“Clinical Developmental & Health Psychology – Lecture 4 (UNIVERSITY OF AMSTERDAM)”

ADHD is classified by two symptom clusters:

1. Inattention
2. Hyperactivity/impulsivity

Additional criteria for ADHD diagnoses is that the symptoms should be pervasive (i.e. symptoms should persist in more than one setting) (1), the symptoms should lead to impairment (2) and at least some of the symptoms should be present before the age of 12 (i.e. age of onset) (3).

There are three presentations of ADHD:

1. Inattentive (30%)
   There is mainly inattention and not necessarily hyperactivity.
2. Hyperactive/impulsive (5%)
   There is mainly hyperactivity and impulsive actions rather than inattention. This is mostly seen in young children.
3. Combined (65%)
   There is a combination of inattentive and hyperactive/impulsive symptoms.

There are several things to know about ADHD:

1. There is substantial heterogeneity within ADHD.
2. The differentiation between ADHD and other disorders is challenging as the presentation of ADHD symptoms can be caused by a lot of things (e.g. anxiety).
3. The prevalence of ADHD appears to decrease from childhood to adulthood.
4. There is a high comorbidity (i.e. 66%).

The prevalence of ADHD in children is 3% to 7%. In adults, the prevalence is 2.5%.

ADHD is a multifactorial disorder (i.e. there are multiple causes). There are several things that contribute to the causal factor of ADHD:

1. Heritability
   There is a high heritability in ADHD, meaning that there is a large genetic component.
2. Prenatal factors
   The prenatal factors of the child influence the development of ADHD (e.g. maternal stress).
3. Interactions with environment (i.e. diathesis-stress model)
   There are genetic vulnerabilities which can be triggered by the environment (i.e. gene-environment interaction).

The ADHD symptoms manifest themselves at different ages (e.g. ADHD in adolescence is associated with different symptoms than ADHD in childhood).

Childhood ADHD is a developmental risk factor for negative outcomes such as traffic incidents (1), substance abuse (2), aggression (3), delinquency (4), sexual risk-taking (5), gambling problems (6), financial risk-taking (7) and food-related risk-taking (8). Prevention and early intervention in childhood ADHD are very important.

There are children who grow out of ADHD when they reach adulthood but many do not. Of the children with ADHD, 20% - 45% meet the full criteria for ADHD as adults. About 25% to 48% of the children with ADHD have impairing symptoms as adults.

Children with ADHD have a delayed cortical development, especially the cortical thickness. The cortical regions are important for executive functions that are impaired in ADHD. This could explain some ADHD symptoms as the maturation of the cortex could alleviate ADHD symptoms.

The birthdate effect refers to the fact that ADHD is more often diagnosed in the youngest children in the class. This may be a wrong social comparison, as the children are compared to other children in the class. However, a younger child has a development that is a little behind compared to the older children in the class. This could lead to an increased rate of false positives when diagnosing ADHD.

The prevalence rates of ADHD in adulthood might be a bit lower than in childhood because adults might match their life’s context with ADHD. This makes ADHD an advantage or a neutral factor, rather than a more negative aspect of life. Adults may learn to deal with ADHD. In short, delayed cortical development (1), the birthdate effect (2) and matching life’s context with ADHD (3) are reasons for the lower prevalence of ADHD in adulthood compared to childhood. Adult-onset of ADHD is likely due to subthreshold childhood ADHD.

It is possible that individuals seeking treatment for late-onset ADHD are valid cases. However, it is more likely that the symptoms are the result of a comorbid disorder (1), the cognitive effects of substance use (2) or non-impairing cognitive fluctuations (3). This means that false positives of late-onset ADHD are common. Nonetheless, it may be possible that there is a distinct adult-onset developmental trajectory with similar phenotypical features of ADHD.

There are a lot of models explaining ADHD. There is no consensus and most models are not mutually exclusive.

