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PSYC2020 > Lecture7 > Flashcards

Lecture7 Flashcards

1
Q

Define Communication; What are some examples of how we communicate?

A

Behaviours used by one member of a species that convey information to another; Turn-taking, intonation, gesture (body language), eye gaze control, touch

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2
Q

Define language

A

A communication system that has symbols (e.g. words) and rules for ways to assemble the symbols (grammar)

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3
Q

What is Aphasia?; What is it not?

A

A loss of language processing ability after brain damage (a neurological disorder); An impairment of intellectual functioning; a psychiatric disturbance; a primary motor or sensory deficit; a developmental disorder

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4
Q

Name the 3 principles underlying classic Aphasia syndromes

A

Localisation of language processors; damage to a single processor can produce multiple deficits (due to connections between modules); language processor localised because of relationship to primary sensory/motor functions

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5
Q

What are the symptoms of Broca’s Aphasia?; What is the deficit?; Where is the lesion?

A

Non-fluent expressive speech; major disturbance in speech production & syntactic production; missing function words; telegraphic speech; comprehension intact; Impaired speech planning & production; Posterior portion of inferior frontal cortex

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6
Q

In 1862, Broca concluded that the integrity of which area was responsible & necessary for articulation?; MRI of Tan’s brain showed lesions extending into where?

A

Left frontal convolution; The deep white matter, including insular cortex & basal ganglia

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7
Q

What are the symptoms of Wernicke’s Aphasia?; What is the deficit?; Where is the lesion?

A

Major disturbances of auditory comprehension; fluent speech; semantic paraphasia; poor repetition & naming; Impaired representation of sound structure of words; Posterior portion of the superior temporal gyrus

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8
Q

“Der aphasische Symptomenkompleks” documented the localisation of the “storehouse of auditory word forms” in what area of the brain?

A

In the posterior portion of the left Superior Temporal Gyrus

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9
Q

What are the symptoms of Conduction Aphasia?; What is the deficit?; Where is the lesion?

A

Disturbance of repetition & spontaneous speech; phonemic paraphasia; Disconnection between sound patterns & speech production mechanisms; Arcuate Fasciculus (white matter tract between Broca’s & Wernicke’s areas - temporal-parietal junction)

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10
Q

What was Lichtheim’s view on word meaning in 1885?; What did his diagram represent?

A

He didn’t consider the function to be localised in one part of the brain but from the combined action of the whole sensorial sphere; Neural networks - a series of nodes which represent meaning as distributed throughout the entire cortex

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11
Q

According to Lichteim’s House Model, a lesion in the Articulate Speech (motor area) causes what?; A lesion in the Auditory Word Forms (auditory area)?; A lesion between Broca’s & Wernicke’s?

A

Broca’s Aphasia; Wernicke’s Aphasia; Conduction Aphasia

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12
Q

Transcortical Sensory Aphasia is a disconnection of what?; What are the symptoms?

A

Auditory & Concept Centres - damage to tracts in posterior Temporo-parietal-occipital junction; Disturbance in single word auditory comprehension & semantic paraphasias, despite fluent grammatical speech, normal recognition of auditorily presented words & intact repetition

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13
Q

Transcortical Motor Aphasia is a disconnection of what?; What are the symptoms?; Where is the lesion?

A

Concept Centre from motor & auditory language centres - between conceptual word/sentence representations & motor speech production; Severe disturbance in initiating responses & spontaneous speech (aka adynamic aphasia), but intact auditory comprehension & repetition; Deep white matter tracts connecting Broca’s area to parietal lobe

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14
Q

What are some issues with Psycholinguistics & Aphasia?

A

Classic aphasic syndromes have limitations; poor classification of patients; lesion overlap/variability; little assistance for treatment planning

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15
Q

Rather than viewing language in terms of production & comprehension, what does Psycholinguistics emphasise?; Such as?

A

Language processing operations; Phonology - sounds that compose language & the rules that govern their combination; semantics - words & their meaning; syntax - methods for combining individual words to convey propositional meaning

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16
Q

According to psycholinguistics, what are the 2 ways to represent sound in speech?

A

Phonemic - smallest unit of sound that can signal meaning (e.g. b in bat or p in pat); allophones are different representations of the same phoneme (same sounds in different orders; e.g. spill, lisp, lips); & Phonetic - how phonemes are produced in different contexts (e.g difference between cave in English & cavé in French)

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17
Q

In regards to Phonology, what do Broca’s aphasics have difficulty in producing?; What about Wernicke’s aphasics?

