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A Dorsolateral Prefrontal Cortex Semi-Automatic Segmenter
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Institution: |
Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta GA 30332 |
Publisher: |
SPIE Medical Imaging |
Publication Date: |
Feb-2006 |
Citation: |
Proceedings of SPIE Medical Imaging 2006; 6144:170-177. |
Keywords: |
Dorsolateral Prefrontal Cortex, Semi-Automatic Segmenter, Segmentation, RuleBasedDLPFCSegmentation |
Appears in Collections: |
NA-MIC, SLICER |
Sponsors: |
NIH Roadmap U54 EB005149 |
Generated Citation: |
Al-Hakim R., Nain D., Melonakos J., Tannenbaum A., Fallon J. A Dorsolateral Prefrontal Cortex Semi-Automatic Segmenter. Proceedings of SPIE Medical Imaging 2006; 6144:170-177. |
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| Paper: | Download, View online |
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Structural, functional, and clinical studies in schizophrenia have, for several decades, consistently implicated dysfunction of the prefrontal cortex in the etiology of the disease. Functional and structural imaging studies, combined with clinical, psychometric, and genetic analysis in schizophrenia have confirmed the key roles played by the prefrontal cortex and closely linked ”prefrontal system” structures such as the striatum, amygdala, mediodorsal thalamus, substantia nigra-ventral tegmental area, and anterior cingulate cortices. The nodal structure of the prefrontal system circuit is the dorsal lateral prefrontal cortex (DLPFC), or Brodmann area 46, which also appears to be the most commonly studied and cited brain area with respect to schizophrenia.1, 2, 3, 4 In 1986, Weinberger et. al. tied cerebral blood flow in the DLPFC to schizophrenia. In 2001, Perlstein et. al. demonstrated that DLPFC activation is essential for working memory tasks commonly deficient in schizophrenia. More recently, groups have linked morphological changes due to gene deletion and increased DLPFC glutamate concentration to schizophrenia.
Additional Material
1 File (189.512kB)
Al-Hakim-SPIE2006-fig8.jpg (189.512kB)