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Published Online: 1 November 1998

Considering the Role of the Amygdala in Psychotic Illness: A Clinicopathological Correlation

Publication: The Journal of Neuropsychiatry and Clinical Neurosciences

Abstract

For many years, the structures of the medial temporal lobe have been implicated in the pathogenesis of schizophrenia. Recent hypotheses, based on data from MRI and functional imaging, propose that disruption of frontotemporal neural networks may be an anatomical substrate of schizophrenia. Many studies have focused on possible abnormalities of the hippocampus within this network. However, the role of the amygdala has been little studied because of the relative complexity of its structure and the paucity of patients with confined amygdaloid lesions. The authors present a case of chronic psychosis in which postmortem findings reveal lesions in and adjacent to the left amygdala. They use this case to review what is known of the functional anatomy of the amygdala and its possible role in some psychoses.

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Go to The Journal of Neuropsychiatry and Clinical Neurosciences
Go to The Journal of Neuropsychiatry and Clinical Neurosciences
The Journal of Neuropsychiatry and Clinical Neurosciences
Pages: 383 - 394
PubMed: 9813783

History

Published online: 1 November 1998
Published in print: November 1998

Authors

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Julie L. Fudge, M.D.
Received November 11, 1997; revised December 11, 1997; accepted April 16, 1998. From the Departments of Psychiatry, Neurobiology and Anatomy, Pathology and Laboratory Medicine, and Neurology, University of Rochester Medical Center, Rochester, New York. Address correspondence to Dr. Fudge, Department of Neurobiology and Anatomy, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642; e-mail: [email protected]
James M. Powers, M.D.
Received November 11, 1997; revised December 11, 1997; accepted April 16, 1998. From the Departments of Psychiatry, Neurobiology and Anatomy, Pathology and Laboratory Medicine, and Neurology, University of Rochester Medical Center, Rochester, New York. Address correspondence to Dr. Fudge, Department of Neurobiology and Anatomy, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642; e-mail: [email protected]
Suzanne N. Haber, Ph.D.
Received November 11, 1997; revised December 11, 1997; accepted April 16, 1998. From the Departments of Psychiatry, Neurobiology and Anatomy, Pathology and Laboratory Medicine, and Neurology, University of Rochester Medical Center, Rochester, New York. Address correspondence to Dr. Fudge, Department of Neurobiology and Anatomy, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642; e-mail: [email protected]
Eric D. Caine, M.D.
Received November 11, 1997; revised December 11, 1997; accepted April 16, 1998. From the Departments of Psychiatry, Neurobiology and Anatomy, Pathology and Laboratory Medicine, and Neurology, University of Rochester Medical Center, Rochester, New York. Address correspondence to Dr. Fudge, Department of Neurobiology and Anatomy, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642; e-mail: [email protected]

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