Memory and Language Flashcards

1
Q

What is the multi-store model?

A

Atkinson and Shiffrin
A model of memory consisting of modality-specific sensory stores, a short-term store of very limited capacity, and a long-term store of essentially unlimited capacity capable of holding information over time.

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2
Q

What is the sensory store of the multi-store model?

A

Consists of an
iconic store - visual.
Echoic store - auditory

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3
Q

What was Sperling’s experiment?

A

Investigating iconic store. Briefly present letters in a grid array. Participants could only report 4 or 5 letters correctly, but in a ‘partial’ report condition, could report most of the letters from the requested line if the delay between removal of the array and presentation of the prompt was less than 1s

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4
Q

What was Treisman’s study on the echoic store?

A

Dichotic listening. Auditory message to one ear, asked to repeat back while ignoring a second message from the other ear. If the second message was identical to the first, but started at a different time, participants only noticed if they started within 2s of each other. Suggests unattended information persists for approx. 2s.

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5
Q

What was Miller’s experiment?

A
  1. Miller: short term memory span Asked subjects to recall digit strings. Typically, could recall 7+-2 digits, same for letters and even words. Words being treated the same as letters suggests that short term memory holds 7+-2 chunks. Can retain information by rehearsing it.
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6
Q

What was Peterson and Peterson’s experiment?

A
  1. Peterson and Peterson: asked participants to remember a stimulus for a few seconds while counting backwards in 3s to prevent rehearsal. Ability to remember a stimulus diminished rapidly, suggesting information decays from the short term store within seconds.
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7
Q

What was Waugh and Norman’s experiment?

A

manipulated speed with which digits were presented to participants, and found that digit recall was more or less unaffected, suggesting that short-term memory forgetting is due to interference from exposure to additional information, rather than the passage of time
Decay hypothesis: fast>slow
Interference hypothesis: fast = slow

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8
Q

What was Rundus’ experiment?

A

Rundus: made people rehearse out loud. The more frequently a word rehearsed, the better it was remembered.

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9
Q

What were the criticism’s of the multi-store model?

A
  1. Model says processing in the short-term store is required for encoding into long-term memory - Patient KF
  2. Assumes short and long term stores are unitary, operating in a single way - patient KF
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10
Q

Who was patient KF?

A

Parieto-occipital lobe damage. Defective short term memory (digit span) but preserved long-term learning and recall. Had worse short-term memory for auditory letters and digits than for visual stimuli - suggests that there may be distinct short-term memory stores for different types of material.

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11
Q

What was the model created aiming to improve the multistore model?

A

Baddeley & Hitch Working memory model

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12
Q

What are the components of the Working Memory model?

A

3 primary components:

  1. Auditory-verbal phonological loop (speech-based)
  2. Visuo-spatial sketchpad
  3. Modality free central executive
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13
Q

What is the role of the central executive?

A

Selecting and initiating cognitive processing routines e.g. manipulation beyond simple repetition

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14
Q

What is the evidence regarding a speech based temporary store existing?

A
  1. Treisman
  2. Miller
  3. Peterson and Peterson
  4. Rundus
  5. Baddeley’s word length and phonological similarity effects
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15
Q

What is the phonological similarity effect?

A

Baddeley
Serial recall of a list of phonologically similar words is significantly worse than from a list of phonologically dissimilar words.
Suggests speech based representations are used in storing the words and that recall requires discrimination between memory traces, which is more difficult for phonologically similar words.

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16
Q

What is the word-length effect?

A

Baddeley
Recall of a list of long words is worse than a list of short words
Confirmed depended on phonological loop by asking participants to silently mouth digits (articulatory suppression) during presentation and recall of words. Eliminated the word-length effect, suggesting that phonological storage capacity is determined by rate of rehearsal.

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17
Q

How did Baddeley structure the phonological loop?

