ADHD And Autism Flashcards
1
Q
ADHD
A
- Persistent pattern of inattention and/or hyperactivity-impulsivity
- Hyperactivity = fidgeting
- Impulsivity = impatience, immediate rewards, dangerous activities etc.
2
Q
Diagnostics subtypes of ADHD
A
- Attendion deficit hyperactivity disorder
- Predominantly inattentive presentation and attention deficit hyperactivity disorder
- Predominantly hyperactive/impulsive presentation
- Combined presentation
3
Q
Diagnosing ADHD
A
- At least 12 years and symptoms from DSM-5 found in two or more contexts/settings
- Higher rate than other psychopathologies.
- Cognitive tests: stroop test, continuous performance, trail making, contextual word association, ADOS
4
Q
Comorbidity of ADHD
A
- Oppositional defiant disorder or conduct disorder
- Anxiety and depressive disorders
5
Q
Prevalence of ADHD + consequences
A
- 5% of school-age children
- 2.5% of adults
- More common in boys than girls but symptoms are not sex specific
- More outbursts, stubbornness, poor self esteem, inattentive = affects academics, hyperactivity = peer/social relationships, work and safety also affected.
6
Q
Biological etiology of ADHD: genetic factors
A
- Most heritable (16% in twin studies)
- Chromosome 16 = most linkage
- Dopamine transporter genes (D4, D5, SNAP-25 - genes that release dopamine)
- Genes identified link to abnormalities in Neurotransmitters: serotonin, dopamine, norepinephrine.
- Environment activates the genes.
7
Q
Biological etiology of ADHD: Neuroscience
A
- Smaller brains (3.2%, with all lobes and global reduction of grey matter as affected areas)
- Peak thickness of the cortex (50%) is reached by 10.5, and not 7.5 yrs.
- Deficit in executive functioning (frontal lobe) = low attention
- Cornico-striatal something
8
Q
Biological etiology of ADHD: Prenatal factors
A
- Smoking/drinking/childbirth complications (low birth weight, respiratory distress and asphyxia) influence genetic predisposition of ADHD.
- Nicotine causes abnormalities in the dopaminergic neurotransmitter system.
9
Q
Biological etiology of ADHD: Environmental toxins
A
- Hyperactivity = from biochemical imbalances caused by food additives/refined sugar cane/lead poisoning.
10
Q
Psychological etiology of ADHD: Parent-child interaction
A
- Parents who have/had ADHD = child has ADHD.
- ADHD = ineffective and inconsistent parenting.
- Authoritarian parenting methods increase hyperactivity = disruptive child > discipline > defiant reaction > acute
- The child’s behavior needs attention from the parents, and that attention may either be rewarding or reinforcing them.
11
Q
Psychological etiology of ADHD: Theory of Mind deficits
A
- Ability to understand one’s own and other people’s mental states.
- Inconsistent evidence for the link with ADHD but consistent with neuroscience view.
12
Q
Treatment of ADHD: Psycho-stimulants (+paradoxical effect)
A
- Increases central nervous system activity.
- Increases alertness, arousal and attention
- Immediate and noticeable improvements in 75% of children
- Ritalin, Dexedrine, Cylert, Adderall
- Side effects: decreased appetite, trouble sleeping, physical growth.
- Long-term
- Learning and growth are at concern.
- Paradoxical effect: abused drugs = restless but not the case.
13
Q
Treatment of ADHD: Alternatives
A
- Strattera: norepinephrine re-uptake inhibitor, for adults, less effective, dangerous side effects (suicidal thoughts)
- Clonidine: decrease aggression, combination with stimulants, adults + high blood pressure.
- Antidepressants: second line, justified only if psycho-stimulants dont work, indirectly affects ADHD.
14
Q
Non-pharmacological treatments for ADHD - Article
A
Methods:
- Review of data available
Results:
- Preschooler = parent training
- School children with moderate impairments = group parent training + classroom behavioral interventions
- Middle school/adolescent children = multimodal interventions (home + school treatment strategies (social skills training))
- Adults = stimulant medication + CBT
15
Q
Autistic Spectrum Disorder (ASD)
A
- Early infancy symptoms can be seen.
- Developmental delays: social, emotional, intellectual, language and communication, and stereotyped/self-injurious behavior patterns.
- Social impairment: non verbal, cannot understand clues, no TOM.
16
Q
Impairments of reciprocal social interaction
A
- Non-verbal behaviors: eye contact, facial expressions.
- No theory of mind
- Lack of interest in social interaction.
