Attention-Deficit Hyperactivity Disorder

Clinical Snapshot

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]

Recognize the Condition

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.

The three ADHD presentations

Predominantly inattentive

Difficulty sustaining attention, organizing tasks, following through on instructions, and a tendency to lose or forget things needed for daily activities. Often under-recognized because it lacks the disruptive behaviour that prompts earlier referral.

Predominantly hyperactive-impulsive

Excessive fidgeting, difficulty remaining seated or waiting a turn, and impulsive speech or actions. Most apparent in younger children and often the presentation that prompts the earliest evaluation.

Combined

Both inattentive and hyperactive-impulsive symptoms meet threshold — the most common presentation overall.^[2]

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.

Risk Factors

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.

Red Flags & Refer

Most ADHD care is non-urgent, but escalate promptly for any of the following:

Signs of stimulant misuse or diversion — repeated early refill requests, specifically requesting a short-acting or crushable formulation without clinical justification, reports from family or pharmacy staff of missing medication, or use at a higher dose or frequency than prescribed. Reassess the regimen and involve the prescriber, and addiction medicine where appropriate, before continuing to dispense as usual.
Cardiovascular symptoms that need urgent evaluation before continuing stimulant or atomoxetine therapy — chest pain, exertional syncope or near-syncope, palpitations, or unexplained dyspnea on exertion. Hold the medication and refer urgently rather than continuing therapy while awaiting workup.
New psychotic symptoms — hallucinations, paranoia, or new-onset mania. Stop the stimulant or atomoxetine and refer promptly for psychiatric assessment.^[3]
Significant growth suppression — height or weight trajectory crossing downward across growth-chart percentiles despite dosing or timing adjustment. Reassess the necessity of continued treatment.
Priapism — an erection lasting over 2 hours is a recognized, though rare, adverse effect of stimulants and atomoxetine and needs emergency medical attention.
New or worsening suicidal thoughts or behaviour, especially around treatment initiation, a dose change, or discontinuation.
Symptoms suggestive of serotonin syndrome when a stimulant or atomoxetine is combined with another serotonergic medication.

Assessment & Diagnosis

Differentiating ADHD from commonly confused presentations

Consider instead of, or alongside, ADHD	Overlapping features	Points that distinguish it from ADHD
Anxiety disorder	Poor concentration, restlessness, difficulty completing tasks.	Inattention is situational and tied to worry rather than pervasive across settings; hyperactivity, if present, reflects anxious arousal rather than a lifelong trait.
Mood disorder (depression or mania/hypomania)	Poor concentration, distractibility, impulsivity (mania), low energy or amotivation (depression).	An episodic course with a clear onset, rather than a lifelong pattern present since early childhood; mood symptoms (elevated or depressed mood, sleep/appetite change) dominate the picture.
Oppositional defiant disorder / conduct disorder	Disruptive behaviour, difficulty following instructions.	Behaviour is defiant and rule-breaking rather than driven by inattention or impulsivity itself — though the 2 conditions frequently coexist and both may need treatment.
Autism spectrum disorder	Inattention, difficulty with transitions, impulsive-appearing behaviour.	Core social-communication deficits and restricted or repetitive behaviours are present, and frequently coexist with ADHD rather than excluding it.
Specific learning disorder	Poor academic performance, apparent inattention during specific tasks (for example, reading).	Difficulty is circumscribed to the affected academic skill rather than pervasive across settings and activities.
Sleep disorder, including obstructive sleep apnea	Inattention, irritability, hyperactivity — a paradoxical hyperactive presentation is common in children with poor sleep.	A sleep history reveals snoring, witnessed apnea, restless sleep, or an inadequate sleep schedule; symptoms often improve substantially once the sleep problem is treated.
Hearing or vision impairment, or thyroid dysfunction	Inattention, apparent difficulty following instructions.	Identified on targeted screening (hearing, vision, thyroid function) — part of the routine ADHD diagnostic workup for exactly this reason.

