What are the main clinical features of ADHD?
- Inattention
- –Poor organisation/planning
- –Poor response inhibition
- –Poor impulse control - Hyperactivity
- –Disorganised
- –Poorly controlled
- –Restless/fidgety - Impulsivity
- –Poor awareness of danger
- –Accident prone
- –Social disinhibition
- –Emotional dysregulation (e.g. anger, extreme emotions)
List some comorbidities of ADHD.
- Sleep disorders (50%)
- Behavioural difficulties (25-50%)
- Specific learning diabilities (25%)
- Developmental coordination disorders (25%)
- Social communication difficulties (25%)
- Anxiety symptoms (20%)
- Tic disorders (20%)
- Mood difficulties (20%)
- Increased psychosocial factors
Describe the prevalence of ADHD (including gender differences).
1-5% population officially (0.4% in Scotland/Glasgow)
Male:female ratio in children: 4:1
Male:female ratio in adults: 1:1
Describe the causes of ADHD.
- Risk factors
- –Boys
- –Poverty
- –Lead exposure
- –Iron deficiency
- –Maternal alcohol during pregnancy - Genetics
- –Dopamine receptor 4 and 5
- –Dopamine transporter
- –Dopamine beta hydroxylase
- –Serotonin receptor 1B
- –Serotonin transporter
- –Synaptosomal associated protein 25 - Environment
- –Low socioeconomic class
- –Low birth weight
- –Maternal smoking
- –Psychosocial adversities - Organic factors
- –Smaller brain volume
- –Smaller basal ganglia
- –Smaller cerebellar vermis
Describe the different subtypes of ADHD, and their prevalence.
- Inattentive ADHD (20-30%)
- –Presents later in adolescence
- –Failure to follow instructions
- –Careless mistakes
- –Forgetfulness
- –Poor organisation
- –Academic difficulties - Hyperactive ADHD (15%)
- –Presents earlier in childhood
- –Running around
- –Frequently interrupts
- –Restlessness
- –Disruptive behaviour - Combined ADHD (50-75%)
- –Meets criteria for both types of ADHD - Unspecified ADHD
- –Significant impairment which does not fit the criteria for either type of ADHD
Describe the pathophysiology of ADHD. (12 marks)
- BRAIN NEUROCHEMISTRY
a) Dysfunction of dopamine/noradrenaline pathways in the prefrontal cortex
- –Dopamine: mesocortical pathway (function: on-task behaviour/cognition, focus)
- –Noradrenaline: locus ceruleus pathway (function: dampens extraneous stimuli, executive operations, response inhibition)
b) Hypoarousal
- –Loss of dopamine/noradrenaline in the arousal network of the prefrontal cortex
- –This means that extraneous information is no longer filtered - leads to inattention
- –This means that there is no response inhibition of other brain areas - leads to hyperactivity and impulsivity
c) Hyperarousal
- –Loss of response inhibition from PFC leads to hyperactivity and impulsivity
- –Signal:noise detection ratio decreases, i.e. inappropriate stimuli can’t be filtered out, which leads to increased activation of receptors - leads to inattention
- BRAIN NEUROPSYCHOLOGY
a) Poor executive function (e.g. organisation, planning) - CHANGES IN BRAIN STRUCTURE
a) Decreased brain volume in certain areas, e.g.
- –Cerebellum
- –Basal ganglia
- –Total cerebrum
- –Right cerebrum
- –Prefrontal cortex
- –Corpus callosum
- –Right caudate
- –Reduced white/grey matter
Outline the treatment options (in order of priority) for ADHD.
- Environmental interventions
- Behavioural interventions
- Psychostimulants (methylphenidate, dexamphetamine)
- Atomoxetine
- Alpha adrenergic agonists (clonidine, guanfacine)
- Anti-depressants (TCAs, MAOIs)
- Dopaminergic drugs (modafinil)
What are the mechanisms of action for the 2 main psychostimulants used to treat ADHD?
