Background: Long-term patients with diabetes and peripheral neuropathy show altered foot biomechanics and abnormal foot loading. This study aimed at assessing muscle performance and ankle mobility in such patients under controlled conditions.
Methods: Forty six long-term diabetes patients with (DN) and without (D) peripheral neuropathy, and 21 controls (C) were examined. Lower leg muscle performance and ankle mobility were assessed by means of a dedicated equipment, with the patient seated and the examined limb unloaded. 3D active ranges of motion and moments of force were recorded, the latter during maximal isometric contractions, with the foot blocked in different positions.
Results: All patients showed reduced ankle mobility. In the sagittal and transversal planes reduction vs C was 11% and 20% for D, 20% and 21% for DN, respectively.Dorsal-flexing moments were significantly reduced in all patients and foot positions, the highest reduction being 28% for D and 37% for DN. Reductions of plantar-flexing moments were in the range 12-15% for D (only with the foot blocked in neutral and in dorsal-flexed position), and in the range 10-24% for DN. In all patients, reductions in the frontal and transversal planes ranged 14-41%.
Conclusion: The investigation revealed ankle functional impairments in patients with diabetes, with or without neuropathy, thus suggesting that other mechanisms besides neuropathy might contribute to alter foot-ankle biomechanics. Such impairments may then play a role in the development of abnormal gait and in the onset of plantar ulcers.
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http://dx.doi.org/10.1186/1471-2474-9-99 | DOI Listing |
Cell Tissue Res
January 2025
Laboratory of Anatomy and Cell Biology, Department of Health Sciences, Kyorin University, 5-4-1 Shimorenjaku, Mitaka, Tokyo, 181-8612, Japan.
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January 2025
Federal State Autonomous Educational Institution of Higher Education "Russian National Research Medical University named after N.I. Pirogov" of the Ministry of Health of the Russian Federation, Separate structural unit "Russian Gerontology Research and Clinical Centre", 16 1st Leonova Street, Moscow, Russia, 129226.
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View Article and Find Full Text PDFVet Res Commun
January 2025
Genetics and Biotechnology, Department of Aquaculture, Faculty of Fish Resources, Suez University, Suez, 43221, Egypt.
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View Article and Find Full Text PDFJ Gerontol B Psychol Sci Soc Sci
January 2025
Centre for Population Health Research and Implementation, Singapore Health Services, Singapore, Singapore.
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Clin Dysmorphol
January 2025
Department of Medical Genetics, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, India.
Introduction: Agrin, encoded by AGRN, plays a vital role in the acetylcholine receptor clustering pathway, and any defects in this pathway are known to cause congenital myasthenic syndrome (CMS) 8 in early childhood with variable fatigable muscle weakness. The most severe or lethal form of CMS manifests as a fetal akinesia deformation sequence (FADS). To date, only one family has been reported with an association of null variants in AGRN and a lethal FADS.
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