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
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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

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3
Q

What are symptoms in younger children?

A
  • Poor concentration
  • Hypervigilance to perceived fear stimulus
  • Stimulus avoidance
  • Excessive worry
  • Denial
  • Rage
  • Social Withdrawal
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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
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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
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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
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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

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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
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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
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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
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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
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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
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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
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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
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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
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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