A

Phonological store perceives speech

Articulatory control process linked to speech production that gives access to the phonological store

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18
Q

How does Baddeley’s structure of the phonological loop explain the phonological similarity effect and the word-length effect?

A

Confusions between similar representations in the phonological store
Takes longer to rehearse longer words via the articulatory control process

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19
Q

What did Baddeley do to elucidate a difference between auditory-verbal and visuospatial short term memory?

A

asked participants to encode material using either rote verbal learning or an imagery strategy. When task was combined with pursuit rotor tracking, performance using the imagery based strategy was disrupted, but not the verbal.

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20
Q

How did Baddeley and Lieberman divide the visuospatial sketchpad?

A
  1. Baddeley and Lieberman: asked participants to encode material using either rote verbal learning or an imagery strategy again. Split concurrent task into visual (making brightness judgments) and spatial (pointing at a moving pendulum while blindfolded, guided by an auditory tone). Learning of the imagery-based strategy was most clearly disrupted by the spatial concurrent task, whist the visual task did not interrupt significantly
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21
Q

What did Logie argue?

A

That the visuospatial sketchpad should be divided into two components: visual cache (passively stores information about visual form and colour, subject to decay and interference by new visual information), and an inner scribe (processes spatial info and allows active rehearsal of information in the visual cache).

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22
Q

Who is patient NL?

A

Preserved perceptual skills, but could not describe details of a scene from memory (fine visual cache, but no inner scribe?)

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23
Q

Who is patient LH?

A

Performed better on spatial processing tasks than visual imagery tasks

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24
Q

How do we measure memory?

