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ADHD: Overview, co-occuring conditions and interventions - Coggle Diagram
ADHD: Overview, co-occuring conditions and interventions
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Causal models of ADHD
Underlying impairments
- ADHD -> Barkey., 1997 - executive function deficit - ‘cool’ EF in dorsolateral prefrontal cortex, and ‘hot’ EF in orbitomedial prefrontal cortex
- ADHD -> Delay aversion (Sonuga-Barke., 2002) which relates to ‘hot’ EF
-> Motivational style is impulsive
-> Prefer rewards sooner rather than later (1 point in 2 seconds, small reward, short delay or 2 points in 30 sec, with a large reward but long delay)
-> Faster decline in the effectiveness of reinforcement as delay between stimulus and reward increases
-> Difficulty learning contingencies between present action and future reward
-> Idle time -> hyperactivity and noisiness increases with ADHD individuals - reduce waiting time with starter activities can scaffold positive behaviour (Imeraj et al., 2016)
Solanto et al., 2001 -
- Compared 45 children with ADHD and 29 CA-controls
- Measures that best discriminated the two groups were -
-> Choice-delay task - larger reward, ADHD 34% and TD 58%
-> SSRT task - ADHD > Stop-signal Rt, ADHD < TD probability of inhibition
- Discriminant functional analysis
-> Probability of inhibition classified 68% correctly
-> % large reward (long delay) choices classified 71% correctly
-> Together classified 87.5% correctly
-> Suggests the two measures account for independent sources of variance in ADHD profile
Castellanos et al., 2006 - multiple pathways models; variation in reaction time, with impulsive responses and inattentive reactionMeasuring EF - Gooch et al., 2016:
- Head Toes Knees and Shoulders - measures cognitive flexibility, inhibition control, sustained attention, language processing demand, motor processing demand
- Visual search - language load, attention switching, memory load, selection of stimuli
- Competing language processing task (CLPT) - verbal working memory
- Inhibition tasks (Chandler., 2010) - stop-signal reaction time
- Working memory, verbal and visuospatial counting and sentence span tests, object mats (Gathercole et al)
Evidence for EF deficits in ADHD -
- Willcutt et al (2005) - robust differences between ADHD and controls on 12 tasks, with a mean effect size d = .54
- Strongest and most consistent effects for response inhibition, vigilance, planning and working memory
EF tasks have difficulty separating where the effect comes from e.g. DLD deficits could be due to language demand rather than the EF demand
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Comorbidity in ADHD - NDC tend to co-occur more often than expected by chance (Pennington., 2006)
Genes act probabilistically and are generalist (Kovas and Plomin., 2007):
- Relationship between traits such as reading ability and inattention is higher in MZ than DZ twins, and this bivariate heritability suggests genetic overlap between NDC (Dyslexia and ADHD; Wilcutt et al., 2000)
- Single cognitive deficit models rarely explain all behavioural symptoms
Multiple deficit models (Pennington., 2006):
- Risk factors act probabilistically to increase the liability of a condition (protective factors decrease the liability) by influencing development of neural systems and cognitive processes
- Shared cognitive processes (Peterson et al., 2017) - EF, Speed of Processing and verbal comprehension
- Levels of analysis - aetiological risk and protective factors (genetic, SE and NSE), neural systems, cognitive processes and behavioural disorders
- The Multiple Deficit Model: Progress, problems and prospects (McGrath et al., 2019)
-> Theory is difficult to falsify and current cross-sectional studies cannot establish casuality
-> Need to focus on explicit promotive and protective factors and the mechanistic connections across these in levels of analyses
Social model of disability -
- Reframes ADHD challenges not as an individual’s internal pathology but as resulting from societal barriers (Oliver., 1990)
-> Person > environment (e.g. rigid structures, lack of understanding, barriers to inclusion)
-> Aligns with the neurodiversity movement which views societal norms, not neurological differences as being the root of many difficulties
- Strengths based perspective - distractibility and impulsivity in ADHD as an evolutionary mismatch of high trait curiosity (Le Cunff., 2024)
Intergenerational transmission of ADHD behaviours: genetic and environmental pathways (Kleppesto et al., 2023):
- Child ADHD behaviours correlated with their mother’s and father’s ADHD behaviours
- Correlations largely due to additive genetic transmission
- Variation in children’s ADHD behaviours was explained by genetic factors active in both generations and genetic factors specific to children, giving a heritability of 57%
- Remaining variance is due to environmental factors
Van Herwegen & Riby et al., 2015:
- Comorbidity can be artifactual e.g. due to diagnostic overlap or being part of a ‘clinical’ sample or use of categorical variables rather than dimensions (Youngstroum et al., 2010)
- However, not all comorbidity can be accounted for this way
- Non-artifactual reasons - phenocopy hypothesis where symptoms mimic those seen in another disorder e.g. motor tics being interpreted as ADHD
-> Could also be due to shared aetiology
-> Could also be that co-occurrence reflects an additive component of two separate diagnoses that represent a true co-occurrence
ADHD is comorbid with a range of conditions, including neurodevelopmental and psychological disorders
- Most commonly comorbid with ODD/CD, ASD, DLD, and Tic disorder
- Children and adults with WS also tend to show ADHD characteristics