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

Practical approachTake a detailed personal and family cardiovascular history — personal history of structural heart disease, arrhythmia, exertional chest pain, or syncope; family history of sudden cardiac death, an inherited arrhythmia syndrome, or cardiomyopathy in a relative under 40-50 years of age — plus a baseline blood pressure, heart rate, height, and weight, reassessed at follow-up.^[4]

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.

Treatment Targets

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.

Choose Initial Treatment

Direct treatment rule

Preschool-age children (under 6 years)

1st line parent training and behaviour management alone — pharmacotherapy is not the first step at this age.^[2]

2nd line — use when moderate-to-severe ADHD symptoms with clear functional impairment persist despite an adequate trial of behavioural therapy: add methylphenidate, specialist-directed, weighing the more limited long-term paediatric stimulant safety data against the expected benefit.^[2]

School-age children, adolescents, and adults

1st line a long-acting stimulant — either a methylphenidate-class or an amphetamine-class agent — combined with behavioural or psychosocial treatment. CADDRA does not favour one stimulant class over the other; individualize by formulation practicality, patient/family preference, and cost.^[2]

2nd line — use when a non-stimulant is preferred as initial therapy instead of a stimulant trial: active or historical psychosis, significant cardiovascular disease or arrhythmia risk, an active substance use disorder or strong diversion concern, prominent comorbid anxiety (favours atomoxetine), or a patient/family preference to avoid a controlled substance. Atomoxetine or guanfacine extended-release are the non-stimulant options.^[2]^[3]

2nd line short- or intermediate-acting stimulants (immediate-release methylphenidate or dextroamphetamine) are used for flexible supplemental dosing — for example, an afternoon top-up — or as an add-on to an established long-acting regimen, rather than as routine monotherapy.^[2]

Switching and escalation triggers

Switch trigger inadequate response, or intolerable adverse effects, after a full 3-4 week trial at an optimized dose of the first stimulant. Switch to the other stimulant class and retitrate before concluding that stimulants have failed.^[2]

Special situation if both stimulant classes fail, are contraindicated, or are not tolerated: move to atomoxetine or guanfacine extended-release, alone or as an adjunct to a partially effective stimulant. Reserve clonidine as a 3rd-line option, particularly for prominent sleep disruption, tics, aggression, or a hyperactivity/impulsivity-predominant presentation, when guanfacine is unavailable or not tolerated.^[2]

Do not skip a baseline cardiovascular history and examination before starting any stimulant or atomoxetine — but do not order a routine ECG in a patient with a normal history and exam, since this is not supported by current evidence and only delays appropriate treatment.^[4]

ADHD pharmacotherapy tracks

Stimulants

Methylphenidate-class and amphetamine-class agents. The most effective agents for core ADHD symptoms and the default 1st-line choice for school-age children, adolescents, and adults. Controlled substances, subject to specific storage, prescribing, and diversion-monitoring considerations.

Non-stimulants

Atomoxetine and guanfacine extended-release. Not controlled substances; slower onset of benefit (weeks rather than days) but a genuine 2nd-line option, and sometimes preferred as 1st-line therapy for the specific situations above.

Adjunct and special-situation agents

Clonidine, bupropion, venlafaxine, tricyclic antidepressants, and — for comorbid aggression or tics only, never as primary ADHD therapy — a second-generation antipsychotic such as risperidone.

Non-Pharmacologic Treatment

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]

