The number of graduating psychiatry residents who choose a career in academic medicine is remarkably small, and the percentage who become National Institutes of Health (NIH)-funded investigators is even smaller. Although this trend for a reduced number of physician-scientists is true in all branches of medicine and has reached criticialproportions, the perception is that this shortage is even more severe in psychiatry. The purpose of this essay is to increase awareness of the problem and begin a discussion of the reasons why the field finds itself in this problematic situation.

First, however, it is important to more clearly define the nature of the problem. At the current time, NIH funding for research and training grants (Research Career Development Awards) has attained unprecedentedly high levels, with the percent of submitted applications that are funded higher than ever thought possible. Physicians who submit NIH grant applications are as successful as their PhD colleagues, dispelling the myth that physicians cannot compete with PhDs for such funding. Others have raised the question as to whether physicians are necessary or even desirable as investigators. In other words, the entire concept of a clinician-scientist is considered by some to be simply passé.

Rumor has it that the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) is on the way. Apart from giving the American Psychiatric Association an enormous financial boost, this should be an opportunity to improve on some of the terrible intellectual lapses of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Revised (DSM-IV-R), to bring DSM and the International Classification of Diseases (ICD) schemes closer together, and to expand on biological and other markers as diagnostic components in the classificatory process. It is hoped that more than the first of these possibilities will be realized.

Since the publication of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, (DSM-III), the DSM manuals have brought a measure of good sense to clinical practice and have improved communication among researchers, so that at least in theory schizophrenia is similar on both sides of the Atlantic, and most probably is similar on both coasts of the United States. The slavish adherence to listed criteria has developed a sense of renewed interest in phenomenology of a practical kind, and exclusion criteria mean that not all individuals who visit a psychiatrist's office can be guaranteed a diagnosis. The distinction between Axis 1 and Axis 2 categories and the removal of any psychoanalytic taints was a stunning acceptance of Jaspers pace Freud.

Although the precise etiologic nature of obsessive-compulsive disorder (OCD), one of the most common psychiatric conditions, is unknown, several findings indicate involvement of the serotonin (5-HT) transporter. Apart from the specific effects of selective 5-HT reuptake inhibitors, other studies show decreased functionality of the platelet 5-HT transporter in OCD. In this report, the authors combine data from two independent studies of patients with OCD, showing both an increased activity of protein kinase type C (PKC) and a decreased activity of protein kinase type A (PKA). The authors propose a unifying hypothesis that OCD might be determined by an imbalance between PKC and PKA, with a prevalence of the former and, more generally, of the phosphoinositide over the cyclic adenosine monophosphate (cAMP) pathway. Should this hypothesis prove correct, the path would be open for new therapeutic interventions in the treatment of OCD.

Over 20 years ago, Monte Buchsbaum first presented metabolic brain images belonging to a patient with schizophrenia at the American Psychiatric Association's annual meeting. This was a truly remarkable achievement brought about by the combined skills of the deoxyglucose technique developed by Lou Sokoloff and colleagues, and the advancement of statistical algorithms for the analysis of computerized images. Positron emission tomography (PET) had arrived, but more importantly, the imaging era of neuropsychiatry was dawning. Since then, we have been treated to a glorious array of technical developments which has seen not only coregistration of functional images (ie, PET) with corresponding structure (magnetic resonance imaging [MRI]), but a proliferation of MRI techniques that allow not only temporal and spatial resolutions undreamed of two decades ago, but permit safe, repeated testing of patients, allowing for experiments of considerable sophistication to be designed.

Now, at any neuroscience meeting, many presentations are accompanied by brain images, often PETs. However, more and more often now we are seeing one form or another of MRI. Such images are displayed from various angles, adorned with multiple colors, and garnished with institutional logos, confirming (and less regularly refuting) the presenter's hypothesis about how the brain is supposed to work in relation to various cerebral functions.

Unraveling the significant complexity of brain-immune interactions could provide essential new insights and potential treatment considerations for the clinical neurosciences. Despite considerable research relating immunological changes to major neuropsychiatric disorders, it has been difficult to establish that immunological processes are involved in the development of central nervous system pathology associated with these disorders. This brief article highlights some of the landmark basic studies and seeks to convey essential principles guiding research in brain-immune interactions. Research in this area often incorporates several disciplines, ranging from psychology and neuroscience to immunology and molecular genetics. The clinical implications of this area of research are discussed, with emphasis on the challenge of disentangling pathogenic factors and valid markers of disease from epiphenomena.

Since before the time of Charcot, nonepileptic seizures (NES) have intrigued and perplexed physicians. With the advent of the electroencephalogram, particularly with the addition of continuous video monitoring, the diagnosis of NES has received increasing evaluation. Characteristic historical features and clinical signs of NES, coupled with new diagnostic techniques, have progressively refined our understanding of the disorder. The treatment of patients who have NES has received much less attention and the prognosis of these patients illustrates the need for a more comprehensive, systematic, and validated intervention. These issues are discussed with an emphasis on the need for future research.

The last decade has seen a shift in the theoretical framework addressing the pathophysiology of psychiatric disorders. During this period, research endeavors have been directed toward investigating the biochemical mechanisms involved in the transduction of information from the cell surface to the cell interior. The emerging picture, supported by growing evidence, is that in addition to neurotransmitters and their receptors, various signal transduction pathways may be linked to the pathophysiology of major psychiatric disorders. In this review, the role of one such pathway—the cyclic adenosine monophosphate (cAMP) signaling pathway—will be highlighted. We review data suggesting the involvement of the upstream and downstream components of this system in the pathophysiology of psychiatric disorders.