Attention-Deficit Hyperactivity Disorder

Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder defined by a persistent pattern of inattention and/or hyperactivity-impulsivity that is inconsistent with the person's developmental stage and directly impairs functioning in 2 or more settings — typically home, school, or work.^[1]

Symptoms usually begin before age 12, though some individuals are not recognized and diagnosed until adolescence or adulthood.^[2] ADHD is a chronic condition for most affected individuals: hyperactive-impulsive symptoms often become less overt with age, but inattention and executive-function difficulties frequently persist into adulthood. People with ADHD carry a higher-than-average burden of comorbid oppositional defiant disorder, learning disorders, and mood, anxiety, and substance use disorders — comorbidities that actively shape diagnostic workup and treatment selection rather than being incidental findings.^[2]

ADHD is diagnosed clinically — there is no laboratory or imaging test that confirms it. The diagnostic threshold requires a persistent pattern of inattentive and/or hyperactive-impulsive behaviours that is excessive for the person's developmental stage, present before age 12, evident in 2 or more settings, and clearly interferes with social, academic, or occupational functioning; the presentation must not be better explained by another psychiatric or medical condition.^[1] Older adolescents and adults (age 17 and older) require a slightly lower symptom count than younger children to meet threshold, reflecting the natural reduction in overtly hyperactive behaviour with age.

How the presentation changes across the lifespan

In preschool and early school-age children, gross motor hyperactivity and impulsivity are often the most visible features. As academic demands increase through school age, inattention, disorganization, and difficulty completing multi-step tasks tend to become more prominent and functionally impairing. In adolescents and adults, overt physical hyperactivity often diminishes into a subjective sense of restlessness or an inability to relax, while inattention, poor time management, and impulsivity in decision-making frequently persist and continue to affect school, work, and relationship functioning.

• Family history of ADHD in a first-degree relative.
• Prenatal exposure to tobacco, alcohol, or other substances.
• Prematurity or low birth weight.
• Significant early childhood adversity, neglect, or trauma.
• Traumatic brain injury.
• Environmental toxin exposure, including lead.
• Certain genetic and neurodevelopmental conditions (for example, fetal alcohol spectrum disorder, fragile X syndrome).
• Male sex.

Differentiating ADHD from commonly confused presentations

History

• Gather information from the patient, family and caregivers, and — with consent — teachers or workplace contacts, since ADHD must be documented in 2 or more settings.
• Characterize the nature, duration, and age of onset of symptoms, and their specific impact on academic, occupational, and social functioning.
• Ask about situations that worsen or improve symptoms.
• Screen specifically for comorbid oppositional defiant disorder, conduct disorder, mood and anxiety disorders, tic disorders, and learning disabilities — refer to a specialist for complex or diagnostically uncertain presentations.
• Take a birth and prenatal history, including prematurity and in utero substance exposure.
• Assess for substance use; a urine drug screen before starting stimulant therapy, and periodically during treatment, is appropriate when substance use is a clinical concern.
• Use standardized, validated rating scales completed by the patient and by 2 or more informants (for example, parent and teacher) — the CADDRA ADHD Assessment Toolkit is a Canadian resource that helps select the appropriate scales and interpret results.^[2]

Physical examination

Assess hearing, vision, thyroid function, and neurologic status, and look for dysmorphic features (suggestive of a genetic syndrome) or signs of anemia — any of these can produce an ADHD-like clinical picture or coexist with it.

Cardiovascular screening before starting a stimulant or atomoxetine

Routine ECG is not recommended before starting a stimulant in a young patient with a normal history and physical examination — current evidence does not show that routine screening ECG prevents adverse cardiac events, and it delays otherwise-appropriate treatment. Reserve ECG and cardiology referral for a patient with a concerning personal or family cardiac history, an abnormal cardiac exam, or known or suspected structural heart disease.^[4]

When testing is not indicated

No blood test, imaging study, or computer-based task diagnoses ADHD — the diagnosis rests entirely on the clinical history and validated rating scales above. Neuroimaging, EEG, and genetic testing are not routinely indicated and should be reserved for when the history or exam suggests an alternative or additional diagnosis, such as a seizure disorder.

