In five patients with long-standing facial palsy we have tried to improve the possibility of elevating the angle of the mouth by bringing regenerating axons from the facial nerve on the normal side through a sural nerve graft to a transplanted free muscle in the paralyzed cheek. In order to expect clinical improvement a sufficient number of axons must grow into and through the sural nerve graft, neuromuscular contacts must be formed, and the transplanted muscle must be vascularized and survive. In order to find out if axons had regenerated, light- and electronmicroscopic examinations of a biopsy from the tip of the sural nerve graft were carried out at the time of muscle transplantation. All the cases showed a very large number of unmyelinated axons located within the fascicles of the sural nerve graft. A considerable fraction of myelinated axons were, however, present particularly in biopsies removed 12-13 months after the nerve operation. There was also a marked increase in endoneurial collagen and at the very tip a neuroma was present. This investigation thus shows that regeneration of a substantial number of axons had occurred and that they had reached the zone which was surgically sutured to the transplanted muscle. One essential requirement for reinnervation of the transplanted muscle therefore exists in these patients, but the clinical outcome has not yet been evaluated due to the short follow-up period.
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http://dx.doi.org/10.3109/02844318209026219 | DOI Listing |
Mod Rheumatol Case Rep
January 2025
Department of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Osaka, Japan.
Peripheral neuropathy is a complication in systemic sclerosis that is occasionally encountered in clinical settings. The mechanisms underlying this condition remain unclear and treatment strategies have not yet been established, making management challenging. Here, we report a case of peripheral neuropathy associated with systemic sclerosis that was successfully treated with corticosteroid therapy despite the absence of conventional inflammatory findings on histopathology or blood tests.
View Article and Find Full Text PDFRinsho Shinkeigaku
January 2025
Department of Neurology, Sumitomo Hospital.
A 78-years-old man was treated for asthma and pansinusitis for >5 years, and mepolizumab was initiated two years previously. Two months after the cessation of mepolizumab treatment, the asthma symptoms worsened and acute progressive muscle weakness and sensory disturbance developed. On day 8 after the onset of weakness and hypoesthesia, the patient presented with complete flaccid tetraplegia and diffuse hypoesthesia of all extremities, without paresthesia or pain, and was admitted to our hospital.
View Article and Find Full Text PDFDiabetol Metab Syndr
January 2025
Department of Endocrinology, Affiliated Hospital 2 of Nantong University, and First People's Hospital of Nantong City, No.666 Shengli Road, Nantong, 226001, China.
Background: Increased glucagon levels are now recognized as a pathophysiological adaptation to counteract overnutrition in type 2 diabetes (T2D). This study aimed to elucidate the role of glucagon in peripheral nerve function in patients with T2D with different body mass indices (BMIs).
Methods: We consecutively enrolled 174 individuals with T2D and obesity (T2D/OB, BMI ≥ 28 kg/m), and 480 individuals with T2D and nonobesity (T2D/non-OB, BMI < 28 kg/m), all of whom underwent oral glucose tolerance tests to determine the area under the curve for glucagon (AUC).
Ann Plast Surg
January 2025
Background: Digital nerve injuries significantly affect hand function and quality of life, necessitating effective reconstruction strategies. Autologous nerve grafting remains the gold standard due to its superior biocompatibility, despite recent advancements in nerve conduits and allogenic grafts. This study aims to propose a novel zone-based strategy for donor nerve selection to improve outcomes in digital nerve reconstruction.
View Article and Find Full Text PDFBrain
January 2025
Department of Neurology, National Taiwan University Hospital, Taipei, 100225, Taiwan.
Hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN) is a neurodegenerative disease caused by mutations in the gene encoding transthyretin (TTR). Despite amyloid deposition being pathognomonic for diagnosis, this pathology in nervous tissues cannot fully account for nerve degeneration, implying additional pathophysiology for neurodegeneration, which, however, has not yet been fully elucidated. In this study, neuroinflammation in ATTRv-PN was investigated by examining nerve morphometry, the blood-nerve barrier, and macrophage infiltration in the sural nerves of ATTRv-PN patients and the sciatic nerves of a complementary mouse system, i.
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