CONDITIONS OF USE: The information in this database is intended to supplement, not substitute for, the expertise and judgment of healthcare professionals. The information is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects, nor should it be construed to indicate that use of a particular drug is safe, appropriate or effective for you or anyone else. A healthcare professional should be consulted before taking any drug, changing any diet or commencing or discontinuing any course of treatment.
There are no well controlled studies with Haldol (haloperidol) in pregnant women. There are reports, however, of cases of limb malformations observed following maternal use of Haldol along with other drugs which have suspected teratogenic potential during the first trimester of pregnancy. Causal relationships were not established in these cases. Since such experience does not exclude the possibility of fetal damage due to Haldol, this drug should be used during pregnancy or in women likely to become pregnant only if the benefit clearly justifies a potential risk to the fetus.
The mechanism of action of all first-generation antipsychotics (FGAs) appears to be postsynaptic blockade of brain dopamine D2 receptors. Evidence supporting this mechanism includes strong antagonism of D2 receptors in both cortical and striatal areas [ 1 ], a high correlation between D2 receptor binding and clinical potency [ 2 ], and a consistent requirement of 65 percent D2 receptor occupancy for antipsychotic efficacy in functional imaging studies [ 3 ]. The nonspecific localization of FGA dopamine binding throughout the central nervous system is consistent with their risk of movement disorders and prolactinemia. Aside from their common activity as D2 antagonists, each FGA has distinct effects on neuronal 5-HT2a, alpha-1, histaminic, and muscarinic receptors, which generally correspond to their individual side effect profiles, as shown in the table ( table 1 ).