Understanding ADHD: Symptoms, and Comorbidity

What is ADHD?

• ADHD is a neurodevelopmental condition.
• DSM-V classifies ADHD as 'attention-deficit/hyperactivity disorder'.
• ICD-10 classifies ADHD as 'hyperkinetic disorder'.
• Common disorder with 3% prevalence in the UK and 5% worldwide.
• ADHD is characterized by developmentally inappropriate and impairing symptoms of inattention, hyperactivity and impulsivity.
• It's more common in boys than girls.
• Childhood onset can persist into adulthood.

Complex Presentations

• Presents as neurodevelopmental problems like social communication, language, and motor difficulties.
• Involves cognitive impairments like those relating to executive function and response inhibition.
• Presents emotionally as emotional lability, irritability, and anxiety linked to later depression.
• Presents behaviourally with aggression and headstrong/hurtful actions linked to later antisocial behaviour.

Comorbidity

• ADHD exhibits significant comorbidity.
• Comorbidity rates are estimated to be 50-66%.
• Co-morbidity occurs across neurodevelopmental disorders like ASD (30%) and learning disability (7-10%).
• ADHD co-occurs with psychiatric and behavioural disorders like conduct problems/antisocial behaviour (40%) and mood disorders (5-20%).

How is ADHD diagnosed?

• Requires careful clinical history from home, school, and clinical observation.
• No genetic test, blood test, or brain scan available.
• Information is gathered from multiple informants across settings.
• Evidence of impairment must be present.
• Includes a developmental history, medical history, family processes, and social circumstances.
• Diagnosis is based on the presence of inattentive and/or hyperactive-impulsive symptoms.
• One symptom pattern may predominate.
• In children, the symptom threshold is 6 symptoms from each domain (inattentive, hyperactivity, or impulsivity).
• In adults, the threshold is reduced to 5 symptoms.

Treatment

• Treatment follows a stepwise approach.
• Guidelines suggest education and support for the family/school including support groups.
• Classroom management strategies, parental psychoeducation, and behavioural management techniques are helpful.
• Medication may be offered if symptoms persist after non-pharmacological intervention.
• Methylphenidate is typically used as a first-line medication.
• Medication is typically used when symptoms are severe, causing major difficulties, and not usually given without behavioural interventions.

Categorical vs. Dimensional Approach

• ADHD acts as a dimensional construct.
• Diagnostic threshold dependent on personal definition.
• Even subthreshold ADHD can still be impairing.
• Dimensionally: Continuously distributed risk dimension.
• Categorical: Clinical decisions are categorical in nature.

Research evidence

• Twin studies suggest the aetiology of ADHD is the same at each extreme.
• Genetic studies suggest genetic risks are similar for those in the general population and those with the disorder.
• Studies suggest that subthreshold ADHD can impact academic achievement, quality of life, and family/peer relationships.

Is ADHD New?

• A mental state resembling ADHD was described in 1798 by Sir Alexander Crichton.
• The Lancet medical journal described children with the clinical features of ADHD in 1902.

Is the rate of ADHD rising?

• Time trend studies show no evidence of increasing ADHD symptoms in the general population.
• There's more awareness and recognition of ADHD.
• Increase in incidence and treatment.

Economic costs of ADHD

• Economic burden extends beyond health care services to education, social and youth justice services.
• UK-annual total cost of £670 million is spent on treatment of ADHD. Children with high hyperactivity need disproportionately more resources.

Definition

• ADHD is a familial neurodevelopmental condition linked with impairment when symptoms cause problems.
• ADHD is highly heritable with mean heritability calculated at 76% from 20 twin studies.
• Many genes show significant evidence of association with ADHD: DRD4, DRD5, 5-HTT, SNAP-25, DAT, DBH and HTR1B.
• Neural dysfunction and abnormalities may be observed in multiple brain regions in ADHD, but none are specific to the condition.
• The prefrontal cortex show differences, with maturation being delayed.
• Overall cortical thickness matches typical development by around 25 years of age.
• Prefrontal cortical thickness matches around 12 years.

Symptoms and Impact

• Impulsivity is characterized by difficulty in inhibiting or modulating responses and blurting out answers.
• Inattention presents as difficulty completing or maintaining activities.
• Externalized symptoms are those that are easily observed.
• Internalized symptoms include problems with organizing, planning, and managing emotions.
• Classification requires one of the symptoms to be present before the age of 12.
• Symptoms must be present in two or more settings.
• Symptoms must interfere with social, work, or school functioning.
• Some people (especially girls or those with higher IQs) are able to compensate and don't need services until later.