A
1. Conscious behavioural methods: 
Objective: accuracy/reaction time
Subjective: remember/know, confidence, qualitative measures
2. Unconscious behavioural methods: priming, conditioning, habits
- Psychophysiological
GSR/HR
- Electrophysiological EEG ECG EMG MEG
- Haemodynamics PET SPECT fMRI
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25
If you are given a list of words to remember and then immediately asked to recall them, you will experience a serial position curve. What does this show?
Primacy effect = remember the first few items better | Recency effect = remember last few items better
26
What did Glanzer and Cunitz do?
Showed that the recency effect can be eliminated if participants counted backwards prior to recall, supporting the link to short-term memory of the recency effect. Showed that counting backwards had no effect on primacy effect, while manipulating word familiarity/presentation rate/age of participant does affect the primacy effect (but not the recency effect) so attributed this to long term memory
27
What separates short term and long term memory experimentally?
Primacy and recency effects | Patient HM
28
Who was patient HM?
Patient who had medial temporal damage and had impaired long-term memory , but normal digit span Intact recency, impaired primacy 1. Impaired explicit memory, not implicit 2. Impaired episodic memory, but not semantic
29
What does fMRI tell us about where in the brain long and short term memories are associated with?
18. fMRI studies: Schacter and Wagner – activity in medial temporal lobe when participants were encoding and/or retrieving information from long-term memory. Henson – asking patients to retain information in short-term storage associated with inferior frontal and parietal cortex.
30
What did Ebbinghaus do?
Taught himself lists of nonsense syllables then repeated them until he could recite them correctly twice. Measured time to learn the lists, then time saved in relearning them after various delays. Retention decreased with a longer retention interval, and rate of forgetting slowed down after the first hour or so.
31
What is the capacity of long term memory?
Theoretically unlimited, realistically limited by number of neurons and synapses in the brain (10^15).
32
What did Standing do?
Tried to locate the limit of capacity of long term memory by testing memory for thousands of pictures, but found good memory for 10,000+
33
What did Lindauer suggest?
That capacity of long term memory may be constrained by the rate of acquisition.
34
How do people forget?
Very rapid over first hour, then logarithmically Primarily due to interference from other experienced events: 1. Proactive interference where previous learning interferes with later learning 2. Retroactive interferemce where later learning interferes with previous learning
35
What did Underwood find?
The more nonsense syllable lists a participant had previously learnt, the more forgetting of new syllables the participant exhibited after 24h - proactive interference
36
What is an example of retroactive interference?
Eyewitness memory for an event can be interfered with by post-event questioning
37
Who split long term memory?
Squire
38
What are the divisions of long term memory?
``` Implicit - Perceptual representation system: Priming - Procedural memory: Motor skills Explicit - Episodic - Semantic ```
39
What are the different memory tasks to test explicit and implicit memory?
23. Schacter: Memory tasks. Ask a participant to study a list of words. Explicit memory task = recognition old or new, cued recall, free recall. Implicit tasks = fragment completion, wordstem completion, degraded word naming.
40
What did Jacoby and Dallas find regarding retaining information in long term memory?
Effect of different levels of processing at encoding. Words encoded using tasks e.g. does it contain an R, does it rhyme with drain, etc. Found that deeper levels of processing improved explicit memory but had little effect on implicit memory.
41
What do medial temporal lobe amnesiacs show about long term memory?
E.g. patient HM Impaired long term memory On pursuit rotor or Gollin figures tasks, performance of amnesics improves over trials, despite the patients being unable to recall having done the test before
42
Define double dissociation
When you can show two mental tasks to be distinct by two lesions leading to contrasting symptoms
43
What does medial temporal lobe damage cause?
Impaired explicit long-term memory
44
Which brain region, when damaged, affects implicit memory?
Occipital E.g. patient HM Impaired long term memory On pursuit rotor or Gollin figures tasks, performance of amnesics improves over trials, despite the patients being unable to recall having done the test before
45
Give two patients that exemplify the double dissociation between explicit and implicit memory