• Decrease or eliminate the core symptoms of ADHD — inattention, hyperactivity, and impulsivity.
• Improve behavioural, academic, and/or occupational performance.
• Improve self-esteem and social and family functioning.
• Prevent or minimize the impact of comorbid mood, anxiety, and substance use disorders.
• Minimize medication adverse effects by using the lowest effective dose.
• Support functioning and quality of life over the long term, since ADHD is a chronic condition for most affected individuals.

• Parent/caregiver behaviour-management training and classroom-based behavioural interventions are the foundation of non-pharmacologic treatment at every age, and are 1st-line therapy on their own in preschool-age children.^[2]
• Cognitive-behavioural therapy, organizational-skills training, and social-skills training can be offered depending on the individual's and family's needs — particularly useful for older children, adolescents, and adults with prominent executive-function or social difficulties.
• Sleep-hygiene strategies specifically targeting bedtime routine and sleep duration can reduce both ADHD symptom severity and sleep problems.
• Regular aerobic exercise can improve core ADHD symptoms, reduce anxiety, and improve cognitive functioning as an adjunct to other treatment.
• Classroom or workplace accommodations — preferential seating, extended time, structured routines, instructions broken into steps — support functioning independent of medication status.
• Elimination diets targeting specific foods, sugars, or additives do not have evidence robust enough to support a specific dietary recommendation — do not present this as an established alternative to evidence-based treatment.
• A digital therapeutic video-game-based intervention (EndeavorOTC) is available in Canada as an adjunct option for adults with ADHD; the related paediatric product (EndeavorRx) is not available in Canada.
• Combining behavioural and pharmacologic treatment is more effective than either approach alone for oppositional behaviours, anxiety symptoms, social functioning, and self-esteem — recommend the combination rather than presenting medication and behavioural therapy as alternatives.^[2]

Breastfeeding

Methylphenidate transfer into breast milk appears low; monitor the breastfed infant for agitation and poor weight gain. Amphetamines (amphetamine, dextroamphetamine, lisdexamfetamine) are transferred into breast milk with unknown infant impact; monitor for insomnia, agitation, irritability, and poor weight gain. There are no reports of atomoxetine use during breastfeeding. Clonidine and guanfacine may reduce milk supply, and clonidine specifically transfers into breast milk and can cause infant hypotension — prefer other options while breastfeeding when possible. Bupropion, venlafaxine, and tricyclic antidepressants can be continued during breastfeeding if the patient has a good response, monitoring the infant for sedation, weight gain, and irritability.

Pediatric

Dosing by age is detailed in the Pharmacologic Treatment Options and Drug Tables sections. Preschool-age children (under 6 years) follow the stepped behavioural-therapy-first approach described in Choose Initial Treatment. Growth (height and weight) monitoring is a required part of paediatric stimulant follow-up — see Monitoring & Follow-Up.

Adults, including adult-onset presentations

ADHD is a chronic condition for most people diagnosed in childhood, and hyperactive-impulsive symptoms often evolve into subjective restlessness and persistent inattention/executive dysfunction rather than resolving. There is also emerging recognition of ADHD identified for the first time in adulthood without a clear childhood diagnosis — evaluate these presentations carefully rather than dismissing them, but apply appropriate diagnostic rigour: rule out a substance use disorder, another psychiatric condition, and medication-seeking behaviour before diagnosing ADHD de novo in an adult. The same stimulant-first treatment approach applies in adults, with adult-specific dosing maximums generally higher than the paediatric maximums (see Drug Tables); limited meta-analytic evidence suggests amphetamine-class agents may have a modest efficacy edge in adults, though this does not override individualized drug selection.

Renal and hepatic impairment

Published dose-adjustment guidance specific to renal or hepatic impairment is limited for the stimulants and alpha2-agonists — consult the current product monograph and use a lower starting dose with closer monitoring when significant impairment is present. Atomoxetine is metabolized primarily via CYP2D6; reduce the dose in significant hepatic impairment and consider a slower titration in patients who are genetically poor CYP2D6 metabolizers, per the product monograph.

