Lecture 14 Flashcards
Wodka et. al 2013
studied language delay
• 535 children with autism who were
– Age 8+
– No phrases by age 4 (37% of 8+-y-o’s)
- 253 (47%) attained fluent speech after age 4
- 372 (70%) could at least produce phrases (multiword utterances)
- Non-verbal IQ, social engagement were predictors
- Stereotypies, sensory sensitivities (sensitive to light or certain kinds of sounds): doesn’t matter
- Good news! Late language is not equivalent to no language in adult life
Echolalia:
type of sterotyped behavior
kids with autism repeat things they’ve heard recently
- Immediate vs. delayed
- Exact vs. mitigated
exact echolalia
exact repition of what they’ve just heard
mitigated echolalia
repetition with some sort of change to it: modified
• Actually, a lot of it is mitigated
– Communicative strategy? Maybe it’s a bit like expressive kids producing entire phrases.
– Tends to disappear as they acquire more
spontaneous speech: this suggestes that maybe early on it’s a stepping stone communicative device
– May be “stepping stone” to help break down larger pieces
autism treatment: intervention guidelines
intensive, early intervention is KEY
– Early
– Intensive (up to 25 h/wk!)
– Involve family
– Social, pragmatic communication: attend to social factors during conversation: real world communication
– Systematic but customized to child (because there’s a wide array of variability)
– Generalization: want children to learn real world skill that can be used outside the treatment context
evaluation of autism treatment
– Until recently, mostly “small N” (where “n” refers to the number of participants) studies
spectrum of treatment
None meet strict criteria for efficacy.
behavioral intervention
address children’s self harming behaviors
reinforcement (reward good behavior), punishment: operant conditioning
Lovaas
applied behavior analysis: discourage negative behaviors and shape kid’s behaviors to more productive forms
have good outcomes in clinical settings
less effective if parents administer these techniques (maybe they don’t have enough time, maybe clinicians are stricter than the parents
developmental social-pragmatic
trying to shape their social and pragmatic development
Multifaceted “TEACCH” approach: looks at multiple facets of development
New study: it improves range of skills
nonverbal autistic intervention
picture communication
if kids can communicate better then…
harmful behaviors may drop (see this in typically developing kids)
autism treatment
• Not just treating language, of course
• ABA: quite good for reducing harmful behaviors
• Medication
– Often, undesirable side effects (weight gain,
dyskinesias)
Medication
– Often, undesirable side effects (weight gain,
dyskinesias - movement disorder )
things that don’t work for autism treatment
• Auditory integration therapy (AIT)
– “uses filtered and modulated music to help
stimulate the audiological and neurological
systems”
• Facilitated communication (FC)
– “Facilitator” offers physical support (usually to type something on a computer) to help the autistic communicate
– May have helped small handful of people (4ish)
– Most scientists think authorship is facilitator’s
specific language impairment (SLI)
• Delayed (not deviant) learning: child’s language skills are worse based on their other cognitive traits
• May originate in toddlerhood (or earlier) with late talkers
– 25-50% of late talkers end up getting SLI diagnosis
- Family history
- Less likely to be caught than articulation problems (Sedaris’ “s”)
- Likely to cascade into reading difficulty: if you can’t read you’ll be really behind with vocab
What does SLI look like?
- no gene for SLI
- Bad at mapping words to meanings
- Circumlocutions: talking around what they want to say
- Syntactic problems (big identifier)
- Pragmatic problems
Syntactic problems SLI
leave off certain kinds of function morphemes: “ the boy go to store”
– Tough time using grammatical syntax
- “He run”
- “Me want cookie”
– Even when you control for language age w/MLU! = compare to normal kids
is this some kind of lesion to the syntactic module?
Circumlocutions in SLI
talking around what they want to say
– SLI kid: “Something round and English” for breakfast ( “ I want an english muffin”)
– Trouble accessing words? [Like anomic adults! = trouble naming things]
pragmatic problems in SLI
– Which can cascade into social difficulties
*Different symptoms in different languages
Where does SLI come from?
• Tip end of distribution of the population? (Hard to say)
- assess normal and SLI kids
• The Brain?
• Genes? (KE family: some members had a really strong language impairment and then had a FOXP2 mutation; Crago & Gopnik, 1994)
– BUT this KE family data smoking gun didn’t work: Lots of SLI kids tested with no FOXP2 mutation
– In mice they took out (lesioned) FOXP2:
– Differences in brain development in multiple
regions
- Deficits in temporal auditory processing (Tallal)
- Trouble with linguistic rules (modular-ish)
In mice they took out (lesioned) FOXP2:
- Difficulty in motor learning (French et al., 2007, Genesis)
- Aberrant vocalizations (Gaub et al., 2010)
- Poor sound-behavior associations (Kurt et al., 2012, PLOS One): learning that a particular sound cues something (sound + electrocution
might explain why mutations in this gene contribute to language difficulties
Surface Hypothesis:
SLI
Hard time processing grammatical morphemes with low perceptual salience (they don’t get stressed in the speech signal)
can’t pick up on those less salient speech sounds
Theory for where SLI comes from:
Deficits in temporal auditory processing (Tallal)
set of tasks where kids have difficulty processing fine grained temporal auditory distinctions: screws up speech perception = screws with the rest of language development = very controversial
Generalized Slowing Hypothesis
SLI
slower at executing a lot of perceptual/motor tasks
bad not just at language learning but also at learning motor sequences
active area of research
SLI Interventions
• Imitation
– Repeat the therapist
• Modeling
– Kid makes new version of what therapist
says
• Recasting
– Restating what kid says: “Me want cookie” and then therapist says “I want a cookie” = reshaping the kid’s sentence to the adult form
• As always, generalization is a toughie
Cerebral palsy
– Impaired motor control
– Comprehension, cognition often OK
Cleft palate
neural tube defect: rare in the U.S.
