Lecture 14 - ADHD Pt 1 Flashcards
1
Q
Why are disorders in children special?
A
- Increased vulnerability
- Less complex/realistic view of themselves/world
- Less self-understadning
- Less past judgements to compare to
- No thoughts on future issues
- Highly dependent on adult
- Events become overly important
- More sensitive to failure/rejection/disappointment
- Problems can become insurmountable
- Behaviour has to be compared to what is appropriate for age/gender
2
Q
Where does vulnerability come from?
A
- Severe marital discord
- Low social class
- Large family size
- Paternal criminality
- Maternal mental disorder
- Foster placement
- Maltreatment & emotional trauma
Combination of adversity = not a single factor
- Factors may lead to other childhood disorders and may influence outcome rather than onset
3
Q
What are symptoms in younger children?
A
- Poor concentration
- Hypervigilance to perceived fear stimulus
- Stimulus avoidance
- Excessive worry
- Denial
- Rage
- Social Withdrawal
4
Q
How does the brain develop in early life? (DESIRE)
A
- includes neuron formation, proliferation, migration, death
- Synapse formation and pruning and myelination
- By age 1 = brain is 70% of adult size, age 2 = 80% and age 5 = 90%
- Following factors are important for brain development:
- Environment
- Stimulation
- Interaction
- Responses
- Experiences
- Diet/growth factors
5
Q
What are the most common disorders in children
A
- Can be diagnosed across whole range, 1 in 10 children have one
- Higher level of conduct, emotion disorders and hyperkinetic disorders like ADHD
- ADHD is more present in boys than girls
6
Q
Is ADHD real?
A
- Chronic condition
- Attention deficit: impulsivity, poor concentration and easily distracted
- Hyperactivity disorder: exaggerated motor activity, fidgeting, aimless running/talking and socially intrusive
7
Q
What does ADHD lead to? (dysfunction)
A
Dysfunction in:
- Problem solving
- Planning
- Orienting
- Alerting
- Cog flexibility
- Decision making
- Sustained attention
- Response inhibition
- Working memory
Relates to frontal cortex and executive functioning
8
Q
What does ADHD lead to? (implication)
A
- Poor academic achievement –particularly reading
- Low intelligence
- Immaturity
- Low self-esteem
- Inability to form normal parental relationships
- Inability to form normal peer/peer relationships
- Negative view by peers
- Increased risk of substance abuse
- Increased risk of anti-social behaviour
- Abnormality is sometimes subtle –extension of normal behaviour
9
Q
How is ADHD diagnosed in DSM?
A
- Split into clusters of symptomology
- child needs to present 6 from attentional cluster and 6 from hyperactivity cluster and presenting for significant amount of time
- Sig amount of symp before age 12 and not better explained by another disorder
- If older than 17 - only need 5 symptoms or more
10
Q
What are the sub-types of ADHD?
A
- Predominantly inattentive: most symptoms are about inattention and <6 of hyperactivity
- Less likely to act out and may sit quietly but are not paying attention = may be overlooked and not notice symptoms of ADHD
- Predominantly hyperactive-impulse: most symptoms are hyperactivity and <6 in inattentional
- Combined Hyperactive-impulsive and inattentive: 6+ symptoms in both categories = most children with ADHD are combined
- Other specified ADHD = last category for ADHD not fitting into other subtypes
- Subtype does not affect treatment type
11
Q
Differential diagnosis in ADHD
A
- Go to GP first to assess hyperthyroidism, anemia, abuse, sleep impairment etc
- Other mental health conditions or fetal alcohol syndrome
- ADHD has comorbidities
- Requires child psychiatrist for final diagnosis
12
Q
What is the epidemiology for ADHD? (Stats)
A
- UK: 0.5/1000 in 1970, but 3/1000 in 1990
- Children in US/UK have greater ADHD than other eastern countries
- 5.2% US adults have ADHD = not just a childhood developmental disorder
- Boys more likely to have ADHD in all sub-types
- Young>old - HI type
- Poor>rich - HI type but rich more likely to receive treatment
13
Q
What was the aetiology of ADHD?
