ADHD 1 Flashcards
characteristics of ADHD - DSM-V
hyperactivity, impulsivity and attentional problems
DSM 5: ADHD – ‘A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development’
- often has difficulty sustaining attention in tasks or play activities (A)
- often fidgets with or taps hands or feet or squirms in seat (H/I)
several symptoms have to be present before age 12 and manifest in more than one context
3 presentations of ADHD in DSM-V
predominantly inattentive
predominantly hyperactive-impulsive
combined
ICD-11
ADHD (2010) - ‘a persistent pattern of inattention and/or hyperactivity-impulsivity that has a direct negative impact on …. functioning’
very similar to the DSM definition - came later than it
prevalence of ADHD in UK - gender difference
5% of children/adolescents in UK
3 : 1 , boys : girls
presents differently in boys (hyperactive) and girls (inattentive)
change in ADHD symptoms with age
symptoms continue into adulthood in 8-43% of cases (gender gap may narrow with age)
some think it can develop in adulthood, not just childhood
activity issues decline with age (hyperactive)
attentional issues remain (inattentive)
maybe gender imbalance in children due to how it is diagnosed
treatments for ADHD
in children over 5, adolescents, and adults:
drug treatment - Adderall (DL-amphetamine) or methylphenidate
these are drugs of abuse (class B) - but are prescribed to children as young as 6
very effective medications - but need non-addictive instead as this could be an issue
estimated medical and non-medical cost of ADHD + reasons why
£2.4billion (children and adolescents in UK)
due to:
- parental income loss
- juvenile detention
- medication costs
- schooling etc.
history of ADHD full timeline (9)
1902 - George Frederic Still - paediatrician described 20 cases of children
1917-28 - encephalitis lethargica epidemic - associated symptoms of ADHD with brain damage - called it postencephalitic-type behaviour disorder
1940/50s - minimal brain damage as a cause of postencephalitic-type behaviour disorder
1960s - minimal brain dysfunction (MBD) - hyperkinetic impulse disorder could occur without brain damage - changed label to dysfunction
1968 - DSM-II : hyperkinetic reaction of childhood - label of MBD as too broad so focus on specific symptoms (esp hyperactivity)
1980 - DSM III - “Attention Deficit Disorder (ADD) (with or without hyper-activity)” - three separate symptom lists for inattention, impulsivity, and hyperactivity - big jump from saying hyperactivity was essential for the disorder previously
1987 - DSM III-R “Attention Deficit Hyperactivity Disorder” - first time having ADHD written in a diagnostic manual, brough the symptom lists together
1994 - DSM - IV - first time ADHD was said to be able to be present in adults as well as children
2013 - DSM - V - very similar to the 1994 definition
history of ADHD - first description
1902 - George Fredric Still
- paediatrician
- described 20 cases of children with: “defect of moral control…. without general impairment of intellect and without physical disease”
- “the immediate gratification of self without regard either to the good of others or to the larger and more remote good of self”
- “fidgety….”
- “a quite abnormal incapacity for sustained attention”
what we now think of as ADHD
“moral control” meaning not considering others as much, not right and wrong
history of ADHD - 1917-1928
epidemic of encephalitis lethargica (brain swelling)
had levels of severity
bad cases = can become rigid - eye muscles become paralysed so the eyes roll and stay open and upwards
many died
many affected children who survived the encephalitis, subsequently showed abnormal behaviour
“Postencephalitic behaviour disorder”:
- children often became: hyperactive, distractible, irritable, antisocial, destructive, unruly, and unmanageable in school
first association with brain damage
because encephalitis = brain swelling –> idea that similar symptoms seen in ADHD may also be associated with brain damage
history of ADHD - 1940s/50s
minimal brain damage
assumption that minimal damage to the brain, even when it cannot be demonstrated objectively, causes postencephalitic-type behaviour disorder
became practice to infer brain damage from behaviour even when there’s no evidence of it - bad practice
history of ADHD - 1960s
Minimal brain dysfunction (MBD)
Became clear that this disorder (“hyperkinetic impulse disorder”) could occur in the absence of explicit brain damage
The Oxford International Study Group of Child Neurology therefore advocated a shift in terminology by replacing the term “minimal brain damage” by “minimal brain dysfunction”
history of ADHD - 1968
change from a broad label (MBD) to more focused in on specific symptoms - especially hyperactivity
DSM-II : hyperkinetic reaction of childhood
(DSM-I had no section about children in it)
history of ADHD - 1980
throughout 70s, developing realisation that attentional problems were as significant, or more significant, than hyperactivity in this patient group
1980 - DSM III - “Attention Deficit Disorder (ADD) (with or without hyper-activity)”
hyperactivity was no longer an essential diagnostic criterion for the disorder
developed three separate symptom lists for:
- inattention
- impulsivity
- hyperactivity
history of ADHD - 1987
DSM III-R “Attention Deficit Hyperactivity Disorder”
brought symptom list together
merge things together into one disorder
history of ADHD - 1994, 2000, 2013
DSM - IV (1994)
- first time ADHD was said to be able to be present in adults as well as children
DSM - IV - TR (2000)
DSM - V (2013)
things ADHD impacts
DSM 5: There is clear evidence that the symptoms interfere with or reduce the quality of:
* social
* academic
* or occupational functioning
impact of ADHD on educational attainment
Fleming et al. (2017):
NHS and Scotland database of school leavers
ADHD vs non-ADHD
Likelihood of Sub-GCSE qualifications
ADHD = poorer academic attainment
impact of ADHD on occupational attainment
