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Traumatic glenohumeral instability represents a commonly encountered clinical scenario. Two case vignettes are presented along with an evidence-based review of epidemiology, pathophysiology, diagnosis, and treatment options.

Meniscus tears in athletes display a variety of clinical presentations. Three different case scenarios are presented along with diagnoses and treatment options, and the best available evidence, at present, is reviewed.

The concept of multiligamentous knee injuries encompasses a large variety of presenting combinations, and the existing published literature lacks adequately sized prospective comparative patient-reported outcome studies to guide clinical decision making. The decisions of operative versus nonoperative management, timing of surgery, repair versus reconstruction, use of allograft versus auto-graft, choice of which ligaments to treat, and rehabilitation protocols remain controversial despite the fact that multiligament injuries have been shown to represent approximately 11-20% of knee ligament sprains presenting for treatment. For the purposes of this manuscript, a multiligamentous knee injury is defined as one complete cruciate tear (grade III) plus a partial or complete collateral tear (grade II or III) or a partial or complete tear of the other cruciate (grade II or III). A surgical treatment algorithm is proposed based upon a review of case series literature and clinical experience in an academic sports medicine practice setting. Use of our proposed surgical algorithms may facilitate clinical decision making in an attempt to restore stability, preserve function, and maximize return to activity.

Fragile X syndrome is a common heritable form of mental retardation in humans. Recent neuroanatomical studies indicate an apparent immature appearance of neurons in fragile X syndrome patients and fragile X mental retardation protein (FMRP)-knockout mice, an animal model of this condition. In this work, we investigated possible alterations in synaptic plasticity in the neocortex of FMRP-knockout mice. Extracellular field potentials were recorded from the deep-layer visual neocortex. Long-term potentiation (LTP) was severely attenuated in brain slices from knockout mice relative to that observed in slices from wild-type mice. Considering that neocortical LTP can involve both NMDA receptor-dependent and -independent mechanisms, we attempted to distinguish the nature of LTP attenuated in the knockout condition. In slices from wild-type mice, LTP was partially attenuated by the NMDA receptor antagonist 3-[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphate (CPP); however, the general metabotropic glutamate receptor (mGluR) antagonist alpha-methyl-4-carboxyphenylglycine (MCPG) strongly attenuated LTP, resulting in a response indistinguishable from that observed in slices from knockout mice. The selective mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) attenuated LTP to a similar degree as did MCPG in wild-type slices, but MPEP did not alter the reduced potentiation in knockout slices. Our results suggest that LTP in layer V visual neocortex depends primarily on mGluR5 activation. Our data also indicate that mGluR5-mediated synaptic plasticity is absent in the neocortex of FMRP-knockout mice. Such an alteration may contribute to the cognitive and learning deficits exhibited in these mice as well as in fragile X syndrome.