behavioural and neurodevelopment disorders Flashcards
1
Q
DSM [broader categories]
behavioural vs neurodevelopmental
A
- neurodevelopment disorders
- intellectual disabilities
- communication disorders
- autism
- ADHD
- specific learning disorder
- motor disorders
- tic disorders
2
Q
ICD-10 [more specific categories]
behavioural vs neurodevelopmental
A
- behavioural disorders in childhood
- conduct disorder
- oppositional defiant disorder
- persuasive developmental disorders
- autism
- hyperkinetic disorders
- ADHD
3
Q
ICD-11
behavioural vs neurodevelopmental
A
- neurodevelopment disorders
- autism
- ADHD
- disruptive behaviour or dissocial disorders
- conduct disorder
- oppositional defiant disorder
4
Q
ADHD, ADD, hyperkinetic disorder
A
- Attention deficit hyperactivity disorder
- Terms used for a syndrome based on (maladaptively) high levels of impulsivity, hyperactivity, and inattention
- ADHD perhaps most common term (Carr, 2011)
- Highly comorbid with conduct disorder (~25% of cases) and ODD
- Associated with a number of ‘secondary’ problems (e.g., academic, relationships)
5
Q
DSM and ICD
ADHD, ADD, hyperkinetic disorder
A
- Some differences
- E.g., age of onset differs, DSM ‘allows’ for comorbidity with autism
- NB. ICD-11 now acknowledges co-occurrence with Autism
- E.g., age of onset differs, DSM ‘allows’ for comorbidity with autism
- 5 (adults) or 6 (children) symptoms of inattention (out of possible 9) and/or hyperactivity/impulsivity (out of possible 9) required
- Think how many potential ‘clusters’!!
- Symptoms present in more than one setting (e.g., at school, with relatives)
- Onset <12 years of age
6
Q
epidemiology & course
ADHD, ADD, hyperkinetic disorder
A
- Worldwide prevalence around 3.4% (Polanczyk et al., 2015)
- Varies due to methodologies but similar in US / Europe, for example
- 25 – 50% will continue with the Dx until adulthood
- But many more will have ADHD in “partial remission”
- More males affected, but perhaps under-recognised in females?
- Females less likely to be referred for Ax / incorrectly diagnosed
- No single cause
7
Q
biological theories
ADHD, ADD, hyperkinetic disorder
A
- Genetic
- Highly heritable (but not 100%)
- Dopamine receptor gene (D4) shows most robustevidence
- Neurotransmitter dysregulation
- Dopamine and noradrenaline systems
-
Hypoarousal hypothesis
- Stimuli not sufficiently arousing, so behaviour is stimulus-seeking
- Not unique to ADHD (e.g., LD, conduct disorders)
7
Q
psychosocial theories
ADHD, ADD, hyperkinetic disorder
A
- Executive function
- Impaired behavioural inhibition
- Reinforced by secondary deficits (e.g., self-regulation ofaffect)
- Impaired behavioural inhibition
- family / systemic factors
- High stress and low support
- Less “effective” parenting, conflict, comorbidity (e.g.,Babinski et al., 2016)
- Cause or effect?
- Environmental risk factors (e.g., alcohol,smoking in pregnancy) but difficult to establish causality (see Thapar et al., 2013)
8
Q
medication
ADHD, ADD, hyperkinetic disorder
A
- Methylphenidate (Ritalin®, Concerta®), atomoxetine, lisdexamfetamine,dexamfetamine
- Generally produce moderate effect sizes for symptom reduction (e.g., Vander Oord et al., 2008)
- Cochrane review of methylphenidate (2015):
- Review including over 12,000 children
- Many small studies, few with long-term follow-up
- 40% funded by industry
- Some risks (e.g., sleeping problems, reduced appetite, compliance)
- May improve teacher-reported symptoms, teacher-reported generalbehaviour, and parent-reported quality of life
9
Q
psychological intervention
ADHD, ADD, hyperkinetic disorder
A
- Individual interventions include:
- Social skills training
- CBT (including behaviour modification)
- Neurofeedback (teaching impulse control)
- Complementary / alternative (e.g., dietary, homeopathic)
- Some support for psychological interventions, particularly BT (e.g., Catalá-López et al., 2017; Fabiano et al., 2009)
- Little evidence for cognitive training, neurofeedback, dietary (e.g., PUFAs), homeopathic and therefore not currently recommended per se (although healthy diet likely to help!)
10
Q
children <5
age difference in intervention [ADHD,autism]
A
- Group parent-training programme to parents / carers as first-line, then considerspecialist advice
- Do not offer medication without specialist opinion
11
Q
children 5+ and young people
age difference in intervention [ADHD,autism]
A
- Psychoeducation + carer support
- Consider parent training / medication / CBT if impairment remains
12
Q
adults
age difference in intervention [ADHD,autism]
A
Consider medication, or non-pharmacological if medication not indicated / accepted
13
Q
what is conduct disorder
A
Repetitive and persistent pattern of behaviour involving:
- Aggression towards people and animals
- Destruction of property
- Deceitfulness or theft
- Serious violation of accepted rules
14
Q
oppositional defiant disorder
A
- ODD is reserved for children who do not meet full criteria for conduct disorder but have regular temper tantrums, refuse to comply with instructions, or may appear to indulge in behaviours that annoy others.
