ADHD in under 18s Flashcards
DSM criteria ADHD
Symptoms of hyperactivity and impulsivity may include [1]:
●Excessive fidgetiness (eg, tapping the hands or feet, squirming in seat)
●Difficulty remaining seated when sitting is required (eg, at school, work, etc)
●Feelings of restlessness (in adolescents) or inappropriate running around or climbing in younger children
●Difficulty playing quietly
●Difficult to keep up with, seeming to always be “on the go”
●Excessive talking
●Difficulty waiting turns
●Blurting out answers too quickly
●Interruption or intrusion of others
Symptoms of inattention may include [1]:
●Failure to provide close attention to detail, careless mistakes
●Difficulty maintaining attention in play, school, or home activities
●Seems not to listen, even when directly addressed
●Fails to follow through (eg, homework, chores, etc)
●Difficulty organizing tasks, activities, and belongings
●Avoids tasks that require consistent mental effort
●Loses objects required for tasks or activities (eg, school books, sports equipment, etc)
●Easily distracted by irrelevant stimuli
●Forgetfulness in routine activities (eg, homework, chores, etc)
Differential diagnosis/comorbid dx
There are several differential diagnoses to be considered. It should be noted that ADHD may also be comorbid with these problems. Differential diagnoses include:
oppositional defiant disorder and conduct disorder 30-40%
anxiety disorders
attachment disorders
bipolar affective disorder
problems with learning, including specific learning difficulties (e.g. dyslexia) and intellectual disability
other problems, including developmental coordination disorder (DCD), sleep disorders and neurological problems such as epilepsy and tic disorders.
Prevalence
5% (0.6% receive diagnosis and treatment)
more common in boys 6:1
more inattentive type in girsl
How to raise awareness/diagnosis and treatment of ADHD
Awareness of ADHD should be raised locally and nationally. We should ensure the delivery of ADHD training to medical students, doctors in training (particularly in psychiatry, paediatrics and general practice), trainee teachers and other health and social care professionals working with children and young people.
ADHD services should be included in development strategies for both child and adult services. ADHD guidelines (NICE in England and Wales and SIGN in Scotland) should be more widely disseminated. We should also foster the development of parent support groups.
persistence of ADHD with age
hyperactivity sx reduce
inattentiveness remains
2/3 continue to have symptoms, 50% functional impairment when older
~3.4% in adult population
significant impact of ADHD
ADHD is associated with problems for the affected child, their family, and wider society.
Children and young people with ADHD can be affected in range of ways. They may:
have low self-esteem
have poor relationships with family and/or friends and peers
underachieve academically (and later in life, when finding an occupation).
Families and carers of children with ADHD suffer a significant emotional burden
(National Collaborating Centre for Mental Health, 2009). Problems include:
strained relationships at home due to difficult parent/child and sibling interactions
marital discord and family breakdown
worry about the lack of understanding about ADHD in schools and in parts of the medical profession (NHS Quality Improvement Scotland, 2008a).
Society is affected more broadly. ADHD is associated with significant financial costs to health, social and educational services. The economic impact of family breakdown, the increased use of state-funded services and the lost contribution to the workforce cannot be underestimated (National Collaborating Centre for Mental Health, 2009).
ADHD in children has been increasingly recognised, diagnosed and treated since the 1960s. Why do you think that is, and what do you think happened to these children in previous decades?
There is no correct answer to this question, and the issue is the subject of debate and controversy. One possibility is that ADHD has appeared more prevalent in recent decades because there is an increased awareness of its presentation and its association with other disorders. Prior to the diagnosis of ADHD, children presenting in this way were likely to have been perceived and treated as badly behaved, and may have been called ‘conduct disordered’ or ‘problem learners’. Comorbid disorders were perhaps more likely to have been recognised and treated. Behavioural parenting approaches may have been recommended, which could have left parents feeling to blame for their child’s presentation.
Can you think of a possible evolutionary advantage of the behaviours we now call ADHD?
Again, there is no correct answer to this question. One hypothesis is based on the finding that the behaviours of ADHD are prevalent and heritable, which suggests that they were previously selectively advantageous behaviours. Hartmann and others propose a ‘hunter versus farmer’ hypothesis. This suggests that people are divided into two groups: those with behaviours with an evolutionary advantage for hunting and the nomadic lifestyle, and those more suited to farming and a more settled lifestyle. What we might call ‘distractibility’ could be framed as an ability to scan and search for novel stimuli and threats. Such distractibility, in addition to impulsivity and risk-taking, would be ideal for hunters but detrimental to farmers (Hartmann, 1997).
Many individuals with ADHD/ADD have been very successful in their chosen paths in life. Well-known names who have been open about their history of ADHD/ADD include Richard Branson, Jamie Oliver, Emma Watson, Rory Bremner and Louis Smith.
Overview Aetiology ADHD
No single risk factor has been associated with ADHD, but many genetic and environmental originating causes appear to be implicated. These interact in complex ways; for example, some environmental triggers may ‘switch on’ particular genes.
It has not yet been possible to construct a comprehensive causal model of ADHD since, in addition to the gene-environment interplay, a model will require integration of the many neural, cognitive and behavioural mechanisms involved. Furthermore, it would need to explain several levels of heterogeneity evident within clinical populations, such as the fact that the inattention and hyperactivity/impulsivity dimensions of ADHD each appear to be linked to different cognitive dysfunctions (Coghill et al, 2005).
This complex picture may explain the wide variation in phenotypes in clinical populations of young people with ADHD. It also provides a rationale for the fact that ADHD is very often associated with a range of other neurodevelopmental and psychiatric comorbidities (as detailed on page 2.7).
