Communication: producing and understanding language

Question 1

What is the main goal of language?

Answer 1

Communication

Question 2

What two large domains does language consist of?

Answer 2

Production (or expression)

Comprehesion (reception)

Question 3

What does language normally rely on?

Answer 3

Symbols - words or signs that refer to objects - and there types of information about them:

1. phonology → the sound of words
2. semantics → the meaning of words
3. grammar → combinatorial rules of word use (syntax)

Question 4

What is the hierarchal structure of language called?

Answer 4

Grammar (syntax)

Question 5

Which of the three rules distinguishes humans from animals?

Answer 5

Grammar

Question 6

Describe signed languages

Answer 6

• Are natural human languages that can be analysed at the same linguistic levels as spoken languages
o Phonology, semantics, morphology and syntax

• Arise spontaneously wherever there are deaf communitieis
• Are different in different countries
• Are distinct from surrounding spoken languages
• Do not impede language development in the audio-vocal domain – in fact may enhance it

Question 7

Watkins, Dronkers, Vargha-Khadem

Who did additional analysis regarding this and when?

Answer 7

2002

Language abilities can be influenced by genetics

KE family (30 members, 15 effected)

the family tree suggests autosomal dominant transmission of an impaired language phenotype

The affected individuals were impaired on EXPRESSIVE LANGUAGE (word and nonword repetition, naming, verbal fluency, derivational morphology) and RECEPTIVE LANGUAGE (receptive vocabulary and grammar, nonword reading and spelling)

The affected individuals were also show to have less grey matter in the caudate nucleus, but according to PET studies - more activation of caudate during word repetition, an impaired function (Watkins 2002)

Linkage and haplotype analysis in the KE family linked their genetic abnormality to 7q31 and SPCH1 region. (Fisher 1998)

Question 8

What case had a similar haplotype to KE family?

Answer 8

Case CS

Question 9

Lai et al

Answer 9

2001
Case CS, unrelated to KE, but with a similar phenotype, was identified and found to have a de novo t(5;7). FOXP2 mutation was identified in CS (Lai et al, 2001) and the gene was found to be expressed in brain areas identified as abnormal in KE family – CS had a de novo translocation between parts of chromosome 5 and 7 that truncated the SPCH1 region. Therefore, FOXP2 is an example of a language-related gene (that encodes for FOXP2, a transcription factor that affects the function of many other genes).

Question 10

Criticism of FOXP2 evidence

Answer 10

FOXP2 appears to have more to do with articulation – it is also majorly involved in normal development, so -/- is bound to have significant impacts upon cognition etc… the actual gene (if it exists) will be downstream of this.

Question 11

What are the two key brain areas of language?

What are they responsible for?

What does damage to these areas cause?

Answer 11

Broca’s area (inferior frontal gyrus; Brodmann areas 44 and 45) → MOTOR SPEECH AREA (helps with speech movement)

Wernicke’s area (posterior section of the superior temporal gyrus; Brodmann area 22) → sensory speech area (helps to understand speech and use correct words to express thought)

Characteristic aphasia

Question 12

Describe Wernicke’s aphasics

Answer 12

Comprehesion is severely impaired, while production remains fluent and grammatically, but lacks meaning

Question 13

Describe Broca’s aphasia

Answer 13

The classic view is that Broca’s aphasics are impaired at speech production (slow, poorly structured speech) and writing, but have normal comprehension
Broca → BROKEN WORDS

Question 14

Caramazza and Zurif

Answer 14

1976
Broca’s aphasics were also shown to have receptive agrammatism - an impairment in syntactic processing (e.g. patients would easily understand sentences like “the boy kissed the girl” but not “the boy was kissed by the girl”)

Question 15

What are the two explanations of agrammatism and Broca’s aphasia?

Answer 15

• Linguistic: (Trace-deletion hypothesis, Grodzinsky, 1990) → the passive construction altered the canonical disposition of subject and object in the sentence (it moved the subject at the end and the object at the beginning)
• Cognitive: processing capacity taken up by the centre-embedded clause → in other words, the patient has to keep the object in mind until the meaning of the sentence is revealed → this requires working memory in the PFC

Question 16

Where is Wernickes area?

Answer 16

Parietal and temporal lobes

Question 17

Where is Broca’s area?

Answer 17

Frontal lobe (B before W)

Question 18

Describe conduction aphasia

Answer 18

If the arcuate fasciculus is cut, thereby disconnecting the two language areas but leaving them intact, a third kind of deficit occurs CONDUCTION APHASIA

Question 19

Describe conduction aphasia

Answer 19

Speech sounds and movements retained, normal comprehension but impaired repetition, however patients can paraphrase them
e.g. hears “the pastry cook was elated” but says “the baker was happy”
They also have impaired naming; frequent phonemic paraphasias (sound-based speech errors, e.g. “wife” for “knife)

Question 20

Buchsbaum

Answer 20

2011

Showed that in conduction aphasia, there is a lesion overlap with phonological working memory

Question 21

Who first predicted conduction aphasia?

Answer 21

Wernicke

Question 22

Who first identified conduction aphasia? When?

