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Background: Reductions in total hippocampus volume have frequently been reported in MRI studies in major depressive disorder (MDD), but reports of differences in total amygdala volume have been inconsistent. Childhood maltreatment is an important risk factor for MDD in adulthood and may affect the volume of the hippocampus and amygdala. In the present study, we examined associations between the volumes of the amygdala subnuclei and hippocampal subfields and history of childhood maltreatment in participants with MDD. Methods: We recruited 35 patients who met the DSM-IV criteria for MDD and 35 healthy controls. We acquired MRI data sets on a 4.7 T Varian Inova scanner. We manually delineated the amygdala subnuclei (lateral, basal and accessory basal nuclei, and the cortical and centromedial groups) and hippocampal subfields (cornu ammonis, subiculum and dentate gyrus) using reliable volumetric methods. We assessed childhood maltreatment using the Childhood Trauma Questionnaire in participants with MDD. Results: In participants with MDD, a history of childhood maltreatment had significant negative associations with volume in the right amygdala, anterior hippocampus and total cornu ammonis subfield bilaterally. For volumes of the amygdala subnuclei, such effects were limited to the basal, accessory basal and cortical subnuclei in the right hemisphere, but they did not survive correction for multiple comparisons. We did not find significant effects of MDD or antidepressant treatment on volumes of the amygdala subnuclei. Limitations: Our study was a cross-sectional study. Conclusion: Our results provide evidence of negative associations between history of childhood maltreatment and volumes of medial temporal lobe structures in participants with MDD. This may help to identify potential mechanisms by which maltreatment leads to clinical impacts., Introduction Major depressive disorder (MDD) causes disability around the world, (1) and its etiology remains uncertain, although changes in the hippocampus and amygdala have been suggested as potentially important. (2) [...]

Background: Imaging studies of pain processing in primary psychiatric disorders are just emerging. This study explored the neural correlates of stress-induced analgesia in individuals with posttraumatic stress disorder (PTSD). It combined functional magnetic resonance imaging (fMRI) and the traumatic script-driven imagery symptom provocation paradigm to examine the effects of trauma-related cues on pain perception in individuals with PTSD. Methods: The study included 17 patients with PTSD and 26 healthy, trauma-exposed controls. Participants received warm (nonpainful) or hot (painful) thermal stimuli after listening to a neutral or a traumatic script while they were undergoing an fMRI scan at a 4.0 T field strength. Results: Between-group analyses revealed that after exposure to the traumatic scripts, the blood oxygen level-dependent (BOLD) signal during pain perception was greater in the PTSD group than the control group in the head of the caudate. In the PTSD group, strong positive correlations resulted between BOLD signal and symptom severity in a number of brain regions previously implicated in stress-induced analgesia, such as the thalamus and the head of the caudate nucleus. Trait dissociation as measured by the Dissociative Experiences Scale correlated negatively with the right amygdala and the left putamen. Limitations: This study included heterogeneous traumatic experiences, a different proportion of military trauma in the PTSD versus the control group and medicated patients with PTSD. Conclusion: These data indicate that in patients with PTSD trauma recall will lead in a state-dependent manner to greater activation in brain regions implicated in stress-induced analgesia. Correlational analyses lend support to cortical hyperinhibition of the amygdala as a function of dissociation., Introduction Despite evidence that pain preferentially recruits affective pain systems in patients with chronic pain (1-3) and strong epidemiological links between disorders of mood, anxiety and chronic pain, (4) imaging [...]

Background: Previous magnetic resonance imaging (MRI) studies of patients with major depressive disorder (MDD) have consistently shown bilateral and unilateral reductions in hippocampal volume relative to healthy controls. Recent structural MRI studies have addressed the question of whether changes in the volume of hippocampal subregions may be associated with MDD. Methods: We used a comprehensive and reliable 3-dimensional tracing protocol that enables delineation of hippocampal subregions (head, body, tail) to study changes in the hippocampus of patients with MDD. We recruited 39 MDD patients (16 medicated, 23 unmedicated) and 34 healthy age- and sex-matched controls. We acquired images using a magnetization-prepared rapid acquisition gradient echo sequence on a 1.5-T scanner with a spatial resolution of 1.5 mm x 0.5 mm x 0.5 mm. We performed volumetric analyses, blinded to diagnosis, using the interactive software package Display. All volumes were adjusted for intracranial volume. Results: We found a significant reduction in the volume of the hippocampal tail bilaterally, right hippocampal head and right total hippocampus in MDD patients. Medicated MDD patients showed increased hippocampal body volume compared with both healthy controls and unmedicated patients. Limitations: This study was cross-sectional. Further prospective studies are needed to determine the direct effect of antidepressant treatment. Conclusion: Our results suggest that decreased hippocampal tail and hippocampal head volumes could be trait changes, whereas hippocampal body changes may be dependent on treatment. We showed that long-term antidepressant treatment may affect hippocampal volume in patients with MDD., Introduction Because of its roles in cognition and regulation of the hypothalamic --pituitary--adrenal (HPA) axis, the hippocampus is one of several limbic structures that has been extensively studied in individuals [...]