A

The correct allophone of a phoneme; mispronunciation of a phoneme; poor phonetic ability & phonemenic selection/discrimination; They select the wrong phoneme; substitute phonemes (i.e. p for b); poor phonemic selection/discrimination but preserved phonetic ability

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18
Q

What are Broca’s aphasics often referred to as?; Though both production & comprehension are impaired, the deficits are…

A

Agrammatic Aphasics (a graded impairment); Dissociable

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19
Q

What do we now know that anterior lesions affecting syntax are also associated with?

A

Comprehension deficits

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20
Q

Lesions resulting in double disassociation of lexical (word form representations) & semantic representations result in what?

A

Intact semantic knowledge but impaired naming (e.g. tip of the tongue & anomic deficits)

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21
Q

Intact naming but impaired semantics (i.e. semantic dementia; often seen in alzheimer’s) result from lesions in what area?

A

Anterior Temporal Lobe

22
Q

Semantic processing can be relatively spared in which aphasics?; Which lesions more often characterise semantic impairments?; When do problems arise for anterior lesioned patients?

A

Anterior lesioned (Broca’s) aphasics; Posterior (Wernicke’s) lesions; When syntax is important in sentence comprehension (e.g. place the blue circle ON TOP OF THE red square)

23
Q

What is the classical characterisation of aphasic deficits?; What is the psycholinguistic characterisation?

A

Production (Broca’s) vs. Comprehension (Wernicke’s); Syntax (Anterior) vs. Semantics (Posterior)

24
Q

Name & describe two articulatory-motor disorders (which are not language disturbances)

A

Dysarthria - disturbance of speech musculature in terms of speed, strength, steadiness, coordination, precision, tone & range of motion (e.g.cerebral palsy); corticospinal tract is commonly affected; Apraxia - articulatory errors increasing with increasing word & phrase length; inability to program speech movements; lesion in left insula/operculum

25
Q

What is Alexia?; What is Agraphia? Can one occur without the other?; Alexia with Agraphia results in the disturbance of what?

A

Acquired impairment in the ability to read; Acquired impairment in the ability to write; Yes, they are dissociable (can have a problem reading but not writing); Word form recognition (finding optical images for words)

26
Q

According to Dejerine, where is the visual image centre of words?

A

Area PC in the left parietal lobe

27
Q

Explain the dual routes to reading

A

Phonological route - convert letter strings to sounds (grapheme-to-phoneme conversion); Direct route - printed words are directly linked to meaning in a visual form system (must have mental store for irregular words, e.g. yacht)

28
Q

What occurs with Surface Alexia patients?; What area is this associated with?; Which route is damaged?

A

They read by sound (grapheme to phoneme) so have difficulty with irregular words but not regular & non-words; Anterior Temporal Lobe; Direct route

29
Q

What do patients with Phonological Alexia have difficulty with?; What are they able to do?; What area is this associated with?

A

Learning new words & pseudowords (both regular & irregular); Read previously learned words via the direct route & extract the meaning directly from the visual form of the word; Lesions to superior temporal lobe & parietal lobe (supramarginal gyrus & angular gyrus)

30
Q

What kinds of errors do patients with Deep Alexia make?; Which routes are damaged?

A

Visual errors (e.g. skate & scale); semantic substitutions relating to target word (e.g. hot when they mean cold); abstract words; better with nouns than verbs as they’re imageable; Both Phonological & Direct routes

31
Q

Explain the subtypes of Agraphia

A

Central Dysgraphia - problems accessing orthographic information from lexical stores or from applying sound-to-spelling phonological rules (i.e. assembling corresponding sounds); Peripheral Dysgraphia - distortions on written letter formation, oral spelling or typing (motor programs)

32
Q

Name the two components of Long Term Memory

A

Declarative (explicit) & Non-declarative (implicit)

33
Q

What are the two components of Declarative memory & their associations?

A

Episodic - events; specific personal experiences from a particular time & place; Semantic - facts; world knowledge, object knowledge, language knowledge, conceptual priming

34
Q

What are the four components of Non-Declarative memory & their associations?

A

Procedural - skills (motor & cognitive); Perceptual Representation System - perceptual priming; Classical Conditioning - conditioned responses between 2 stimuli; Non-associative Learning - habituation, sensitisation

35
Q

What is Sensory Memory?; How is it processed?

A

Sensory memory trace, like an echo lasting just a few milliseconds; Via cranial nerves to primary cortical areas: iconic/visual - retina>primary visual cortex; echoic/auditory - cochlea>primary auditory cortex

36
Q

Short Term Memory has limited…; It decays quickly without…; What is the average span in the number of items recalled?

