In addition to these methodological issues, it is important to bear in mind that imaging findings do not tell us about causal mechanisms. They tell us about associations between a condition and brain involvement, but do not help distinguish between cause, effect, or epiphenomena (for a review of this issue, see: Peterson BS100). For example, from the studies of prenatal cocaine and methamphetamine exposure, we might speculate that the findings identified in fMRI43 MRS85, DTI37 and cerebral blood flow41 studies could well represent either direct effects or involvement of compensatory mechanisms related to other (as yet unknown) areas of the brain. Nor do we know the developmental course of these findings; whether these alterations were present at birth, how the early brain changes from prenatal exposure might impact normative processes of brain development and maturation, and how the postnatal environment may be involved in shaping brain architecture, structure and function. To date, there are no repeated measures studies of children with prenatal drug exposure that would enable us to know whether neuroimaging findings persist over time or if other findings