Impact of Quadriceps Tendon Graft Thickness on Electromechanical Delay and Neuromuscular Performance After ACL Reconstruction.

Background: Both partial- and full-thickness quadriceps tendon (QT) graft harvests are used for anterior cruciate ligament reconstruction (ACLR). Purpose: To evaluate the impact of QT graft harvest depth (full or partial thickness) on electromechanical delay (EMD), peak torque (PT), and rate of torque development (RTD) after ACLR. Study Design: Controlled laboratory study. Methods: A total of 26 patients who underwent either partial-thickness (n = 14) or full-thickness (n = 12) autograft QT ACLR were recruited between June and November 2021 (>1 year before participation). Patients performed isokinetic knee extension testing with surface electromyography of the quadriceps muscles. Mixed repeated-measures analysis of variance with least significant difference post hoc testing was used to determine significant differences (mean difference [MD] ± SE) or interactions for all variables. Results: A significant speed×depth interaction was seen for the vastus medialis (P = .005). Pairwise analyses showed significantly longer EMD for the partial-thickness graft than the full-thickness graft (MD ± SE, 19.92 ± 6.33 ms; P = .006). In the partial-thickness graft, the EMD was significantly longer at 90 deg/s versus 180 deg/s (MD ± SE, 19.11 ± 3.95 ms; P < .001) and 300 deg/s (MD ± SE, 16.43 ± 5.30 ms; P = .006). For PT, the full-thickness graft had a significantly lower PT on the operated versus nonoperated side at all speeds (MD ± SE: 90 deg/s, -57.0 ± 10.5 N·m, P < .001; 180 deg/s, -26.0 ± 10.2 N·m, P = .020; 300 deg/s, -20.3 ± 8.9 N·m, P = .034). For RTD, the full-thickness graft showed significantly Slower RTD for the operated versus nonoperated side at all time points (MD ± SD: RTD0-25 (0-25% of the range of motion), -131.3 ± 50.9 N·m/s, P = .018; RTD25-50, -197.0 ± 72.5 N·m/s, P = .014; RTD50-75, -113.3 ± 39.8 N·m/s, P = .013; RTD75-100, -149.4 ± 35.9 N·m/s, P < .001). Conclusion: Compared with partial-thickness QT, full-thickness QT showed a shorter vastus medialis EMD at higher loading, and therefore greater stiffness, as well as slower RTD and lower PT across all testing speeds. Clinical Relevance: The impact of full-thickness QT autograft on EMD and neuromuscular performance should be considered for ACLR.

The Associations Between Quadriceps Tendon Graft Thickness and Isokinetic Performance.

BACKGROUND: Anterior cruciate ligament reconstruction (ACLR) using the quadriceps tendon is an increasingly popular technique. Both partial-thickness quadriceps tendon (PT-Q) and full-thickness quadriceps tendon (FT-Q) graft depths are employed. HYPOTHESIS/PURPOSE: This study was designed to assess isokinetic peak torque, average power, and total work during knee extension in patients with FT-Q or PT-Q grafts for ACLR. We hypothesized that both groups would show lower isokinetic values for the operated side, with greater deficits in the FT-Q group than in the PT-Q group. STUDY DESIGN: Cohort study; Level of evidence, 3. METHODS: A total of 26 patients who underwent ACLR with either an FT-Q or PT-Q graft were recruited between June 2021 and November 2021. Patients underwent isokinetic knee extension testing at > 1 year after surgery. Mixed repeated-measures analysis of covariance with least square difference post hoc testing was used to determine significant differences or interactions for all variables. RESULTS: Peak torque was significantly lower for the operated limb than the nonoperated limb in the FT-Q group (mean difference [MD] ± standard error [SE], -38.6 ± 8.3 Ncm [95% CI, -55.7 to -21.5 Ncm]; P < .001; d = 0.90) but not in the PT-Q group (MD ± SE, -7.3 ± 7.7 Ncm [95% CI, -23.2 to 8.5 Ncm]; P = .348; d = 0.20). Similarly, average power for the operated limb was lower than that for the nonoperated limb in the FT-Q group (MD ± SE, -53.6 ± 13.4 W [95% CI, -81.3 to -26.9 W]; P < .001; d = 0.88) but not in the PT-Q group (MD ± SE, -4.1 ± 12.4 W [95% CI, -29.8 to 21.5 W]; P = .742; d = 0.07), and total work was lower for the operated limb compared with the nonoperated limb in the FT-Q group (MD ± SE, -118.2 ± 27.1 J [95% CI, -174.3 to -62.2 J]; P < .001; d = 0.96) but not in the PT-Q group (MD ± SE, -18.3 ± 25.1 J [95% CI, -70.2 to 33.6 J]; P = .472; d = 0.15). CONCLUSION: The FT-Q group showed significant deficits in the operated limb compared with the nonoperated limb for all isokinetic variables. In contrast, no significant differences were found between the nonoperated and operated limbs for the PT-Q group.

