Evaluating the Diagnostic Performance of MRI for Identification of Meniscal Ramp Lesions in ACL-Deficient Knees: A Systematic Review and Meta-Analysis.

BACKGROUND: Despite vigorous efforts to delineate the efficacy of magnetic resonance imaging (MRI) for the diagnosis of meniscal ramp lesions, there is still a great deal of uncertainty regarding its diagnostic performance. Therefore, we conducted a systematic review and meta-analysis to investigate the diagnostic performance of MRI for detecting ramp lesions in anterior cruciate ligament (ACL)-deficient knees. METHODS: We performed a systematic search of MEDLINE via PubMed, Scopus, Web of Science, and Embase and included all articles, published before October 20, 2022, comparing the accuracy of MRI with that of arthroscopy as the gold standard for diagnosis of ramp lesions. We performed statistical analysis using Stata and Meta-DiSc software. Quality assessment of the included studies was performed using the QUADAS-2 (Quality Assessment of Diagnostic Accuracy Studies-2) tool. RESULTS: This meta-analysis evaluated 21 diagnostic performance comparisons from 19 original research articles (2,149 patients). The pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and area under the summary receiver operating characteristic (SROC) curve for diagnosing a ramp lesion were 0.70 (95% confidence interval [Cl], 0.66 to 0.73), 0.88 (95% Cl, 0.86 to 0.89), 6.49 (95% Cl, 4.12 to 10.24), 0.36 (95% Cl, 0.28 to 0.46), 24.33 (95% Cl, 12.81 to 46.19), and 0.88, respectively. Meta-regression using different variables yielded the same results. CONCLUSIONS: MRI exhibited a DOR of 24.33 and moderate sensitivity, specificity, and accuracy for diagnosing ramp lesions in ACL-deficient knees. However, arthroscopy using a standard anterolateral portal with intercondylar viewing is recommended to confirm a diagnosis of a ramp lesion. LEVEL OF EVIDENCE: Diagnostic Level III. See Instructions for Authors for a complete description of levels of evidence.

Intra-accumbal orexinergic system contributes to the stress-induced antinociceptive behaviors in the animal model of acute pain in rats.

Stress and pain are interleaved at numerous levels - influencing each other. Stress can increase the nociception threshold in animals, long-known as stress-induced analgesia (SIA). Orexin is known as a neuropeptide that modulates pain. The effect of stress on the mesolimbic system in the modulation of pain is known. The role of the intra-accumbal orexin receptors in the modulation of acute pain by forced swim stress (FSS) is unclear. In this study, 117 adult male albino Wistar rats (270-300 g) were used. The animals were unilaterally implanted with cannulae above the NAc. The antagonist of the orexin-1 receptor (OX1r), SB334867, and antagonist of the orexin-2 receptor (OX2r), TCS OX2 29, were microinjected into the NAc in different doses (1, 3, 10, and 30 nmol/0.5 µl DMSO) before exposure to FSS for a 6-min period. The tail-flick test was carried out as an assay nociception of acute pain, and the nociceptive threshold [tail-flick latency (TFL)] was measured for 60-minute. The findings demonstrated that exposure to acute stress could remarkably increase the TFLs and antinociceptive responses. Moreover, intra-accumbal microinjection of SB334867 or TCS OX2 29 blocked the antinociceptive effect of stress in the tail-flick test. The contribution of orexin receptors was almost equally modulating SIA. The present study's findings suggest that OX1r and OX2r within the NAc modulate stress-induced antinociceptive responses. The intra-accumbal microinjection of orexin receptors antagonists declares inducing antinociceptive responses by FSS in acute pain. Proposedly, intra-accumbla orexinergic receptors have a role in the development of SIA.

The stress-induced antinociceptive responses to the persistent inflammatory pain involve the orexin receptors in the nucleus accumbens.

Stress suppresses the sense of pain, a physiological phenomenon known as stress-induced analgesia (SIA). Brain orexin peptides regulate many physiological functions, including wakefulness and nociception. The contribution of the orexinergic system within the nucleus accumbens (NAc) in the modulation of antinociception induced by forced swim stress (FSS) remains unclear. The present study addressed the role of intra-accumbal orexin receptors in the antinociceptive responses induced by FSS during the persistent inflammatory pain model in the rat. Stereotaxic surgery was performed unilaterally on 106 adult male Wistar rats weighing 250-305 g. Different doses (1, 3, 10, and 30 nmol/ 0.5 µl DMSO) of orexin-1 receptor (OX1r) antagonist (SB334867) or OX2 receptor antagonist (TCS OX2 29) were administered into the NAc five minutes before exposure to FSS for a 6-min period. The formalin test was carried out using formalin injection (50 µl; 2.5%) into the rat's hind paw plantar surface, which induces biphasic pain-related responses. The first phase begins immediately after formalin infusion and takes 3-5 min. Subsequently, the late phase begins 15-20 min after formalin injection and takes 20-40 min. The findings demonstrated that intra-accumbal microinjection of SB334867 or TCS OX2 29 attenuated the FSS-induced antinociception in both phases of the formalin test, with the TCS OX2 29 showing higher potency. Moreover, the effect of TCS OX2 29 was more significant during the early phase of the formalin test. The results suggest that OX1 and OX2 receptors in the NAc might modulate the antinociceptive responses induced by the FSS.