Discontinuation and drug holidays

A planned 2-3 week medication-free period once a year, typically over a school holiday, can help reassess whether ongoing treatment is still needed, but an extended holiday, such as an entire summer, is not generally recommended for a child with moderate-to-severe symptoms who is doing well on treatment. Taper clonidine by 0.1 mg per week and guanfacine by 1 mg per week when discontinuing — abrupt withdrawal of either can cause rebound hypertension. Consider tapering a stimulant that has been used at a high dose or for longer than 3 months, since abrupt discontinuation can cause withdrawal symptoms in some patients; atomoxetine is associated with less discontinuation-related difficulty than the other agents.

1. Confirm the diagnosis, adherence, correct administration timing, and that the dose was genuinely optimized over a full 3-4 week trial before concluding a medication has failed.
2. If response is inadequate at the optimized dose of the first stimulant, switch to the other stimulant class (methylphenidate to amphetamine, or amphetamine to methylphenidate) and retitrate.
3. If both stimulant classes have failed, are contraindicated, or are not tolerated, trial atomoxetine or guanfacine extended-release, alone or as an adjunct to a partially effective stimulant.
4. Screen for untreated comorbidities (anxiety, mood disorder, learning disorder, substance use, sleep disorder) and psychosocial stressors that can mimic or worsen an apparent treatment failure.
5. Reassess for genuine nonadherence or diversion as a cause of apparent non-response before adding or escalating therapy further.
6. For a partial responder with tolerable adverse effects, consider adding a low-dose alpha2-agonist adjunct rather than repeatedly escalating the primary agent.
7. Refer to psychiatry, developmental pediatrics, or a specialized ADHD clinic for complex, treatment-refractory, or diagnostically uncertain presentations.

• Ordering a routine ECG in a patient with a normal cardiac history and examination before starting a stimulant — not supported by current evidence, and it delays otherwise-appropriate treatment.^[4]
• Skipping baseline blood pressure, heart rate, height, weight, and a genuine personal/family cardiac history before starting a stimulant.
• Crushing or chewing an extended- or controlled-release stimulant capsule or tablet not designed for that — check the specific formulation's handling instructions, since some beads can be sprinkled on food and others cannot.
• Assuming a generic bilayer methylphenidate product is automatically clinically interchangeable with a brand-name long-acting product — CADDRA notes differences in absorption profile that have caused symptom destabilization in some patients after a switch.^[2]
• Giving the last daily stimulant dose too late in the day, causing insomnia.
• Treating growth suppression or appetite loss as an automatic reason to stop medication without first trying dose/timing adjustment, meal-timing strategies, or a planned drug holiday.
• Stopping guanfacine or clonidine abruptly instead of tapering — both can cause rebound hypertension.
• Skipping the diversion-risk conversation (secure storage, not sharing medication) at initiation of any stimulant.
• Starting medication in a preschool-age child without first trying, or concurrently offering, behavioural parent training.
• Combining a stimulant or atomoxetine with an MAOI, or starting either within the required washout window of MAOI use.
• Dismissing a possible adult-onset ADHD presentation solely because there is no documented childhood diagnosis, rather than evaluating it on its own merits.
• Selecting a stimulant or non-stimulant without first checking for comorbid tics, anxiety, or a substance use history — these should actively shape, not just follow, the drug choice.

How to use this table: doses are CADDRA-based and require patient-specific confirmation, including renal/hepatic adjustment where relevant. Select any drug name to open its complete Pharmasist Drug Database page.

Amphetamine-based agents

Contraindicated with MAOIs — allow the required washout period before starting either. All amphetamine-class agents share a broadly similar adverse-effect and interaction profile.

Methylphenidate-based agents

Contraindicated with MAOIs. Can raise phenytoin, phenobarbital, and tricyclic antidepressant levels, and can reduce warfarin metabolism, increasing INR. Formulations below are not interchangeable with one another.

Alpha2-adrenergic agonists

Norepinephrine reuptake inhibitor

Antidepressants (off-label adjunct/3rd-line options)

Considered less effective than stimulants for core ADHD symptoms; used mainly for a comorbid indication or when stimulants, atomoxetine, and guanfacine/clonidine are unsuitable.

Second-generation antipsychotics (adjunct only — not a primary ADHD treatment)

Evidence note: drug inventory, dosing, adverse effects, and comments reflect CADDRA-based Canadian practice, cross-checked against current primary literature.^[2]