HM lost explicit not implicit | MS lost implicit but not explicit
46
Define episodic memory
Memory of specific events or episodes occurring in a particular time and place
47
Define semantic memory
General knowledge about objects, people, facts, concepts, meanings, without awareness of where or when the information was learned Stored in the lateral temporal cortex
48
What did Jacoby and Dallas fine regarding episodic and semantic memory?
Double dissociation: reading a word out of context improved semantic memory, whereas generating word themselves improved subsequent episodic memory.
49
What did Vargha-Khadem et al show?
Children with selective hippocampal damage showed impaired episodic, but performed well on tests regarding semantic.
50
Explain the double dissociation shown by dementia
Alzheimer's --> medial temporal lobe atrophy Early semantic Dementia --> lateral temporal lobe atrophy. Simons et al, asked patients to perform a semantic task and later tested episodic memory for same drawings. Alzheimer's = impaired semantic and preserved episodic. Semantic dementia = preserved episodic, impaired semantic.
51
What is the problem with studying patients with Semantic dementia?
Lateral temporal lobe damage so often also have language issues and can't do word related tasks
52
What are the two major forms of amnesia?
Retrograde (forgetting of events occurring prior to trauma) | Anterograde (inability to retain new information in a permanent form)
53
What are the causes of amnesia?
Anoxia, ischaemia, encephalitis, alcoholism and associated dietary insufficiency (thiamine deficiency in Korsakoff's syndrome) and neurosurgery. Alzheimer's.
54
Where does the pathology of Alzheimer's strike?
Hippocampus and entorhinal cortex within the parahippocampal gyrus of the medial temporal lobe
55
What is the difference between forgetting and amnesia?
Forgetting prevents the brain being burdened with useless information. Amnesia is a pathological memory loss.
56
What was resected in patient HM?
Bilateral medial temporal lobe: hippocampus, amygdala, overlying temporal cortex
57
How was HM studied?
1. Impaired long term - Showed intact digit and spatial span 2. Impaired explicit - Deficit in matching to sample after delay, but not immediately, showing that he understood the task 3. Impaired episodic 4. Severe anterograde 5. Mild retrograde
58
What does a right sided medial temporal lobe resection result in?
Non verbal memory deficit
59
What does a left sided unilateral medial temporal lobe resection result in?
Verbal memory deficit
60
What does the Corsi block tapping test test?
Spatial span Subject must copy a sequence tapped out by the examiner on the blocks. Numbers visible tot he examiner but not the subject.
61
Who is patient NA?
Patient with diencephalic amnesia Lesion of mediodorsal nucleus of the thalamus Severe anterograde amnesia
62
What can Korsakoff syndrome cause?
Thiamine deficiency Damage to medial thalamus, fornix and mammillary bodies Diencephalic amnesia
63
Which characteristic lesion causes selective loss of short term memory? What else happens?
Temporo-parietal junction | Often conduction aphasiac.
64
Where might short term memory in vision be stored?
Unimodal association areas related to the particular modality in question e.g. post parietal in case of spatial span
65
What are agnosias?
Higher level sensory deficits | Inability to recognise things
66
Define prospagnosia
Patient can't see faces
67
What are the two main types of visual agnosia?
Associative: patient cannot recognise objects, name them, or use them appropriately, but can draw them accurately Apperceptive: patient can name if the appropriate perceptual cues are present, but cannot draw the object, or name it if it is presented in an unusual view
68
What is an example of a condition where procedural memory is impaired?
Huntington's | Perform better on word recognition
69
What are the types of amnesias?
1. Medial temporal lobe 2. Diencephalic 3. Selective short term loss 4. Loss of special knowledge systems (agnosias/apraxias/aphasias) 5. Procedural
70
Which brain structures underly declarative and procedural memory?
``` Declarative = temporal lobe, diencephalon Procedural = basal ganglia and cerebellum ```
71
What is DNMS and what does it show?
Delayed non matching to sample Impaired recognition memory Monkeys have to remember having seen a junk object over longer and longer delays. At the choice stage, monkey has to choose between the junk object or a novel object. Has to choose novel object, indicating that he remembered which of the objects was familiar. Large impairments following combined damage to hippocampus, amygdala, entorhinal and perirhinal cortex
72
How do you show that moneys with MTL damage have intact skill learning?
