ABSTRACT
BACKGROUND: Fluoroscopically guided cooled genicular nerve radiofrequency ablation (RFA) is an increasingly performed procedure for chronic, refractory knee pain due to osteoarthritis. Traditionally, partial sensory denervation has been accomplished through ablation of the superomedial, superolateral, and inferomedial genicular nerves. However, recent cadaveric studies have demonstrated additional sensory nerves and significant anatomic variation that impact current protocols. OBJECTIVE: We describe an updated cooled genicular nerve radiofrequency ablation protocol that accounts for varied nerve location of the superomedial, superolateral, and inferomedial genicular nerves, as well as capture of the terminal articular branches of the nerves to the vastus intermedius, vastus lateralis, and vastus medialis. Furthermore, we describe an adjusted technique for inferomedial genicular nerve capture that mitigates the risk of pes anserine tendon injury. DESIGN: Technical report and brief literature review. METHODS: Cadaveric studies relating to the sensory innervation of the anterior knee joint were reviewed, and a more accurate and comprehensive cooled genicular nerve radiofrequency ablation (CRFA) protocol is proposed. CONCLUSIONS: Based on recent, rigorous anatomic dissections of the knee, the proposed genicular nerve CRFA protocol will provide more complete sensory denervation and potentially improve clinical outcomes. Prospective studies will be needed to confirm the hypothesis that this protocol will result in improved effectiveness and safety of genicular nerve RFA.
Subject(s)
Chronic Pain/surgery , Knee Joint/innervation , Knee Joint/surgery , Osteoarthritis, Knee/surgery , Catheter Ablation/methods , Dissection/methods , Humans , Prospective StudiesABSTRACT
Diabetic retinopathy (DR) is the leading cause of blindness in the working-age population in the U.S. The vision-threatening processes of neuroglial and vascular dysfunction in DR occur in concert, driven by hyperglycemia and propelled by a pathway of inflammation, ischemia, vasodegeneration, and breakdown of the blood retinal barrier. Currently, no therapies exist for normalizing the vasculature in DR. Here, we show that a single intravitreal dose of adeno-associated virus serotype 2 encoding a more stable, soluble, and potent form of angiopoietin 1 (AAV2.COMP-Ang1) can ameliorate the structural and functional hallmarks of DR in Ins2Akita mice, with sustained effects observed through six months. In early DR, AAV2.COMP-Ang1 restored leukocyte-endothelial interaction, retinal oxygenation, vascular density, vascular marker expression, vessel permeability, retinal thickness, inner retinal cellularity, and retinal neurophysiological response to levels comparable with nondiabetic controls. In late DR, AAV2.COMP-Ang1 enhanced the therapeutic benefit of intravitreally delivered endothelial colony-forming cells by promoting their integration into the vasculature and thereby stemming further visual decline. AAV2.COMP-Ang1 single-dose gene therapy can prevent neurovascular pathology, support vascular regeneration, and stabilize vision in DR.