A
- PCB
- Foetal exposure to alcohol
- Maternal smoking
- Pregnancy and delivery complications = nonsig evidence
- Psychological adversity = nonsig evidence
- Children born preterm/born low birth weight = more likely to have diagnosis of ADHD
14
Q
What are the pre/neo-natal effects for aetiology?
A
- Foetal exposure – toxins such as PCBs, lead, mercury
- Maternal alcohol – hyperactivity, impulsivity (FAS)
- Maternal tobacco – 2.7 fold increase in ADHD reduces placental function
- Link between nicotine and dopamine function can affect neuronal proliferation/differentiation
- Hypoactivity of dopamine/noradrenaline
- Birth complications – pre-eclampsia, hypoxia, prematurity, maternal age/health,malnutrition, duration of labour
- IUGR: intrauterine growth retardation
- All lead to low birth weight
15
Q
What are the genetic aetiologies?
A
- High heritability - 75%
- High MZ twin concordance
- Many candidate gene association studies and Genome wide association studies
- Numerous candidates
- genetic candidates have high biological efficacy
- Linked to dopamine function: receptors and transporters
- Linked to Serotonin function: receptors and transporters
- Linked to noradrenergic function: transporters
- D4 receptor gene strongest candidate
16
Q
Why are CNVs a risk?
A
- Looking at alterations in gene structure
- Significantly higher rate of large, rare CNVs in ADHD children than in healthy controls
- Significant overlap with CNVs implicated in autism and schizophrenia
- Overlapping genetic aetiology for some common neurodevelopmental disorders
- Genes within these CNVs proposed as candidates for risk of psychiatric disorders
- But many cases do not possess these CNVs (in fact the majority do not) – clearly just a part of the overall genetic risk
- Findings provide genetic evidence of an increased rate of large CNVs in individuals with ADHD and suggest that ADHD is not purely a social construct
17
Q
What is a study looking at the diathesis/stress model in aetiology of ADHD?
A
- Looked at CNVs and repeated sequences and categorised them into short/long versions of the dopamine transporter gene
- Compared this to pre-natal smoking in mother
- If you have long form of gene without smoking = no different to people without ADHD BUT if she does there are higher manifestations
- Need gene/env interaction to manifest ADHD
18
Q
What was a study looking at biological aetiology?
A
- Longitudinal MRI assessment between 7-12 years old in patients and ADHD
- Delay in brain maturation in ADHD
- Reduced total brain volume in ADHD
- Reduced right frontal cortex volume, caudate and cerebellum - size difference maintained
- Hypofunction in PFC during tasks assessing ADHD-related functions
19
Q
What is the continuation of ADHD into adulthood?
A
- Majority of children with ADHD do not have ADHD in adulthood = brain catches up
- Majority of adults with ADHD did not have ADHD in childhood
- Insufficient methodologies do not show the nature of late-onset symptoms
- Adult-emergent symptoms that were previously surpassed due to lower env demands
- Mimics that were not properly assessed
- Childhood-onset was not properly detected due to failure to come to clinical attention
20
Q
What are the adult emergent ADHD symptoms?
A
- Slightly different pattern to childhood ADHD (less hyperactivity) (more I than HI or C types)
- Sluggish Cognitive Tempo (SCT)
- Gender difference not as clear cut (referral bias?)
- High co-morbidity (bipolar, substance abuse)
- Current treatments similar
- Diagnosis accuracy
21
Q
Why is it hard to accurately diagnose ADHD in adults based upon self-report alone?
A
- Retrospective recall of childhood symptoms is used to diagnose ADHD in adults.
- But, parental-and self-report retrospective recall of childhood ADHD symptoms is poor
- Adults with ADHD both overreport and underreport current ADHD symptoms and associated impairment, while adults without ADHD overreport ADHD symptoms