Pharmacologic Treatment Options

Drug / intervention	Role	Dose / use	Important adverse effects	Teaching points
Lisdexamfetamine Preferred	1st-line long-acting amphetamine-class stimulant — a prodrug formulation with lower misuse/diversion potential	Children, adolescents, and adults (6 years and older): start 20-30 mg PO once daily in the morning; increase by 10 mg every 7 days; maximum 60 mg per day.	Appetite suppression, insomnia, irritability, headache, increased heart rate and blood pressure	Requires enzymatic conversion to active dextroamphetamine, which blunts the effect of tampering — a reasonable 1st choice when diversion risk is a specific concern.
Mixed salts amphetamine (extended-release) Preferred	1st-line long-acting amphetamine-class stimulant	Children 6-12 years: start 5-10 mg PO once daily in the morning, increase by 5 mg every 7 days, maximum 30 mg per day. Adolescents 13 years and older, and adults: same titration, maximum 20-30 mg per day.	Appetite suppression, insomnia, irritability, increased heart rate and blood pressure	Capsule contents can be sprinkled on food but should not be divided or stored once opened.
Methylphenidate (long-acting) Preferred	1st-line long-acting methylphenidate-class stimulant — several distinct Canadian formulations are available (see Drug Tables)	Formulation-dependent; representative example (controlled-release capsules): 10-20 mg PO once daily in the morning, increase by 5-10 mg every 7 days, maximum 60 mg per day in children/adolescents or 80 mg per day in adults.	Appetite suppression, insomnia, irritability, increased heart rate and blood pressure	Formulations are not interchangeable with each other — confirm which specific product is intended before dispensing or switching.
Methylphenidate (immediate-release) Alternative	2nd-line short-acting agent — flexible dosing or an add-on to a long-acting regimen	5 mg PO 2-3 times daily, increase by 5 mg every 7 days, maximum 60 mg per day.	Appetite suppression, insomnia, irritability, increased heart rate and blood pressure	Give the last daily dose before 4 p.m. where possible to avoid insomnia.
Atomoxetine Alternative	2nd-line non-stimulant — preferred initial therapy for active/historical psychosis, significant cardiovascular risk, active substance use disorder, or comorbid anxiety	Children/adolescents under 70 kg: 0.5 mg/kg/day PO for 10 days, then 0.8 mg/kg/day for 10 days, then 1.2 mg/kg/day; maximum 1.4 mg/kg/day, up to 100 mg per day. Adolescents 70 kg and over, and adults: 40 mg per day PO for 10 days, then 60 mg per day for 10 days, then up to 80-100 mg per day if needed.	Nausea, decreased appetite, sedation, dizziness; rare hepatotoxicity and suicidal ideation	Not a controlled substance. Requires 3-4 weeks for full benefit — set this expectation explicitly.
Guanfacine (extended-release) Alternative	2nd-line non-stimulant — monotherapy or adjunct to a stimulant, particularly useful for aggression, impulsivity, tics, or sleep disruption	Children 6-12 years: start 1 mg PO daily, increase by 1 mg every 7-14 days, maximum 4 mg per day. Adolescents 13-17 years: maximum 7 mg per day as monotherapy, or 4 mg per day as an adjunct to a stimulant.	Somnolence, headache, fatigue, hypotension, bradycardia	Health Canada indication is limited to ages 6-17. Taper by 1 mg per week when discontinuing to avoid rebound hypertension.
Clonidine Alternative	3rd-line non-stimulant/adjunct — sleep disruption, tics, aggression, or a hyperactivity/impulsivity-predominant presentation	Start 0.05 mg per day PO; usual maintenance 0.003-0.01 mg/kg/day (0.05-0.4 mg per day), once daily or in divided doses.	Hypotension, sedation, dizziness, dry mouth	Taper by 0.1 mg per week when discontinuing to avoid rebound hypertension. Less selective than guanfacine, with more sedation and hypotension.
Bupropion Special situation	Off-label 3rd-line/adjunct option, particularly with comorbid depression or an interest in smoking cessation	Children: 2-3 mg/kg/day PO. Adults: usual 200-300 mg per day PO in 2 divided doses; single doses should not exceed 150 mg.	Agitation, insomnia, dry mouth, lowered seizure threshold	Avoid in a seizure disorder, eating disorder, or significant head-injury history. May take 2-4 weeks for effect on ADHD symptoms.
Risperidone Special situation	Adjunct only, for comorbid aggression, severe impulse-control problems, or a tic disorder when stimulant/non-stimulant therapy alone is insufficient — not a primary ADHD treatment	Start 0.25-0.5 mg PO at bedtime, increase weekly by up to 0.5 mg per day in divided doses; usual maintenance 0.75-1.5 mg per day.	Weight gain, sedation, extrapyramidal symptoms, hyperprolactinemia	Reserve for behavioural symptoms unresponsive to core ADHD therapy — does not treat inattention itself.

