Magnetization transfer imaging reveals the brain deficit in patients with treatment-refractory depression

Huaxi MR Research Center, Department of Radiology, West China Hospital of Sichuan University, Chengdu, 610041, PR China.
Journal of Affective Disorders (Impact Factor: 3.38). 03/2009; 117(3):157-61. DOI: 10.1016/j.jad.2009.01.003
Source: PubMed


Studies on treatment resistant depression (TRD) using advanced magnetic resonance imaging techniques are very limited.
A group of 15 patients with clinically defined TRD and 15 matched healthy controls underwent magnetization transfer imaging (MTI) and T1-weighted (T1W) imaging. MTI data were processed and analyzed voxel-wised in SPM2. A voxel based morphometric (VBM) analysis was performed using T1W images.
Reduced magnetization transfer ratio was observed in the TRD group relative to normal controls in the anterior cingulate, insula, caudate tail and amygdala-parahippocampal areas. All these regions were identified within the right hemisphere. VBM revealed no morphological abnormalities in the TRD group compared to the control group. Negative correlations were found between MRI and clinical measures in the inferior temporal gyrus.
The cross-sectional design and small sample size.
The findings suggest that MTI is capable of identifying subtle brain abnormalities which underlie TRD and in general more sensitive than morphological measures.

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    • "Some years later, the same authors did another data analysis and noted enlarged cerebroventricles and reduced gray matter in several regions of the left and right hemisphere in TRD subjects compared to the other two groups combined (Shah et al., 2002). Zhang et al. (2009) also examined brain structure in subjects who were already known to suffer from TRD. Using magnetization transfer imaging, they noted differences between TRD subjects and healthy individuals in several regions in the right hemisphere. "
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    ABSTRACT: The search for potential biomarkers of psychiatric disorders is a central topic in biological psychiatry. This review concerns published studies on potential biomarkers of treatment-resistant depression (TRD). The search for biomarkers of TRD in the bloodstream has focused on cytokines and steroids as well as brain-derived neurotropic factor. Additional approaches to identifying biomarkers of TRD have dealt with cerebrospinal fluid analysis, magnetic resonance imaging, and positron emission tomography. Some studies have also investigated potential genetic and epigenetic factors in TRD. Most studies have, however, used a post hoc experimental design that failed to determine the association between biomarkers and the initial risk of TRD. Particular attention in future studies should be on shifting the experimental paradigm toward procedures that can determine the risk for developing treatment resistance in untreated depressed individuals.
    Full-text · Article · Jun 2013 · Frontiers in Psychiatry
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    • "Major depression is a common condition and a leading cause of disability worldwide [1]. Approximately 5% of American adults are affected by depression each year, 30% of whom fail to respond to two or more types of antidepressant, a phenomenon termed treatment-resistant depression (TRD) [2-7]. The pathogenesis of major depressive disorder (MDD) and the pathogenic mechanism of TRD remain unclear. "
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    ABSTRACT: Background White matter abnormalities can cause network dysfunction that underlies major depressive disorder (MDD). Diffusion tensor imaging (DTI) is used to examine the neural connectivity and integrity of the white matter. Previous studies have implicated frontolimbic neural networks in the pathophysiology of MDD. Approximately 30% of MDD patients demonstrate treatment-resistant depression (TRD). However, the neurobiology of TRD remains unclear. Methods We used a voxel-based analysis method to analyze DTI data in young patients with TRD (n = 30; 19 males, 11 females) compared with right-handed, age- and sex-matched healthy volunteers (n = 25; 14 males, 11 females). Results We found a significant decrease in fractional anisotropy (FA) (corrected, cluster size >50) in the left middle frontal gyrus (peak coordinates [−18 46–14]), left limbic lobe uncus (peak coordinates [−18 2–22]), and right cerebellum posterior lobe (peak coordinates [26–34 -40]). There was no increase in FA in any brain region in patients. We also found a significant negative correlation between mean regional FA values in the three areas and Beck Depression Inventory symptom scores. Conclusions We found significant differences in white matter FA in the frontal lobe, limbic lobe and cerebellum between TRD patients and controls. These data suggest that abnormalities of cortical-limbic-cerebellar white matter networks may contribute to TRD in young patients.
    Full-text · Article · Mar 2013 · BMC Psychiatry
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    • "Shan et al. have identified gray matter density or volume reductions in ACC, frontal, temporal, and parahippocampal areas [Shah et al., 2002]. In our previous study of TRD using magnetization transfer imaging [Zhang et al., 2009], reduced magnetization transfer ratio, indicative of abnormalities of brain tissue composition, was observed in the ACC, insular and parahippocampal areas. Other attempts to find metabolic or functional alterations in TRD have revealed increased blood flow in hippocampus-amygdala in TRD compared to both NDD and healthy controls [Hornig et al., 1997], and hypometabolism in cingulate, insula, frontal, and temporal areas in TRD, in association with different components of the severity and course of illness [Kimbrell et al., 2002]. "
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    ABSTRACT: Treatment-refractory depression (TRD) represents a large proportion of the depressive population, yet has seldom been investigated using advanced imaging techniques. To characterize brain dysfunction in TRD, we performed resting-state functional MRI (rs-fMRI) on 22 TRD patients, along with 26 matched healthy subjects and 22 patients who were depressed but not treatment-refractory (NDD) as comparison groups. Results were analyzed using a data-driven approach known as Regional Homogeneity (ReHo) analysis which measures the synchronization of spontaneous fMRI signal oscillations within spatially neighboring voxels. Relative to healthy controls, both depressed groups showed high ReHo primarily within temporo-limbic structures, and more widespread low ReHo in frontal, parietal, posterior fusiform cortices, and caudate. TRD patients showed more cerebral regions with altered ReHo than did NDD. Moderate but significant correlations between the altered regional ReHo and measures of clinical severity were observed in some identified clusters. These findings shed light on the pathophysiological mechanisms underlying TRD and demonstrate the feasibility of using ReHo as a research and clinical tool to monitor persistent cerebral dysfunction in depression, although further work is necessary to compare different measures of brain function to elucidate the neural substrates of these ReHo abnormalities.
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