Medial Elbow Pain Syndrome: Current Treatment Strategies.

Medial elbow pain is a common presentation that can be a challenge to appropriately treat for the orthopedic surgeon. Causes include medial epicondylitis, ulnar neuritis, ulnar collateral ligament injury, flexor pronator strain, or snapping medial triceps. A good outcome is typically achieved with adequate treatment of tendon degeneration at the common flexor tendon origin. Mainstay treatment is nonoperative modalities such as stretching, rest, activity modification, therapy, and injections. If nonoperative management fails, intermediate interventions such as extracorporeal shockwave therapy, platelet-rich plasma injections, prolotherapy, and ultrasound-guided percutaneous tenotomy can be attempted. Surgical treatments are dictated based on the severity of the pathology, involvement of soft tissues, and concomitant pathology. Medial elbow complaints can be multifactorial and require a broad differential diagnosis. [Orthopedics. 2023;46(2):e81-e88.].

Optical and SPION-enhanced MR imaging shows that trans-stilbene inhibitors of NF-κB concomitantly lower Alzheimer's disease plaque formation and microglial activation in AßPP/PS-1 transgenic mouse brain.

Alzheimer's disease (AD) is associated with a microglia-dependent neuroinflammatory response against plaques containing the fibrous protein amyloid-ß (Aß). Activation of microglia, which closely associate with Aß plaques, engenders the release of pro-inflammatory cytokines and the internalization of Aß fibrils. Since the pro-inflammatory transcription factor NF-κB is one of the major regulators of Aß-induced inflammation, we treated transgenic amyloid-ß protein protein/presenilin-1 (AßPP/PS1) mice for one year with a low dose (0.01% by weight in the diet) of either of two trans-stilbene NF-κB inhibitors, resveratrol or a synthetic analog LD55. The 3D distribution of Aß plaques was measured ex vivo in intact brains at 60 µm resolution by quantitative magnetic resonance imaging (MRI) using blood-brain barrier-permeable, anti-AßPP-conjugated superparamagentic iron oxide nanoparticles (SPIONs). The MRI measurements were confirmed by optical microscopy of thioflavin-stained brain tissue sections and indicated that supplementation with either of the two trans-stilbenes lowered Aß plaque density in the cortex, caudoputamen, and hippocampus by 1.4 to 2-fold. The optical measurements also included the hippocampus and indicated that resveratrol and LD55 reduced average Aß plaque density by 2.3-fold and 3.1-fold, respectively. Ex vivo measurements of the regional distribution of microglial activation by Iba-1 immunofluorescence of brain tissue sections showed that resveratrol and LD55 reduced average microglial activation by 4.2- fold and 3.5-fold, respectively. Since LD55 lacked hydroxyl groups but both resveratrol and LD55 concomitantly reduced both Aß plaque burden and neuroinflammation to a similar extent, it appears that the antioxidant potential of resveratrol is not an important factor in plaque reduction.