1
Q
3 types of ADHD
A
- inattentive
- hyperactive
- combined
2
Q
general ADHD DSM criteria
A
- either 6 (or more) inattention symptoms or 6 (or more) hyperactivity/impulsivity symptoms
- some hyperactive-impulsive or inattentive symptoms that caused impairment have been present for at least 6 months and before 12 years of age
- persistent not situational: some impairment from the symptoms is present in two or more settings
- functional impairment: there must be clear evidence of clinically significant impairment in social, academic, or occupational functioning
- the symptoms do not occur exclusively during the course of a pervasive developmental disorder, SZ, or other psychotic disorder and are not better accounted for by another mental disorder
3
Q
inattention DSM
A
- often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities
- often has trouble holding attention on tasks or play activities
- often does not seem to listen when spoken to directly
- often doesn’t follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace
- often has trouble organising tasks and activities
- often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time
- often loses things necessary for tasks and activities
- is often easily distracted
- is often forgetful in daily activities
4
Q
hyperactivity/impulsivity DSM
A
- often fidgets with or taps hands or feet, or squirms in seat
- often leaves seat in situations when remaining seated is expected
- often runs about or climbs in situations where it is not appropriate
- often unable to play or take part in leisure activities quietly
- is often “on the go” acting as if “driven by a motor”
- often talks excessively
- often blurts out an answer before a question has been completed
- often has trouble waiting his/her turn
- often interrupts or intrudes on others
5
Q
ADHD demographics
A
- peak onset between the age of 3 and 4 - but often diagnosed later than this
- affects 3-5% children, prevalence higher in areas of low SES
- male/female ratio - 4:1 for the hyperactivity/impulsivity type, 2:1 for the inattention type
- comorbidity: 50% of children also show another psychiatric disorder
6
Q
ADHD in adolescence and adulthood
A
- persists in adolescence for around 50-80% of inds & in adulthood for around 30-50% of inds
- inattentiveness increases, hyperactivity decreases
- persistent ADHD more likely in those with comorbid disorders
- highly associated with criminal activity, substance misuse and long-term unemployment
7
Q
ADHD clusters in families
A
- increased risk for first and second order degree relatives (Faraone et al., 1995)
- siblings are 3-5 times more at risk (Biederman et al., 1992; Faraone et al., 1993)
- concordance is higher in MZ twins (50-80%) than DZ twins (33%) (Bradley & Golden, 2001)
8
Q
7 candidate genes
durston & konrad (2007)
A
- 5 are linked to dopaminergic system (esp. DAT-1 and DRD4)
- 2 are linked to the serotonergic system
9
Q
matthews et al. (2014) on the genetic basis of ADHD
further reading
A
- twin study (burt, 2009) : 70-80%
- family studies (e.g. biederman et al., 1992): 2-8 fold increase for parents and siblings
- adoption studies (sprich et al., 2000) support genetic etiology
- genome studies 4 regions (5p12, 10q26, 12q23, and 16p13) with evidence of linkage (fisher et al., 2002)
- smalley et al. (2002) supported this especially with region 16p13
- but not supported in meta-analysis (neale et al., 2010) finding no genome-wide significant association
- candidate genes more common approach (look at dopamine and serotonin transporters)
10
Q
environmental risk factors
A
- alcohol and nicotine use by mother during pregnancy
- but mothers themselves more likely to have ADHD and ADHD increases the use of substance
- low birth weight and premature birth
- obstetric complications
- maternal stress
- exposure to lead during childhood
11
Q
endophenotypes
viding & blakemore (2007)
A
- eritable (correlate with the gene), vulnerability traits that mark a risk for the development of the disorder
- should co-occur with the disorder e.g. should correlate with symptoms, although given heterogeneity of ADHD may be unlikely to be present in all inds
- should be heritable e.g. identical twins should be more similar than non-identical twins
- should show familial susceptibility e.g. non-affected relatives should also exhibit the endophenotype to a greater extent than in the general population
12
Q
cognitive theories
A
- inhibition
- arousal state regulation
- reward processing
13
Q
inhibition & ADHD
barkeley (1997)
A
- weak inhibitory control leads to difficulties with: WM, self-regulation of affect/motivation/arousal, internalisation of speech, reconstitution
- beh of those with ADHD is controlled by immediate events and reinforcers due to impaired ability to represent goals, plans and temporal sequence
- issues with planning as don’t have inhibitory control to follow what’s in the environment at that very moment
14
Q
nigg (2005) and EFs in ADHD
A
- common to find worse performance on EF tasks in ADHD children than controls
- EFs most affected: spatial working memory, response suppression (inhibition measure), signal detection
- meta-analysis
- most effected is not inhibition as Berkeley proposed but it is still an EF
- stroop interference is a measure of inhibition but fairly low down the list
15
Q
reward processing in ADHD
sagvolden et al. (1998)
A
- ADHD have issues in lots of areas but key area of issue is reward processing in this theory
- this can be seen by reward discounting task: all ppts more likely to go for lower amount if delay is longer but overall ADHD showed greater delay aversion
16
Q
key brain areas of reward system
A
- orbitofronal cortex
- ventromedial prefrontal cortex
- anterior cingulate cortex
- striatum
- amygdala
17
Q
matthews et al. (2014) on reward processing in ADHD
further reading
A
sensory/reward theories are bottom-up theories which are often associated with problems with emotions e.g. anger, mood and affect regulation
