Psych 373 exam 2

autism spectrum disorder

-persistent deficits in social communication and interaction across multiple contexts

- restricted repetitive patterns of behavior, interests, or activities

DSM 5 criteria for ASD diagnosis

- must have symptoms in both domains

- sx present in early developmental period

- cause clinically significant impairment in social, occupational, or other area of function

-disturbances not explained by intellectual disability or global dev delay

specifiers of ASD

current severity

co-occuring intellectual or language impairment

ASD: persistent deficits in social comm or social interaction

*Must have all three*

- lack of social reciprocity

- def in nonverbal communicative beh

- lack of developing, maintaining, and understanding rel

ASD : restricted, repetitive patterns of beh, interests or activities

** at least two**

- stereotypes or rep motor patterns

- use of obj

- insistence on sameness

- routines

- fixated interests that are unusual in intensity

- hyper or hypo sensitivity to stimuli

DSM 5 changes in ASD diagnosis

- eliminated subtypes (diagnosis often changed, cultural issues, unreliable, dev issues)

- from 3 domains to 2 domains (communication and interaction used to be separate) -- not supported by research

prevalence of ASD

about 1% in US (1 in 68 kids)

- increase 600x since 1966

gender differences in ASD

boys 4 times more likely than girls to get diagnosed with ASD

why has there been an increase in ASD diagnosis?

- better awareness and ability to diagnose

- changes in environment

two patterns of symptom onset

1. sx onset in the first year

2. regression or loss of skills during first 3 years (25%)

early signs of ASD (1 year)

- not making eye contact

- not responding to parent's voice

- not responding to name

- not smile or laugh in response to others

most useful predictors of ASD prognosis

- IQ > 70

- communicative speech by age 5

common co-occuring disorders with ASD

intellectual disability (70%)

language disorders

epilepsy

joint attention

ability to coordinate attention with social partner to pay attention to the same thing

- decreased in ASD

attachment pattern in ASD

once thought that ASD kids couldn't form secure attachments, but they can

- those w lower IQ or higher severity are less likely to form secure attachment

- difficulty understanding and responding to social info

- express attachment differently

-Strange situation might not work to test them

language deficits in ASD

-lack of gesturing (only use instrumental gestures)

- unusual rhythm or intonation of speech

- pronoun reversal

- pragmatic issues: use of appropriate language to social situation

language issues in ASD

- expressive: dont use facial expressions

- receptive

- pragmatic: don't use appropriate language

echolalia

parroting speech, repeating what they have heard immediately or on delay

self-stimulatory behavior in ASD and possible explanations

example of hand flapping

- CNS craves stimulation

- env too stimulating so they use self stim to block out

ASD: sensory overresponsivity

negative response to or avoidance of sensory stimuli accompanied by overreactive brain responses

ASD: sensory dominance

tendency to focus on certain types of sensory input over others

ASD: stimulus overselectivity

tendency to focus on one feature of an object while ignoring others

"mind blindness" theory of autism

- difficulty with ToM and understanding states of mind

- shown in difficulty with Sally-Ann task

sally-anne task

way to test ToM in kids with autism

- dolls: doll puts marble in box and then leaves, other doll moves marble to bag, ask child where the first doll will look for the marble

- kids with ASD say she will look in the bag bc they know its there -- can't take her position to know that she doesn't know the marble got moved

- typical 4 year olds can do this task

- some kids with ASD and high intelligence can figure out task but not through understanding of ToM

false photograph task

- like the Sally Anne task but camera records scene and then objects are moved; ask where in picture objects will be located?

- ASD children do better on false photograph task than Sally Ann task (better at taking perspective of mechanical object)

theories of cognitive deficits in ASD

- mind blindness

- executive function - central coherence

Executive function theory of ASD

- issues with working memory and inhibitory control

- higher order planning and regulatory beh

ASD: central coherence

strong tendency of humans to interpret stimuli in relatively global way that takes broader context into account

- kids with ASD fail to use contextual cues

- make it difficult to process emotions

which symptoms are unique to ASD and which aren't?

- lack of ToM is specific

- executive function is not specific

common medical issues in kids with ASD

- motor and sensory impairments

- seizures (25%)

- sleep disturbances (65%)

- gastrointestinal issues

reasons for sex difference in ASD

- more prevalent in kids w high IQ than ID

- diagnosis bias

- extreme male brain theory of ASD: high end of spectrum of understanding object world and low end of understanding social world

when can ASD be reliably detected?

