Chronic low back pain (CLBP) is a debilitating, painful, and costly condition. Implantable neuromuscular electrical stimulation targeting the multifidus musculature is growing as a non-pharmacologic option for patients with recalcitrant nociceptive mechanical CLBP who have failed conservative treatments (including medications and physical therapy) and for whom surgery is not indicated. Properly selecting patients who meet specific criteria (based on historical results from randomized controlled trials), who diligently adhere to implant usage and precisely implement neuromuscular rehabilitation, improve success of significant functional recovery, as well as pain medication reductions.
View Article and Find Full Text PDFLumbar radiculopathy due to impingement of nerve roots from facet hypertrophy and/or disc herniation can often coincide with vertebrogenic low back pain. This is demonstrated on MRI with foraminal stenosis and Modic changes. We examine the potential of using a combination of basivertebral nerve ablation (BVNA) and lumbar laminotomy as an alternative to traditional spinal fusion in specific patient populations.
View Article and Find Full Text PDFIntroduction: Sacroiliac joint (SIJ) pathology is typically diagnosed and treated with fluoroscopy-guided intraarticular injections. Most practitioners use only an anteroposterior (AP) or oblique view. Although injection into the periarticular space may yield adequate pain relief, intraarticular needle placement is imperative to identify SIJ pathology and plan future management.
View Article and Find Full Text PDFChronic low back pain is a worldwide leading cause of pain and disability. Degenerative disc disease has been the presumptive etiology in the majority of cases of chronic low back pain (CLBP). More recent study and treatments have discovered that the vertebral endplates play a large role in CLBP in a term defined as vertebrogenic back pain.
View Article and Find Full Text PDFBackground: X-linked hypophosphatemia (XLH) is the most common inherited form of renal phosphate wasting and inherited rickets. Patients have hyperplasia of fibrochondrocytes in tendons and ligaments, causing the structures to thicken and calcify. Thickening of the lamina, hypertrophy of facet joints, and calcification of spinal ligaments are sequelae of this condition and can result in central or foraminal stenosis that compresses nerve roots or the spinal cord.
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