Most antidepressants and other psychotropics in clinical use are available as generic formulations (Table). The availability of lower-priced, generic drugs can benefit patients and third-party payers, but it should not be assumed that all generic drugs are equally beneficial. There are numerous reports in the literature of unexpected and untoward consequences that occur when a generic drug is substituted for the original brand-name drug. A previously stable clinical response may suddenly deteriorate, or the patient may experience new or more severe adverse events (AEs). The United States Food and Drug Administration requires that manufacturers of generic drugs demonstrate that their formulation has pharmacokinetic properties similar (or bioequivalent) to the brand-name drug. Bioequivalency studies are conducted in healthy volunteers, not in patients who would be treated with that drug. Moreover, bioequivalency studies are conducted on a current lot of the branded drug and do not account for variability between lots of the generic formulation. The manufacturer is only required to submit bioequivalency data that support the Abbreviated New Drug Application (ANDA); the FDA does not require disclosure of failed bioequivalence studies. Unlike brand-name drugs, lengthy and costly clinical studies are not required to show that the generic drug is effective and safe.

Although the FDA has taken the position that bioequivalence and therapeutic equivalence are equal, many questions related to the use of generic drugs remain unanswered. The following question-and-answer session is an excerpt of an interview with Pierre Blier, MD, PhD, conducted by Diane Sloan, PharmD, which addresses the issue of generic substitution of psychotropic drugs.

Depersonalization disorder (DPD) is characterized by a subjective sense of detachment from one's own being and a sense of unreality. An examination of the psychobiology of depersonalization symptoms may be useful in understanding the cognitive-affective neuroscience of embodiment. DPD may be mediated by neurocircuitry and neurotransmitters involved in the integration of sensory processing and of the body schema, and in the mediation of emotional experience and the identification of feelings. For example, DPD has been found to involve autonomic blunting, deactivation of sub-cortical structures, and disturbances in molecular systems in such circuitry. An evolutionary perspective suggests that attenuation of emotional responses, mediated by deactivation of limbic structures, may sometimes be advantageous in response to inescapable stress.

Objective: To better understand the efficacy and tolerability of atypical antipsychotics among racial groups, we reviewed data from four short-term (4–6 weeks), fixed-dose, placebo-controlled trials of ziprasidone for black, white, and overall populations of patients with schizophrenia.

Methods: Efficacy of ziprasidone in the black, white, and overall schizophrenic populations was compared to placebo using standard efficacy measures (Positive and Negative Syndrome Scale [PANSS] total, PANSS negative, Brief Psychiatric Rating Scale [BPRS], Clinical Global Impression-Severity [CGI-S], CGI-Improvement [CGI-I]).

Results: Black patients receiving ziprasidone demonstrated statistically significant improvements from baseline in PANSS total, PANSS negative, and BPRS, and improvements in CGI-S and CGI-I (n=99–149) compared with placebo (n=41–66); improvements were comparable to those observed in the overall population (n=451–639) and the white population (n=310–430). Interaction effect (treatment by race) was not significant for any efficacy variables. Ziprasidone was well-tolerated among black patients (n=175). Adjusted mean (least squares mean) overall weight gain in black patients receiving ziprasidone (n=124) was 1.8 kg. There were no increases in total cholesterol, triglycerides, or random glucose in the black population.

Conclusion: Ziprasidone has similar efficacy and safety in black patients with schizophrenia compared with patients in the white and overall populations.

Introduction: Concomitant psychotropic medication (CPM) treatment is common in persons with major depression (MDD). However, relationships with patient characteristics and response to treatment are unclear.

Methods: Participants with nonpsychotic MDD (N=2682) were treated with citalopram, 20–60 mg/day. Sociodemographic, clinical, and treatment outcome characteristics were compared between those using CPMs at study entry or during up to 14 weeks of citalopram treatment, and non-users.

Results: About 35% of participants used a CPM. Insomnia was the predominant indication (70.3%). CPM users were more likely to be seen in primary care settings (69.3% versus 30.7%), be white, of non-Hispanic ethnicity, married, and have a higher income, private insurance, and certain comorbid disorders. CPM users had greater depressive severity, poorer physical and mental functioning, and poorer quality of life than non-users. Response and remission rates were also lower. CPM users were more likely to achieve ≥50 mg/day of citalopram, to report greater side effect intensity, and to have serious adverse events, but less likely to be intolerant of citalopram.

Conclusion: CPMs are associated with greater illness burden, more Axis I comorbidities (especially anxiety disorders), and lower treatment effectiveness. This suggests that CPM use may identify a more difficult to treat population that needs more aggressive treatment.

The basic science literature is replete with descriptions of naturally occurring or experimentally induced pathological grooming behaviors in animals, which are widely considered animal models of obsessive-compulsive disorder (OCD). These animal models rely largely on observed similarities between animal behaviors and human OCD behaviors, and on studies of animal pathological grooming disorders that respond to serotonin enhancing drugs. However, current limitations in assessment of complex cognition and affect in animals precludes the field's ability to match the driving primary processes behind observable phenomenology in animal “OCD” with human behavioral disorders. We propose that excessive grooming behaviors in animals may eventually prove to be equally, or possibly more relevant to, other conditions in humans that involve pathological grooming or grooming-like behaviors, such as trichotillomania, body dysmorphic disorder, olfactory reference syndrome, compulsive skin-picking, and onychophagia. Research is needed to better understand pathological grooming behaviors in both humans and animals, as animal models have the potential to elucidate pathogenic mechanisms and inform the treatment of these psychiatric conditions in humans.