LAUSR

increased ratio of 5HT2-D2 antagonism as the mechanism for production of OCS due to SGAs. Aripiprazole has a higher 5HT2/D2 antagonism ratio because of its full antagonist action on 5HT2 and partial agonist action on D2, which may explain the production of OCS in our case. The synergistic effect of preexisting high 5HT2-D2 antagonism ratio of olanzapine may have contributed to it. Olanzapine has lesser D2 affinity (as compared with haloperidol and risperidone) and has not shown efficacy in the treatment of OCS. Whether the resultant reduction of D2 receptor antagonism due to olanzapine withdrawal had any effect in OCS accentuation in our case remains to be seen. Other possible mechanisms, for example, histaminergic, cholinergic, and glutamatergic pathways, have not yet been explored adequately. There is also a possibility of genetic vulnerability leading to the production of OCS under the influence of atypical antipsychotics. Some such candidate polymorphisms have been identified in genes SLC1A1,GRIN2B, andDLGAP3. Overall, none of the available hypotheses could convincingly explain this paradox, and a further scientific inquiry is required in this regard. The United States Food and Drug Administration has recently issued a warning that impulse control disorders (ICDs) including pathological gambling, compulsive eating, shopping, and sexual behaviors have been reported with the use of aripiprazole. Whether such ICDs lie within the obsessivecompulsive spectrum is still debatable due to lack of evidence from basic neurosciences. Research into the mechanisms through which aripiprazole leads to OCS and ICDsmay provide a potential connecting link between the two. In summary, aripiprazolemay be associated with OCSs in some patients, and clinicians need to be careful about this potential adverse drug reaction while prescribing this drug.