A

Capacity; Rehearsal (cues don’t help); 7 plus or minus 2 items

37
Q

What can be retained with Long Term Memory?; It persists without constant…; Can be called up with…

A

Many facts & experiences; Rehearsal; A cue or hint

38
Q

What results have been found in list-learning tasks?

A

A gradual increase in performance (i.e. recall); After a distractor/interfering list is presented, performance decreases back to first trial; there’s an increase in following trial but still some decay in memory trace

39
Q

Explain the Serial Position effects; What effects occur if distracting items are introduced at the end of the list?

A

Primacy - beginning of list is easier to recall (there’s enough memory capacity to transfer to LTM); recency - end of list items are available in STM as there’s no decay yet; It eliminates recency but not primacy effect

40
Q

How has evidence supporting the distinction between STM & LTM been weakened?

A

Some memories are neither short or long term (e.g. where you parked the car this morning or dinner consumed last night); these are too long to be STM but weren’t rehearsed so will fade over hours or days

41
Q

Describe Working Memory; How can this be tested?; Lesions to what area can impair performance?

A

The temporary storage of information while we actively attend to or work on it; In the delayed response task (responding to the same stimulus as presented a short time earlier); Prefrontal Cortex

42
Q

What type of memory was effected when 29 y.o patient H.M underwent surgery which damaged the bilateral medial temporal lobe; What difficulties were demonstrated?; What was still intact?

A

Declarative Memory; Couldn’t remember meeting people minutes after meeting them, couldn’t form long-term memories, reported age as 27; Biographical knowledge up to the time of surgery & procedural memory

43
Q

What 5 main findings were generated based on studies of patient H.M?

A

Memory is a distinct biological function; amnesia spares short-term & working memory; amnesia is an impairment of declarative & episodic memory; hippocampus is a core structure supporting memory; hippocampus supports permanent consolidation of memories

44
Q

What is Anterograde (going forward) Amnesia?; As well as the hippocampus, what other areas have been observed to be affected?

A

The inability to form new memories after brain damage has occurred (e.g. H.M); Thalamus, Hypothalamus & Pretectum

45
Q

In the delayed non-matching-to-sample task, monkeys had to remember the old object, reject it & choose the new one to get more food. How did monkeys with bilateral temporal lesions perform compared to intact monkeys with 90% correct performance?

A

Performance was ok at short delays but there were increasing decrements with longer delays

46
Q

When patient N.A suffered a fencing foil to the forebrain, damage was found in the mediodorsal nuclei & mammillary bodies but intact hippocampus formation. What did this result in?; What did his occasional ability to recall something spontaneous demonstrate?

A

Retrograde Amnesia - initial inability to recall personal or global events for 2 years prior to injury (this shrank in 2 wks); recall of daily events were initially poor; That memories can be accessed unknowingly by cues or triggers in the environment

47
Q

Describe Retrograde (going backward) Amnesia

A

Loss of memory for events before the brain damage

48
Q

Despite patient K.C suffering damage to medial temporal lobe, frontal, parietal & occipital cortices, what normal functions existed?; What type of amnesia did he suffer?; What was still intact?; This suggests….

A

IQ of 94, normal language, good reasoning & concentration; Retrograde - no recall of personally experienced events, though could recall facts; could learn new info but couldn’t recall how he’d acquired it; Semantic memory for general world knowledge prior to accident; Episodic & semantic memories are dissociable

49
Q

What are the 3 contemporary classes of theory regarding Semantic memory?

A

Distributed model - semantic memory is not localised to any particular structure (all connected); distributed-plus-hub model - anterior temporal cortex is a hub in mediating abstract conceptual representations; embodied cognition - the meaning is represented in the same sensory or motor structures that mediate perception & action (somatotopic)

50
Q

Describe Procedural Memory; When patient H.M performed the Mirror Tracing task, what was found?; What about the Perceptual Priming task (determining objects from fragments)?

A

Ability to develop motor skills (e.g. riding a bike); Performance improved over 3 days but he couldn’t remember performing the task; Also improvement but no memory of performing the task

51
Q

Although patient H.M showed intact Pavlovian classical conditioning, attaining & retaining a conditioned eyeblink response to a tone, he showed what?; What does this evidence support?; What is essential for eyeblink conditioning?

A

No memory of performing the task; The concept of dissociable memory systems; An intact cerebellum

PSYC2020 (11 decks)

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