Klein et al. (2012)
Adults (mean age 41) diagnosed with ADHD at 6 -12 years of age (vs controls)
results:
employment: 84% ADHD and 95% control
occupational level: 4.7 ADHD and 3.0 control ( done on a scale)
median salary: $60k ADHD and $100k control
impact of ADHD on peer relations
Hoza et al (2005)
children with ADHD (7.0-9.9 years of age) and same sex classmates
ADHD kids were found to be less popular, more rejected - similar number were average and unclassified
impact of ADHD on physical health problems
Lange et al. (2016)
Accidents over the last 12 months requiring medical treatment in children with ADHD (10.4 years old) and controls
ADHD = 23%
Control = 15.3%
OR for accidents was 1.60 (95% confidence interval [CI] = 1.34-1.91)
impact of ADHD on mental health problems (4)
Larson et al (2010)
study of around 5000 kids with ADHD
age 6-17
much higher rates of anxiety and depression in kids with ADHD than in others
anxiety:
17% ADHD
2% other
depression
14% ADHD
2% other
autism
6% ADHD
1% other
Tourette’s
~1% ADHD
minimal other
therefore hard to study due to many comorbidities
impact of ADHD on drug addiction
Levy et al (2014)
ADHD as a kid = more likely to have non-alcohol based drug dependence
ADHD ~ 11%
control ~ 2%
2 classical theories of ADHD
frontal cortex
dopamine
frontal cortex theory of ADHD - task used to compare frontal cortex damage and ADHD
evidence from:
Neuropsychology
Structural imaging
Functional imaging
the symptoms of ADHD are similar to the changes following frontal cortex damage
Impulsivity – Iowa Gambling Task:
- disadvantageous or advantageous decks of cards used - either lose or gain overall
- disadvantageous has higher win per card but also much higher loss per 10 cards
- tendency to be pulled towards the possibility of big gains from individual cards rather than overall gain = cognitive impulsivity in ADHD
Bechara et al (1994) - frontal cortex damage:
- controls = normal or brain damage
- target = frontal cortex damage - patient EVR and EVR-type participants (EVR had damage to ventromedial prefrontal cortex)
- controls made more advantageous choices than the target group with frontal brain damage
Miller et al (2013) - ADHD:
- people with ADHD made fewer advantageous choices than control group
- delay aversion in ADHD - want rewards ASAP
as similar patterns are seen in frontal brain damage and ADHD - investigate the correlation
Barkley’s theory of ADHD
behavioural disinhibition theory of ADHD (executive)
sees poor behavioural inhibition as the central deficiency in ADHD
accounts for attentional and kinetic symptoms
self-control
clinical case of frontal cortex damage
Phineas Gage
frontal lobe damage caused behaviour change
MRI study of frontal cortex
structural observations
frontal lobe grey matter volume is lower in those with ADHD
functional study of frontal cortex
PET scan (positron emission tomography)
- use atom with unstable nucleus which decays, producing positrons
- detected by a ring of detectors
- this goes into a coincidence processing unit, producing an image of where activity is in the brain - using computer algorithms
study:
- injected glucose (which was associated with fluorine - radioactive source)
- therefore found which brain areas were active on the scan
- kids did a continuous performance task repetitively
results:
anterior and posterior frontal brain regions = had significantly different normalized rates of glucose metabolism in patients (teenagers with ADHD) compared with controls
3 forms of evidence for dopamine theory of ADHD
evidence:
medication
imaging
reward/reinforcement
how many prescriptions for methylphenidate are written per year in the UK
922,200 prescriptions (might be more now)
evidence for dopamine theory - DA increasing drugs
test of DA levels in ADHD
Micro-dialysis
A small, semi-permeable probe is inserted into a specific brain site
Fluid is perfused through the probe and chemicals in the extracellular fluid diffuse across the membrane and are collected
Samples are then analysed using chromatography methods (e.g. HPLC)
Dopamine levels in the striatum after i.p. D-Amphetamine or methylphenidate = a lot higher
ADHD and increased dopamine reuptake
as the drugs used raise dopamine - have low DA in the brain
could be explained by reuptake being too high
SPECT scans used - single photon emission tomography (similar to PET) - use atoms which produce gamma radiation as it decays - less precise than PET as one atom is used not 2 - lower resolution (about 1cm - PET is about 0.5cm) - camera that moves rather than in a ring
IPT used - binds tightly to dopamine transporter - attached to a gamma radiation source
showed much greater radiation in drug-naive children with ADHD (never had ADHD med) vs a control
= more DA transporters in ADHD in forebrain
particularly in basal ganglia - big part of DA system
ADHD, DA, and changes in response to reward
rat study
children reinforcement study
study with food and sex in rats:
- rats given food = increase in DA
- rats increase in DA with sex - knowing a female is there causes increase - big spike when they see them
Douglas and Parry (1983)
disruption of learning by non-contingent reinforcement
method:
- 66 elementary school children (mean age around 9.5 years old)
- 33 with ADHD, 33 without
- had to release a response key when a stimulus light came on (reaction time task)
3 conditions: - rewarded on every trial when they got faster (continuous)
- rewarded on every other trial when they got faster (partial)
- rewarded randomly (non-contingent)
Reward = “very good”, “excellent” or “very fast”
results:
- control: faster reaction time at reward than baseline and extinction in all conditions
- ADHD: same pattern as control in continuous and partial condition
- ADHD in non-contingent condition: much slower reaction time at reward than baseline or extinction
conclusion:
non-contingent reinforcement schedule resulted in slower mean reaction times in the ADHD sample - also delay aversion
