Coghill 2007.

Study characteristics
Methods	12‐week randomised, placebo‐controlled, double‐blind cross‐over trial with 3 interventions: MPH 0.3 mg/kg MPH 0.6 mg/kg placebo
Participants	Number of participants screened: not stated Number of participants included: 75 (all boys) Number of participants followed up: not stated Number of withdrawals: not stated Diagnosis of ADHD: DSM‐IV (combined type); ICD‐10 (hyperkinetic disorder) Age: mean not reported (range 7‐15 years) IQ: > 80 MPH‐naive: 100% Ethnicity: not stated Country: UK Setting: outpatient clinic Comorbidity: ODD (41.3%), CD (28%), depressive disorder (4%), generalised anxiety disorder (2.7%), separation anxiety disorder (4%), tic disorder (2.7%), social phobia (1.3%) Comedication: not stated Other sociodemographics: none Inclusion criteria Eligible boys (scoring 1.5 SD from the mean on both CPRS Short Version, and CTRS Short Version) were interviewed by an experienced child and adolescent psychiatrist using the K‐SADS‐PL Those meeting criteria for hyperkinetic disorder (HD F 90) (ICD‐10) and combined subtype (DSM‐IV) were invited to participate Exclusion criteria History of neurological impairment/learning disability IQ < 80 Chronic physical illness Sensory or motor impairment Current or previous exposure to stimulant medication Abuse of any illegal drugs
Interventions	Participants were randomly assigned to 1 of 3 possible drug condition orders: 0.3 mg/kg/dose MPH or 0.6 mg/kg/dose MPH and placebo Administration schedule: twice daily Duration of each medication condition: 4 weeks Washout before trial initiation: no Titration period: none Treatment compliance: assessed by pill count and clinical enquiry but not further described
Outcomes	ADHD symptoms CGI, Parent Version and Teacher Version (10 item): rated by parents and teachers, each after 4 weeks
Notes	Sample calculation: no Ethics approval: yes Key conclusions of trial authors Chronic MPH (MPH administered two cross‐over periods in a row) predominantly enhanced neuropsychological functioning on "recognition memory" component tasks with modest "executive" demands Neuropsychological measures offer only modest contributions to the prediction of clinical responses to MPH in ADHD Comment from trial authors Doses (0.3 mg/kg and 0.6 mg/kg) were chosen to reflect low‐ and high‐dose regimens, respectively Exclusion of MPH non‐responders/children who have previously experienced AEs while taking MPH before randomisation: no Any withdrawals due to AEs: no Funding source: supported by a local trust through a Tenovus Scotland initiative Email correspondence with trial authors in 2013. Emailed trial authors twice with a request for additional information regarding protocol and number of participants on which analyses were based. Have not received a reply
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Participants were randomly assigned by an independent clinical trials pharmacist (using a computer‐generated random number sequence with block design to ensure equal numbers in each treatment arm)
Allocation concealment (selection bias)	Low risk	Participants were randomly assigned by an independent clinical trials pharmacist
Blinding of participants and personnel (performance bias) All outcomes	Unclear risk	Placebo‐controlled, double‐blind, no further information
Blinding of outcome assessment (detection bias) All outcomes	Low risk	Clinical status was assessed by interview conducted by an experienced, blinded child and adolescent psychiatrist. Double‐blind
Incomplete outcome data (attrition bias) All outcomes	High risk	No description about how many participants were included in analyses Selection bias (e.g. titration after randomisation → exclusion of MPH non‐responders or placebo responders): not stated
Selective reporting (reporting bias)	Unclear risk	No protocol identified