BACKGROUND Attainment of extremity immobilization in orthopedic trauma patients experiencing psychosis is often uniquely challenging. Many fractures, including those of the distal humerus, require a period of immobilization postoperatively to optimize fracture healing. Patients with Parkinson's disease have also been shown to have lower rates of union after fracture compared to the general population. The combination of Parkinson's disease and associated psychosis requires heightened attention to those parameters that may hinder fracture healing, such as inadequate immobilization of the fracture. Botulinum toxin has previously been described as a potential adjunctive therapy for fracture immobilization but has not yet been described in the setting of distal humerus fractures. CASE REPORT A 75-year-old woman with Parkinson's disease-associated psychosis presented 2 weeks after open reduction and internal fixation of a distal third humeral shaft fracture due to failure of fixation and episodes of violent hallucinations. The patient underwent irrigation and debridement, and revision open reduction and internal fixation. Given her uncontrolled hallucinations, intramuscular botulinum toxin injections were given to the right triceps, biceps, and brachialis muscles to aid in the immobilization of the right extremity and protect the surgical site during the perioperative period. The patient subsequently followed up at the clinic 3 months postoperatively with ongoing fracture healing, evidenced by bridging callous and bone formation on radiographs, as well as a return of motion to the extremity. CONCLUSIONS Botulinum toxin may be a safe and effective adjunct for fracture immobilization in patients who are difficult to immobilize and have high fixation failure risk.
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http://dx.doi.org/10.12659/AJCR.939680 | DOI Listing |
Am J Med Genet A
January 2025
Hayward Genetics Center, Tulane University School of Medicine, New Orleans, Louisiana, USA.
RAC1 encodes the protein RAS-related C3 Botulinum Toxin Substrate 1 (RAC1), which plays a pivotal role in various cellular functions. Pathogenic variants in RAC1 are linked to the rare intellectual developmental disorder, autosomal-dominant 48 (MRD48). We present one case with typical phenotype and two cases with a mild phenotype.
View Article and Find Full Text PDFCNS Neurol Disord Drug Targets
January 2025
The Movement Disorders Unit, Shaare Zedek Medical Center, Jerusalem.
Background: Botulinum Toxin type A (BonTA) is the preferred treatment for Cervical Dystonia (CD). However, the success rate is often suboptimal. One of the reasons for treatment failure is the in accuracy of injections.
View Article and Find Full Text PDFNat Struct Mol Biol
January 2025
Department of Physiology and Biophysics, University of California, Irvine, Irvine, CA, USA.
Botulinum neurotoxins (BoNTs) rank among the most potent toxins and many of them are produced by bacteria carrying the orfX gene cluster that also encodes four nontoxic proteins (OrfX1, OrfX2, OrfX3 and P47). The orfX gene cluster is also found in the genomes of many non-BoNT-producing bacteria, often alongside genes encoding oral insecticidal toxins. However, the functions of these OrfXs and P47 remain elusive.
View Article and Find Full Text PDFInt J Colorectal Dis
January 2025
Department of Surgery, Azienda Sanitaria Provinciale Crotone, 88900, Crotone, Italy.
Purpose: Chronic constipation is a common symptom. Constipation due to pelvic floor disorders remain a therapeutic challenge. Biofeedback therapy is considered as the first-choice treatment for pelvic floor disorders, whenever dedicated expertise is available.
View Article and Find Full Text PDFJ Struct Biol
January 2025
Department of Biochemical Engineering, University College London, London, United Kingdom.
Despite sharing ∼ 43 % sequence identity and structurally similar individual domains, botulinum neurotoxin (BoNT) serotypes A and E have differences in their properties and domain positioning. BoNT/E has a faster onset of action than BoNT/A. This difference is proposed to be due to conformational differences between BoNT/E and the other BoNT serotypes.
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