- Created by: embarry27
- Created on: 06-12-19 10:14
- ADHD is characterised by developmentally inappropriate levels of hyperactivity, impulsivity and attention (APA, 2013).
- World prevalence of ADHD at about 5% (Polanczyk et al, 2007).
- ADHD was originally seen as a disorder of childhood but now its lifelong prevalence is widely acknowledged.
- The DSM-5 distinguishes between 3 subtypes of ADHD: hyperactice/impulsive, inattentive and combined type
- Hyperactive/impulsive: high acivity levels cause difficulty
- Inattentive: problems with maintaining attention - inattention is greater than expected for their developmental age
- Combined type: they have difficulty with both attention and activity
- Study by Gaub et al (1996) where ADHD children were rated by teachers on areas of behavioural, academic and social functioning, and compared to controls.
- Inattentive: impaired in all areas but more appropriate behaviour and fewer externalising problems than other subtypes
- Hyperactive/impulsive: displayed externalizing and social problems, but no different from controls in learning or internalizing problems.
- Combined type: severe and pervasive difficulties across domains.
Diagnosis of ADHD
- DSM-5 states patients must have experienced a minimum of 6 symptoms of inattention or 6 symptoms of hyperactivity/imulsivity
- - inattentive symptoms include: often easily distracted, often doesn't seem to be listening when spoken to directly, often has trouble organizing tasks and activities
- hyperactivity/impulsivity symptoms include: often talks excessively, is often impatient, finds it difficut to resist temptations
- Symptoms must be present by age 12, be pervasive across settings, and associated with substantial impairment in functioning (APA, 2013).
- Subtypes aren't always stable though. A child may have only one type in childhood, but have both in adolescence.
Genetic risk factor for ADHD
Farone et al (2005)
- Note that from 20 twin studies, the heritability estimate of ADHD is around 0.76, making it one of the most heritable psychiatric conditions
- But, they note that many candidate genes have been identified so there is no single gene identified as a risk factor.
- They identified eight genes thought to be invloved and these are related to dopamine and serotonin. Dopamine part fits with the fact that methylphenidate (a dopamine agonist) seems to reduce ADHD symptoms (Spencer et al, 2005).
Brain structure in ADHD
- ADHD has been associated with reduced global brain volume (Castellanos et al, 2002), but also more specific regional abnormalties.
- There are various theories for what brain structures are implicated in ADHD
- Executive Function (EF)
- Delay aversion
- Dual pathway model
- Temporal processing deficits
Brain structure - executive functioning (EF)
Lawrence et al (2004)
- study looking at EF in lab (Stroop test and WSCT) compared with real world context (playing challenging videogames and route taking at the zoo)
- children exhibited deficits in EF function and processing speed on both lab and real world tasks, BUT deficits weren't evident across all measures - selective impairments
- EVAL: analysis as a function of ADHD subtype was not used - is EF deficit seen in all cases of ADHD?
Klingberg et al (2005)
- computer based training has indicated changes in EF and behaviour
Brain structure - reward processing
Rhein et al (2015)
- fMRI study- ADHD in adolescents is associated with enhanced neural responses in frontostriatal circuitry to anicipation and receipt of reward
- modified version of Monetary Incentive Delay task (MID) - ppts asked to respond to a target as a fast as possible - if they did so in a given time window, they would get a reward
- showed ADHD is characterized by increased reward-related neural responses during anticipaton and receipt
- unaffected siblings of participants with ADHD also had increased neural responses in some areas (although to lesser extent) suggesting that familial factors play a role in this increased sensitivity of the reward system
- enhanced neural responses in frontostriatal circuitry to anticipation and receipt of reward
Brain structure - delay aversion and impulse drive
Miranda et al (2009)
- children made to play spaceship game where they could shoot 1 spaceship, or wait to shoot 2, where they could gain more points. (1 point after 2s or 2 points after 30s).
- children with ADHD tend to choose smaller sooner (**) over larger later (LL) rewards more than controls.
- support for a two component model in which IDIR and DA both contribute
- siblings of ** reponders more likely than those of non-** reponsers to be ** responsers themselves suggesting that DA may mediate family based influences in ADHD
- may be that IDIR and DA are elements of the same neuro-developmental mechanism and IDIR is a developmental precursor of DA.
- IDIR hypothesised to be ground in disrptions of neuro-circuitry of the dopamine modulated, pre-frontal brain reward circuits.