Special Populations

Pregnancy: for mild-to-moderate symptoms without significant functional impairment, non-pharmacologic treatment is preferred. When pharmacotherapy is genuinely needed, individualize the risk-benefit discussion — a large observational cohort found that amphetamine/dextroamphetamine use was not associated with an increased risk of cardiac or major congenital malformations, and methylphenidate use was not associated with an overall increased risk of major malformations, though it appeared associated with a higher risk of cardiac malformations specifically; caution is advised, particularly in the first trimester.^[5] There are no published reports of lisdexamfetamine use in pregnancy — apply the same caution as for other amphetamines. Avoid atomoxetine, at least in the first trimester, given insufficient safety data. Clonidine has not been associated with birth defects, though first-trimester data are limited; there are no data on guanfacine in pregnancy. Bupropion, venlafaxine, and tricyclic antidepressants appear less effective for ADHD than stimulants and non-stimulants, but can be used with caution if the patient has a separate indication for one of them. Avoid risperidone for the ADHD indication in pregnancy — safety data are insufficient and its ADHD-specific benefit is limited.

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.

Monitoring & Follow-Up

Cardiovascular

Blood pressure and heart rate at baseline, then within the first 2 weeks of starting or changing a stimulant dose, then every 3 months. Discontinue and consider cardiology consultation for sustained tachycardia, a new arrhythmia, or systolic blood pressure persistently above the 95th percentile for age.^[4]

Growth (children and adolescents)

Height and weight at baseline, then every 3-6 months, plotted on growth charts against age/sex norms. Long-term cohort data have not consistently reproduced the modest growth-rate reduction seen in earlier stimulant trials, but ongoing monitoring is still warranted.^[6]^[7]

Psychiatric and sleep

Ask about insomnia, anxiety, irritability, tics, and mood at 1 week, then monthly for the first 3 months, then every 6 months. Ask specifically about suicidal thoughts at initiation, at every dose change, and at discontinuation.

Efficacy

Use standardized rating scales completed by 2 or more informants (for example, home and school) at initiation and at each dose change, then periodically once stable.

Diversion and misuse

Ask about medication storage and security, refill timing, and any behaviours suggestive of misuse at every dispensing encounter — a community pharmacist is often best positioned to notice an emerging pattern.

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.

Treatment Failure / Next Step

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.
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.
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.
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.
Reassess for genuine nonadherence or diversion as a cause of apparent non-response before adding or escalating therapy further.
For a partial responder with tolerable adverse effects, consider adding a low-dose alpha2-agonist adjunct rather than repeatedly escalating the primary agent.
Refer to psychiatry, developmental pediatrics, or a specialized ADHD clinic for complex, treatment-refractory, or diagnostically uncertain presentations.

Common Errors to Avoid

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.

Clinical Decision Algorithm

Initial treatment selection by age

ADHD confirmed: DSM-5-TR criteria met, symptoms present before age 12, evident in 2 or more settings, causing functional impairment

Preschool-age (under 6 years)

1st line: parent training and behaviour management alone

Moderate-to-severe symptoms with clear functional impairment despite adequate behavioural therapy: add methylphenidate, specialist-directed

School-age children, adolescents, and adults

Baseline cardiovascular history/exam, height/weight, and comorbidity screen

No psychosis history, no significant cardiovascular risk, no strong diversion concern

1st line: a long-acting stimulant (methylphenidate-class or amphetamine-class) plus behavioural treatment

Active/historical psychosis, significant cardiovascular risk, active substance use disorder, or strong diversion concern

1st line instead: atomoxetine or guanfacine extended-release plus behavioural treatment

