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Neurotropism and infiltration by of peripheral nerves causing neuropathy are well established, but reports of central nervous system (CNS) damage are exceptional. We report CNS magnetic resonance imaging (MRI) abnormalities of the brain and spinal cord as well as lesions in nerve roots and plexus in leprosy patients. Eight patients aged between 17 and 41 years underwent detailed clinical, histopathological, and MRI evaluation. All had prominent sensory-motor deficits with hypopigmented and hypo/anesthetic skin patches and thickened peripheral nerves. All demonstrated DNA in affected peripheral nerve tissue. All received multidrug therapy (MDT). Two patients had brainstem lesions with enhancing facial nuclei and nerves, and one patient had a lesion in the nucleus ambiguus. Two patients had enhancing spinal cord lesions. Follow-up MRI performed in four cases showed resolution of brainstem and cord lesions after starting on MDT. Thickened brachial and lumbosacral plexus nerves were observed in six and two patients, respectively, which partially resolved on follow-up MRI in the two cases who had reimaging. The site and side of the MRI lesions corresponded with the location and side of neurological deficits. This precise clinico-radiological correlation of proximal lesions could be explained by an immune reaction in the gray matter corresponding to the involved peripheral nerves, retrograde axonal and gray matter changes, or infection of the CNS and plexus by lepra bacilli. Further study of the CNS in patients with leprous neuropathy is needed to establish the exact nature of these CNS MRI findings.
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http://dx.doi.org/10.4269/ajtmh.17-0945 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
November 2025
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Background And Objectives: Myelitis is a relatively common clinical entity for neurologists, with diverse underlying causes. The aim of this study was to describe the incidence of myelitis, its causes, clinical presentation, and factors predicting functional outcomes and relapses.
Methods: Using the Swedish National Patient Registry, we identified all adult patients in Stockholm County between 2008 and 2018 using International Classification of Diseases, 10th Edition (ICD-10) codes likely to include myelitis.
J Spinal Cord Med
September 2025
Department of Surgery, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec, Canada.
Study Design: A retrospective study with a crossover design.
Objectives: Maintaining mean arterial pressure (MAP) is crucial in the early management of SCI, yet the role of oral midodrine in this setting remains unclear. This study evaluates whether midodrine facilitates IV vasopressor weaning within 24 hours of initiation.
Sci Prog
September 2025
Department of Neurology, University of Afyonkarahisar Health Sciences, Afyonkarahisar, Türkiye.
A considerable number of individuals are diagnosed with idiopathic trigeminal neuralgia. In order to achieve a more complete understanding of the pathophysiology, it is essential to adopt a range of novel approaches and utilize new animal models. This study investigated changes in the messenger RNA (mRNA) expression of ion-channels in a newly developed animal model of trigeminal neuropathic pain induced by cervical spinal dorsal horn compression.
View Article and Find Full Text PDFEur Spine J
September 2025
Consultant Neurosurgeon, Centre for Functional Neurosurgery, University Hospital Southampton NHS Foundation Trust, Southampton, UK.
Stem Cell Rev Rep
September 2025
Stem Cells and Metabolism Research Program (STEMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, 00014, Finland.
Mutations in Delta Like Non-Canonical Notch Ligand 1 (DLK1), a paternally expressed imprinted gene, underlie central precocious puberty (CPP), yet the mechanism remains unclear. To test the hypothesis that DLK1 plays a role in gonadotropin releasing hormone (GnRH) neuron ontogeny, 75 base pairs were deleted in both alleles of DLK1 exon 3 with CRISPR-Cas9 in human pluripotent stem cells (hPSCs). This line, exhibiting More than 80% loss of DLK1 protein, was differentiated into GnRH neurons by dual SMAD inhibition (dSMADi), FGF8 treatment and Notch inhibition, as previously described, however, it did not exhibit accelerated GNRH1 expression.
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