Lifesaver motor-skill task | Measured by improved ability of monkeys to retrieve a sweet from a bent stick
73
How do you show monkeys with MTL damage have mild retrograde amnesia?
Mild retrograde amnesia – monkeys trained on concurrent object discriminations pre surgery at 2/4/6/8/10/12 w. Impairment only on object discriminations post-surgery that were learnt 2-8 weeks before surgery.
74
Which area of the brain is associated with recognition memory?
``` Rhinal cortex (perirhinal and entorhinal) within MTL May be connected to a larger system within the temporal loves important for storing knowledge about objects that may be analogous to a semantic knowledge or specialised knowledge system in humans. Entorhinal = major input to hippocampus Perirhinal = receives information from unimodal polymodal association areas ```
75
Which area of the temporal lobe is associated with emotional memory?
Amygdala Subjects may recognise a particular stimulus and remember previous interactions with it but have no motivational memory of it.
76
What does the hippocampus do?
Encode memories that are then laid down in the cortex
77
Where is the hippocampus?
The most medial aspect of the temporal lobe (along with the dentate gyrus)
78
How many layers of cortex are there in the hippocampus?
3 - primitive allocortex
79
What lies between the temporal neocortex and the hippocampus/dentate gyrus?
Subiculum and parahippocampal cortex - also primitive cortex. Some of PH transitional 4-5 layered cortex
80
What is the ridge formed by the hippocampus invaginating into the lateral ventricle called?
Ammon's horn
81
What are the 3 areas of the hippocampus? What is the cell type?
CA1 CA2 CA3 - pyramidal output cells
82
What is the cell type of the dentate gyrus?
Granule cells (input)
83
What is the hippocampal formation?
Hippocampus + dentate gyrus + subiculum
84
What are the 3 afferent connections of the hippocampal formation?
1. All major cortical association areas --> entorhinal cortex --> afferents of dendrites of dentate granule cells 2. Subcortical structures including the septum, anterior thalamus and amygdala 3. Non-specific arousal systems including the cholinergic, serotonergic and noradrenergic pahtways
85
What is the performant pathway
All major cortical association areas --> entorhinal cortex --> afferents of dendrites of dentate granule cells Called performant as the fibres perforate the hippocampal fissure in reaching their destination
86
Draw the trisynaptic circuitry of the hippocampus
Perforant path | Mossy fibres
87
Where do the cells of the performant pathway synapse?
Dendrites of the dentate granule cells | Apical dendrites of the CA3 pyramidal cells
88
Where do the mossy fibres of the hippocampus project?
Dentate granule cells to CA3 pyramidal cells
89
Where do the Schaffer collaterals project?
CA3 pyramidal cells to the CA1 pyramidal cells
90
Where does CA1 connect to?
Schaffer collaterals going in, connects to subiculum
91
What are the efferent connections of the hippocampal formation?
1. Entorhinal cortex and subiculum to neocortex 2. CA3 and subiculum through fimbria-fornix to structures like the hypothalamus, mammillary bodies, anterior thalamus, nucleus accumbens
92
Descibe Papez circuit?
Mamillary bodies to anterior thalamus then to cingulate cortex back to entorhinal cortex into hippocampus and via fornix to mammillary bodies
93
Which cell fields of the hippocampus are particularly prone to ischaemia and what does this cause?
CA1 | Profound loss of ability to lay down declarative memories, in particular episodic
94
What happened to patient RB?
Damage to CA1 of the hippocampus. Episodic memory defect.
95
Discuss the Morris water maze
Rats trained to escape from a pool of opaque water by swimming to a submerged platform in opaque water. Rat started from different positions around the edge of the pool on different trials, so learns to swim to the submerged platform based on knowledge about the position of the platform wrt landmarks around the outside of the maze. Hippocampal lesions impair learning of the task, and even when it is eventually acquired, subsequent retention tests show that the lesioned rat has poor memory for the location of the platform. If the subject is trained first, prior to the lesion, there is a much weaker deficit on subsequent retention test post lesion. So appears to be more important in the laying down of the memory trace, rather than its retrieval.
96
What is the evidence that the human hippocampus is involved in spatial memory?
38. Human hippocampus is activated during navigation | 39. London taxi drivers show altered hippocampal volume
97
What did Gaffan think the hippocampus does?
Binds together the disparate aspects of a memory (from all sensory areas) into a coherent memory trace - an episode
98