Stimulant trial, response assessment, and switching

Long-acting stimulant started at a low dose

Titrate weekly based on response and tolerability for 3-4 weeks

Adequate response, tolerable adverse effects

Continue at the optimized dose; add a short-acting stimulant dose only if a specific coverage gap remains

Inadequate response, or intolerable adverse effects, at the optimized dose

Switch to the other stimulant class and retitrate

Second stimulant trial adequate

Continue at the optimized dose

Second stimulant trial also inadequate, not tolerated, or contraindicated

Trial atomoxetine or guanfacine extended-release, alone or as an adjunct; reassess the diagnosis and screen for comorbidities

Suspected misuse or diversion

Signs suggesting possible misuse or diversion: early refill requests, requests for a specific short-acting/crushable formulation, missing medication, or third-party reports

Assess further: collateral history, urine drug screen if indicated, screen for a comorbid substance use disorder

Misuse or diversion confirmed, or high suspicion

Switch to a lower-misuse-potential agent (for example, lisdexamfetamine or a non-stimulant), tighten prescribing (shorter intervals, no early refills), and consider an addiction medicine referral

Low suspicion, isolated incident

Reinforce storage/diversion counselling and continue routine monitoring

Drug Tables

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.

Drug	Dosage	Duration of action	Adverse effects	Drug interactions	Comments
Dextroamphetamine (immediate-release)	Children/adolescents: 2.5-5 mg PO twice daily (morning and noon); increase by 2.5-5 mg every 7 days; maximum 20-30 mg per day Adults: Same starting dose and titration; maximum 50 mg per day	About 4 hours	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression, rebound hyperactivity	Avoid MAOIs (hypertensive crisis risk). Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs (serotonin syndrome risk). TCAs and antipsychotics such as chlorpromazine can alter stimulant levels. Acidifying agents (fruit juice, ascorbic acid) decrease absorption; alkalinizing agents (sodium bicarbonate) increase absorption.	Onset usually within the first week. Monitor for abuse/dependence potential and for emergence of manic or psychotic symptoms.
Dextroamphetamine sustained-release spansules	Children/adolescents: 10 mg PO once daily in the morning; increase by 2.5-5 mg every 7 days; maximum 20-30 mg per day Adults: Same starting dose and titration; maximum 50 mg per day	6-8 hours	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression, rebound hyperactivity	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. TCAs and antipsychotics can alter stimulant levels. Acidifying/alkalinizing agents affect absorption as above.	Onset usually within the first week. Capsule contents can be sprinkled on soft food such as applesauce, ice cream, or yogurt.
Lisdexamfetamine	Children, adolescents, and adults (6 years and older): 20-30 mg PO once daily in the morning; increase by 10 mg every 7 days; maximum 60 mg per day	13-14 hours	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. TCAs and antipsychotics can alter stimulant levels.	A prodrug requiring enzymatic conversion to active dextroamphetamine — tampering does not produce a proportionally faster or stronger effect, a genuine advantage when diversion risk is a concern. Capsule contents can be mixed with water or sprinkled on soft food; a chewable tablet formulation is also available.
Mixed salts amphetamine (extended-release)	Children 6-12 years: 5-10 mg PO once daily in the morning; increase by 5 mg every 7 days; maximum 30 mg per day Adolescents 13 years and older, and adults: Same starting dose and titration; maximum 20-30 mg per day	12 hours	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. TCAs and antipsychotics can alter stimulant levels.	Capsule contents can be sprinkled on applesauce and eaten immediately without chewing; doses should not be divided or stored once opened.

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.