Genetic factors
Twin, family and adoption studies suggest that mean heritability is 76% (Coghill et al, 2008), which is similar to the figure for schizophrenia. ADHD therefore appears to be more attributable to genetic factors than depression (39%), generalised anxiety disorder (32%) and breast cancer (27%).
Parental ADHD increases the risk of developing the condition eight-fold (Spencer et al, 2002). There are many common genetic variants; each genetic component exerts very weak effects and none are necessary or sufficient to explain ADHD.
Molecular genetic studies suggest candidate genes coding for neurotransmitter receptors and transporters in several systems:
dopaminergic: DRD4, DRD5, DAT1
serotonergic: HTR1B, 5-HTT/SLC6A4
noradrenergic: ADRA2A, NET1/SLC6A2.
There are many mechanisms by which neurotransmitters, and their respective receptors and transporters, may exert their influence. For example, serotonin and noradrenaline can have both facilitatory and inhibitory impacts on dopamine transmission.
Other candidate genes relate to neuronal transmission (e.g. SNAP-25) and plasticity. Genome wide association studies (GWASs) suggest that neuronal migration, cell adhesion and cell division may also be implicated.
environmental factors
Prenatal factors
Intrauterine exposure to toxins is associated with ADHD. Exposure to cigarettes or alcohol increases the risk for developing ADHD by two to three times (Spencer et al, 2002). These risks are particularly high if the foetus has the DAT1 dopaminergic genotype (Coghill et al, 2008).
Brain injury in utero is associated with ADHD.
Perinatal factors
Prematurity and hypoxia are associated with ADHD.
Low birth weight increases the risk of ADHD by a factor of 3 (Spencer et al, 2002).
Postnatal and early life factors
Early life damage to the developing brain (e.g. head injury) is associated with ADHD.
Other ‘insults’ to the developing brain include exposure to early adversity and emotional neglect (Kreppner et al, 2001). Several areas of the brain, including the prefrontal cortex, require particular experiences for normal neurological development, especially in the first two years of life. These include a safe, calm environment and an attentive, responsive primary caregiver.
Socio-economic status and maternal age contribute very little to the risk of developing ADHD (Spencer et al, 2002).
A link has been found between hyperactivity and some additives and preservatives in the diet (McCann et al, 2007). Some children with ADHD have idiosyncratic reactions to certain natural and/or artificial foodstuffs.
Pathophysiology
Structural and functional neuroimaging studies and electrophysiology have shown the following brain abnormalities in ADHD (Tripp & Wickens, 2009):
overall reduction in brain size; regional thinning in cortical thickness in childhood that largely resolves during adolescence
reduced dimensions of several brain regions, including the caudate nucleus, prefrontal cortex white matter, corpus callosum and cerebellar vermis
reduced connectivity in frontostriatal white matter tracts and reduced activation in prefrontal and striatal regions
various morphological and functional differences in other areas, including the motor cortex and the temporal and parietal lobes.
There also appears to be altered dopamine, noradrenaline and serotonin transmission in many of these regions.
A complete causal model for ADHD has not yet been possible for several reasons:
Different dimensions of ADHD may be associated with different cognitive deficits. Inattention may be associated with deficits in executive function and working memory, whereas hyperactivity and impulsivity may be related to dysfunctions of reward mechanisms. Not everyone with ADHD performs poorly on standard neuropsychological tests (Taylor et al, 2004).
Various cognitive deficits within individuals with ADHD may not be correlated. ADHD may be the outcome of a variety of anomalies in separate neural networks.
Several single-cause models have been suggested, which are probably best viewed as complementary approaches:
Executive function deficits, including weaknesses in response inhibition, vigilance, working memory and planning (Willcutt et al, 2005).
Motivational deficits, particularly an altered response to reinforcement, i.e. being less able to delay gratification (Nigg, 2005).
A comprehensive modelling framework requires biological, cognitive and behavioural levels, with a separate domain for environmental influences that can interact at any of these levels (
Parent/carer interview
The following points should be covered in a parent/carer interview:
Presenting complaint (parental report of child’s symptoms)
Nature and frequency of symptoms.
How or if the symptoms vary across situations.
Impact upon social functioning at home and nursery/school.
Impact upon learning or academic functioning.
History of presenting complaint
When symptoms first become a problem.
Total duration of symptoms.
Obstetric and perinatal history
Maternal stress during pregnancy.
Maternal exposure to alcohol, cigarettes or medication.
Pre-term delivery.
Neurological insults at delivery, e.g. hypoxia.
Developmental history (chronology of evolving difficulties)
Baby’s temperament, sleeping and feeding.
Quality of care and attachment to main carer.
Acquisition of developmental milestones.
Significant events and transitions.
School (including nursery)
General behaviour.
Academic progress (school reports).
Relationships with peers and with adults.
Concerns raised with parents.
Medical history
Medical problems (particularly neurological problems and tic disorders). Associated conditions (e.g. developmental coordination disorder). Medications and allergies.
Family history
ADHD or other neurodevelopmental disorder (or history that suggests a disorder, as these are unlikely to have been diagnosed in older generations).
Psychiatric illness.
Sudden cardiac death (impacts on use of stimulant medication).
Assessment of family functioning
Relationships within the family and who is at home.
Child management styles.
Marital conflict or stress
child/young person interview
Things to look out for in the child/young person include:
their activity level
the degree of focus on tasks and on the conversation
their social communication skills
any evidence of tics.
Note that most children with ADHD will be more settled in a one-to-one situation
rating scales
Conners parent rating scale