– Physically impossible to produce certain
sounds
– Again, cognition and comprehension fine
Functional articulation disorders (NotOtherwiseSpecified)
we don’t know why they have language learning issues
could be Otitis media? (ear infections) = compromised hearing
stuttering
– Starts after speech sounds acquired
– Part-word repetitions
• Not just individual word repetitions “And…and this one time” • But also “t-t-t-t-time” (stuck on certain kinds of speech sounds)
– Children often very aware (unlike other disorders): teased
– Many resolve in a few years (speech therapy)
clues to language problems
how do you know if your kid has a language disorder?
- No babbling by 12 months
- No conventionalized gestures by 12 months (waving, pointing)
- No spoken words by 18 months
- Less than 50 words, no 2-word combos by 24 months
- Speech or language regression
First steps when encountering language problems
– Is it a hearing problem? (audiologist)
– Evaluation, possible therapy (speech language pathologist)
– Testing: lots of options, varying in content validity
– Watch out for language variation that’s not a disorder (different dialects)
Studies of children who had prenatal or
perinatal brain injury
– Before language production started
– Not necessarily before getting language input
• Range of lesion locations and sizes
• Big questions: does L or R hemisphere
damage matter for language ability?
• Is impairment related to lesion size?
Brain lesions Methodological problems:
– Small N
– Huge variability in:
• Timing of lesion
• Underlying cause (Stroke? Seizures?)
– Sensitivity of testsExtreme views of language specialization:
– Equipotentiality
– Determinism
– emergentism
equipotentiality
extreme empiricist:any area of the brain can do langauge with equal facility
somehow it just ends up being the left temporal reasons: it’s “lucky”
determinism
extreme nativism: dedicated chunk of brain tissue that ALWAYS does language, necessary for language
emergentism
compromises: it’s a constant interaction of the developing brain and the input that you’re getting
maybe the left hemisphere has slight early advantage and that’s why it emerges as the language region for most people, BUT it’s not the only region that can do language
Brain lesions
• Early work: Bates and colleagues
Large set of kids with similar etiology
• By about age 6, most had recovered to low normal levels
• No relationship to hemisphere damaged
• Lesion size x performance:
– U-function: tiny and large did better (brain has to completely reorganize), medium did worse (brain keeps trying to “limp along” instead of just starting over) (consistent with animal lit–”fresh start” H)
– Later in development, U-function did not hold
Brain lesions long-term
• The happy story:
Temporary impairment
• Then recover to normal by about age 6
• BUT
• Studies after age 6 show overall below normal
IQ (verbal and performance)
• Artifact of more impaired kids continuing to
see doctors and it’s just a drop out effect that makes it looks like kids are getting worse?
Brain lesions long-term
Levine et al.
• After initial recovery of function, is there a
decline in IQ later in development for kids
with unilateral focal lesions?
• Levine et al. examined 15 kids who were IQ tested pre- age 7 and post- age 7
– Unusual–a longitudinal study: hard to keep track of people over the span of years
• 12 of 15 showed an IQ decline
• Equivalent declines in verbal and performance
what does a decline in IQ mean?
• IQ tests have age-based norms
– A 2-y-o who performs like a UCSD undergrad has a higher IQ than that undergrad*
- may just be not gaining skills as rapidly as their age cohort (so still improving, but not as fast as normal)
- IQ tests have more abstract reasoning content: may be that they have a deficit in abstract learning from the beginning and this just the first instance of that particular deficit being visible
Relationship to lesion size? in brain lesions long term
smaller is worse
maybe cause the brain doesn’t “give up” and move on but just keeps limping along
SLI vs FL (focal lesion) vs WS (williams syndrome)
• Reilly et al. used narrative speech
study 1
Look at this picture book and explain story
– Tests both formal language (e.g., syntax)
and cognitive abilities (understanding the
story)
• Do SLI kids look like
– FL kids?
– WS kids?
Study 1: SLI vs. early lesions • Measures: – Story length – Complexity of sentences – Rate of morphological errors
• Assessment
– Count total # of propositions
– Count errors, divide by prop. count
– Assess diversity of syntactic constructions
Results:
story length:
• both SLI, FL below typically developing kids at age 4-6 • Lesion group approached normal at 10-12
proportions of errors:
• SLI, FL below typical at age 4-6 • Lesion group approached normal at 10-12
frequency of complex syntax:
• both SLI, FL below typical at age 4-6 • Lesion group approached normal at 10-12
suggests that language impairment is worse than missing part of your brain!!!!
Reilly et al. used narrative speech
study 2
SLI vs. Williams (WS)
Measures:
– Story length
– Morphological errors
– Narrative coherence (major points, theme)
Results:
• SLI: more morphological errors at 4-6 than WS
• both are at about the same level on complex syntax
• But WS has harder time maintaining
structure of narrative (boy looks for frog)
• WS use more social evaluation devices
- Voices, sfx, exclamations–audience attention
Overall picture for SLI
• Grammatical competence really poor
– Worse than focal brain injury!!
• Narrative skills not so bad
applied behavior analysis: ABA
• quite good for reducing harmful behaviors
– If can communicate better, aggression, inappropriate behavior may drop
– Functional analysis: what’s motivation/function of bad behavior? Can we shape into better behavior
Predictors of autism
Non-verbal IQ, social engagement