The functional working memory (WM) model states that ADHD symptoms are the result of overwhelmed demands on impaired working memory. According to this model, the working memory demands are too high for children with ADHD, which leads them to seek behavioural ways to compensate for ADHD (e.g. hyperactivity). This hyperactivity also stimulates their brain. It activates brain-based arousal mechanisms that support the executive and supervisory attentional component of working memory. In other words, children become hyperactive to remain focused on a task.

Evidence for this comes from the fact that working memory is impaired in children with ADHD and that there is a better working memory performance in children with ADHD with a higher activity level. This implicates that children with ADHD must be allowed to move. However, there is high heterogeneity within ADHD thus this may not work for all children with ADHD.

Children with ADHD show hypoactivation in the frontoparietal and ventral attentional networks involved in executive function and attention and a hyper-activation in the sensorimotor and default mode network. Adult ADHD is mostly associated with hypoactivity in the frontoparietal system and hyperactivity in the visual network, dorsal attention network and default mode network.

The delay aversion theory states that ADHD symptoms represent a choice to avoid delay because delay is seen as aversive. This implies that ADHD is associated with problems with dealing with delayed rewards (e.g. financial risk-taking).

The dual pathway model states that ADHD is explained by impairment in executive functioning (1) and the motivational and reward system (2). The functional working memory model is reflected in the impairment in executive functioning. The delay aversion theory is reflected in the impairment in the motivational and reward system.

There is an impairment in executive functions in children with ADHD and children with ADHD have an aberrant reward sensitivity (i.e. completely different reward sensitivity). Children with ADHD require more reinforcement to reach optimal performance. The most impaired executive function is visuospatial working memory.

Typically developing children already have optimal performance with feedback only. However, the performance of children with ADHD improves with reward and there is more improvement with higher rewards but the performance of children with ADHD does not normalize, regardless of the reward.

Typically developing children have better working memory than children with ADHD. The performance on a working memory task of typically developing children is similar over time. The children with ADHD have a decrease in performance over time. However, when given a high reward, the performance over time normalizes in children with ADHD. This implies that children with ADHD need more motivation, especially on long tasks. It is wise to apply strategies to diminish working memory demands.

Diminishing working memory demands can be done by dividing the tasks into multiple steps (1), by providing structure (2), using to-do lists (3), keep instructions short and repeat them (4), ignore motor activity (5) and prevent distraction (6). Improving motivation can be done by using reward systems (1), reinforce desired behaviour immediately (2), make desired behaviour explicit (3), create attractive tasks (4) and anticipate for problems (5).

Patients often experience that the services provided by health care are not aimed specifically at ADHD. This lack of support contributes to people with ADHD experiencing more severe problems with age.

The definition of impairment is difficult in ADHD because ADHD symptoms are continually distributed throughout the population. Young children with ADHD are more likely to show externalising symptoms. At a later age, it is more likely that inattention is the main problem rather than hyperactivity. ADHD is more often diagnosed in boys than girls, probably because boys more often show hyperactivity.

Secondary ADHD refers to ADHD acquired at a later age due to brain injury. The comorbidities of ADHD change over time. At a young age, oppositional defiant disorder is more common whereas substance use disorder is more common at a later age. ADHD may mimic disruptive mood dysregulation disorder and bipolar disorder in the presence of severe emotional dysregulation.

ADHD medication is not associated with increased risk of substance abuse. ADHD treatment appears to reduce impairment and symptoms but not necessarily functioning in the long-term. It appears as if people who remit from ADHD do so because of maturation of higher cognitive functions but remain at ADHD level regarding lower cognitive functions. Impairments in executive functioning do not distinguish the ADHD remitters and the non-remitters.

Rule-breaking behaviour disorders (e.g. ODD, CD) predict a more severe symptomatology (1), more severe functional impairments (2), higher persistence of ADHD in adulthood (3) and worse outcome of the disorder (4). These disorders also mediate the risk for the development of other disorders.