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.

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.

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.