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Clinical Psychology > ADHD And Autism > Flashcards

ADHD And Autism Flashcards

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1
Q

ADHD

A
  • Persistent pattern of inattention and/or hyperactivity-impulsivity
  • Hyperactivity = fidgeting
  • Impulsivity = impatience, immediate rewards, dangerous activities etc.
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2
Q

Diagnostics subtypes of ADHD

A
  1. Attendion deficit hyperactivity disorder
  2. Predominantly inattentive presentation and attention deficit hyperactivity disorder
  3. Predominantly hyperactive/impulsive presentation
  4. Combined presentation
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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
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4
Q

Comorbidity of ADHD

A
  • Oppositional defiant disorder or conduct disorder
  • Anxiety and depressive disorders
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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.
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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.
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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
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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.
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9
Q

Biological etiology of ADHD: Environmental toxins

A
  • Hyperactivity = from biochemical imbalances caused by food additives/refined sugar cane/lead poisoning.
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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.
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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.
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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.
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13
Q

Treatment of ADHD: Alternatives

A
  1. Strattera: norepinephrine re-uptake inhibitor, for adults, less effective, dangerous side effects (suicidal thoughts)
  2. Clonidine: decrease aggression, combination with stimulants, adults + high blood pressure.
  3. Antidepressants: second line, justified only if psycho-stimulants dont work, indirectly affects ADHD.
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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

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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.
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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
Q

Biological etiology of ASD: Brain abnormalities

A
  • 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
Q

Cognitive etiology of ASD: Executive functioning

A
  • 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
Q

Cognitive etiology of ASD: Theory of Mind

A
  • Failed to develop
  • Sally-Anne false belief task (marble vs box)
  • Awkward moment test (tv commercial)
28
Q

Cognitive etiology of ASD: Empathizing-systematizing theory

A
  • Superior skills in systematizing - analyzing or constructing systems - noting regularities, rules and structures.
  • Explains inability to generalize.
29
Q

Issues with treatment

A
  • 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
Q

Treatment: Medication

A
  • 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
Q

Treatment: Behavioral training

A
  • 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
Q

Treatment: Inclusion strategies

A
  • Support through important life transitions.
  • Supported employment: support to employee and employer.
33
Q

DSM

A
  • Criteria and symptoms for each disorders.
  • 2013
  • Largely subjective (up for interpretation)
  • Clear boundaries for diagnosis.

Clinical Psychology (7 decks)

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