DAILY / MAY 7, 2012, VOL. 2, NO. 20   Send Feedback l View Online
Psychiatric News Update
The Voice of the American Psychiatric Association and the Psychiatric Community
twitter facebook facebook
2012 APA's Annual Meeting Special Edition
Schizophrenia Expert Proposes New Model for Understanding Psychosis

Carol TammingaPsychosis may be essentially a disorder of learning and memory mediated by impaired glutamate signaling in the hippocampus, causing disruptions in synaptic encoding of memories, said Carol Tamminga, M.D., who delivered a lecture in APA’s Distinguished Psychiatrist Lecture Series at APA’s annual meeting in Philadelphia. This model for understanding psychosis has important implications for treatment, she said.

Tamminga is a professor and chair of the Department of Psychiatry and chief of translational neuroscience research in schizophrenia at the University of Texas Southwestern Medical School.

In her lecture, titled “Schizophrenia as a Learning and Memory Disorder,” Tamminga provided an overview of the hippocampus and its principal role in modulating memory and learning. She noted that scientists first became interested in exploring this role in the 1950s when Henry Gustav Molaison, an epilepsy patient, had his hippocampus removed in an effort to cure his seizures. In fact, Molaison’s seizures ceased, but he was left without the ability to form memories; he could retain working memory for 10 to 15 memories but was unable to encode declarative memory.

Tamminga outlined the most recent research using hippocampal imaging studies in schizophrenia to identify specific alterations relevant to learning and memory, especially involving the CA3 region of the hippocampus. The latter, she said, normally allows the brain to “scroll through past memories” and form associations with the present. But in patients with psychosis, there appears to be an increase in baseline blood perfusion and decreases in task-related activation.

“Our model for psychosis is that increased CA3-associated activity generates mistakes of association, which are laid down in memory despite their psychotic content,” Tamminga told psychiatrists at the meeting. In other words, overactivation in the CA3 region may cause the brain to form spurious associations that get encoded as memories.

Moreover, this model of psychosis as a disorder of learning and memory mediated by impaired glutamate signaling in the hippocampus appears to account for all forms of psychosis—whether it appears in schizophrenia, bipolar disorder, or epilepsy.

The model has important implications for treatment. These include use of CBT, cognitive remediation or “brain training” exercises; pharmacologic treatments to decrease excitability in the CA3 region including dopamine antagonists and cholinergic agonists; and transcranial magnetic stimulation or other forms of neuromodulation.



 subscribe to blog rss

>>subscribe to blog via email

Copyright © 2012 American Psychiatric Association. All rights reserved.