Psychiatry Gets More Scientific

Jeffrey A. Lieberman, MD


June 17, 2013

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In This Article

Early Identification in Mental Disorders

Hello. This is Dr. Jeffrey Lieberman of Columbia University, speaking to you for Medscape. Today I am going to talk about a study that recently appeared in Neuron[1] and was published by a research group at Columbia, of which I am a member.

The article is titled, "Imaging Patients With Psychosis and a Mouse Model Establishes a Spreading Pattern of Hippocampal Dysfunction and Implicates Glutamate as a Driver." The first author is my colleague and former student, Scott Schobel, a talented young psychiatric researcher, and the senior author is Dr. Scott Small, a colleague of mine in the Department of Neurology, with whom we collaborate closely.

The reason I wanted to talk about this paper today is that it illustrates 2 things that are fundamentally important to where psychiatry is going. First, the study illustrates the potential power of early identification and intervention in mental disorders and, in this case, in the area of psychotic disorders and schizophrenia in particular. Second, the research reported in this paper illustrates what is called translational research -- the ability to take a clinical problem and to study it preclinically in animals using basic science techniques or to take studies that come from basic science in the laboratory and move them into human studies.

In this case, the article describes a line of investigation that attempted to develop a biomarker to identify individuals who were in the prodromal phase, at risk for the imminent onset of a psychotic episode, and with a presumptive diagnosis of schizophrenia. This was prompted by the fact that the early identification intervention movement, which is focused on the prodrome of psychotic disorders, has devised a strategy to identify people using behavioral, subjectively reported criteria.

The problem with this approach is that it identifies some people who go on, in the ensuing 1-3 years, to have a diagnosable psychotic disorder. But it also identifies many people who don't. So it produces an unacceptably high false positive rate.

It occurred to us that what we needed to enhance the specificity of these diagnostic criteria was some laboratory-based measure that could identify which of the individuals meeting the behavioral criteria for being high risk would, indeed, go on to develop these disorders; in other words, to identify the true positives as opposed to the false positives. To do so, we used a technique that Scott Small developed to distinguish individuals who were suffering from minimal cognitive impairment and who would go on to develop Alzheimer dementia from those who were having benign senile forgetfulness or "senior moments."


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