Racemic methylphenidate remains the drug of choice for attention‐deficit hyperactivity disorder (ADHD). Methylphenidate appears to produce psychostimulation by inhibiting the presynaptic uptake of impulse‐released dopamine. The absolute bioavailability of methylphenidate in humans is quite low and variable: mean 23 per cent for the therapeutic (+)‐isomer and 5 per cent for the (−)‐isomer. The primary site of presystemic metabolism may be the gut and/or intestinal wall. Brain concentrations of methylphenidate average eight times that of blood. A Tmax of 1·5–2·5 h, a Cmax of 6–15 ng/ml and a T1/2 of 2–3·5 h are typical. The area under the plasma concentration–time curves for immediate‐release versus sustained‐release formulations are nearly identical, but the relative efficacy is unresolved. Dextroamphetamine has generally been found to compare favourably with methylphenidate in ADHD; it acts through release of newly synthesized dopamine. Levoamphetamine is present as a minor component in a combination product (Adderall®), but the rationale for inclusion of the levo isomer remains unclear. Pemoline appears to both release and block the uptake of dopamine. Though rarely exhibiting sympathomimetic side‐effects, potential hepatotoxicity relegates pemoline to a second‐line status. © 1997 John Wiley & Sons, Ltd.