Week 12 - Neurodevelopmental Disorders Flashcards
(16 cards)
Introduction
Conditions stemming from brain development differences
Onset - childhood (persists to adulthood)
Predictable developmental sequence disrupted, which has cascading effects
‘Abnormal’ - must consider what is typical at each stage (things may be delayed but not abnormal)
Attention-Deficit/Hyperactivity Disorder DSM
Kids must show 6 symptoms (adults only 5) in either 1 and/or 2
A. Inattention and/or hyperactivity that interferes with functioning
- 1. Inattention - 6+ sxs for at least 6 months, inconsistent with development period, pervasive
- 2. Hyperactivity - 6+ sxs for at least 6 months, inconsistent with development period, pervasive
B. Symptoms present prior to 12
C. Symptoms present in 2+ settings
D. Interferes with functioning
E. Not better explained
Specify - combined, inattentive, hyperactive/impulsive
- Inattentive most common
- Combined often comorbid with conduct and oppositional disorder (also trouble interacting with peers)
ADHD Inattention criteria
Inattention - 6+ sxs for at least 6 months, inconsistent with development period, pervasive
1. No attention to detail
2. Can’t sustain attention
3. Doesn’t listen when spoken to
4. Fails to finish/follow through
5. Difficulty organising
6. Reluctant to engage in sustained mental effort
7. Loses things
8. Easily distracted
9. Forgetful in daily activities
ADHD Hyperactivity criteria
Hyperactivity - 6+ sxs for at least 6 months, inconsistent with development period, pervasive
1. Fidgets/taps/squirms
2. Leaves seat when inappropriate
3. Runs/climbs when inappropriate
4. Can’t play quietly
5. Often on the go (like a motor)
6. Talks excessively
7. Blurts out before Q is complete
8. Can’t wait their turn
9. Interrupts others
ADHD - what’s not in the DSM
Emotion dysregulation - these kids have a tougher time
Groups (based on temperament) - irritable, emotionally balanced, energetic
ADHD prevalence
8% in children, 3% in adults (7% with sig. symptoms)
2 boys:1 girl (girls may cope better, criteria may be flawed)
US 12-16%, other countries 6-7% (likely diagnostic differences such as preferring ADHD to conduct dx)
ADHD course and comorbidity
Course - symptoms appear at 3-4, 65-80% continue into adolescence, 50% into adulthood
- Persistence linked to low SES, severity, ODD, conduct dx, MDD
- Associated with job instability, substances, divorce
- Impulsivity decreases, inattention persists
Comorbidity - ODD, conduct dx, irritability, antisocial behaviour, ASD, intellectual disability, anxiety, mood dx
- Hard to distinguish ADHD given amount of comorbidity
ADHD influences
Biological - genetic contribution up to 80% (higher than most conditions), polygenic
- delays PFC development - affects DA system (lower levels of DAT gene)
Environmental - toxins (lead, AFO food colourant, sodium benzoate, maternal smoking), diet (tend to be picky eaters, NOT causal)
- Also prenatal maternal inflammation, perinatal ischemia, preterm birth
Gene-Environment Interactions - environment only matters to already vulnerable kids (no shared environment influences)
- parent-child relationship interacts with neurobiological factors (parents give more negative commands due to sxs, parent may also have ADHD)
ADHD treatment
Stimulant medications (Ritalin, Dexedrine, Vyvanse)
- interact with DA system
- 80% of ADHD kids given stimulants
- better than placebo and other treatments short-term
- reduces risk of substance use
Behaviour treatment (parent training, reinforcement programs)
- intensive programs may be as effective as meds short-term
Adults - CBT to increase attention
Combined treatments - maybe superior to meds/behaviour alone in short-term
Diet in ADHD
Food additives may have an influence BUT - most kids don’t respond to Feingold diets, elimination diets showed different kids responded to different foods (and not just processed)
Vitamin D supplements may help if vitamin D is sufficient in the first place
No conclusive evidence that refined sugar contributes
ASD history
Autism spectrum disorder - new label to DSM5
Takes over from several disorders that were ‘pervasive developmental disorders’
- Autistic disorder, Asperger’s, pervasive developmental disorder NOS, childhood disintegrative disorder, Rett syndrome (now a genetic disorder)
Asperger’s - not a diagnosis anymore but still used for identity, familiarity, advocacy
Autism Spectrum Disorder DSM
A. Social communication/interaction deficits across contexts:
- 1. Social-emotional reciprocity deficits
- 2. Nonverbal communication deficits
- 3. Relationship development, maintenance, understanding deficits
B. Repetitive, restricted behaviour patterns
- 1. Repetitive motor/speech
- 2. Insistance on sameness
- 3. Fixated and restricted interests that are abnormally focused
- 4. Hyper- or hypo-reactivity to sensory input
C. Sxs present early in development
D. Clinically sig. life impairment
E. Not better explained (intellectual disability often co-occurs - look for social communication issues)
Specify severity - requiring support, substantial support, very substantial support
ASD prevalence
1% (4.2B:1G) - girls may mask better, or criteria are flawed
Higher rates in transgender adults
33% have intellectual disability (IQ interaction)
Co-occurring conditions - ADHD, intellectual disability, anxiety, MDD, epilepsy, sleep problems, sight/hearing problems, GI problems
ASD biological influences
Genetic contribution - as high as 81% (identical twin 70-90% chance, 0-10% for fraternal twins)
Neurobiological condition - small number of rare genetic variants in approx. 100 genes (6% risk), 1000+ common variants (smaller risk but combine for more cases)
- Early overgrowth in brain area of DM, language, social behaviour
- Later shrinkage in emotion and memory areas
- Low levels of oxytocin in ASD children
ASD environmental influences
Maternal factors - gestational hypertension, overweight, preeclampsia, 35+ YO, short or long gap between pregnancies, valproic acid
Older paternal age
ASD treatment - applied behavioural analysis
ABA - skill building, reduce problem behaviours, communication training, socialisation
- ABC model as foundation
- ABA is best practice, but unregulated (anyone can practice)
Critiques - use of punishment, wanting compliance
Controversy - QOL issues stem from environment mismatch, not ASD itself (some say ASD does not require treatment and that ABA stigmatises them by forcing them to be ‘normal’)