When was this model updated, by whom? Describe the new model

Answer 22

1885
Ludwig Lichthein - published the Wernicke-Lichtheim model (or classical model of aphasia)
Was revisited in 1965 by Geschwind - Wernicke-Lichtheim/Geschwind house model
Auditory input from A1 → WA (extraction of meaning) → travels to BA via the AF and association cortex (which also projects to BA) to form concepts → BA (instructions for speech) motor input to M1

Question 23

Describe primary progressive aphasia

Answer 23

• language capabilities become slowly and progressively impaired
• results from neurodegenerative diseases, e.g. AD
• Cases are described as “PNFA” vs. “SD” or “non-fluent” vs. “fluent” (analogous to stroke aphasia)
• there is also a third variant → lopopenic progressive aphasia → hesitant anomic speech, word retrieval and sentence repetition impairment

Question 24

Describe LPE

Answer 24

• slow speech due to long word-finding pauses
• normal grammar and articulation except phonological paraphasias
• impaired repetition and comprehesion for sentences but preserved for single words
• moderately impaired. naming
• deficit in phonological loop functions:
  1. severely impaired digit, letter and word span tasks
  2. word length effect (longer = harder)
  3. no benefit of phonological discriminability (e.g. W, Z, Q easier than B, T P)

Question 25

Gorno-Tempini et al

Answer 25

2004 patterns of atrohpy in PPA - left perislyvia region and anterior temporal lobes were atrophies - but different patterns of atrophy in different clinical types of PPA

Question 26

Wilson et al 2010 results

Answer 26

Patients with the: - Non-fluent variant – syntactic errors, reduced complexity of speech, slow rate, distortions - Semantic variant – normal rate, very few speech or syntactic errors – but showed retrieval deficits - Logopenic variant – speech rate intermediate, distortions and syntactic errors less common than in non-fluent

Question 27

What did Dejerine describe and when?

Answer 27

1892 | visual word-form dyslexia/alexia = deficits in reading whole words or even letters

Question 28

Gaillard 2008

Answer 28

showed that the VWFA (visual word form area), a major component of the reading network, which is damaged in pure alexia patients, was mainly linked to the occipital cortex through the inferior longitudinal fasciculus, and to perisylvian language areas (supramarginal gyrus) through the arcuate fasciculus.

Question 29

What are the aquired dyslexias? (lost some aspect of reading due to brain damage)

Answer 29

Surface dyslexia Phonological dyslexia Deep dyslexia

Question 30

Describe surface dyslexia

Answer 30

o Can read words or pseudo words with regular pronunciation o Cannot read familiar words with irregular pronunciation o Deficit for words with unusual spelling-to-sound (YACHT, TWO) CANT READ IRREGULAR WORDS

Question 31

Describe phonological dyslexia

Answer 31

o Cannot read unfamiliar or pseudo words (MAVE, NUST) o Can read familiar words, even with irregular pronunciation (BLOOD, YACHT, MAUVE) o Deficits in converting spelling-to-sound CANT READ NON-WORDS

Question 32

Describe deep dyslexia

Answer 32

``` o Cannot read pseudo words o Phonol & semantic errors o Multiple deficits? o Examples:  Signal  “single”  Fridge  “oven”  Sympathy  “orchestra” ```

Question 33

What are the two routes of reading? | Decribe these in the acquired dyslexias

Answer 33

By sound or by sight • Surface dyslexics use letter-sound correspondence to read words and non-words • Phonological dyslexics rely on sight vocab and cannot convert letter to sound • Deep dyslexics have problems with both sight and sound reading routes o Additional impairment with function words (it, and, when) and make semantic errors o E.g. “inn”  “pub”, but unable to read “in”

Question 34

Draw the model of reading

Answer 34

On the notes

Question 35

Which hemisphere is normally dominant with regard to language?

Answer 35

Left

Question 36

How can the lateralisation of speech and other functions be established?

Answer 36

Wada test → a barbiturate (normally sodium armobarbital) is injected into one of the internal carotids, suspending the function of one of the hemispheres for 4-8 mins, during which the preservation of various functions can be asseses

Question 37

Which patients is the laterality of language apparent in?

Answer 37

Split-brain patients If they are presented with an object in their left visual field, which is processed in the right hemisphere, they report nothing seen, but can draw it with their left hand. If the split is parietal, they eventually come up with a word through description of the picture, but not if the split is complete, which suggests that the anterior corpus callosum transfers semantic information.

Question 38

Do lesions during childhood impair language learning? What does this suggest?

Answer 38

Lesions sustained in childhood do not impair language learning, which suggests capacity for plasticity in immature brain. However, there is a critical period for language acquisition.

Question 39

Describe the case of Genie

Answer 39

This is illustrated by the case of Genie, who was confined from age 2 in a room and restrained to a chair, not spoken to and punished for making sounds. She was discovered at age 13.5 and fostered into a normal linguistic environment. She acquired some English words after puberty, but had phonological problems and her morphology and syntax were limited to simplest aspects.

Question 40

Describe second language learning

Answer 40

Earlier exposure to a second language leads to greater fluency.

Question 41

Johnson and Newport

Answer 41

1989 Adults outperform children during early stages of language learning, but this effect is temporary, as shown by Johnson and Newport in their 1989 paper. They studied comprehension of grammar by Chinese and Korean immigrant to the US, and, controlling for years of exposure, showed that test score decreased approximately linearly with age of arrival from 2 to 16, and then remained more or less stable throughout adulthood

Question 42

Newport

Answer 42

1990 | . Newport (1990) also found that age of acquisition effects mastery of sign language.

Question 43

Describe what happens when there is no common language to a group of people

Answer 43

Language is key to people and when there is no common language for a group of people, one is created. Pidgin - rudimentary (simplified) language developed by a group of speakers from different linguistic backgrounds. Children of pidgin speakers develop a more complex elaboration of the pidgin (Bickerton, 1983) with rich syntactic forms, known as creole.