Our standpoint for characterization of any drugs on sleep is based on three issues: 1) Assessment of drug induced effects on sleep in healthy young volunteers leads to unbiased conclusions about the pharmacological effects of a compound per se. 2) Working hypothesis underlying the scenario states that electrophysiological changes are directly related to the biochemical changes each compound induces in the brain. 3) Only changes on sleep macrostructure do not provide enough information for documenting pharmacological effects on sleep EEG. From a pharmacological perspective, second generation antipsychotic, as a class, may be defined in part as agents with simultaneously serotonin 2A and dopamine 2 antagonist properties. However, no two agents have exactly identical properties, including multiple pharmacologic actions at serotonin and dopamine receptor subtypes and multiple pharmacologic actions at other neurotransmitter receptors. Current knowledge about the parts played by the different transmitters on the control of the sleep-wake continuum, although important, is far for being clearly established. Availability of EEG sleep data on the effects of antipsychotic drugs is more than sparse. No attempts have been made to determine short-term, intermediate-term, or long-term effects. Questions of rebound following withdrawal or of tolerance have not been addressed. Up to date the most robust finding dealing with sleep EEG changes and second generation of antipsychotics is the increase of slow wave sleep (SWS) after drugs, as olanzapine, which show potent 5HT2A/2C antagonism activity. Further adequately designed, justified and analysed studies are certainly needed to advance in the field.