using the lesion overlay method, which are was found to be damaged in ALL patients with apraxia of speech?

A

precentral gyrus of the insula

51
Q

using voxel based lesion symptom mapping, which areas were proposed as key comprehension regions. What are their specific functions in relation to comprehension?

A

perisylvian areas:

  • MTG - BA21/37 - comprehension and naming
  • ASTG - BA 22 - comprehension of simple sentences
  • STS + AG - BA39 - STM
  • inferior frontal areas around brocha’s area - BA 45/47/46 - working memory
52
Q

Describe the cortical language circuit in auditory sentence comprehensoin.

A

Top-down semantic processes:

  • frontal cortex projects to ASTG and MTG which projects back to frontal cortex. also projections from A1 to ASTG.
  • ventral route
  • develops early - 1-5 years

syntactical relations:

  • frontal cortex projects to ASTG and back to frontal cortex. Also projections from A1 to ASTG.
  • ventral and dorsal routes
  • develops later

auditory-to-moto mapping:

  • A1 to PSTG to PMC
  • dorsal route
53
Q

What is primary progressive aphasia, and what are the subtypes (describe only main features).

A

PPA is focal dementia presented as an isolated and progressive language impariment.

non-fluent PPA:

  1. agrammatism in language
  2. apraxia of speech

semantic variant of PPA/semantic dementia:

  1. impaired confrontation naming
  2. impaired single word comprehension

Lopogenic variant:

  1. impaired single word retrieval in spontaneous speech
  2. impaired repetition of sentences and phrases
54
Q

how do we know our eyes moved, or an object moved?

A

Remember where you told your eye to move - efferent copy, which is sent to parietal cortex - updating the maps of where things are and compensating for retinal motion.

55
Q

Describe what the experiment by Bisiach and Luzzatti (1978; experiment on Piazza Del Dumo), Marshall and Halligan (1988; experiment with house on fire), and the Stroop effect revel about visual processing in hemispatial neglect.

A

Bisiach and Luzzatti (1978) showed that knowledge from both sides of the patient was in their memory, but unable to access it all normally from their imagery.

Marshall and Halligan (1988) showed unconcious processing of neglected sitmuli.

Stroop effect - fast processing of congruent stimuli, even though words are ‘negelcted’

56
Q

It’s likely that we have different coordinate frames for object recognition. What does hemispatial neglect reveal about these coordinate frames? What are these coordinate frames?

A

Hemispatial neglect reveals that we do in fact have 3 coordinate frames for object recognition, as they can individually be impaired in this disorder.

viewer centered representations - coordinate relative to visual field

stimulus centered representations - processing orientation fo shapes

object-centered representations - defined by the canonical orientation fo the object, irrespective of the orientation or location fo the object relative to the viewer. suggests a separate map for word recognition.

57
Q

Describe the symptoms and identify the neuropathology of Alzheimer’s Disease.

A 
•	Symptoms
-	Memory loss
-	word finding problems 
-	Inability to perform simple tasks
-	Vegetative 
• Neuropathology – amyloid plaques + neurofibrillary tangles
58
Q

Describe the symptoms and identify the neuropathology of Parkinson’s Disease.

A 
•	Symptoms: 
-	Motor deficits 
-	Slowed mental processing,
-	Attention impairments
-	Memory problems with recall 
•	Loss of dopaminergic cells in substania niagra, results in decreased input to cortex from thalamus – blocking of motor signals
•	Neuropathology – lewy bodies
59
Q

Describe the symptoms and identify the neuropathology of Huntington’s Disease.

A
  • Symptoms: twitches in face and hands and tremors through body
  • Loss of striatal GABA neurons, meaning overall increased input to cortex,
60
Q

Describe the symptoms of each variant of FTD and identify the neuropathology.

A

• Neuropathology – Pick’s bodies
• Variants:
- Behavioural variant – personality changes, executive function decline
- Semantic variant – progressive loss of semantic knowledge
- Progressive non-fluent aphasia – non-fluent speech, agrammatic

61
Q

Describe apperceptive agnosia and associative agnosia

A

Apperceptive agnoasia
• Visual form → cant discriminate shapes, read, draw, identify faces
• Perceptual categorisation deficit → difficulty with variations in viewpoints

Associative agnosias
• Visual object agnosia → inability to recognise objects
• Prosopagnosia → inability to recognise faces
• Alexia → inability to read
• Topographical → inability to recognise familiar environments or landmarks.

62
Q

Describe 2 conditions that are characterised by episodic deficits

A
  • Korskoff syndrome → anterograde and retrograde amnesia caused by damage to diencephalon in alcoholism
  • Retrograde amnesia → thalamic stroke. Autobiographical and personal semantics severely impaired
63
Q

What is Semantic dementia and HSVE

A
  • Semantic dementia → loss of semantic knowledge, non category specific, loss of word meanings, inability to identify objects
  • HSVE → can be category and modality specific loss of semantic
64
Q

Describe brochas aphasia, wernikes aphasia and conduction aphasia

A
  • Brocha’s aphasia → non-fluent (apraxia, dyspraxia), anomia, agrammatsm
  • Wernicke’s aphasia → anomia, fluent grammatical speech, impaired reading + comprehension
  • Conduction aphasia → impaired repetition, phonemic parapraxis
65
Q

Describe the 3 types of primary progressive aphasia.

A
  • Non fluent → agrammatism, apraxia of speech
  • Semantic variant of PPA – impaired confrontation or naming + single word comprehension
  • lopogenic → impaired single word retrial in spontaneous speech, repetition.

PSYC3914 (1 decks)

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