2004
DOI: 10.1111/j.1742-1241.2004.00224.x
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Imaging in psychiatric illnesses

Abstract: Brain imaging has given new insights into the structure and function of the brain in psychiatric illnesses. The conditions studied include Alzheimer's disease, Schizophrenia, depression and psychopathic disorders. Emerging technologies in the field of brain imaging have helped in the understanding of pathophysiology, aetiology, diagnosis, treatment response and prognosis of certain psychiatric disorders. This article summarizes the literature available and the potential clinical applications.

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Cited by 12 publications
(2 citation statements)
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References 80 publications
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“…A correlation was only found after reduction of intersubject variation in CMR glc by scaling to the global CMR glc . Scaled CMR glc showed a significant correlation with depression scores in some areas, which have been shown to be affected in depression in former studies: the orbitofrontal cortex, the cingulate gyrus, and the hippocampal region (Gupta et al, 2004;Kimbrell et al, 2002). It should be noted that scaling of CMR glc to global CMR glc can result in scaling artefacts as described for example in the study by Borghammer et al (2008).…”
Section: Discussionmentioning
confidence: 87%
“…A correlation was only found after reduction of intersubject variation in CMR glc by scaling to the global CMR glc . Scaled CMR glc showed a significant correlation with depression scores in some areas, which have been shown to be affected in depression in former studies: the orbitofrontal cortex, the cingulate gyrus, and the hippocampal region (Gupta et al, 2004;Kimbrell et al, 2002). It should be noted that scaling of CMR glc to global CMR glc can result in scaling artefacts as described for example in the study by Borghammer et al (2008).…”
Section: Discussionmentioning
confidence: 87%
“…Although hyperactivation of brain regions has been reported (Callicott et al, 2000;Manoach et al, 2001;Quintana et al, 2001), recent meta-analyses suggest that the most consistent finding is hypoactivation, or increased variability, in frontal and temporal lobes for SP compared with HNV (Davidson & Heinrichs, 2003;Glahn et al, 2005). Although the exact mechanism or mechanisms producing the hypoactivation in SP are still being debated (Callicott et al, 1998;Callicott & Weinberger, 1999Davidson & Heinrichs, 2003;Gupta et al, 2004;Weinberger et al, 1996), possible explanations include disease-related neuronal pathology, neuronal pathology resulting from secondary disease characteristics, inefficient cognitive strategies, medication effects, and differences in behavioral performance.…”
Section: Introductionmentioning
confidence: 99%