The information in this column is not intended as a definitive treatment strategy but as a suggested approach for clinicians treating patients with similar histories. Individual cases may vary and [...]

A new 1H-MRS filtering strategy for selective measurement of glycine (Gly) in human brain in vivo at 3.0T is proposed. Investigation of multiple refocusing following a 90° excitation pulse indicated that triple refocusing is most effective for suppression of the strongly coupled resonances of myo-inositol (mI) at the Gly 3.55-ppm resonance. The echo times of the triple refocusing were optimized, with numerical analysis of the filtering performance, as {TE1, TE2, TE3} = {67, 62, 69} ms. Compared with the 90°-acquired mI signal the mI suppression ratios of the filter were 170 and 1000, in terms of peak amplitude and area, respectively, between 3.51 and 3.59 ppm. From LCModel analyses, using density-matrix calculated spectra as basis functions, the concentration of Gly in parieto-occipital cortex of healthy adults was estimated to be 0.5 ± 0.1 mM (mean ± SD, n = 6), with reference to creatine at 8 mM. Magn Reson Med, 2007. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

The proton NMR transverse relaxation time T2 of glutamate (Glu) in human brain was measured by means of spectrally selective refocusing at 3.0 T in vivo. An 81.4-ms-long dual-band Gaussian 180° RF pulse, designed for refocusing at 2.35 and 3.03 ppm, was employed within point-resolved spectroscopy (PRESS) to generate the Glu C4-proton target multiplet and the total creatine (tCr) singlet. Six optimal echo times (TEs) between 128 and 380 ms were selected from numerical analysis of the filtering performance for effective detection of the Glu signal with minimal contamination from glutamine (Gln), N-acetylaspartate (NAA), and glutathione (GSH). The magnetization of Glu and tCr was extracted from spectral fitting of experimental and calculated spectra. Apparent T2 values of Glu and tCr were estimated as 201 ± 18 and 164 ± 12 ms for the medial prefrontal (PF) cortex, and 198 ± 22 and 169 ± 15 ms (mean ± SD, N = 5) for the left frontal (LF) cortex, respectively. With water segmentation data, the magnetization values of Glu and tCr of the two adjacent voxels, calculated from the T2 values and spectra following the thermal equilibrium magnetization, were combined to give the Glu and tCr concentrations as 10.37 ± 1.06 and 8.87 ± 0.56 mM for gray matter (GM), and 5.06 ± 0.57 and 5.16 ± 0.45 mM (mean ± SD, N = 5) for white matter (WM), respectively. Magn Reson Med, 2006. © 2006 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

An optimized single-shot proton double-quantum (DQ) filter for the quantification of γ-aminobutyric acid (GABA) levels in human brain is reported. It is demonstrated that creation of DQ coherences following dual-resonance-selective refocusing gives a theoretical editing efficiency of 50% for the detection of the GABA resonance at 3.01 ppm. The sequence times are optimized with both numerical and experimental analyses of the editing performance, giving an experimental editing efficiency of 42%. It is acknowledged that homocarnosine is partially coedited, leading to a 20% contribution to the edited signal; however, macromolecule contamination is negligible in vivo under these experimental conditions. The GABA concentration in human prefrontal cortex is estimated to be 0.8 ± 0.1 μmol/g (mean ± SD, n = 6), with reference to the internal standard creatine at 9 μmol/g. Magn Reson Med 54:272-279, 2005. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

An optimized single-shot proton double-quantum (DQ) filter for the quantification of gamma-aminobutyric acid (GABA) levels in human brain is reported. It is demonstrated that creation of DQ coherences following dual-resonance-selective refocusing gives a theoretical editing efficiency of 50% for the detection of the GABA resonance at 3.01 ppm. The sequence times are optimized with both numerical and experimental analyses of the editing performance, giving an experimental editing efficiency of 42%. It is acknowledged that homocarnosine is partially coedited, leading to a 20% contribution to the edited signal; however, macromolecule contamination is negligible in vivo under these experimental conditions. The GABA concentration in human prefrontal cortex is estimated to be 0.8 +/- 0.1 micromol/g (mean +/- SD, n = 6), with reference to the internal standard creatine at 9 micromol/g., (2005 Wiley-Liss, Inc)