Drug	Dosage	Duration of action	Adverse effects	Drug interactions	Comments
Methylphenidate immediate-release tablets	Children, adolescents, and adults (6 years and older): 5 mg PO 2-3 times daily; increase by 5 mg every 7 days; maximum 60 mg per day	3-4 hours	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels. Reduces warfarin metabolism, increasing INR. Carbamazepine decreases methylphenidate levels.	Give the last daily dose before 4 p.m. where possible to avoid insomnia. Doses above 60 mg per day usually do not add further benefit in children.
Methylphenidate sustained-release tablets	Children/adolescents (6 years and older): Once titrated to 20 mg per 8 hours of the immediate-release product: 20 mg PO once daily in the morning; maximum 60 mg per day	About 8 hours	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels. Reduces warfarin metabolism, increasing INR. Carbamazepine decreases methylphenidate levels.	Titrate using the immediate-release product first, then switch once the effective immediate-release total reaches 20 mg per 8 hours. Adult dosing for this specific formulation is not well established — use the equivalent immediate-release approach and consult the product monograph.
Methylphenidate controlled-release capsules (Biphentin)	Children/adolescents 6-17 years: 10-20 mg PO once daily in the morning; increase by 5-10 mg every 7 days; maximum 60 mg per day Adults: Same starting dose and titration; maximum 80 mg per day	10-12 hours (about 40% immediate-release, 60% gradual release)	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels. Reduces warfarin metabolism, increasing INR.	Capsule contents can be sprinkled on soft food such as applesauce, ice cream, or yogurt.
Methylphenidate controlled-release capsules (Foquest)	Children/adolescents 6-17 years: 25 mg PO once daily in the morning; increase by 10-15 mg every 5 days; maximum 70 mg per day Adults: Same starting dose and titration; maximum 100 mg per day	16 hours (about 20% immediate-release, 80% delayed controlled-release)	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels. Reduces warfarin metabolism, increasing INR.	Patients already taking methylphenidate can be converted to the next lower strength based on their total daily methylphenidate dose. Capsule contents can be sprinkled on soft food.
Methylphenidate bilayer controlled-release tablets (Concerta)	Children/adolescents 6-17 years: 18 mg PO once daily in the morning; increase by 9-18 mg every 7 days; maximum 54 mg per day Adults: Same starting dose and titration; maximum 72 mg per day	12 hours (about 22% immediate-release, 78% long-acting release)	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels. Reduces warfarin metabolism, increasing INR.	Generic bilayer products are bioequivalent by regulatory standard, but CADDRA notes an earlier peak concentration, a shorter duration of effect, and reports of symptom destabilization after switching between brand and some generics — confirm the specific product with the prescriber before substituting.
Methylphenidate delayed-release and extended-release capsules (Jornay PM)	Children, adolescents, and adults (6 years and older): 20 mg PO between 6:30-9:30 p.m.; increase by 20 mg every 7 days; maximum 100 mg per day or about 3.7 mg/kg/day	8-10 hour delay, followed by controlled release	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels. Reduces warfarin metabolism, increasing INR.	The only formulation given in the evening — designed to produce symptom control starting the next morning. Beads can be sprinkled on applesauce but should not be chewed. Do not convert directly from another methylphenidate product using a simple ratio — discontinue the prior product and retitrate from the starting dose.
Methylphenidate extended-release oral suspension (Quillivant ER)	Children 6-12 years: 20 mg PO once daily in the morning; increase by 10-20 mg every 7 days; maximum 60 mg per day	12 hours (about 20% immediate-release, 80% long-acting release)	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels.	Health Canada indication is restricted to ages 6-12 years. The oral suspension and the chewable tablet formulation of the same brand are not interchangeable — confirm which specific product is intended.
Methylphenidate extended-release chewable tablets (Quillivant ER)	Children 6-12 years: 20 mg PO once daily in the morning; increase by 10-20 mg every 7 days; maximum 60 mg per day	8-12 hours (about 30% immediate-release, 70% long-acting release)	Anorexia, insomnia, weight loss, irritability, dizziness, headache, abdominal pain; rare psychotic reactions, tachycardia, hypertension, growth suppression	Avoid MAOIs. Theophylline may increase tachycardia/palpitation risk. Caution with SSRIs/SNRIs. May increase phenytoin, phenobarbital, and tricyclic antidepressant levels.	Health Canada indication is restricted to ages 6-12 years. Not interchangeable with the oral suspension formulation of the same brand.

