26.4 - Communication: Producing and Understanding Language Flashcards

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1
Q

What are 3 important types of information found in language?

A
  • Phonology = Sounds of words
  • Semantics = Meaning of words
  • Grammar = Combinatorial rules (syntax)
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2
Q

What aspect of human language can animals not learn?

A

They can learn individual words, but they cannot learn syntax.

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3
Q

What is the name for the structure of a sentence?

A

Grammar (or syntax)

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4
Q

What is recursion?

A

Embedding linguistic units within each other in a sentence.

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5
Q

Summarise the main differences between language in apes and in children.

[EXTRA?]

A
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6
Q

Is language unique to humans?

A

Yes, but it relies on other parts of cognition (e.g. memory) that are shared with other animals.

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7
Q

Are there currently any animal models of language?

A

No

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8
Q

What is aphasia?

A

The inability to comprehend or formulate language because of damage to specific brain regions.

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9
Q

What are the classic aphasias?

A
  • Broca’s aphasia (non-fluent)
  • Wernicke’s aphasia (fluent)
  • Conduction aphasia
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10
Q

What is non-fluent aphasia and what causes it?

A
  • Lesions of Broca’s area
  • Features:
    • Disjointed speech
    • Uses mostly content words (nouns, names, etc.), not many function words
    • Poor articulation, but this is not consistent between patients so it is not a motor problem
    • Repetition of speech is impaired
    • Patients struggle to find words or name objects
    • Comprehension is spared, but have problems understanding syntax (i.e. may struggle with certain sentence structures)
    • Patient is aware of deficit
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11
Q

Where is Broca’s area?

A

Left inferior frontal gyrus (Brodmann areas 44 and 45) of left cerebral hemisphere

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12
Q

What is fluent aphasia and what causes it?

A
  • Lesions of Wernicke’s area
  • Features:
    • Fluent speech
    • Impaired comprehension
    • Repetition of speech is impaired
    • Normal articulation
    • Grammatically correct sentences without meaning
    • Patient is unaware of deficit
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13
Q

Where is Wernicke’s area?

A

Posterior part of superior temporal gyrus (Brodmann area 22) of left cerebral hemisphere

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14
Q

Draw the position of Wernicke and Broca’s areas and what the consequence of their lesion is.

A
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15
Q

What are some types of errors that patients with Wernicke’s aphasia may make?

A
  • Semantic paraphasia -> When an entire word is substituted for the intended word (e.g. orange instead of apple)
  • Phonemic paraphasia -> When part of a word is substituted with a non-word that preserves at least half of the segments and/or number of syllables of the intended word (e.g. wife instead of knife).
  • Neologisms -> Making up a word.
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16
Q

What aphasia is hemiplegia associated with?

[EXTRA]

A
  • Hemiplegia is paralysis on one side of the body.
  • It causes weakness, problems with muscle control, and muscle stiffness.
  • It is more commonly associated with non-fluent (Broca’s) aphasia, because Broca’s area is much closer to the motor cortex, so it is more likely to be lesioned too.
17
Q

Describe how limits of comprehension in a patient with non-fluent (Broca’s) aphasia. Give some experimental evidence.

A
  • Although patients with lesions in Broca’s area generally have relatively normal comprehension, they are impaired at syntactic processing due to their problems with grammar
  • Much like with their use of mostly content words in speech, they also struggle to understand grammar (e.g. some tenses) when listening
  • (Caramazza & Zurif, 1976):
    • Presented patients with three simple sentences like “the boy ate the apple”, “the boy kissed the girl” and “the boy was kissed by the girl”
    • The patients understood the first two sentences, since they can understand the subject words and can infer the meaning from the word order and logic
    • However, they struggle to understand the third sentence due to the passive voice
    • The two explanations are:
      • The object of the verb has moved (Trace-deletion hypothesis, Grodzinsky, 1990)
      • There is a lack of working memory to process this syntax
18
Q

Describe a model of the of the language systems in the brain (derived from observations of patients with aphasia).

A

Geschwind model (1960s) explains that when speaking a heard word:

  • Auditory cortex passes auditory information to Wernicke’s cortex
  • Wernicke’s cortex accesses the meaning of the word
  • Wernicke’s area communicates with Broca’s area via the arcuate fasciculus
  • Broca’s area stores motor information associated with that word and outputs to the motor cortex
  • This leads to the speech of that word
19
Q

What is conduction aphasia?

A
  • It is an aphasia due to lesions in the arcuate fasciculus (connecting Wernicke’s and Broca’s areas).
  • More recently this idea has been challenged and it is thought that it could also be due to lesions of other areas such as the left superior temporal gyrus/left supramarginal gyrus.
  • The superior temporal gyrus/left supramarginal gyrus are involved in phonological working memory (processes that underlie the short-term maintenance of language sounds for processes like memory during a sentence), while the arcuate fasciculus is involved in integrating the auditory and motor systems.
  • These lesions result in an inability to repeat things exactly (e.g. “the football player celebrated” becomes “the sportsman cheered”)
  • Also show impaired naming, especially phonemic paraphasis (e.g. they may say “wife” instead of “knife”)
  • Speech is fluent and grammatical, and auditory comprehension normal -> Since Wernicke’s and Broca’s areas are mostly undamaged
20
Q

Give some experimental evidence for the lesion that causes conduction aphasia.