Influence of co-occurrence on psychological profiles:
- Inhibitory control can be worsened by ASD, however, comorbidity may also have an additive or compensatory effect in some tasks (Nyden et al., 2010 - Tower of London task)
- ASD children show impaired conflict monitoring and response preparation, whereas ADHD children showed impaired attention orienting and inhibitory control
- Children with both had an additive profile
- Delay aversion in ADHD is not always picked up in ASD samples, but both appear to be less motivated in situations where social rewards can be gained
ODD and ADHD -
- ODD did not have the same EF impairments as ADHD, but both have deficit around inhibitory control
- ODD more associated with verbal WM impairments than the ADHD group, suggesting that the additive effect on memory results in true comorbidity between the two
Social cognition - ASD and ADHD have been suggested to have similar patterns of ToM impairments but literature is mixed, but the weight of the literature suggests that this is not the case and it is unique to ASDEmotion cognition - evidence for some impairment in the ADHD and comorbid group, but ASD showed no impairment
- Additive comorbidity - ASD had lowered response to face-sensitive components with gaze direction, whereas ADHD has response to upright and inverted faces, and comorbid diagnosed children showed both impairments
Experience of ADHD - What’s it like to have ADHD / Let’s talk about ADHD / ADHD voices / NeuroSense ADHD
Behavioural characteristics and consequences -
- Procrastination and struggles with motivation with tasks and academics - low self-esteem as a result
- It is invisible and affects all aspects of life - need adaptations and support, does not mean they are lazy
- Inattention harder to diagnose - behaviours are not taken as unintentional
- Presents mainly with inattention and hyperactivity / impulsivity, but has a range of consequences socially, academically, professionally and emotionally
- It is heterogeneous and variable
- Difficulties with reading, spelling and motor skills, as well as difficulties with emotional regulation and control and socialising
- Range of executive functional deficits - organising, inhibition control and attention sustaining / switching - hard to control behaviour (prefrontal cortex, major deficit with inhibitory control)
- Affects learning and development as there is difficulty with focusing on learning, concentration and recalling information, as well as being categorised as having bad behaviour which is actually just difficulty with emotion regulation
-> Higher incidence of anxiety and depression
-> Hard to pay attention for whole lesson, unless the activity is rewarding in which case hyperfocus occurs where the individual cannot move on from a task
- However, flexible thinking and creativity are a big strength
- Several mechanisms involved in interactive framework - genetic variation, toxins, trauma and pregnancy issues (environment) - not caused by parenting
- Support - building in strategies such as routines can help to support with attention and working memory load
-> Introduce structures of answering questions, varying tasks and physical activities
Interventions
Medication - ADHD is an impairment in the regulation of neurotransmitters, and dopamine and norepinephrine have been linked to prefrontal cortex (EF) - MPH moderates levels of DA and NE
- Pietrzak et al., 2006 - 66% of studies show positive effect of MPH on cog outcomes
- Waschbusch et al., 2009 - placebos can produce positive changes in MH conditions
-> Parents / teachers evaluate children with ADHD more positively when they believe they are being treated with a stimulant
-> No sig chance in child behaviour or cognition
- Bussing et al (2012) - willingness to use (higher in adults)
How do stimulants work - Hawk et al., 2018: N = 82, 9-12 years with ADHD
- Randomised double-blind placebo controlled trial, MPH
- Cognition - inhibitory control (e.g. SST), attention and working memory
- Outcomes - maths productivity and teacher ratings
- Cognitive processes mediate clinical improvement of stimulant treatment, and inhibitory control and working memory could be mechanisms of treatment response in ADHD
- Has some effect, but it is not always due solely to EF and cognitive changes
Multimodal treatment study of children with ADHD (MTA trial., 1999):
- Randomised controlled trial (RCT) - due to effect of intervention, removes systematic interventions, more ethical to include multiple interventions
- 579 children aged 7-9 years; combined type of ADHD
- This study uses multiple interventions and compares them
4 conditions (14 months):
- Medication management (MM) - individually titrated doses
- Behavioural management (BM) - family / parent i.e. positive attention and rewards, and in school (i.e. daily report card and summer camp)
- Combination treatment (CT) - integrated M and BM - communication between teacher and clinicians
- Control condition (CC) - regular community care
- Monitored behavioural symptoms, social skills and relationships and educational achievements
- Longitudinal study
All groups < ADHD symptoms:
- CT -> lower levels of medication (BM more important here)
- MM and CT > BM and CC in reduction of symptoms (hyperactivity, internalising symptoms, arguing and social skills)
- No untreated control group - CC often medicated (not ideal control)
- Generalisability to other subtypes
Molina et al (2009) - MTA at 8 years
- Medication use decreased by 62%
- Early ADHD symptoms are prognostic
- Storebo et al (2015)
- Some sustained difference on ADHD symptoms (decline and stabilise)
- Impact on academics still - need other targeted educational support
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