In a recent discussion with David Silbersweig, co-director of the Functional Neuroimaging Laboratory, Weill Medical College of Cornell University, he suggested that there was a convergence emerging between neuropsychiatric and psychodynamic models of psychosis. We are to participate in a panel on neuropsychoanalytic perspectives to be held at NYU in the Spring 2006. The following is an earlier study from their functional neuroimaging lab demonstrating, I believe, that emotions may be critical in the formation of hallucinations & delusions. The popular view of schizophrenia as a neurocognitive disorder is seriously called into question by the research. Those of us who have been emphasizing the significant role of affects/emotions in the initiation as well as the course of psychotic disorders have a strong research base to substantiate these positions.
Annals of the New York Academy of Sciences 877:562-574 (1999) © 1999 New York Academy of Sciences
Mesolimbic Activity Associated with Psychosis in Schizophrenia: Symptom-specific PET Studies, JANE EPSTEINa, EMILY STERN and DAVID SILBERSWEIG
Functional Neuroimaging Laboratory, Weill Medical College of Cornell University, New York, New York 10021, USA
Address for correspondence: Functional Neuroimaging Laboratory, Box 171, Weill Medical College of Cornell University, 525 E 68th St., New York, NY 10021. Voice: 212-746-3976; fax: 212-746-8892; [mailto:jeps@hanazono.med.cornell.edu ]jeps@hanazono.med.cornell.edu
ABSTRACT
Hallucinations and paranoid delusions are prominent among the positive symptoms of schizophrenia. Such psychotic symptoms are notable for their aberrant representations of, and relation to, the external world and for the emotional/motivational valence associated with the representations. As mesolimbic structures, including the amygdala and ventral striatum, are thought to play a significant role in imparting emotional valence to external stimuli, we here examine the mesolimbic findings of H215O PET studies designed to probe the functional neuroanatomy of psychosis.
Patients with schizophrenia (including those with active hallucinations, those with active paranoid delusions, and those without active positive symptoms at the time of scanning) and healthy control subjects were studied. An event-related PET paradigm was used to identify the neural correlates of hallucinations, and a modified emotional stroop paradigm (with threat versus neutral words) was used to test the hypothesis that paranoid patients would have increased mesolimbic activity in response to threat, and even in response to neutral stimuli.
The findings suggest that the positive psychotic symptoms of hallucinations and delusions share similar functional neuroanatomical features of increased mesotemporal and ventral striatal activity in the setting of decreased prefrontal activity. The pattern is evident even in a neutral context, unlike the case for normal subjects, who show such features only in response to threat. The implications of these findings for a pathophysiology of psychosis will be discussed in the context of the behavioral neuroanatomical literature in animals and humans.
Brian Koehler
Anxiety--What Happens in the Brain
Robert Sapolsky, Ph.D., (NARSAD 2004 Distinguished Investigator) of Stanford University, notes that the neurobiological aspects of anxiety are now becoming clearer, with attention focused on the effects of stress and trauma upon the amygdala, its role in mediating conditioned fear, and how repeated major stressors can increase amygdaloid activation of the autonomic nervous system. Specifically, this involves stress enhancing synaptic strength in the amygdala and causing amygdala neurons to form new dendritic branches. The stress effects seem to be mediated by glucocorticoids, the adrenal steroid hormones secreted during stress. Dr. Sapolsky is constructing stress-inducible vectors that will be introduced into the amygdala to express genes that will block amygdale hyperexcitation during a stressful event, or to block downstream steps that mediate the stress-induced increase in amygdala activation. He hopes to better understand fear and anxiety, as well as improve gene therapy for trauma and anxiety.