Is the hippocampus used to retrieve memories?
For a short time, but eventually only need the cortex
99
How is the perforant path --> dentate gyrus synapse strength altered?
Synapse strength increase if an activated afferent in the perforant path synapses onto an already strongly activated post-synaptic neuron
100
How is the differential input of perforant pathway neurons strengthened?
Mutual inhibition between output neurons- inhibitory interneurons at each stage receive input from the previous stage but also from their own output neurons, resulting in a competitive mechanism of inhibition Inhibition between pathways
101
What is the difference between how the cerebellum learns and how the hippocampus learns?
Hippocampus: no teacher signal (like a climbing fibre) that can unconditionally set or correct the output firing of each neuron
102
How does the hippocampus guide storage of memories?
Thought to be the pathway that the hippocampus back projects to the neocortex
103
What did Bliss and Lomo demonstrate?
LTP dentate gyrus and hippocampus proper: increases in amplitude of electrically evoked responses following brief strains of tetanic stimulation. Pathway specific Lasts up to many days experimentally
104
Why might LTP be a good synaptic model for learning and memory?
Rapidly induced Long lasting Synapse specific Can be associative (not in dentate gyrus or CA3, but in CA1). Seen in other structures including the neocortex and cerebellum
105
What does associative mean?
If a weak input is paired with a strong one, both sets of synapses subsequently show LTP
106
What are the 3 types of glutamate receptors?
Kainate Quisqualate NMDA
107
Which glutamate receptor is involved in LTP? How do we know?
NMDA Specific NMDA antagonist, AP5, can block LTP development in the CA3-CA1 pathway when D-L AP5 is infused constantly into the ventricles close to the hippocampus, it impairs the learning of the same water maze task, described earlier, that is normally impaired following lesions of the hippocampus
108
How does LTP work?
When the post synaptic cell is already active/depolarised Mg2+ is removed from blocking the NMDA receptor Ca2+ can move through the NMDA receptor as well as monovalent ions. Ca2+ --> activated Ca2+ dependent processes that modify the synaptic efficiency of the cell.
109
What is the function of the rhinal cortex?
Encoding new information | Storage of recently acquired memories: declarative semantic
110
Define aphasia
Impairment in language in presence of normal speaking apparatus
111
Where in the brain is language controlled?
Left frontal lobe: Broca's area, and Wernicke's area (left superior temporal lobe)
112
Define Broca's aphasia
Speech laboured and slow, articulation impaired. Often can communicate, as selection of words esp nouns is correct, even though they are difficult to understand. Impaired at verbs and repeating complex sentences. But can comprehend the words they hear.
113
What did Broca's famous patient with aphasia say?
Tan
114
Where is damaged in Broca's aphasia?
``` Broca's area Surrounding frontal fields Underlying white matter Insula and basal ganglia (damage restricted to Broca's area produces a far less severe and transient aphasia) ```
115
Define Wernicke's aphasia
Speech effortless at a normal rate, but content unintelligible because of frequent wrong words and phonemes Difficulty comprehending sentences
116
Where is the damage for Wernicke's aphasia?
Posterior sector of left auditory association cortex | Middle temporal gyrus and underlying white matter in severe, persistent cases
117
Why are Broca's aphasics impaired in understanding complex sentences?
Impaired in short term memory, so impaired when elements need to be linked together in different parts of the sentence
118
What connects the areas of language processing?
Arcuate fasciculus
119
What is conduction aphasia?
Damage to the arcuate fasciculus fibre tract Produces impairment in repetition of the spoken word in the absence of spontaneous speech deficits or word comprehension.
120
What are the studies demonstrating hemispheric specialisation of language?
Aphasic patients Study of split brain subjects WADA procedure
121
What did split brain patients show us?
Asked to examine an object that they were allowed to examine with either their left or right hand (but not see). Object in right hand named appropriately, object in left hand couldn't be named. Based on fact that left hand somatosensory info interpreted by the right brain. Showed with tachistoscopic presentation that the left hemisphere can respond to written commands, while the right hemisphere responds primarily to non-verbal stimuli
122
Why is the right hemisphere important for language?
Prosody - emotional and tonal colouring of language.
123
What is the effect of right hemisphere damage on speech?