Facts and Figures

• 5% of children and adolescents are affected worldwide.
• 1% have severe hyperkinetic disorder.
• Symptoms persist into adulthood for up to 60% of sufferers.

Heterogeneous Nature of ADHD

• ADHD has various subtypes and possible aetiologies.
• Neurological mechanisms involve areas of the brain like the prefrontal cortex and anterior cingulate.
• Genetics play a role
• Genetics (dopamine and NE system) and environmental factors contribute.
• Environmental factors include low weight at birth, being premature, maternal depression or smoking during pregnancy, paternal antisocial behaviour, toxins exposure, TBI and family instability.

Gender gap in ADHD

• A gender-based referral bias may exist.
• Diagnosed three times more often in boys than girls.
• Hyperactivity symptoms more pronounced in boys.
• More externalizing symptoms like aggression, defiance, and conduct problems in boys.
• Diagnosed twice as often in males (22%) than females (11%) in child case studies.
• More internalizing symptoms like depression and anxiety in girls.
• Greater risk of criminal activity
• This can lead to overdiagnosis
• Less aggression (in non-referred populations)
• Increased rates of self-injury and suicide

Comorbidities

• Comorbidities present throughout the lifespan include Tourette’s syndrome, general learning disability, ASD (very common in childhood), dyslexia/dyscalculia, conduct disorder, oppositional defiant disorder, disruptive mood dysregulation disorder and chronic tic disorder.

Diagnosis

• The overall most common comorbidity is anxiety disorder.
• Substance use disorder is more common in adulthood and is comorbid with ADHD.
• Bipolar disorder and borderline personality disorder are comorbid disorders.
• Tests to diagnose children and adolescents use pre-interview parental questionnaires.
• QbTest and Neuropsychology tests are digitized.
• Using behaviour rating scales and teacher questionnaires give a broad overview.
• School observations, medical examinations, parent interviews and child interviews are also important.
• Diagnosis should take into account all available tools.
• Assessors must be well trained for an accurate >90% diagnosis.
• Patient pathways are explained in Children NICE guidelines.

Treatment

• Medication is the first line of treatmen for moderate to severe ADHD
• Medication is the last choice of treatment for mild ADHD
• Only some conditions related to ADHD require intervention
• Up to 80% of patients respond to stimulant treatment.
• ADHD doesn't automatically justify medication with symptoms capable of being managed with time.
• Patients have found ways to compensate for their impairments.
• Lifestyle changes can improve symptoms.
• Physical activity and exercise can be most effective to compensate symptoms.
• Treating underlying issues.
• An individual approach to treatment should be taken. Successful treatment requires effectiveness and and should be multimodal.
• These treatments should consist of psychoeducation, psychosocial intervention and pharmacotherapy.

Pharmacotherapy

• Medications include methylphenidate, dexamfetamine and lisdexamfetamine.
• Effect size of methylphenidate: 0.9 (inattention),0.75 (aggression).
• Non-Stimulants include: Atomexetine (effect size: 0.7) and Guanfacine.
• Medication can cause unfounded fears of side effects, lack of belief that medication is needed, and expectation of a miracle cure or instant effects.

DA and NE in ADHD

• ADHD is most likely due to decreased activity in neuron-to-neuron chemical communication.
• Norepinephrine reuptake blocker, atomoxetine, causes NE and DA levels to increase in the prefrontal cortex.
• Methylphenidate blocks the transporter for dopamine and norepinephrine.
• Amphetamines block the transporter for dopamine, serotonin, and norepinephrine
• The immediate effect is to increase the synaptic concentration of monoamines, producing a post-synaptic effect
• Cortical striatal circuits are tightly regulated by feedback from inhibitory dopamine receptors in the presynaptic nerve terminal, which regulate the synaptic neurotransmitter.

Methylphenidate Side Effects

• More common side effects include a decreased appetite and sleep disturbance.
• Less common side effects include increased blood pressure/pulse, headaches/dizziness, stomach aches/nausea/dry mouth, arrhythmia/tachycardia and anxiety/irritability/depression.

Dexamfetamine Side Effects

• More common: increased blood pressure, heart rate, insomnia, nausea, tachycardia, euphoria, restlessness, overstimulation, tic exacerbation and depression / anxiety / irritability.
• Less common: headaches, increased sweating, stomach cramps, psychosis and chest pain.

Atomoxetine Side Effects

• More common: decreased appetite/anorexia, increased blood pressure/pulse and headache.
• Uncommon: suicidal thoughts, aggression, migraine and hepatotoxicity. Non-Pharmacological Interventions may not have any effect on ADHD symptoms.