T2 Mapping of Patellar Cartilage After a Single First-Time Episode of Traumatic Lateral Patellar Dislocation.

BACKGROUND: In most cases, lateral patellar dislocation (LPD) is accompanied by chondral injury and may initiate gradual degeneration of patellar cartilage, which might be detected with a T2 mapping, a well-established method for cartilage lesions assessment. PURPOSE: To examine short-term consequences of single first-time LPD in teenagers by T2 mapping of the patellar-cartilage state. STUDY TYPE: Prospective. POPULATION: 95 patients (mean age: 15.1 ± 2.3; male/female: 46/49) with first-time, complete, traumatic LPD and 51 healthy controls (mean age: 14.7 ± 2.2, male/female: 29/22). FIELD STRENGTH/SEQUENCE: 3.0 T; axial T2 mapping acquired using a 2D turbo spin-echo sequence. ASSESSMENT: MRI examination was conducted 2-4 months after first LPD. T2 values were calculated in manually segmented cartilage area via averaging over three middle level slices in six cartilage regions: deep, intermediate, superficial layers, and medial lateral parts. STATISTICAL TESTS: ANOVA analysis with Tukey's multiple comparison test, one-vs.-rest logistic regression analysis. The threshold of significance was set at P < 0.05. RESULTS: In lateral patellar cartilage, a significant increase in T2 values was found in deep and intermediate layers in both patient groups with mild (deep: 34.7 vs. 31.3 msec, intermediate: 38.7 vs. 34.6 msec, effect size = 0.55) and severe (34.8 vs. 31.3 msec, 39.1 vs. 34.6 msec, 0.55) LPD consequences as compared to controls. In the medial facet, only severe cartilage damage showed significant prolongation of T2 times in the deep layer (34.3 vs. 30.7 msec, 0.55). No significant changes in T2 values were found in the lateral superficial layer (P = 0.99), whereas mild chondromalacia resulted in a significant decrease of T2 in the medial superficial layer (41.0 vs. 43.8 msec, 0.55). DATA CONCLUSION: The study revealed substantial difference in T2 changes after LPD between medial and lateral areas of patellar cartilage. EVIDENCE LEVEL: 2 TECHNICAL EFFICACY STAGE: 2.

Amino acid metabolism in glioma: in vivo MR-spectroscopic detection of alanine as a potential biomarker of poor survival in glioma patients.

PURPOSE: Reprogramming of amino acid metabolism is relevant for initiating and fueling tumor formation and growth. Therefore, there has been growing interest in anticancer therapies targeting amino acid metabolism. While developing personalized therapeutic approaches to glioma, in vivo proton magnetic resonance spectroscopy (MRS) is a valuable tool for non-invasive monitoring of tumor metabolism. Here, we evaluated MRS-detected brain amino acids and myo-inositol as potential diagnostic and prognostic biomarkers in glioma. METHOD: We measured alanine, glycine, glutamate, glutamine, and myo-inositol in 38 patients with MRI-suspected glioma using short and long echo-time single-voxel PRESS MRS sequences. The detectability of alanine, glycine, and myo-inositol and the (glutamate + glutamine)/total creatine ratio were evaluated against the patients' IDH mutation status, CNS WHO grade, and overall survival. RESULTS: While the detection of alanine and non-detection of myo-inositol significantly correlated with IDH wildtype (p = 0.0008, p = 0.007, respectively) and WHO grade 4 (p = 0.01, p = 0.04, respectively), glycine detection was not significantly associated with either. The ratio of (glutamate + glutamine)/total creatine was significantly higher in WHO grade 4 than in 2 and 3. We found that the overall survival was significantly shorter in glioma patients with alanine detection (p = 0.00002). CONCLUSION: Focusing on amino acids in MRS can improve its diagnostic and prognostic value in glioma. Alanine, which is visible at long TE even in the presence of lipids, could be a relevant indicator for overall survival.

Dynamics of γ-aminobutyric acid concentration in the human brain in response to short visual stimulation.