- DA emerges over time and this may be as children with IDIR perform poorly in delay-rich settings and come to associate such situations with failure and disappointment
Brain structure - dual pathway model
Sonuga - Barke (2003)
- The model reconciles the ideas of executive dysfunction (EDF) and delay aversion - previously thought to be competing accounts of ADHD
- Two dissociable pathways mediated by distinctly different psychological processes and rooted in functionally segregated, though conceptually related, brain circuits
- EDF deals with cognitive deficits and delay aversion with motivational deficits
Brain structure - temporal processing
Huang et al (2012)
- in duration discrimination tasks, children consistently performed worse than controls
- time processing in probands with a family history of ADHD is more seriously affected than those without family history suggesting an effect of genetics
- multiple difficulties with time production, time reproduction and duration discrimination associated with ADHD.
Smoking and prematurity
Langley et al (2012)
- no difference found between maternal and paternal smoking suggesting that it is not genetic.
- Thapar et al (2009) found that smoking in pregnancy was only related to ADHD symptoms in offspring who were genetically related to their mothers (e.g. not from egg donation)
Johnson et al (2010)
- children born pre-term and more likely to have LBW are 4x more likely to be diagnosed with ADHD (particularly inattentive subtype)
- but longitudinal study (Heinonen et al, 2010) found no association with being born pre-term... was found for gestational age though -> 3x more likely to meet clinical cut off for ADHD.
- Thought maybe to be due to effect of foetal growth restriction on brain development (Mallard et al, 1995)
- There's insufficient evidence to implicate diet deficiencies as a causal factor in ADHD (Thapar et al, 2013).
- It's unclear whether diet is a primary cause of nutritional deficiencies or whether the nutrients are metabolized differently in some children with ADHD (Burgess et al, 2000)
- although not offered as an intervention in NICE guidelines, parents often report diet can exacerbate symptoms. Food colourings have been found to increase hyperactivity in both typically developing children and children already displaying high levels of hyperactivity (Tarver et a, 2014)
- Johnston et al (2007) ~ relationship most likely to be bidirectional - parents respond to genetically determined negative behaviour of the child in a way that serves to maintain or exacerbate the child's behaviour... so not thought to cause ADHD as such
Kennedy et al (2016)
- Early-life institutional depriation is associated with ADHD later in childhood and adolescence
- looked at UK adoptees vs Romanian adoptees (low deprivation related risk vs high deprivation related risk)
- found ADHD in the low deprivation related risk group was similar to the general population in adolescence and adulthood.
- the high deprivation related risk group were respectively, nearly four, and over seven times more likely to meet criteria, than the low deprivation group.
- the study shows powerful association of early experience with later development, suggesting a role for alterations to brain structure and function.
Nigg et al (2010)
- 16 studies reviewed
- seem to point to interaction of genotype with psychosocial factors in the development of ADHD
- the environmental main effects were usually strong but gene main effects usually non-significant in these studies
- also suggests the eitiological influences on inattention vs hyperactivity may be distinct
- but the study only looked at a small fraction of the relevant genes and environments.... it's one for future work!
Hoza et al (2005)
- children with ADHD (compared to controls) were:
- lower on social preference
- higher on social impac
- less well liked
- more often rejected
- had fewer dyadic friends
- More likely to be nominated by peers as someone they'd least like to be friends with
ADHD affects functioning
- Poor motor co-ordination
- might be due to inhibitory control deficits (Mostofsky et al, 2003)
- can result in things like poor handwiriting and performance in sports
- School Performance
- underachievement observed from pre-school through to adolescence (Frazier et al, 2007)
- EF deficits may play a larger role in academic functioning deficits (Daley et al, 2010)
- Emotional Functioning
- emotion regulation a key factor predicting later adverse life events (Barley et al, 2010)
- Substance Misuse
- Later problems with this. about 1/4 with substance dependece will also have ADHD - unsure to what extent this is due to comorbidiy with conduct disorder, but independent effect of ADHD also evicent (Szobot et al, 2007)
- ADHD is highly co-morbid with disruptive behaciour disorders including oppositional defiant disorder (ODD) and conduct disorder (CD) with as many as 50% showing one of these (Biederman et al, 1991)
- Mood and anxiety disorders also commonly observed in children with ADHD.
- Clinically referred sample: 50% also had a mood disorder while 33% displayed anxiety disorders (Wilens et al, 2002)