17
Q
Impairments in communication
A
- Delay in spoken language development, or inability to sustain a conversation.
- Failure to follow rules of pitch, intonation or stress. May sound monotonous and uninterested. Grammar is immature.
- Echolalia: immediate imitation of words and sounds just heard.
- Pronoun reversal: refer to themselves as he/she/you
18
Q
Impairments in imagination and flexibility of thought
A
- Specific and detailed interest in a few toys.
- Sameness is a need: if a disturbance in routine = distress.
- Strong attachment to inanimate objects.
- Rarely indulge in symbolic play.
- Self-stimulatory body movements (clapping, rocking etc).
19
Q
Intellectual deficits
A
- 80% show IQ lower than 70.
- Perform better on visuospatial ability than tests on social understanding and verbal ability.
- Savant syndrome: excel in one particular task/area.
20
Q
Diagnostics
A
- Symptoms present in the early developmental period.
- Hard to diagnose: manifest from a range of severity, hard to distinguish symptoms, behavior patterns may change with age, comorbidity with other disorders (epilepsy/adhd).
21
Q
Prevalence of ASD
A
- 0.5% of births.
- 80% are boys.
- Equal over all socio-economic classes and racial groups.
- 0.2% increase gradually = unknown reasons
22
Q
Biological etiology of ASD: Genetic factors
A
- Highly heritable
- Co-occurs with genetic disorders: PKU, fragile X syndrome, Tuberous sclerosis.
- ASD = deletion on chromosome 16 and an abnormality in gene sequencing on chromosome 5.
23
Q
Biological etiology of ASD: Biochemical factors
A
- Abnormalities in brain neurotransmitters that regulate and facilitate normal adaptive brain functioning.
- Serotonin and dopamine are essential for effective cognitive, behavioral and motor functioning and mood regulation.
24
Q
Biological etiology of ASD: Perinatal factors
A
- Maternal infections, intrauterine exposure to drugs, maternal bleeding after first trimester, depressed maternal immune functioning during pregnancy.
- Not the primary cause of the disorder.
25
Biological etiology of ASD: Brain abnormalities
- Limbic system, cerebellum, larger brain size, enlarged ventricles.
- Cerebellum = deficits in motor skills: balance, dexterity and grip.
- Limbic systems: neurons dense, shorter and less developed.
- Decreased activation of the prefrontal cortex and amygdala: low theory of mind.
- Abnormal EEG patterns in frontal/temporal lobes.
26
Cognitive etiology of ASD: Executive functioning
- Difficulty in problem solving, planning, initiating, organizing, monitoring, and inhibiting complex behaviors.
- Difficult to assess - require integration of a range of basic cognitive abilities such as attention, memory, sequencing events, inhibiting responses etc
27
Cognitive etiology of ASD: Theory of Mind
- Failed to develop
- Sally-Anne false belief task (marble vs box)
- Awkward moment test (tv commercial)
28
Cognitive etiology of ASD: Empathizing-systematizing theory
- Superior skills in systematizing - analyzing or constructing systems - noting regularities, rules and structures.
- Explains inability to generalize.
29
Issues with treatment
- Individuals dont like changes in their routines.
- Respond poorly to attempts at communication - programmes need to start at the basics.
- Interest in a very limited range of events and objects - hard to find effective reinforcers that will reward them.
- Selective attention - unlikely they will learn anything and generalize it to other situations.
- Idiosyncratic social and communicative skills mean they are treated with suspicion and reserve by everyone else.
30
Treatment: Medication
- Anti-psychotic drugs are common - haloperidol and risperidone.
- Reduce repetitive and stereotyped behaviors, social withdrawal, aggressive symptoms etc.
- Serious side effects: dizziness, increased appetite, weight gain, jerky movement disturbance.
- Opioid receptor antagonist naltrexone also beneficial in controlling hyperactivity and self-injurious behavior.
31
Treatment: Behavioral training
- Develop basic self help, social and communication skills.
- Conditioning-based approach - reinforce basic behavioral skills.
- Reduces frequency of disruptive/inappropriate behaviors.
- Modeling is used to promote appropriate behaviors.
- Best long-term option, but requires big commitment/effort from trainer.
- Alternative: train parents.
32
Treatment: Inclusion strategies
- Support through important life transitions.
- Supported employment: support to employee and employer.
33
DSM
- Criteria and symptoms for each disorders.
- 2013
- Largely subjective (up for interpretation)
- Clear boundaries for diagnosis.
