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Schizophrenia Research Forum: Researcher Profile - Tonya White
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Researcher Profile - Tonya White

First Name:Tonya
Last Name:White
Title:Associate Professor of Child and Adolescent Psychiatry and Radiology
Advanced Degrees:M.D., Ph.D.
Affiliation:Erasmus University Medical Centre
Email Address:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 20 October 2005]
View all comments by Tonya White
Clinical Interests:
Research Focus:
Neurodevelopment, Brain imaging
Work Sector(s):
Web Sites:
Reasearcher Bio
Tonya White, M.D. is currently an assistant professor in the Department of Psychiatry at the University of Minnesota. She graduated from the University of Utah with a Bachelors of Science in Electrical Engineering. She then obtained her Masters Degree in Electrical Engineering from the University of Illinois in Champaign/Urbana and her medical degree from the University of Illinois College of Medicine. She completed her residency in pediatrics, psychiatry, and child and adolescent psychiatry (‘Triple Board Program’) at the University of Utah. Following three years as a junior faculty member in the combined Creighton-Nebraska Department of Psychiatry, she completed a research fellowship in neuroimaging under Dr. Nancy C. Andreasen at the University of Iowa. Dr. White is currently board certified in adult psychiatry and pediatrics. She is board eligible in child and adolescent psychiatry.

Dr. White was recruited to Minnesota in 2001 to join a team of researchers Dr. Charles Schulz has assembled to study psychotic disorders. Tonya’s research interests include the use of neuroimaging tools to study functional brain connectivity in normal development and in pediatric neuropsychiatric disorders, primarily psychotic disorders. Her goals are to merge different imaging modalities (structural imaging, fMRI, diffusion tensor imaging) to better identify and treat children at risk.

Top Papers
White T, Magnotta, V (2006) The application of magnetic resonance imaging to to develop anatomically correct brain models, International Journal for Bioelectromagnetism (In Press).

White T, Andreasen NC, Nopoulos P, Magnotta, V (2003) Gyrification abnormalities in childhood and adolescent onset schizophrenia. Biological Psychiatry 52: 418-426.

White T, Andreasen NC, Nopolous P, Arndt S (2002) Brain volumes and surface morphology in monozygotic twins. Cerebral Cortex 12: 486-493.

Gray D, Parker-Cohen NY, White T, Clark ST, Seiner SH, Achilles J, McMahon WM (2001) A comparison of individual and family psychology of adolescents with chronic fatigue syndrome, rheumatoid arthritis, and mood disorders, J Dev Beh Pediatrics 22: 234-242.

White T, O’Leary DS, Magnotta V, Flaum M, Arndt S, Andreasen NC (2001) Anatomic and functional variability: The effects of filter size in fMRI data analysis. NeuroImage, 13: 577-588.

Stephan KE, Magnotta VA, White T, Flaum M, O’Leary DS, Andreasen NC (2001) Effects of olanzapine on cerebellar functional connectivity in schizophrenic patients during a simple motor task. Psychological Medicine, 31: 1065-1078.

White T, Schulz, SK (2000) Naltrexone in a 3½-year-old boy with self injurious behavior: Am J Psychiatry, 157: 1574-1582.
If resources were not limited, what research projects would you pursue?
I would pursue a comprehensive study of the neurochemical, neurostructural and neurofunctional development of the prefrontal cortex. This would be accomplished in a large group of healthy children and adolescents to better understand normal development. In addition, a group of subjects at high risk would also be evaluated and followed longitudinally. One arm of the study would include a cognitive intervention at an earlier age, being a time when there is greater inherent plasticity.
What is your leading hypothesis?
That the constellation of symptoms associated with schizophrenia (i.e., negative and positive symptoms, cognitive decline, and disruptions of thought), are attributed to alterations in connectivity between brain regions. One area that is our current focus involves white matter development.
What piece of missing evidence would help prove it?
Studies that clearly deliniate the disconnection hypothesis of schizophrenia, especially within a developmental framework. Thus, in essence, a longitudinal study of the development of brain connectivity in healthy controls versus those who later develop schizophrenia.
What is your fallback position?
My fallback question, is can the inherent plasticity of the developing brain be utilized to either prevent, or to decrease the morbidity of those who sufferer from schizophrenia. Although this question is best addressed with a clear understanding of the etiology of the illness, it is not a strict requirement.

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