Methylphenidate:
1. Blocks the dopamine transporter, i.e. inhibits dopamine reuptake
Dexamphetamine:
- Blocks the dopamine transporter, i.e. inhibits dopamine reuptake
- Facilitates dopamine release from presynaptic storage vesicles
List some side effects of psychostimulants in ADHD treatment.
- Misuse of dexamphetamine (controlled substance)
- Increased BP/heart rate
- Sleep difficulties/insomnia
- Anorexia
- Loss of appetite
- Growth retardation
- Sadness
- Irritability
- Abdominal pain
- Headaches
Describe the mechanism of action of atomoxetine.
- Noradrenaline reuptake inhibitor
2. Focussed on prefrontal cortex - avoids rewards pathway, so there is no risk of addiction
What are the advantages of atomoxetine as compared to psychostimulants?
- Long half life (once a day dosing)
- No abuse
- No drug holidays needed
- Effective for comorbidities too
List the side effects of atomoxetine. Which are the 3 most significant ones?
- Mood swings (e.g. rage)
- Suicidal tendencies
- Hepatic impairment
- Nausea/vomiting
- Abdominal pain
- Weight loss
- Headaches
- Excessive tiredness/insomnia
- Constipation
- Increased HR/BP
What is the mechanism of action of adrenergic drugs in ADHD treatment?
Alpha adrenergic agonists bind to noradrenaline receptors in the prefrontal cortex and stimulate them
What are the side effects of adrenergic drugs in ADHD treatment?
- Sedation
- Dizziness
- Hypotension
What are the side effects of anti-depressants in ADHD treatment?
- Anticholinergic effect
- Cardiac effects
- Seizures
What are the side effects of dopaminergic drugs in ADHD treatment?
- GI problems
- Loss of appetite
- Abdominal pain
- Dry mouth
- Tachycardia
Outline the environmental interventions that can be used to treat ADHD.
- Provide a calm environment
- Avoid distracting stimuli
- Avoid asking child to be still and quiet for too long
- Maintain structure and supervision
Outline the behavioural interventions that can be used to treat ADHD.
- Encourage consistency
- Don’t personalise behaviour problems
- Positive reinforcement for good behaviour (also applies to parents)
- Parents should be firm and in control without being coercive
- Set clear rules with consequences
- Use routines, countdowns, reminders
- Use quiet time, planned ignoring, time out
- Provide feedback after observing parents
What factors constitute a diagnosis of ADHD?
- Presence of risk factors
- –Family history
- –Male gender
- –Low birth weight
- –Epilepsy
- –Maternal smoking - Presence of clinical features, which fulfill the following criteria:
- –Present before 7yo
- –Excessive for child’s age and development
- –Pervasive (present in more than one environment)
- –May get worse in the afternoon
- –Have a significant impact on the child’s development
How is ADHD diagnosed?
- Information is collected from different sources
- –Direct observation
- –Education
- –Structured questionnaires
- –Parents
- –Teachers - Information is needed about:
- –Pregnancy and development
- –Past medical history (especially head injuries)
- –Family history
- –Educational attainment
- –Behaviour in school
- –Other emotional problems
- –Hearing/vision screening
What are the normal brain changes associated with adolescence?
- Decreased grey matter (PFC matures last - this causes reckless behaviour in adolescents)
- Increased white matter (rapid myelination)
- No change in gyrification
- Cortical thinning
- Increased ventricular size
- Decreased connectivity
- Decreased brain volume
What features might increase the risk of ADHD persisting into adulthood?
- Comorbidities:
- –Organic disorders
- –Psychiatric disorders (e.g. ODD, OCD)
- –Learning difficulties
- –Predominant symptoms - Progressive reduction in cerebellar/hippocampal volumes
- Maternal depression
- Martial discord
- Negative parent-child interaction
- Family socio-economic disadvantage
- Familial ADHD
Describe the risks of adult ADHD.
- 4-5x increased risk of dying in a RTA
- 3x increased risk of illegitimate children
- Increased risk of criminality
In children with ADHD, what proportion of them will continue to have ADHD into adulthood?
15-60%