OBJECTIVE: To find a possible quantitative relation between activation-induced fast (< 10 s) changes in the γ-aminobutyric acid (GABA) level and the amplitude of a blood oxygen level-dependent contrast (BOLD) response (according to magnetic resonance spectroscopy [MRS] and functional magnetic resonance imaging [fMRI]). MATERIALS AND METHODS: fMRI data and MEGA-PRESS magnetic resonance spectra [echo time (TE)/repetition time (TR) = 68 ms/1500 ms] of an activated area in the visual cortex of 33 subjects were acquired using a 3 T MR scanner. Stimulation was performed by presenting an image of a flickering checkerboard for 3 s, repeated with an interval of 13.5 s. The time course of GABA and creatine (Cr) concentrations and the width and height of resonance lines were obtained with a nominal time resolution of 1.5 s. Changes in the linewidth and height of n-acetylaspartate (NAA) and Cr signals were used to determine the BOLD effect. RESULTS: In response to the activation, the BOLD-corrected GABA + /Cr ratio increased by 5.0% (q = 0.027) and 3.8% (q = 0.048) at 1.6 and 3.1 s, respectively, after the start of the stimulus. Time courses of Cr and NAA signal width and height reached a maximum change at the 6th second (~ 1.2-1.5%, q < 0.05). CONCLUSION: The quick response of the observed GABA concentration to the short stimulus is most likely due to a release of GABA from vesicles followed by its packaging back into vesicles.

Macromolecular-Suppressed GABA-Edited MR Spectroscopy in the Posterior Cingulate Cortex of Patients With Acute Mild Traumatic Brain Injury.

BACKGROUND: Mild traumatic brain injury (mTBI) causes a number of molecular and cellular alterations. There is evidence of an imbalance between the main excitatory (glutamate, Glu) and the main inhibitory (gamma-aminobutyric acid [GABA]) neurotransmitters following mTBI. In vivo human GABA-Glu balance studies following mTBI are sparse. PURPOSE: To investigate the effect of acute mTBI on the GABA concentration measured in the posterior cingulate cortex (PCC) of pediatric patients by using the macromolecular (MM)-suppressed GABA J-editing technique. STUDY TYPE: Prospective patient and phantom. PARTICIPANTS: A total of 14 pediatric patients (mean age 16.0 ± 1.7) with acute mTBI (<3 days after trauma; Glasgow Coma Scale 15) and 16 healthy volunteers (mean age 16.9 ± 2.8). Phantom: 524 cm3 sphere containing 10 mM glycine, 10 mM GABA. FIELD STRENGTH/SEQUENCE: A 3 T, MEGA-PRESS pulse sequence. ASSESSMENT: GABA spectra were processed in Gannet software. MM-suppressed GABA editing efficiency was derived from the phantom study. Absolute GABA and glutamate + glutamine (Glx) concentrations were quantified using different types of correction and compared between groups. N-acetyl aspartate (NAA) and choline (Cho) levels relative to tCr were also compared. STATISTICAL TESTS: Shapiro-Wilk test, Mann-Whitney U test, Student t-test, Pearson or Spearman correlations. P < 0.01 was considered statistically significant. RESULTS: The MM-suppressed GABA editing efficiency was 0.63. GABA signal fit error was <16% for all participants. The GABA concentration in the PCC of the mTBI group was significantly different from that in healthy controls: GABA/tCr was higher by 27%, absolute GABA concentration with different types of correction was higher by ≈17%. No significant differences were observed in Glx concentrations (P ≥ 0.32) or in Glx/tCr (P ≥ 0.1), NAA/tCr (P = 0.55), and Cho/tCr levels (P = 0.85). DATA CONCLUSION: We report an increase in the GABA concentration in the PCC region in acute mTBI pediatric patients. This may suggest activation of GABA synthesis and impairment of the GABAergic system after acute mTBI. EVIDENCE LEVEL: 3 TECHNICAL EFFICACY: Stage 1.

3T MEGA-PRESS study of N-acetyl aspartyl glutamate and N-acetyl aspartate in activated visual cortex.

OBJECTIVE: To measure N-acetyl aspartyl glutamate (NAAG) and N-acetyl aspartate (NAA) concentrations in visual cortex activated by a continuous stimulation in a 3 T field. METHODS: NAAG and NAA spectra were obtained with MEGA-PRESS pulse sequence (TE/TR = 140/2000 ms; δONNAAG/δOFFNAAG = 4.61/4.15 ppm; δONNAA/δOFFNAA = 4.84/4.38 ppm) in 14 healthy volunteers at rest and upon stimulation by a radial checkerboard flickering at a frequency of 8 Hz. Spectra of all subjects were frequency and phase aligned and then averaged. Additionally, to obtain the time-dependency data, spectra were divided into time sections of 64 s each. The intensities of NAA, NAAG and lactate + macromolecular (Lac + MM) signals were defined by integration of the real part of spectra. The heights of the central resonance of NAAG and NAA signals were measured. RESULTS: The NAAG and NAA concentrations, measured with 2.5% and 0.5% error, respectively, were unaffected by visual activation. A significant increase in the Lac + MM signal by ~ 12% is clearly observed. No stimulation-induced time dependency was found for NAAG or NAA, while the increase in Lac + MM was gradual. The concentration values in visual cortex are in good agreement with the 7 T MRS measurements: [NAAG] = 1.55 mM, [NAA] = 11.95 mM. CONCLUSION: The MEGA-PRESS pulse sequence together with the spectral preprocessing techniques allowed to demonstrate that the concentrations of NAAG and NAA in the visual cortex remain constant during continuous visual stimulation within the margin of error. An increase in the lactate signal intensity signifies the activation of the anaerobic glycolysis in activated visual cortex.