5. Patients with anterior right hemisphere damage – inappropriate intonation 6. Posterior right hemisphere damage – difficulty interpreting emotion in others speech. May also have difficulty incorporating sentences into a coherent narrative and using appropriate language in social settings
124
What is the WADA procedure?
Inject short acting anaesthetic (e.g. sodium amytal) into left or right carotid artery, so anaesthetising ipsilateral hemisphere. Ask patients questions to assess ability to speak. 140 right handers, 96% speech representation on left. 122 left handers, 70& speech representation left, 15% bilateral.
125
What were the two further aphasias Lichtheim described? How did he explain them?
Transcortical motor aphasia Transcortical sensory aphasia Explained them as suggested disconnection of language centres from 'concept' centres - e.g. auditory images of words, or motor images of words
126
Describe transcortical motor aphasia
Speak non fluently but can repeat even very long phrases | Damage to frontal lobe anterior to Broca's
127
Describe transcortical sensory aphasia
Poor comprehension but can repeat sentences and even make grammatical corrections to a sentence they don't understand Damage to cortex near the junction of temporal, parietal and occipital lobes.
128
What is the Wernicke-Geschwind model?
Spoken word --> auditory cortex --> Wernicke's area (process to recognise the words) Written word --> visual cortex --> processed in angular gyrus then --> Wernicke's area Wernicke's --> arcuate fasciculus --> Broca's area --> cranial nerves --> speak
129
Where is the angular gyrus?
Anterolateral parietal lobe, near superior border of temporal lobe
130
What does fMRI for language show?
- Passively viewing words minus at rest: activation in striate (V1) and extrastriate cortex - Listening to words minus at rest: activation of primary and secondary auditory cortex including Wernicke’s area - Neither of these areas activated by non-word stimuli - Repeating written or spoken words minus activity following passively viewing or listening to words= primary motor, supplementary motor, Broca’s area - Generating new words minus repeating words – frontal and temporal cortex.
131
What are the problems with the Wernicke-Gerschwind model?
- Informaiton coming through visual cortex doesn't go through the angular gyrus or Wernicke's area, there is an alternative route to anterior speech areas - Considerable overlap between speech production and word comprehension such that these abilities are not completely independent - Doesn't include subcortical structures - Cortico-cortical connections from visual and auditory regions to speech zones and the arcuate fasciculus can apparently be removed without incurring aphasia
132
Define anomia
Category specific naming deficits (but still know what it is)
133
What do anomias and modality specific deficits argue against?
A single semantic or comprehension system
134
When is episodic memory lost?
ECT or closed head injury
135
What are the cingulate and parahippocampal gyri for and where are they?
Medial wall of hemisphere | Involved in a mixture of functions: olfaction, recognition memory, emotion
136
Where is the hippocampal formation?
Medial temporal lobe inferior horn
137
What is the complex layer of primary visual cortex?
Layer IV - thalamic input
138
What are secondary areas?
Enable different components of a single modality to be processed together
139
Which modalities are combined in the parietal-temporal-occipital association area?
Auditory, visual, somatosensory
140
Which association area is Broca's area in?
Premotor association cortex
141
What are the highest level association areas?
Prefrontal | Limbic
142
Where is the cingulate gyrus?
Above the corpus callosum, posteriorly continues around the callosum and downwards to become continuous with the parahippocampal gyrus on the medial part of the temporal lobe
143
Where is olfaction processed?
Anterior part of parahippocampal gyrus - entorhinal cortex
144
Where do you do deep brain stimulation to treat intractable depression?
Subgenual cortex of the cingulate gyrus below the genu of the corpus callosum
145
What connects the cingulate cortex and the parahippocampal gyrus?
Cingulum - a large white matter tract
146
What does the cingulate gyrus do?
Anterior cingulate = emotion
147
What are the two regions of the parahippocampal gyrus?
1. Pyriform cortex anteriorly (uncus and primary olfactory cortex) 2. Entorhinal cortex - recognition memory
148
Which part of the prefrontal cortex is associated with visual attentional control?
Ventrolateral
149
What are the outputs of the orbitofrontal cortex?
Cingulate cortex, amygdala and hypothalamus especially, also hippocampus Nucleus accumbens, via which can influence action
150
Which thalamic nuclei are associated with the frontal cortical area motor control?