18
Q
arousal state regulation in ADHD
bellato et al. (2020)
A
- reduced autonomic arousal during slow tasks & boring situations –> inattention
- impulsivity/hyperactivity may be attempts to up-regulate arousal; self-stimulation –> slower & more variable/less accurate performance
- difficulties in down-regulating arousal during stressful or -ve situations –> challenging behs e.g. tantrums, aggressivity (too much arousal)
- account for behavioural symptoms of ADHD
19
Q
tamm et al. (2012)
RT variability as a marker of arousal regulation
A
- within-subject fluctuations in performance speed over a short period of time e.g. due to mind wandering
- deviation of RT in controls is pretty stable
- ADHD it is much more variable
- marker of arousal regulation
- lapses of attention as a marker
20
Q
kofler et al. (2013)
RT variability as a marker of arousal regulation
A
- meta-analysis found increased RT variability in people with ADHD (especially in children, but also in adults): medium-to-large effect
- is the increased RT variability specific to ADHD? - yes, but not entirely. statistically significant differences were found between children with ADHD and those with other clinical conditions. but not in adults
- no differences in RT variability between ADHD presentations - between inattentive, hyperactive, or combined
21
Q
heterogeneity in EF
A
- some children with ADHD who perform better than TD controls
- cannot say that all children with ADHD have issues with executive control
22
Q
triple route model
sonuga-barke et al. (2010)
A
- 9 tasks designed to tap three domains (inhibitory control, delay aversion/reward processing and timing)
- number of ADHD patients (including affected siblings) with a ‘deficit’ in each of the neuropsychological domains was calculated using cut-offs based on the lowest 10% of scores in the control group
- 71% of inds with ADHD displayed performance below the cut-offs in something but not necessarily the same one
- of those, more than 70% performed below cut-off in just one of the three domains
23
Q
positive aspects of ADHD
sedgwick (2019)
A
- some aspects of ADHD are adaptive e.g. they help people to succeed in certain situations
- group of adults with ADHD identified several aspects of ADHD which were considered beneficial, including “cognitive dynamism, courage, energy, humanity, resilience and transcendence”
- other adaptive traits with ADHD are creativity and imaginative problem-solving, sense of humour, perseverance, and acceptance
24
Q
neurobiological theories of ADHD
A
- delayed brain maturation
- different connectivity
- dopamine dysregulation
25
grey matter
| shaw et al. (2007)
* delayed maturational hypothesis
* difference in age when attaining peak cortical thickness - across all cortical regions, ADHD brain developed a bit later
* delay was even more obvious in PFC
26
delayed maturational hypothesis
| rubia (2007)
* ADHD symptoms described as age-inappropriate
* symptoms improve in adulthood
* do children with ADHD simply display a delay in brain maturation? - recent findings suggest yes
* delayed maturational hypothesis could specific to ADHD (not found in children with childhood onset SZ or autism)
* so the delayed brain maturation can act as an endophenotype
27
white matter
| castellanos et al. (2002)
* structural MRI reveals in brain volume in many areas, especially white matter reduction
* key areas: total cerebral volume, total white matter, frontal white matter, parietal white matter, temporal white matter, smaller subcortical areas (caudate, cerebellum)
28
connectivity
| sonuga-barke & castellanos (2007); fair et al. (2010)
* default mode network = 'a network of brain regions that are active when an individual is not focused on the outside world and the brain is at wakeful rest'
* this network that is at work when you're at rest, not engaging in tasks/world around you
* in ADHD it has been proposed that activity in the default mode network persists into, or reemerges in task-related active processing, producing attention lapses and deficits in performance
* differences between ADHD & TD in frontal lobe
29
pharmacology & ADHD
| durston & konrad (2007)
* typical treatment = methylphenidate or amphetamine
* example of methylphenidate is RITALIN
* these drugs stimulate the release and inhibit the reuptake of catecholamines (dopamine and noradrenaline)
* enhances activity in these NT systems
* effectiveness of treatment --> ADHD linked to dysfunction of catecholaminergic system, especially dopaminergic system
30
dopamine dysregulation hypothesis of ADHD
* hypodopaminergic state in the prefrontal cortex. not enough/reduced amount of dopamine in PFC --> inattentiveness and lock of cognitive control
* hyperdopaminergic state in the striatum (part of basal ganglia, includes caudate nucleus and putamen. too much --> hyperactive behaviours
31
review against hypothesis of dopaminergic dysfunction in ADHD
* gonon (2009)
* "the dopaminergic hypothesis of attention-deficit/hyperactivity disorder needs re-examining"
* doesn’t fully explain ADHD
32
other NT dysfunctions associated with ADHD
| (not dopamine)
* norepinephrine/noradrenaline
* serotonin (linked with aggressive behaviour)
* can use these for critical analysis of dopamine dysregulation theory, dopamine has been focused on due to RITALIN impacting dopamine pathways
33
factors result of too little dopamine in PFC
* inattention
* poor executive function
34
factors result of delayed brain maturation
* poor executive function
* hyperactivity
35
factors outcome of atypical connectivity in default mode network
* inattention
* atypical arousal regulation
36
factors result of too much dopamine in striatum
* hyperactivity
* atypical reward processing
37
factor result of a smaller cerebellum
issues with timing
Understanding neurodevelopmental disorders
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