Alpha2-adrenergic agonists

Drug	Dosage	Duration of action	Adverse effects	Drug interactions	Comments
Clonidine	Starting dose: 0.05-0.1 mg per day PO Usual maintenance: 0.003-0.01 mg/kg/day (0.05-0.4 mg per day), once daily or in divided doses	Onset usually 2-3 weeks	Hypotension, sedation, dizziness, dry mouth; may worsen depression	Avoid with TCAs. Additive CNS depression with other sedating agents, including alcohol.	Improves hyperactivity and impulsivity more than inattention. Use caution in cardiovascular disease or depression. Taper by 0.1 mg per week when discontinuing to avoid rebound hypertension.
Guanfacine (extended-release)	Children/adolescents 6-12 years: 1 mg PO once daily; increase by 1 mg every 7-14 days; maximum 4 mg per day Adolescents 13-17 years: Maximum 7 mg per day as monotherapy, or 4 mg per day as an adjunct to a stimulant	Onset usually after 2 weeks	Somnolence, headache, fatigue, upper abdominal pain, irritability, emotional lability, nightmares, bradycardia, mild hypotension	Avoid with TCAs. Additive CNS depression with other sedating agents. Strong CYP3A4 inhibitors (for example, clarithromycin, ketoconazole) significantly increase guanfacine levels; strong CYP3A4 inducers (for example, carbamazepine, rifampin, phenytoin, phenobarbital, systemic dexamethasone) significantly reduce them. Caution with beta-blockers and other agents that lower heart rate or blood pressure, and with QT-prolonging agents.	A selective alpha2A-adrenoceptor agonist — less sedation and hypotension than clonidine. Health Canada indication limited to ages 6-17. Monitor blood pressure and heart rate during and after discontinuation until they normalize. Taper by 1 mg per week when discontinuing.

Norepinephrine reuptake inhibitor

Drug	Dosage	Duration of action	Adverse effects	Drug interactions	Comments
Atomoxetine	Children/adolescents under 70 kg: 0.5 mg/kg/day PO for 10 days, then 0.8 mg/kg/day for 10 days, then 1.2 mg/kg/day; maximum 1.4 mg/kg/day, up to 100 mg per day Adolescents 70 kg and over, and adults: 40 mg per day PO for 10 days, then 60 mg per day for 10 days, then up to 80 mg per day if needed, maximum 100 mg per day	Requires 3-4 weeks for full benefit	Headache, rhinorrhea, upper abdominal pain, nausea, sedation, vomiting, decreased appetite, dizziness, fatigue, emotional lability, small increases in heart rate/blood pressure; rare suicidal ideation, sudden cardiac death, hepatotoxicity, QTc prolongation	Contraindicated with MAOIs. CYP2D6 inhibitors (fluoxetine, paroxetine, quinidine) increase plasma levels. Concurrent salbutamol may increase heart rate.	Not a controlled substance. Normal or rapid CYP2D6 metabolizers may titrate to 1.2 mg/kg/day more quickly; slow metabolizers need a slower titration.

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.

