Child aphasia & other disorders

Brain & LanguageLING 411, NSCI 411/611

Harry HowardTulane University

Come See a Movie With

Neuroscience Majors

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TUNA Members

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7:00 pm in Paterson Lounge

The Tulane University Neuroscience Association is hosting a showing of the film The Jacket. Come enjoy some food

with us while we watch.

LING 411, NSCI 411/611

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Q2 answers Transcortical sensory aphasia

(1 pt each) Broca’s aphasia

(2 pts each)

PATIENT’S COMPREHENSION

OF SOMEONE’S SPEECH

impaired spared, but patient may

misunderstand reversible, passive, and object-gap sentences

PATIENT’S PRODUCTION OF SPONTANEOUS

SPEECH

fluent impaired/non-fluent,

agrammatism, telegraphic, perseveration

PATIENT’S REPETITION OF

SOMEONE’S SPEECH spared, echolalia impaired

PATIENT IS CONCERNED ABOUT

IMPAIRMENT

unconcerned; does not correct errors

very concerned, to point of depression/suicide; tries to correct

errors

LING 411, NSCI 411/611

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Milestones [See Hoff 01:7]

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Normal language developmentAge Language milestone

0-3m cooing

4-20m from babbling to words in L1/L2

21-36m

acquisition of structure of L1/L2

3-10ygrammatical refinement & expansion of vocabulary of L1/L2

11-14y

foreign accent in L2

15y + L2 is increasingly difficult

LING 411, NSCI 411/611

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How lateralization develops Equipotentiality hypothesis (Lenneberg 1967) LH & RH have equal potential for language at birth

Invariance hypothesis LH is specialized for language at birth

LING 411, NSCI 411/611

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Evidence from processing studies with children Molfese, Freeman & Palmero (1975) found that 10m showed same lateralization for speech vs. non-speech sounds as 4y-11y and adult

Dichotic listening shows right ear advantage for children as young as 2y

LING 411, NSCI 411/611

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Evidence from childhood aphasia & brain injury prior to language

Few children get aphasia It invariably follows LH but not RH injury

Children get more non-fluent/Broca aphasia; adults get more fluent/Wernicke aphasia

Recovery is faster in children, see next slide

LING 411, NSCI 411/611

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Effect of LH lesion at ageAge Effect of LH lesion

0-3m50% no effect, 50% delayed onset of language but normal development

4-20m “

21-36m

L1 lost, reacquired with repetition of all stages

3-10y aphasiac symptoms but with full recovery

11-14y

aphasiac symptoms no longer recovered from fully

15y +aphasiac symptoms persist (usually irreversible if more than 3-5m)

LING 411, NSCI 411/611

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ConclusionsAge Organization of hemispheres

0-3mno lateralization of language (equipotentiality)

4-20m “

21-36m LH begins to assume responsibility

3-10yLH takes over more responsibility, but language can still be re-established in RH if LH is damaged

11-14y LH becomes dominant (invariance)

15y + LH dominant in 97% population

LING 411, NSCI 411/611

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Basic processes in neurological development Neural plasticity

Children’s brains are more plastic than adults The brain grows redundant connections among neurons from fetal development to 2y

Connections that are used are stabilized; most others are erased (pruned)

Changes in functional asymmetry The child initially uses both hemispheres because the LH isn’t ready yet (LH > grammar), or

The child uses both hemispheres until the acquisition of grammar causes a shift to LH specialization (grammar > LH)

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The critical/sensitive period It appears that there is a period during which children must be exposed to language for language to develop at all

What experiment would you do to test this prediction? Wild/feral children Genie Late acquisition of sign language L2, for & against

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The genetics of language development It is a maturational process, the course and timing of which is determined by the unfolding of a genetic blueprint.

Twin studies suggest that syntactic development is more controlled by genetics than vocabulary development. -- What does this mean in our terms?

Genetic language impairments, known as ‘specific language impairment’ or ‘developmental dysphasia’ see upcoming slides

LING 411, NSCI 411/611

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A story told by a 4.5y child with SLI The man got on the boat. He jump out the boat. He rocking the boat. He drop his thing. He drop his other thing. He tipping over. He fell off the boat.Lindner & Johnston (1992), cited in Hoff (2001:354)

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Sentences produced by a 16y with SLI Then he went home and tell mother - his mother - tell what he doing that day.

Then about noontime those guy went in and eat and warm up.

That boy climbing a rope to get to the top the rope.

He want play that violin. Those men sleeping. That man in a dark room. Can I play with violin?

Weiner (1974), cited in Hoff (2001:355)

LING 411, NSCI 411/611

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Specific language impairment/ Developmental dysphasia

Cognition normal, as measured by IQ tests

slower at processing information

Language Acquisition is delayed or deviant but with no obvious

neurological cause

In English, this is seen in problems with inflectional morphology, but languages with richer morphologies (Italian, Hebrew) do not show this problem

SLI runs in families: Gopnik found it in 16/30 members of a single family over 3 generations

Several analyses have been proposed some features of morphology are missing (number & tense) inflectional morphology is not salient phonologically difficulty processing stimuli presented rapidly

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Language and other species Primates The birds & the bees

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The origin of language Evolutionary psychology Language is an adaptation

Modularity: language is a mechanism specifically adapted for communication, i.e. a cognitive module [and a kind of mutation]

Non-modularity: language evolved gradually by adding new communicative functions to existing neural hardware; there is no neural mechanism dedicated exclusively to language

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Next time I am away next week; you will see two videos

Bellugi et al. "Williams syndrome" Q5 on Tuesday Oct 24, on this week’s material