Intradural symptomatic arachnoid cyst formation following non-instrumented lumbar decompression.

PURPOSE: Intradural arachnoid cyst is a rare complication of lumbar puncture, post-trauma or post-intraoperative durotomies. We aim to estimate the incidence of early intradural arachnoid cyst radiologically in non-instrumented posterior lumbar decompression among symptomatic patients, and establish clinical correlation. MATERIALS AND METHODS: Patients who underwent lumbar decompression without instrumentation at a tertiary spinal service between December 2014 and January 2018 were identified. When MRI scans were performed post-operatively within 14 days, imaging, medical and operative records were reviewed by two consultant neuroradiologists. RESULTS: 488 operations were included. 46 operations were followed by an early MRI scan. 59% were requested to investigate new or ongoing pain. Ten demonstrated an intradural arachnoid cyst - seven had no documented durotomy. Eight were primary operations, three were emergency operations. Statistically, we have not identified durotomy, primary-vs-revision surgery, and elective-vs-emergency surgery as risk factors. Two patients required revision operations, of these, one had a repeat post-operative scan, where the cyst resolved following further decompression at the index level, without intradural exploration. CONCLUSIONS: Intradural arachnoid cyst may complicate posterior lumbar decompression. To our knowledge, this is the first study to assess its incidence as an early post-operative radiological finding, which is likely to be commoner than we recognise. It may be a cause of persisting post-operative pain.

Sarcoidosis--the greatest mimic.

Little is known regarding the exact pathogenesis of sarcoidosis, but it is widely recognized that it affects multiple organs. The presentation and imaging features can be nonspecific, and this is the reason why it is a great mimic of other diseases. Diagnosis of sarcoidosis is often prompted initially by clinical suspicion. Imaging plays a crucial role in both detection and monitoring of disease process. This review is a case-based systemic approach looking at various systemic manifestation of the disease presenting real clinical encounters using various imaging modalities.

Red blood cell arginase suppresses Jurkat (T cell) proliferation by depleting arginine.

BACKGROUND: Transfusion of packed red blood cells (PRBC) suppresses immunity, but the mechanisms are incompletely understood. PRBCs contain arginase, an enzyme which converts arginine to ornithine and depletes arginine in vitro. Arginine depletion suppresses proliferation of Jurkat T cells in other models. We hypothesize that PRBC arginase-mediated arginine depletion will suppress proliferation of T cells. METHODS: A transfusion model was designed adding PRBC to culture RPMI media with or without an irreversible arginase blocker (nor-NOHA), incubating for 6-48 hours and then removing the PRBCs. Amino acid concentrations in the media were measured using liquid chromatography mass spectrometry. T cells were then added to the pre-conditioned media, cultured for 24 hours, and proliferation was measured. RESULTS: PRBC depleted arginine significantly and increased ornithine in media compared to baseline PRBC treated wells and significantly decreased T cell proliferation. These effects were enhanced with volume of PRBC exposure. Nor-NOHA inhibition of arginase restored T cell proliferation in PRBC treated cultures. CONCLUSIONS: Jurkat T cell proliferation was impaired by PRBC in clinically relevant volumes. The mechanism influencing T cell impairment appears to result from arginine depletion by arginase. Arginine depletion by PRBC arginase may be a novel mechanism for immunosuppression after transfusion.