Over the last two decades, there has been a resurgence of interest in cerebral mechanisms underlying many psychiatric disorders. The changes in our understanding of the syndrome called obsessive-compulsive disorder (OCD) reflect this shift of perspective. Although OCD remains a syndrome that is quintessentially psychiatric, it has been increasingly recognized that it also has a neurological dimension that merits study in its own right, using the concepts and tools of clinical neurology.

This article presents an overview of sensorymotor aspects of obsessive-compulsive disorder (OCD). These phenomena have received less attention than obsessions and compulsions, but are nonetheless important in the development, maintenance, phenomenology, and treatment of the disease. In many individuals, seemingly disparate sensory-motor symptoms can be conceptualized as part and parcel of OCD. Sensory-motor aspects are discussed within the context of faulty information processing and related to neuropsychiatric systems characteristic of OCD. As the pathophysiology of OCD is highly extensive, not all sensory-motor symptoms discussed here will be observed in every individual.

Various schemes have been developed in attempts to define meaningful subtypes of obsessive-compulsive disorder (OCD). A factor analytic approach presumes that the symptom of the disorder can be described by several independent symptom dimensions. The purpose of this study was to explore the neural correlates of three symptom dimensions that were derived from previous factor analyses. Positron emission tomography was used to measure relative regional cerebral blood flow (rCBF) in 14 subjects with OCD while they engaged in a continuous performance task. Clinical indices, including factor scores, we ascertained via structured interviews plus administration of the Yale-Brown Obsessive-Compulsive Scale and checklist. The severity of Factor 1 (religious/aggressive/sexual obsessions and checking) was positively correlated with rCBF in striatum bilaterally. In addition, distinct trends were observed for the other two Factors. These findings provide initial support for a modular neurobiologic model of OCD, where dysfunction within separate component systems may principally mediate independent symptom factors. More important, this nove strategy may represent a powerful new approach to interpreting brain imaging studies of neuropsychiatric diseases.

Brain lesions cause different level change in cerebral function. They may conflict with the existing antagonistic mechanisms between the dorsal and ventral brain. At a clinical level, a dorsal brain lesion may constitute praxis disorders, while a ventral lesion may represent preventive inhibition. Further instinctive symptoms originate in the cingulate gyrus and its connections with the thalamic peduncle. This area may be an importan obsessive-compulsive disorder (OCD) pathway, that is utilized therapeutically during neurosurgical interventions in OCD.

The etiology and treatment of obsessive-compulsive disorder has been explained from a social learning and neurobiological model. In this article a third model is proposed: the biobehavioral model, which encompasses a learning and neurochemical viewpoint. The authors suggest that behavior therapy and medications may operate in the same manner and that behavior therapy may need to be reconceptualized. Animal and human research supporting the interaction of behavioral change and neurochemical processes is presented. The authors also posit that urges precede anxiety and that compulsions are performed in response to the anxiety. Also, obsessions are viewed as secondary to compulsions. The mechanism of how behavior and cognitive-behavioral therapy may produce neurochemical changes is discussed.

Various theories exist concerning the philosophical, biopsychosocial, and anatomic aspects of obsessive-compulsive disorder (OCD). The heterogeneous symptomatology of OCD and the complex interaction between the brain as a physical structure and the mind demands a theory fo OCD that recognizes the disorder as a unified emergent property. A unified theory of OCD is proposed, which incorporates the neurochemical, neuroanatomic, and psychatric underpinnings of this disorder, explor the methods by which OCD pathologies impact the neuroanatomic circuits of the brain, and explains how, through its symptmatology, OCD is “communicated” by the mind to the outside world.

In Washington these days, there is no shortage of people willing to dispense advice about what clinicians can do to impact national mental health policy. The advice and comments that follow reflect one perspective, but it is not that of a psychiatrist, a psychopharmacologist, a nurse, a social worker, or a member of any medical profession. Rather, it is the view of one of the legions of Washington bureaucrats with fancy titles and delusions of grandeur. The difference is that this view happens to have a chemical basis—it comes from a person with a decade of experience dealing firsthand with both manic-depressive illness and mental health policy.