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Case 1.14
Published in Monica Fawzy, Plastic Surgery Vivas for the FRCS(Plast), 2023
Saltatory conduction allows the action potentials to transmit along the only uninsulated areas along the axon, termed the nodes of Ranvier, to speed transmission from 10 m/s in an unmyelinated nerve to 150 m/s in a myelinated nerve.
Neurologic Diagnosis
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Demyelination may result in marked slowing of conduction, conduction block, and increased susceptibility to changes in temperature. In normal myelinated fibers, impulses conduct rapidly from one node of Ranvier to the next by saltatory conduction. In demyelinated nerve fibers, conduction between nodes is delayed or, as with unmyelinated nerve fibers, becomes nonsaltatory and continuous, therefore much slower across the demyelinated segments. The delay in conduction may result in markedly prolonged distal latencies, marked slowing of segmental conduction velocity, and temporal dispersion and a lower amplitude of the action potential across the involved segment.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
MS, a chronic demyelinating disease of the CNS, is an autoimmune disease characterised by degeneration of the myelin sheath. The name comes from the pathophysiology of the disease. The myelin sheaths degenerate in multiple areas, until they form hardened plaques called scleroses. Plaques are found in the brain and spinal cord of MS sufferers. Demyelination prevents saltatory conduction and reduces nerve transmission. Symptoms include muscle weakness, altered sensation and blurred vision. Acute episodes are followed by periods of remission, but frequency and severity of the attacks increases with time.
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
Damage and loss of oligodendrocytes after SCI leads to demyelination and disrupted saltatory conduction, which contribute to a proportion of functional deficits that are seen in individuals with SCI [126]. In order to reverse the functional consequences of demyelination, regenerative approaches have been investigated. After SCI, a degree of myelin remodeling occurs through the recruitment of endogenous progenitors such as oligodendrocyte progenitor cells (OPCs) and injury–activated ependymal cells [56,127–129]. These endogenous precursors can further be experimentally stimulated to strengthen the spontaneous response [130–133]. Notably, some studies suggest that the inherent, non-stimulated response may be sufficient. In this regard, the Tetzlaff lab has demonstrated the importance of distinguishing which axons become remyelinated during regenerative mechanisms [134]. Specifically, they have shown that the intact, functional axons that remain post-SCI become remyelinated by endogenous cells, whereas the demyelination that is seen can be attributed to the severed axons, which are no longer functional. Therefore, they suggest that the injured spinal cord does not have a population of axons remaining that would benefit from transplant-mediated remyelination [134]. Future studies should elaborate on this work by distinguishing which axons (healthy vs. nonfunctional) become remyelinated by transplanted cells.
Remyelination therapies for multiple sclerosis: optimizing translation from animal models into clinical trials
Published in Expert Opinion on Investigational Drugs, 2021
Rujapope Sutiwisesak, Terry C. Burns, Moses Rodriguez, Arthur E. Warrington
The pathology of MS is characterized by areas of progressive demyelination or ‘plaques’ at multiple sites within the CNS [6]. Although demyelination is the main pathology, MS lesions occur in both white and gray matter. A healthy myelin sheath, formed by oligodendrocytes in the CNS, enables efficient nerve impulse transmission by utilizing saltatory conduction and maintaining axonal health [7]. Damage to myelin sheaths results in axonal conduction block in the early stages of disease. Axonal damage is usually acute and reversible but axonal loss and dysfunction are the causes of permanent neurological deficits. Progressive neurodegeneration can result from untreated or chronic disease progression. As such, a central goal of MS treatments is axonal preservation, which could be achievable by preventing ongoing damage to myelin sheaths and promoting remyelination.
Ultrastructural and morphometric alterations to the peripheral nerve following the administration of immunosuppressive agent tacrolimus (FK506)
Published in Ultrastructural Pathology, 2021
Ferda Topal Celikkan, Nazli Hayirli Ozyol, Hilal Nakkas, Oya Evirgen
G-ratio, which is frequently used as a structural and functional indicator of optimal axonal myelination, is an important parameter for the exploration of the myelinated nerve fibers during the evaluation of damage and regeneration processes. In peripheral nerves, G-ratio of myelinated axons, which is considered normal in the range between 0.60 and 0.80, is optimal for the saltatory conduction speed of nerve impulses.20–23 We found that G-ratio of control and experimental groups were in normal range and there was no statistically significant difference between the groups. This indicates that despite the presence of statistically significant increase in fiber diameter, axonal diameter, and myelin thickness in 2-week tacrolimus-treated group, still myelinated fibers have optimal myelination in order to facilitate nerve impulse conduction.