contrast, an earlier double-blind, placebo-controlled trial of pindolol or placebo in conjunction with ﬂuvoxamine showed no differences between groups (Mundo et al 1998). A second approach to treatment refractory OCD outlined by McDougle et al (2000) includes the use of low-dose dopamine antagonists added to existing regimens of SSRIs. Second-generation antipsychotics, for example, may improve the treatment response when added to an SSRI that is only producing a partially favorable response (Starcevic 2005). In a double-blind, placebo-controlled trial, McDougle et al (2000) found that low-dose risperidone was effective in reducing OCD features when added to an SSRI. Similarly, in a double-blind, placebo-controlled study of treatment- refractory subjects with OCD already taking ﬂuoxetine, paroxetine, sertraline, or clomipramine, Bystritsky et al (2004) reported that the addition of the second-generation antipsychotic olanzapine to an SSRI in a double-blind, randomized trial was superior to the placebo group. Some controlled evidence supports the use of intravenous clomip- ramine for treatment-refractory OCD (Fallon and Mathew 2000). Finally, in some severe, treatment-refractory cases, stereotactic cingulotomy or other neurosurgical intervention can be associated with improvement in OCD, although these procedures tend to be reserved for extreme cases (Chang et al 2003; Cosgrove and Rauch 2003; Jung et al 2006). Despite the use of both psychotherapy and pharmacotherapy in OCD, the response to treatment is often suboptimal (McDougle et al 1993), even with augmentation techniques (Bystritsky et al 2004). In fact, according to some estimates, approximately 40% (Dell’Osso et al 2006) to 60% (Fallon and Mathew 2000; Pallanti et al 2002) of patients with OCD have an inadequate response to SSRIs. Further, even some reduc- tion in OCD features still may leave patients with consider- able morbidity (Fallon and Mathew 2000). The prevalence of inadequate response to available OCD treatments argues for a need to consider alternative approaches to the management of OCD. One such potential treatment warranting consideration for use in adult OCD is the SSRI escitalopram. Pharmacology and mechanism of action of escitalopram The SSRI citalopram is a racemic preparation (Lader et al 2004) composed of both right (R) and left (S) stereoisomers (Burke and Kratochvil 2002) in a 1:1 ratio (Sanchez et al 2003). However, biochemistry in vivo appears to be enan- tiomer selective, possibly responding preferentially to only one stereoisomer (Burke and Kratochvil 2002), consistent with findings that it is the S-enantiomer of citalopram Neuropsychiatric Disease and Treatment 2007:3(4) Escitalopram for OCD (ie, escitalopram) that inhibits serotonin reuptake (Hyttel et al 1992). In fact, citalopram’s R-enantiomer appears to be relatively inactive (Dhillon et al 2006). Not only may it be inactive, but ﬁndings suggest that the R-enantiomer of citalopram may actually interfere with the action of the S-enantiomer. For example, Sanchez et al (2003) reported that R-citalopram signiﬁcantly interfered with the anxiolytic- like effect of escitalopram in an animal model. The interference effect of R-citalopram may not extend to other SSRIs, as suggested by ﬁndings showing that R-citalopram did not appear to inhibit the behavioral effects of ﬂuoxetine (Storustovu et al 2004). However, ﬁndings showing that R-citalopram can interfere with S-citalopram provide a rationale for the possibility that S-citalopram could have superior clinical efﬁcacy compared with citalopram, which contains both R and S enantiomers. Moreover, the behavioral effect of escitalopram in the fear conditioned stress animal model of anxiety was greater than the behavioral effect of the dose- equivalent racemic preparation of citalopram, an observation providing additional evidence that the enantiomer speciﬁcity of escitalopram carries an advantage over citalopram, even though citalopram contains escitalopram (Sanchez et al 2003). Finally, equivalent doses of escitalopram increase frontal extracellular serotonin more than does citalopram (Baldwin and Nair 2005). Used in adults for the treatment of depressive and anxiety disorders (Burke 2002), the SSRI escitalopram is simply the S-enantiomer of citalopram (Burke and Kratochvil 2002), a development designed to take advantage of physiological stereoisomer speciﬁcity by producing a drug preparation consisting of only one stereoisomer. Like other SSRIs, escitalopram initiates its biological effects by binding to the serotonin transport molecule (Burke 2002) and increasing the concentration of serotonin in the synapse. A notable feature of escitalopram is that it is the most selective of all the SSRIs, having little or no afﬁnity for 144 other binding sites (Sanchez et al 2003). In addition, escitalopram binds to both the primary, high-afﬁnity site on the serotonin transporter protein, which inhibits serotonin reuptake, and to a low-afﬁnity site that alters binding at the primary site (Dhillon et al 2006). Consistent with ﬁndings showing that R-citalopram is relatively inactive (Dhillon et al 2006), escitalopram binds more than 30 times more potently to the serotonin transporter receptor than does R-citalopram (Burke 2002), providing further support that stereoisomers have biological relevance. Other neurotransmitter receptors may be affected differently by R-citalopram and escitalopram. For example, Sanchez et al (2003) reported that citalopram 457