Purpose: To investigate potential pathological differences in major brain metabolites in burning mouth syndrome (BMS). Materials and Methods: We prospectively evaluated eight patients and six healthy controls with sin...Purpose: To investigate potential pathological differences in major brain metabolites in burning mouth syndrome (BMS). Materials and Methods: We prospectively evaluated eight patients and six healthy controls with single voxel magnetic resonance (MR) spectroscopy throughout 2017 using 3-Tesla MR unit. Metabolite levels measured from the left posterior paracingulate white matter. Raw images were processed with Tarquin version 4.3.10 and area under curve values were automatically calculated for GABA (γ-Aminobutyric acid), Ins (myo-inositole), tNAA (N-Acetylaspartate), tCho (total choline), tCr (total creatine) and GLx (glutamine + Glutamat). Major metabolite levels and all metabolites ratio to tCr calculated and compared between two groups using Mann-Whitney U test. Results: GABA/tCR value of the patients (0.589 ± 0.194, median = 0.515) was significantly higher than control group (0.230 ± 0.067, median = 0.220) (P = 0.002). tNAA/tCR value of the patients (1.106 ± 0.218, median: 1.205), was significantly lower than the control group (1.538 ± 0.401, median: 1.705) (P = 0.028). No significant difference was observed between two groups in terms of all other metabolites (P > 0.05). Conclusion: We demonstrated increased GABA and decreased NAA in the left posterior paracingulate region in BMS patients. We suggest that these metabolite alterations in central nervous system might play a key role in the etiology of the disease by inhibiting the suppression of burning sensation.展开更多
文摘Purpose: To investigate potential pathological differences in major brain metabolites in burning mouth syndrome (BMS). Materials and Methods: We prospectively evaluated eight patients and six healthy controls with single voxel magnetic resonance (MR) spectroscopy throughout 2017 using 3-Tesla MR unit. Metabolite levels measured from the left posterior paracingulate white matter. Raw images were processed with Tarquin version 4.3.10 and area under curve values were automatically calculated for GABA (γ-Aminobutyric acid), Ins (myo-inositole), tNAA (N-Acetylaspartate), tCho (total choline), tCr (total creatine) and GLx (glutamine + Glutamat). Major metabolite levels and all metabolites ratio to tCr calculated and compared between two groups using Mann-Whitney U test. Results: GABA/tCR value of the patients (0.589 ± 0.194, median = 0.515) was significantly higher than control group (0.230 ± 0.067, median = 0.220) (P = 0.002). tNAA/tCR value of the patients (1.106 ± 0.218, median: 1.205), was significantly lower than the control group (1.538 ± 0.401, median: 1.705) (P = 0.028). No significant difference was observed between two groups in terms of all other metabolites (P > 0.05). Conclusion: We demonstrated increased GABA and decreased NAA in the left posterior paracingulate region in BMS patients. We suggest that these metabolite alterations in central nervous system might play a key role in the etiology of the disease by inhibiting the suppression of burning sensation.