[EXTRA]

A

(Buchsbaum, 2011):

  • Mapped the areas of lesion in patients with conduction aphasia and found the most common areas of overlap
  • Mapped the active areas in healthy patients performing a phonological working memory task
  • The area that was most overlapping between the two groups was determined to be Area Spt (which is involved in phonological working memory)
21
Q

What is primary progressive aphasia?

A

Neurodegeneration of the language network characterised by:

  • Impaired usage, retrieval or comprehension of words (aphasia)
  • Language disorder is the principal deficit (primary)
  • Neurodegenerative (progressive)
22
Q

What are 3 variants of primary progressive aphasia?

A
  • Progressive Non-Fluent/Agrammatic Aphasia (PNFA) -> Non-fluent
  • Semantic Dementia (SD) (a.k.a. fluent) -> Fluent
  • Logopenic Progressive Aphasia (LPA) -> Slow speech due to struggle to find words
23
Q

Compare the symptoms of PNFA (progressive non-fluent/agrammatic aphasia) and SD (senile dementia).

(i.e. compare non-fluent vs fluent primary progressive aphasia)

A
24
Q

Describe the symptoms of LPA (logopenic progressive aphasia).

A
  • Slow speech rate due to long word-finding pauses -> The patients struggle to find words from memory
  • Normal grammar and articulation except phonological paraphasias
  • Impaired repetition and comprehension for sentences but preserved for single words
  • Moderately impaired naming
  • Deficit in phonological loop functions:
    • Severely impaired digit, letter, and word span tasks (even with pointing response)
    • Word length effect (longer = harder)
    • No benefit of phonological discriminability (e.g. W, Z, Q easier than B, T, P) -> Words starting with different sounds are usually easier to distinguish, but not in these patients
25
Q

Summarise the patterns of atrophy in different types of primary progressive aphasia. Give some experimental evidence.

A

(Gorno-Tempini, 2004):

  • Mapped the areas of the brain that were most commnoly atrophied in NFPA, SD and LPA
  • NFPA featured atrophy of the left inferior frontal and insular cortex
  • SD featured atrophy of the anterior temporal lobes
  • LPA featured atrophy of the posterior temporal lobe and inferior parietal lobule
26
Q

Give some experimental evidence for syntax processing in different types of primary progressive aphasia.

[EXTRA?]

A

(Wilson, 2010):

  • Tested the comprehension of different sentences in patients with NFPA and LPA
  • Patients with NFPA showed the greatest inaccuracy when presented with sentences with a complex syntax (e.g. passive tense)
  • Patients with LPA showed the greatest inaccuracy when presented with long sentences
  • This suggests that NFPA features impairment of syntactic processing, while LPA features cognitive memory deficits
27
Q

Is it just grey matter that is affected in primary progressive aphasia?

A

No, it can also be the white matter, especially the dorsal pathways (arcuate fasciculus) between language areas.

28
Q

Summarise the main ways in which syntactic processing (i.e. understanding sentence structure) may be impaired in aphasias.

A
  • Syntactic processing impaired in non-fluent (Broca’s) aphasia and non-fluent PPA
  • Disconnection of arcuate fasciculus or damage to posterior STG (or both) impairs phonological working memory (conduction aphasia)
  • Arcuate fasciculus function correlates with syntactic comprehension in PPA
29
Q

Summarise the role of Broca’s area and Wernicke’s area.

A
  • Broca’s area is involved in speech production
  • Wernicke’s area is involved in language comprehension
30
Q

How can you remember each of the PPA disorders?

A
  • NFPA is essentially like Broca’s aphasia
  • SD is essentially like Wernicke’s aphasia
  • LPA is essentially like conduction aphasia
31
Q

What is a Specific Language Impairment (SLI)?

A
  • AKA developmental language disorder, impairment, or dysphasia.
  • Identified in children when there is an unexplained and language-specific impairment compared to other children the same age.
  • A subset of SLI’s may also be associated with more general (non-language) perceptual impairments, specifically a disorder of rapid auditory temporal processing and/or magnocellular visual function. Some children show improved language function after training in these perceptual skills.
  • Associated with reduced structural and functional left hemisphere asymmetry in frontal language brain regions.
32
Q

Give two examples of the involvement of genetics in specific language impairments.

[IMPORTANT?]

A
  • KE family in the UK (Watkins et al., 2002):
    • Affected family members are impaired on expressive and receptive language tasks.
    • Reduced grey matter in Caudate Nucleus and increased in Putamen.
  • FOXP2 transcription factor gene
    • The first connection between a gene and language function (Lai et al., 2001)
    • Heterozygous FOXP2 mutation is highly predictive of SLI
    • FOXP2 is expressed in brain areas identified as abnormal in KE family
    • Variants of FOXP2 also associated with other language and reading disorders
33
Q

How is speech processing related to memory?

[IMPORTANT]

A
  • Memory also plays an important role in language production and understanding, as semantic memory provides the meaning for words (with damage leading to semantic dementia and a ‘word salad’ which can also relate to Wernicke’s (fluent) aphasia).
  • Working memory is linked with the coherence of ideas and the following through of a thought pattern, and provided by the frontal lobes, as well as providing an important aspect of comprehension, especially while reading as an internalised form of language generated by visual, rather than spatial, aspects in a convergence of the cortical areas.
34
Q

What is dyslexia?

[IMPORTANT]

A
  • Dyslexia is trouble with reading despite normal intelligence
  • The causes may be developmental or acquired
  • Posterior parietal cortex lesions may be causes of acquired dyslexia. This is due to its role in the direction of attention, as is necessary for reading and speech in particular.