Separate N-acetyl aspartyl glutamate, N-acetyl aspartate, aspartate, and glutamate quantification after pediatric mild traumatic brain injury in the acute phase.

PURPOSE: To separately measure N-acetyl aspartul glutamate (NAAG), N-acetyl aspartate (NAA), aspartate (Asp), and glutamate (Glu) concentrations in white matter (WM) using J-editing techniques in patients with mild traumatic brain injury (mTBI) in the acute phase. METHODS: Twenty-four patients with closed concussive head injury and 29 healthy volunteers were enrolled in the current study. For extended 1 H MRS examination, patients and controls were equally divided into two subgroups. In subgroup 1 (12 patients/15 controls), NAAG and NAA concentrations were measured in WM separately with MEGA-PRESS (echo time/repetition time [TE/TR] = 140/2000 ms; δONNAA / δOFFNAA = 4.84/4.38 ppm, δONNAAG / δOFFNAAG = 4.61/4.15 ppm). In subgroup 2 (12 patients/14 controls), Asp and Glu concentrations were acquired with MEGA-PRESS (TE/TR = 90/2000 ms; δONAsp / δOFFAsp = 3.89/5.21 ppm) and TE-averaged PRESS (TE from 35 ms to 185 ms with 2.5-ms increments; TR = 2000 ms) pulse sequences, respectively. RESULTS: tNAA and NAAG concentrations were found to be reduced, while NAA concentrations were unchanged, after mild mTBI. Reduced Asp and elevated myo-inositol (mI) concentrations were also found. CONCLUSION: The main finding of the study is that the tNAA signal reduction in WM after mTBI is associated with a decrease in the NAAG concentration rather than a decrease in the NAA concentration, as was thought previously. This finding highlights the importance of separating these signals, at least for WM studies, to avoid misinterpretation of the results. NAAG plays an important role in selectively activating mGluR3 receptors, thus providing neuroprotective and neuroreparative functions immediately after mTBI. NAAG shows potential for the development of new therapeutic strategies for patients with injuries of varying severity.

T2 measurement and quantification of cerebral white and gray matter aspartate concentrations in vivo at 3T: a MEGA-PRESS study.

PURPOSE: To measure the transverse relaxation rate (T2 ) of aspartate (Asp) from Asp-edited MEGA-PRESS spectra and use the measured T2 values to estimate the Asp concentrations in gray matter (GM)- and white matter (WM)-dominant brain regions. METHODS: Since Asp-edited MEGA-PRESS spectra contain non-overlapped Asp signals, TE-dependence arising from J-evolution can be considered using phantom MEGA-PRESS spectra acquired with the same parameters as in vivo spectra. Four TE values (90, 115, 140, and 150 ms) were selected from numeric analyses for effective detection of the edited Asp multiplet at ~2.71 ppm. The T2 relaxation time was measured in the anterior cingulate cortex (ACC) of 16 healthy volunteers. Absolute cerebral Asp concentrations were measured with Asp-edited MEGA-PRESS in the ACC and left centrum semiovale (CS) of 44 healthy volunteers at TEs of 90, 115, 140, and 150 ms. RESULTS: The in vivo and phantom T2 values of the edited Asp signals were 165 ± 37 ms and 313 ± 27 ms, respectively. The cortical GM concentration quantified was significantly greater than the WM concentration (2.80 ± 0.31 mM vs. 1.01 ± 0.18 mM). CONCLUSION: MEGA-PRESS is the most common editing method used for low-concentration metabolites detection. Estimation of the absolute Asp concentrations has potential in many research applications, such as studying the processes underlying the reduction of N-acetyl aspartate as well as studying mitochondrial diseases etc. The T2 measurement method described has been successfully applied for edited Asp signals. This method can also be used for other strongly J-coupled signals.