Background: Blockade of the suprascapular nerve is an effective diagnostic tool in the workup and potential treatment of shoulder pain. For chronic shoulder pain, peripheral nerve stimulation has been shown to provide significant, sustained pain relief. However, no literature to date has described peripheral nerve stimulation for the treatment of oncologic shoulder pain.
Objectives: We describe two cases of chronic oncologic-related shoulder pain that responded to posterior suprascapular peripheral nerve stimulator placement to facilitate future progress and discussion in the fields of peripheral nerve stimulation and oncology pain.
Methods: Two subjects with chronic shoulder pain underwent ultrasound-guided peripheral nerve stimulation therapy at the suprascapular nerve.
Results: At follow-up visits (30 and 98 days after procedure), both subjects reported greater than 50% pain relief as measured by the numerical rating scale (NRS).
Conclusions: Peripheral nerve stimulator placement at the suprascapular nerve is a feasible procedure to treat oncologic shoulder pain via the described technique. Both subjects experienced clinically significant pain relief and decreased oral analgesic medication intake, and decreased medication-related side effects. This warrants further investigation including large comparative, prospective studies to better assess efficacy and safety of this approach.
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http://dx.doi.org/10.1016/j.inpm.2024.100421 | DOI Listing |
Sci Rep
December 2024
Department of Orthopaedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
Chronic complete spinal cord injury (SCI) is difficult to treat because of scar formation and cavitary lesions. While human iPS cell-derived neural stem/progenitor cell (hNS/PC) therapy shows promise, its efficacy is limited without the structural support needed to address cavitary lesions. Our study investigated a combined approach involving surgical scar resection, decellularized extracellular matrix (dECM) hydrogel as a scaffold, and hNS/PC transplantation.
View Article and Find Full Text PDFJ Med Case Rep
December 2024
Division of Infectious Diseases, Denver Health Medical Center, Denver, CO, USA.
Background: Leprosy (Hansen's disease) is an infectious disease most common in resource-limited countries caused by the acid-fast bacilli Mycobacterium leprae and Mycobacterium lepromatosis that frequently affects the skin and peripheral nerves. Prompt diagnosis and treatment with multidrug therapy is crucial to reduce disease transmission and sequelae, which include nerve function impairment, ocular injury, and stigmatizing physical deformities. Traditional treatment of multibacillary leprosy consists of 12-24 months of multidrug therapy with dapsone, rifampin, and clofazimine.
View Article and Find Full Text PDFIntroduction: Available therapies for peripheral nerve injury (PNI) include surgical and non-surgical treatments. Surgical treatment includes neurorrhaphy, grafting (allografts and autografts) and tissue-engineered grafting (artificial nerve guide conduits), while non-surgical treatment methods include electrical stimulation, magnetic stimulation, laser phototherapy and administration of nerve growth factors. However, the treatments currently available to best manage the different PNI manifestations remain undetermined.
View Article and Find Full Text PDFJ Oral Maxillofac Surg
December 2024
PhD Adjunct Professor, in Oral and Maxillofacial Surgery, School of Dentistry, University of Pernambuco - UPE, Recife, Pernambuco, Brazil. Electronic address:
Background: Fluoxetine, a serotonin reuptake inhibitor antidepressant, raises extracellular serotonin levels and promotes angiogenesis and neurogenesis. Numerous animal models have shown its beneficial effects on recovery from peripheral nerve injury.
Purpose: The primary objective of this study was to analyze the influence of fluoxetine on the sensory-motor function recovery of the sciatic nerve in Wistar rats after axonotmesis.
Neurobiol Dis
December 2024
Department of Neurology, University Hospital of Wuerzburg, Germany. Electronic address:
DYT-THAP1 dystonia is a monogenetic form of dystonia, a movement disorder characterized by the involuntary co-contraction of agonistic and antagonistic muscles. The disease is caused by mutations in the THAP1 gene, although the precise mechanisms by which these mutations contribute to the pathophysiology of dystonia remain unclear. The incomplete penetrance of DYT-THAP1 dystonia, estimated at 40 to 60 %, suggests that an environmental trigger may be required for the manifestation of the disease in genetically predisposed individuals.
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