12 to 18 months

- usually no signs before 6 months

savants

kids with ASD that have high levels of abilities in specific areas of function

- memory, math, drawing or music

- about 5% of the 1%

problems in early development in kids with ASD

- health problems prenatally and at birth

-pre term birth, bleeding during pregnancy, viral infection

- mother age, fever, hypertension, obesity

genetic causes of ASD

lots of evidence for strong genetic influence

- MZ twin studies 70 to 90%

- lots of family member have broader autism phenotype

broader autism phenotype

family members show minor impairment in social, communicative and repetitive behaviors

- more common in biological than adoptive parents

molecular genetic causes of autism

susceptibility genes: might make someone more likely to get autism, not a single gene but interaction of genes

- chromosomes 2, 7, and 15

ASD: abnormalities in brain development

- abnormal brain growth 1 to 5 years

- cellular abnormalities

- cerebellum, medial temporal lobe, limbic structures

- issues in connectivity of brain account for wide spread of symptoms

- overgrowth of gray and white matter

tract abnormalities in ASD

corpus callosum, frontal lobe, interhemispheric connections

- issues with default mode network

what gray and white matter overgrowth in ASD means

not enough pruning of synaptic connections

temporal lobe limbic circuits

emotional regulation

learning

memory

emotional processing

goals of ASD treatment

minimize core problems and maximize independence

- enhance learning, reduce maladaptive beh, educate and support parents

behavioral intervention for ASD

intensive assessment of deficits and excesses

shape and selectively reinforce comm skills

generalizability of skills

why is early intervention important in ASD?

extreme neuroplasticity in brain allows for new brain connections to form and potential for long term and wide spread effects

examples of beh deficits and excesses treated in ASD behavioral treatment

deficits: social response, self help, language, communication

excessive: self injurous behavior, inappropriate disruptive social beh, self stim behaviors

where should educational placement be for kids with asd?

in least restrictive environment

discrete trial training v incidental training

discrete: step by step approach to presenting stimulus and requiring specific response

incidental training: capitalize on natural opportunities

most effective treatments for asd are:

- early

- intensive

- low student-teacher ratio

- high structure

- family inclusion and edu

- generalizable

- on going assessment and data keeping

how much tx should kids with asd get a week? how much do most receive?

at least 25 hours per week

1.5 hours a week

medication for asd

psychotropic meds (antidepressants, stimulants, antipsychotics)

Childhood onset schizophrenia (COS)

neurodevelopmental disorder expressed in abnormal mental function and disturbed beh

positive sx of COS

delusions

hallucinations

disorganized speech

disorganized or catatonic behavior

negative sx of COS

flat affect

diminished goal-directed activity

continuous signs of disorder for at least 6 months

differences bw ASD and COS

later onset than ASD

less ID

less social and language difficulty

more hallucinations and delusions

DSM 5 criteria of COS

criterion a: sev disturbance in sensory function and behavior

criterion b: social or occupational disfunction

criterion c: duration (at least 6 months)

criterion d: shizoaffective and mood disorder exclusion

criterion e: substance abuse exclusion

delusion

disturbance in thinking involving disordered thought and strong false beliefs

hallucinations

disturbances in perception (see, hear, sense things that aren't there)

precursors to COS

speech issues

learning problems

maturational delays

motor dev issues

unusual thought content

substance abuse

genetic risk

prevalence of COS

adult onset is 1%, even lower in kids (1 in 10,000)

comorbidities with COS

mood disorder

ODD

ASD

sex differences in boys and girls

boys diagnosed earlier, more common to have early onset in bosy

outcomes of early onset COS

when followed into adulthood

25% recovered

25% improved

25% continuing chronic course

- earlier onset associated with poor outcomes

COS case study: Mary

- history of withdrawn beh before onset

- difficulty making friends

- academic difficulty

- delusions: though devil was trying to kill her

- disorganized thought and language

- suicide attempt

neurodevelopmental model of schizophrenia

genetic vulnerability and early neurodev insults result in impaired connections bw brain regions

biological factors to COS

- strong genetic contribution( 88% in MZ twin studies)

- children whose parents have schizophrenia are at higher risk

adoption studies in COS

studied kids who have COS but were adopted by parents who dont

- resembled biological parents more than adoptive parents

possible bio causes of cos

- abnormal dopamine receptor function

- abnormalities in frontal and temporal-limbic sx

- enlarged ventricles

pregnancy and birth complications in COS

- anoxia

- exposure to toxins ot trauma in prenatal or postnatal period

- maternal diabetes, LBW, older parents

family climate in COS

- communcation deviance: communication seems incoherent to observer, attention and thought disturbances