Ventrolateral and ventroanterior
151
Which thalamic nuclei are associated with the frontal cortical area planning and cognition?
Medial dorsal
152
Which thalamic nuclei are associated with the parietal somatosensory function?
Ventroposterior
153
Which thalamic nuclei are associated with the parietal multimodal sensory integration function?
Pulvinar
154
Which thalamic nuclei are associated with the temporal recognition function?
Pulvinar
155
Which thalamic nuclei are associated with the temporal emotion function?
Anterior
156
Which thalamic nuclei are associated with the occipital vision function?
Lateral geniculate
157
Which thalamic nuclei are associated with the occipital visual association function?
Pulvinar
158
What is the structure of the fimbria-fornix?
One fimbria leaves each temporal lobe, forms fornix, two fornices merge to form one fornix that follows the inferior aspect of the corpus callosum towards the hypothalamus Fibres exchanged between two sides at the fornical commissure, linking the two hippocampi Continues forwards to split on the anterior commissure Post-commissural part runs to the mammillary body
159
Where is the subiculum?
Cortex between the hippocampus and the parahippocampal cortex
160
What has the CA2 area been implicated in in animals?
Social memory
161
What is the sulcus associated with the hippocampal formation?
Collateral sulcus
162
What is the artery near the hippocampal formation?
Anterior choroidal artery
163
What projects into the fimbria/fornix?
CA3 pyramidal cells
164
Where is the amygdala?
Grey matter Deep to primary olfactory cortex of the uncus at the temporal pole Can see in coronal slices at the level of hypothalamus and anterior temporal lobe
165
What is in the same plane as the hypothalamus?
Third ventricle
166
What is the hypothalamus bordered by?
Optic chiasm ant Mammillary bodies post Can normally also see infundibulum/pituitary stalk between these
167
What is the nucleus accumbens close to?
Amygdala Caudate and putamen Anterior limb internal capsule
168
What might the nucleus accumbens be related to in pathology?
Schizophrenia | Drug addiction
169
Where does the forebrain cholinergic system arise from?
Septal nuclei and basal forebrain
170
Where do the midbrain dopaminergic systems arise from?
Substantia nigra --> motor loops basal ganglia | Ventral tegmental area -->nucleus accumbens --> motivation
171
Where do the midbrain/pontine NA systems arise from and what do they do?
Locus coerulus Attention Makes signal to noise ratio more
172
Where does the serotinergic system arise from?
Raphe nuclei medulla
173
What is the target of ecstasy?
Medullary serotoninergic system
174
What are neuroleptics?
Block dopamine D2, used to treat Schizophrenia
175
What is medial temporal sclerosis?
Hippocampal sclerosis Most common cause of intractable temporal lobe epilepsy. Primarily involves dentate gyrus, CA1 CA4 and CA3 to a lesser degree. Neuronal cell loss, gliosis and sclerosis. Managed medically initially, but after temporal lobectomy or selective amygdalo-hippocampectomy performed.
176
What are colloid cysts of the third ventricle?
Epithelial-lined cysts attached to antero-superior portion of ventricle 3 Hydrocephalus Hyper attenuated on non-enhanced CT As close to foramen of munro, can occasionally cause sudden obstructive hydrocephalus and present with thunderclap headache or unconscious collapse. Headaches tend to be positional
177
What are T1 weighted images?
Dark fluid Brighter white matter Darker grey matter Most useful for visualising anatomy
178
What are T2 weighted images?
Bright fluid Darker white matter Brighter grey matter Most useful for determining ongoing athology
179
What is fMRI?
Ultra-fast brain scans repeated many times to find changes correlated with a task. Signals that change with the task highlighted as activations. Identifying the differences between MRI signals that are influenced by local magnetic environment (amounts of oxy vs deoxyhaemoglobin - changes in blood flow in response to local metabolic demand cause local changes)
180
What is diffusion weighted imaging?
Look for movements of water in specific direction. Signal is lost from moving water, so it is dark. Water between white matter fibres cannot move easily perpendicular to those fibres, so remains relatively bright. Acquiring images in many directions allows a map of white matter fibres to be created. Make into tractography. Use to avoid major tracts when performing surgery.
181
What is proton MR spectroscopy?
Gives a localised, quantitative chemical readout of important brain metabolites. Altered in tumours.
182
Is the hippocampus lateral or medial to the lateral ventricle?
Medial
183
What is stained for in the pink/purple hippocampal cross section?
Nucleic acid/nuclei/cell bodies