- ODD is common in preschool children and may predict later conduct disorder
15
Q
prevalence and course of CD
A
- Relatively common, 4-16% in boys, 1-9% in girls (Loeber et al., 2000)
- Median age of onset 11.6 years (Nock et al., 2006)
- In the majority of individuals the disorder remits, but some may go onto meet criteria for antisocial personality disorder
- Studies suggest that CD, but not ADHD, predicts antisocial personality disorder, but only in lower SES families (Lahey et al., 2005), or if parents have antisocial personality disorder or low verbal IQ (Lahey etal., 1995)
- Like with ADHD, causal links with genetic, neuropsychological andprenatal factors
16
Q
presentation of ODD and CD in boys
A
- aggressive and violent behaviours
- fighting
- stealing
- damage to property
- school problems
17
Q
presentation of ODD and CD in girls
A
- petty theft
- lying
- running away from home
- avoiding school
- prostituition
18
Q
what is autism? and what is it not
A
- A (neuro)developmental ‘disorder’
- On a spectrum of difficulties
- Some difficulties shared; to different degrees
- It is not an illness or disease, it means the brain works differently* Individuals with autism can live a full life, and it is different for everyone
Language
- Autistic Spectrum Disorder (medical name – but term disorder not recognised by everyone)
- Autistic Spectrum Condition (often preferred)
- Move towards ‘neurodiversity’
- Is not necessarily associated with above or below average intelligence
18
Q
characteristics- ‘Triad of impairment’
autism
A
- Social interaction
- Difficulty ‘reading’ other people
- Emotion recognition in others
2.Social communication
- Difficulties interpreting both verbal and non-verbal language
- Range from no speech to not understanding some jokes (e.g., non-literal)
3.Repetitive behaviours / interests (DSM-5, but disputed!)
- Prefer routine / predictability
- Prefer to eat same food, travel same way
- May have focused interests
- (Sensory sensitivity)
19
Q
prevalence & course
autism
A
- Worldwide prevalence around 1% but highly variable (see Baxter etal., 2015)
- Cultural differences
- Different diagnostic criteria
- Less data in older people and low- and middle-income countries (LMIC)
- Onset in childhood but follows a persistent course
- More common in males (4:1 or 5:1), BUT…
- Delayed or even missed diagnosis in girls
- Core triad may be similar, but other areas (e.g., restricted interests, attention problems) may be different (e.g., Holtmann et al., 2007)
20
Q
genetic factors
autism
A
- Autism has a prenatal origin but precise cause has not been determined
- E.g., has been associated with greater maternal age, use of medication / alcohol, obstetric complications
- Consensus that evidence is insufficient to support a contributory link
- Highly heritable (but not 100%)
- “Stronger environmental component than previously believed” (Tchaconas & Adesman, 2013, p. 130)
- Several genes involved in synaptic plasticity, i.e., multifactorial (see Bourgeron, 2015)
21
Q
what are the cognitive factors
autism
A
- weak central coherenece
- theory of mind [ToM] deficit
- executive dsyfunction
22
Q
weak central coherenece
autism: cognitive factors
A
- Bias away from integrating contextual information for meaning (detail focus)
- Remembering the gist of a story, not elements
Happé (1997):
- Pronounce tear: ‘In her eye there was a big tear’
- Pronounce tear: ‘In her dress there was a big tear’
- Most of the participants with ASC (including those who passed ToM tasks)made relatively little use of context
23
theory of mind deficit
| autism: cognitive factors
- Impairments in attributing thoughts and feelings to others
- Tested, classically, with ‘False Belief’ tests (e.g., Sally-Ann)
- Majority of autistic children predict Sally’s behaviour onbasis of reality, BUT ToM may be less affected in those whoare older or with higher IQ
24
executive dsyfunction
| autism: cognitive factors
- Umbrella term for functions such as planning, working memory, impulse control, set shifting, and so onMay be necessary for development of ToM (see Ozonoff etal., 1991)
- Particularly associated with repetitive behaviours
25
psychological interventions
| autism
- Psychosocial interventions that:
- increase the understanding, sensitiveness and responsiveness to child’s patterns of communication and understanding
- Include techniques that expand child’s communication, interactive play and social routines
- Interventions for life skills
- Interventions for co-existing problems (both mental health and medical)
- E.g. CBT
- Interventions for sleep problems / feeding problems
26
ABA interventions
| autism
- Historically there has been much research into ABA as an interventiontechnique
- ABA (applied behavioural analysis) is a term for interventions that arebased on observing and understanding behaviours.
- Because of it’s broad approach, which first emerged in the mid 20th century, ABA has changed over time and ranged from:
- Using encouragement and rewards, and making changes in the environment
- To... trying to ‘treat’ autism, and even using cruel methods as punishment
- Views on ABA are strongly polarised, and whilst it has developed substantially many are fundamentally against it’s approach