Drug	Dosage	Duration of action	Adverse effects	Drug interactions	Comments
Bupropion	Children: 2-3 mg/kg/day PO Adults: Usual 200-300 mg per day PO in 2 divided doses	May take 2-4 weeks for effect	Agitation, dry mouth, insomnia, headache, constipation, nausea, vomiting, nervousness, sweating, hypertension, tachycardia; dose-related seizure risk	CYP2D6/2B6/3A4 inducers (carbamazepine, phenytoin, rifampin) decrease bupropion levels. Inhibits CYP2D6, raising venlafaxine and tricyclic antidepressant levels. Avoid with MAOIs. Additive seizure-threshold lowering with other agents such as tramadol, ciprofloxacin, or theophylline.	Avoid in a seizure disorder, eating disorder, or significant head-injury history. Single doses should not exceed 150 mg; seizure risk increases above 300 mg per day.
Venlafaxine	Adults: Start 37.5-75 mg PO daily for 1 week; titrate gradually to 150-300 mg per day	May take up to 4 weeks for optimal effect	Nausea, drowsiness, nervousness, dizziness, dry mouth; may increase blood pressure at higher doses	CYP2D6/3A4 inhibitors (clarithromycin, erythromycin, fluoxetine, paroxetine) increase levels. Avoid with MAOIs.	Evidence for ADHD is more limited than for stimulants or atomoxetine; considered mainly in adults with a separate indication for venlafaxine.
Tricyclic antidepressants (desipramine, imipramine, nortriptyline)	Dosing: Individualized and specialist-directed — consult the current product monograph	Less effective than stimulants for core symptoms	Anticholinergic effects, sedation, orthostatic hypotension, cardiac conduction effects; overdose is cardiotoxic	Avoid with MAOIs. Bupropion inhibits CYP2D6, raising TCA levels. Additive QT-prolongation risk with other QT-prolonging drugs.	Reserve for patients who cannot take stimulants, atomoxetine, or bupropion — supporting trial evidence is older and has significant design limitations. Obtain a baseline ECG and periodic ECG monitoring given cardiac conduction risk, especially where overdose risk is a concern.

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

Drug	Dosage	Duration of action	Adverse effects	Drug interactions	Comments
Risperidone	Starting dose: 0.25-0.5 mg PO at bedtime; increase weekly by up to 0.5 mg per day in 2 divided doses Usual maintenance: 0.75-1.5 mg per day PO	Not applicable — not a core ADHD treatment	Weight gain, drowsiness, headache, orthostatic hypotension, dyspepsia, dose-related extrapyramidal effects, hyperprolactinemia	CYP2D6/3A4 inhibitors (clarithromycin, erythromycin, fluoxetine, paroxetine) increase effect/toxicity; CYP2D6/3A4 inducers (carbamazepine, phenytoin, rifampin) reduce effect.	Used only for comorbid behavioural symptoms — hyperactivity, impulsivity, aggression, tics — when stimulant therapy alone is ineffective or not tolerated; does not treat core inattention. Counsel on antipsychotic-associated body-temperature dysregulation (hydration, sun protection).

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

References

Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents — American Academy of Pediatrics (Wolraich ML, Hagan JF Jr, Allan C, et al.). Pediatrics 2019;144(4):e20192528
Canadian ADHD Practice Guidelines, 4.1 Edition — Canadian ADHD Resource Alliance (CADDRA). CADDRA, 4.1 ed., January 2020
Psychosis with Methylphenidate or Amphetamine in Patients with ADHD — New England Journal of Medicine (Moran LV, Ongur D, Hsu J, et al.). N Engl J Med 2019;380(12):1128-1138
Cardiac risk assessment before the use of stimulant medications in children and youth: a joint position statement — Canadian Paediatric Society, Canadian Cardiovascular Society, and Canadian Academy of Child and Adolescent Psychiatry (Hamilton R, Gray C, Belanger SA, et al.). J Can Acad Child Adolesc Psychiatry 2009;18(4):349-355
Association Between Methylphenidate and Amphetamine Use in Pregnancy and Risk of Congenital Malformations — JAMA Psychiatry (Huybrechts KF, Broms G, Christensen LB, et al.). JAMA Psychiatry 2018;75(2):167-175
Effects of Stimulant Medication on Growth Rates Across 3 Years in the MTA Follow-up — Journal of the American Academy of Child and Adolescent Psychiatry (Swanson JM, Elliott GR, Greenhill LL, et al.). J Am Acad Child Adolesc Psychiatry 2007;46(8):1015-1027
Long-term safety of methylphenidate in children and adolescents with ADHD: 2-year outcomes of the ADDUCE study — The Lancet Psychiatry (Man KKC, Hage A, Banaschewski T, et al.). Lancet Psychiatry 2023;10(5):323-333

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.