- expressed emotion: tend to blame child for symptoms

best treatment method of kids with COS

antipsychotic meds combined with psychotherapy, edu support, and social support

type of drug used to treat COS

antipsychotics: tranquilizers

- bad motor side effects

Atypical antispychotics can act on positive and negative sx but have bad side effects

psychosocial treatments for COS

family educational: reduce blame, stress, increase support and understanding

behavioral: inc social and self help skills

difference bw COS and adolescent onset sx

early onset sx manifest in early signs of deficits in social function (withdrawal, isolation, poor social skills)

- nonpsychotic sx: delays, peer difficulty, school problems

adolescent onset with chronic course

ADHD

persistent, age-inappropriate sx of inattention and /or hyperactivity-impulsivity that cause impairment

history of ADHD

first described in germany 1775

1950s: focus on hyperactivity/hyperkinesis

1960s-70s: Virginia Douglass (studies on regulating activity)

2 categories of sx for ADHD

hyperactivity-impulsivity

inattention

inattention

inability to sustain attention or stick to tasks, difficulty following directions and resisting distraction, difficulty planning and organizing

types of memory/attention affected by inattention

- working memory: 7+/- 2 pieces of info in head

- selective attention: focus on relevant info and ignore irrelevant

- sustained attention: maintain persistent focus of attention across time

attentional capacity

amount of info we can remember and attend to for a short amount of time

where is main deficit in inattention for ADHD? what about in hyperactivity-impulsivity?

sustained attention

undercontrol of motor beh, poor inhibition, inability to inhibit dominant response in response to social conditions

hyperactivity-impulsivity

undercontrol of motor behavior, poor inhibition, inability to delay response or gratification, inability to inhibit dominant response in accordance with social demands

how can we distinguish bw hyperactivity and high activity levels?

quality of activity: hyperactivity is intense overactivity that is not goal directed or focused

inhibitory control

stop dominant response and engage in less rewarding experience

types of impulsivity

delay and inhibition

DSM 5 diagnostic criteria for ADHD

Persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning

I. 6 sx of inattention

2. 6 sx of hyperactivity for under 17, 5 for over 17

3. 6 months at impairing levels

4. sx prior to age 12

5. multiple settings

6. impairment

7. not better explained by another disorder

DSM 5 inattention sx

- have to have 6 for 6 months that interfere with function

fail to pay close attention, make careless mistakes

difficulty sustaining attention

not listening when spoken to

does not follow directions, fails to finish hw

has difficulty organizing tasks

avoids tasks that req sustained effort

loses things

easily distracted by extraneous stimuli

forgetful in daily activities

hyperactivity-impulsivity sx for ADHD

6+ for under 17, 5 for over 17 for 6 months

fidgets or squirms

leaves seat

runs about or climbs

unable to engage in leisure activity

on the go, acting like driven by motor

talks excessively

blurts out

difficulty waiting turn

interrupts others

DSM 5 specifiers for ADHD

combined presentation

ADHD-I: meet criteria for inattention but not HAI in last 6 monts

ADHD-HAI: meet criteria for HA-I but not inattention in last 6 months

specify severity

specify partial remission

what is the most common specifier of ADHD?

ADHD-C

subgroups of ADHD-I

1. clinically significant sx of inattention and substantial but subclinical sx of HAI

2. Sluggish Cognitive Tempo

3. group who once met criteria for ADHD_C but had age-related reduction in hyperactivity

Sluggish Cognitive Tempo

variant of ADHD-I

- day dreamers, mentally foggy, easily confused, spacey

ADHD: changes from DSM 4 to 5

- now listed under neurodevelopmental disorder

- examples added to criterion sx to facilitate application across lifespan

- age of onset criterion changed from 7 to 12

- subtypes replaced w specifiers

- symptom threshold change made for adults

how stable are ADHD specifiers over lifetime?

Not stable -- diagnosis will often change (50% of the time)

what is wrong with DSM 5 diagnosis of ADHD?

- age insensitive

- categorical view of ADHD: have or don't have no in between

common comorbidities with ADHD

80% of kids have co-occuring disorder

- ODD (35-70%)/CD(30-50%)

- Learning disorder (dyslexia)

- anxiety disorder

- depression

- bipolar

cognitive deficits in ADHD

poor executive function: cognitive processes, language, motor, emotional

executive function

cog processes that activate, integrate, and amange other brain functions; multiple streams of info, revise plans, filter distractions

cognitive processes that are part of executive function

working memory

mental computation

planning

flexible thinking

language process that are part of executive function

verbal fluency

self-directed speech

motor processes that are part of executive function

allocation of effort

response inhibition

motor coordination and sequencing