In structural magnetic resonance imaging (MRI) studies of depression, it is reported that there is decreased brain volume in the frontal cortex, hippocampus, striatum, and limbic areas like the subgenual cingulate cortex (Bremner et al, 2000; Bremner, 2002; Bremner et al, 2002; Anand and Shekhar, 2003) . Typically, total brain volume is not significantly decreased. Functional studies in depression, including functional MRI (fMRI), single-photon emission-computed tomography (SPECT), and positron emission tomography (PET), have demonstrated decreased activation in the dorsolateral frontal and anterior cingulate cortex with increased activation of the limbic and paralimbic areas (e.g., amygdala, hippocampus, anterior temporal lobes, thalamus, and basal ganglia) (Soares and Mann, 1997; Anand and Shekhar, 2003).
In anxiety, fMRI studies revealed increased activation in the amygdala (Rauch et al, 2000) . Studies using emission tomography blood flow showed increased glucose metabolism in the orbitofrontal cortex, anterior cingulate cortex, caudate nucleus, and thalamus in obsessive compulsive disorder (Rauch et al, 2001). Utilizing PET and SPECT in neurochemical studies, it has been demonstrated there is a decrease in benzodiazepine receptors throughout the brain, particularly in the hippocampus and precuneus in those with a panic disorder or generalized anxiety disorder (Malizia et al, 1998). Additionally, magnetic resonance spectroscopy (MRS) studies have revealed decreased GABA levels in panic disorder (Goddard et al., 2001).
There is evidence of brain changes occurring in the limbic-cortical-striatal-pallidal-thalamic circuit in both anxiety and depression. These structures include frontal cortex, hippocampus, thalamus, amygdala, putamen, caudate, and basal ganglia (Sheline, 2003) . A complete correspondence between structural impairment in the limbic-cortical-striatal-pallidal-thalamic circuit and resulting depression and anxiety is not confirmed. It is likely that a structural impairment in this circuit results in an increased vulnerability to depression and anxiety (Sheline, 2003).
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