ABSTRACT
Proton magnetic resonance spectroscopy (1H-MRS) has shown inconsistent alterations in the brain metabolites of individuals with chronic pain. We used 3T 1H-MRS to investigate the brain metabolites in the anterior cingulate cortex and thalamus of 22 patients with chronic mild pain and no gait disturbance and 22 healthy controls. The chronic-pain group included patients with chronic low back pain and/or osteoarthritis but none suffering from hypersensitivity. There were no significant between group-differences in glutamate, glutamate plus glutamine (Glx), N-acetylaspartate, glycerophosphorylcholine (GPC), glutamine, creatine plus phosphocreatine, or myo-inositol in the anterior cingulate cortex, but the patients showed a significant decrease in GPC, but not other metabolites, in the thalamus compared to the controls. The GPC values in the patients' thalamus were significantly correlated with pain components on the Short-Form McGill Pain Questionnaire (SF-MPQ-2) and affective empathy components on the Questionnaire of Cognitive and Affective Empathy (QCAE). The GPC in the patients' anterior cingulate cortex showed significant correlations with cognitive empathy components on the QCAE. Myo-inositol in the controls' anterior cingulate cortex and Glx in the patients' thalamus each showed significant relationships with peripheral responsivity on the QCAE. These significances were not significant after Bonferroni corrections. These preliminary findings indicate important roles of GPC, myo-inositol, and Glx in the brain of patients with chronic mild pain.
ABSTRACT
Proton magnetic resonance spectroscopy (1H-MRS) has shown inconsistent alterations in brain metabolites of adults with autism spectrum disorder (ASD). We investigated brain metabolites in the medial prefrontal cortex and amygdala of 24 drug-naive adults with ASD and no intellectual disability and 24 non-ASD control subjects, using 3 T 1H-MRS. Adults with ASD showed no significant differences from control in glutamate, glutamate plus glutamine, N-acetylaspartate, glycerophosphorylcholine plus phosphorylcholine, creatine plus phosphocreatine, or myo-inositol in either region. However, ASD subjects did show significant correlations of localized brain metabolites with autistic traits, empathy deficits, and personality traits using the Autism-Spectrum Quotient, Questionnaire of Cognitive and Affective Empathy, Interpersonal Reactivity Index, and NEO Personality Inventory-Revised. These findings should be taken as preliminary or exploratory.
ABSTRACT
BACKGROUND: The brains of patients with depression exhibit many changes in various regions. Recently, proton magnetic resonance spectroscopy has been used to measure brain metabolites, using saturation bands to shape the volume of interest. Our a priori hypothesis was that myo-inositol and glutamate were downregulated in the hippocampus and amygdala in depression. METHODS: We measured brain metabolites from the medial prefrontal cortex, hippocampus, and amygdala of 22 drug-naïve, first-episode patients with major depressive disorder and 27 healthy control subjects using 3T proton magnetic resonance spectroscopy. RESULTS: Compared with healthy control subjects, patients showed statistically significant reductions in myo-inositol levels in all three regions and reductions in glutamate levels in the medial prefrontal cortex. Furthermore, we found significant decreases in the ratios of glutamate to creatine plus phosphocreatine in the medial prefrontal cortex and amygdala. Additionally, the ratios of glutamine to creatine plus phosphocreatine were also decreased in all three regions examined, although not all the participants presented reliable data. Finally, glutamate levels in the medial prefrontal cortex and amygdala have significant correlations with executive function and those in the hippocampus with memory function. Hippocampal myo-inositol was significantly related to blood cortisol. CONCLUSIONS: Our findings indicated abnormal myo-inositol, glutamate, and glutamine levels in the brains of major depressive disorder patients.
Subject(s)
Amygdala/metabolism , Depressive Disorder, Major/metabolism , Glutamic Acid/metabolism , Glutamine/metabolism , Hippocampus/metabolism , Inositol/metabolism , Adult , Female , Humans , Magnetic Resonance Spectroscopy/methods , Male , Middle Aged , Prefrontal Cortex/metabolism , Temporal Lobe/metabolismABSTRACT
PURPOSE: To determine if magnetic resonance (MR) imaging T2 mapping can be used to quantify histologic tendon healing by using a rabbit Achilles tendon transection model treated with platelet-rich plasma (PRP). MATERIALS AND METHODS: Experiments were approved by the Institutional Animal Care and Use Committee. The Achilles tendons of 24 New Zealand white rabbits (48 limbs) were surgically transected, and PRP (in the test group) or saline (in the control group) was injected into the transection site. The rabbits were sacrificed 2, 4, 8, and 12 weeks after surgery. Thereafter, T2 mapping and histologic evaluations were performed by using the Bonar scale. A mixed-model multivariate analysis of variance was used to test the effects of time and PRP treatment on the T2 value and Bonar grade, respectively. The correlation between the T2 value and Bonar grade was also assessed by using the Spearman correlation coefficient. RESULTS: The Bonar scale values decreased in both groups during tendon healing. The T2 value also shortened over time (P < .001 for both groups). The T2 values were positively correlated with the Bonar grade (ρ = 0.78, P < .001). Both the T2 value and Bonar scale value were lower in the PRP group than in the control group at 4, 8, and 12 weeks; however, there was no significant effect of PRP treatment on the T2 value or Bonar grade. CONCLUSION: The T2 value changes reflected histologic tendon healing. While T2 and Bonar grade were lower at all time points in tendons treated with PRP, there was no significant difference between the treatment and control tendons.