63,64,66,69,71,75,229 This is important because hippocampal neur

63,64,66,69,71,75,229 This is important because hippocampal neurogenesis has been shown to be required for antidepressant response.74 Few studies have examined the effects of pharmacological treatment on brain structure and function in

patients with trauma-related mental disorders. We studied a group of patients with depression and found no effect of fluoxetine on hippocampal volume, although there were increases in memory function230 and hippocampal activation measured with PET during a memory encoding task. Depressed patients with a history of childhood trauma were excluded, and we subsequently have found Inhibitors,research,lifescience,medical hippocampal volume reductions at baseline in women with early abuse and depression but not in women with depression without early abuse;198 this suggests that the study design of excluding patients with early trauma may account for the negative result. Other studies in depression showed that smaller hippocampal volume was a predictor of Inhibitors,research,lifescience,medical resistance to antidepressant treatment.231 Smaller orbitofrontal cortex volume is associated with depression; one study in geriatric depression found smaller orbitofrontal cortex volume,

while length of antidepressant exposure was correlated with larger orbitofrontal volume.232 Several studies have looked at functional brain imaging Inhibitors,research,lifescience,medical response to antidepressants in depression. Single photonemission computed tomography (SPECT) blood flow studies in depression showed that antidepressants increased anterior cingulate, right putamen, and right thalamus function.233 SPECT Xenon-133 studies showed reduced prefrontal function at baseline in depression, with treatment responders showing

Inhibitors,research,lifescience,medical reduced perfusion in prefrontal cortex compared with non-responders after treatment.234 In a fluorodeoxyglucose Inhibitors,research,lifescience,medical (FDG) PET study of brain function patients with depression treated with fluoxetine who had a positive response to treatment had limbic and striatal decreases (subgenual cingulate, hippocampus, insula, and pallidum) and brain stem and selleck chemical dorsal cortical increases (prefrontal, parietal, unless anterior, and posterior cingulate) in function. Failed response was associated with a persistent 1-week pattern and absence of either subgenual cingulate or prefrontal changes.235 Sertraline resulted in an increase in middle frontal gyrus activity in depression measured with PET FDG, as well as increased function in right parietal lobe and visual association cortex.236 Successful paroxetine therapy of depression was associated with increased glucose metabolism measured with PET in dorsolateral, ventrolateral, and medial aspects of the prefrontal cortex, parietal cortex, and dorsal anterior cingulate. Areas of decreased metabolism were noted in both anterior and posterior insular regions (left) as well as right hippocampal and parahippocampal regions.

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