Animal models of obsessive-compulsive disorder may be derived naturally or generated experimentally. Either may be considered a full or partial model, depending on the extent of resemblance to human OCD. Although many models appear to be valid at first glance, complete models should demonstrate “compelling similarities” in all areas examined. Partial models may have only one or two OCD-like features; however, they still provide some opportunities for research. Criteria to consider when evaluating potential models are etiology, symptomatology, and use in indicating methods of therapy and prevention. Demonstration of common underlying physiological mechanisms, patterns of development and expression, and familial associations are some specific elements to consider when assessing the relevance of more complete models.

Cognitive aspects of OCD are difficult, if not impossible, to explore in animals at present and may be quite different from what is found in humans. It is hard to imagine that animals experience ego-dystonicity; however, dogs with acral lick dermatitis (ALD) that have been scolded by their owners will resort to licking themselves when out of sight, implying that they know it is wrong. Because of the difficulty in evaluating an animal's internal state, some adopt the position that there is no complete animal model of OCD and that animal models are at best partial models. However, children who exhibit compulsive behaviors frequently do not experience accompanying obsessions. Even the expression of OCD in children—for example, licking and walking in geometric designs—resembles what is seen in animals.

In the descriptions that follow, only directly comparable aspects of compulsive behavior in animals will be discussed. Naturally occurring models that appear to correspond most closely to full models may be useful in understanding the fundamental mechanisms underlying OCD and the OC spectrum, including genetics and neurobiology. Experimental models, which may be either full or partial models, could contribute similarly or provide limited but specific information in a targeted area of study, depending on the extent of their similarity to OCD.

A growing body of evidence suggests that obsessive-compulsive disorder (OCD) may be associated with alterations of the serotonin (5-HT) system and that the dorsal raphe nucleus (DRN) may play a role in OCD. In this report, we review this evidence and explore the possible roles of 5-HT and DRN as they relate to OCD.

Although considered rare and intractable until relatively recently, obsessive-compulsive disorder (OCD) is now recognized as a common condition that can be treated. Clomipramine initially dominated the treatment of OCD, but the introduction of the selective serotonin reup-take inhibitors (SSRIs) now allows OCD to be treated without the unpleasant adverse effects associated with the high doses of clomipramine necessary in OCD. Double-blind, placebo-controlled, and active treatment comparison trials showing the efficacy of fluvoxamine and fluoxetine in particular now provide good reasons to consider SSRIs as first-line therapy for OCD.

The obsessive-compulsive spectrum can be divided into two subclusters: disorders of impulsivity and neurologic disorders (Figure 1). This article examines autism (from the neurologic cluster) and pathologic gambling and compulsive shopping (from the impulse side of the spectrum). These three disorders are major mental health problems, impacting on society, the affected individuals, and their families. In addition, these three disorders are underrecognized and underdiagnosed. In this article, we outline and review the phenomenology, psychopathology, and treatment options of these three disorders.

Body dysmorphic disorder (BDD) is characterized by excessive preoccupation with an imagined or greatly exaggerated defect in appearance, and often by related rituals or pursuit of medical or surgical treatments. The frequent comorbidity of BDD with obsessive-compulsive disorder (OCD) and the phenomenological similarities between these two disorders suggest that they may be related. BDD reportedly responds to oral clomipramine (CMI).

We present here two case studies of patients meeting DSM-IV criteria for BDD with comorbid delusional disorder, somatic type, to whom we administered pulse-loaded intravenous (IV) CMI (150 mg on day 1, 200 mg on day 2). After a 4.5-day drug holiday, both patients continued on oral CMI. As reflected in modified Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) scores, both patients' BDD improved by about one third within 4.5 days of the second IV dose. Improvement continued over 2 months on oral CMI, and comorbid major depression present in one patient remitted. By the end of 8 weeks of oral CMI, the patients' modified Y-BOCS scores had decreased about 55%, and their social functioning had markedly improved.

As in OCD, pulse-loaded, IV CMI may produce a much faster response than oral CMI or selective serotonin reuptake treatment and can be well tolerated. This treatment approach to BDD deserves further study in a prospective, randomized controlled trial.