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2 results

  • Chapter 9 - Pathology

  • John A. Jarratt, Emeritus, Sheffield Teaching Hospitals NHS Foundation Trust
  • Book:
    Essential Electromyography
    Published online:
    14 September 2023
    Print publication:
    05 October 2023, pp 27-28

  • Summary

    Muscle disease tends to be patchy, hence the term ‘sampling’, which is often applied to the technique of electromyographic investigation. The susceptibility of muscle pathology to electromyographic diagnosis relies on type 1 fibres being affected because motor units containing these fibres are the first to be recruited. Myelinated nerve fibres may undergo demyelination or degeneration depending upon whether the myelin or the axon is primarily affected. Severely demyelinated nerves are unstable and degenerate. Disease of nerve cell bodies cause centripetal degeneration in the longest axons, the so-called dying-back neuropathy. Severe trauma to a nerve causes distal degeneration, also known as Wallerian degeneration.

  • 17 - Axon degeneration and rescue

  • from Section B1 - Neural repair
    • By John W. Griffin, Departments of Neurology and Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD, USA, Ahmet Höke, Departments of Neurology and Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD, USA, Thien T. Nguyen, Departments of Neurology and Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD, USA
  • Edited by Michael Selzer, University of Pennsylvania, Stephanie Clarke, Université de Lausanne, Switzerland, Leonardo Cohen, National Institute of Mental Health, Bethesda, Maryland, Pamela Duncan, University of Florida, Fred Gage, Salk Institute for Biological Studies, San Diego
  • Book:
    Textbook of Neural Repair and Rehabilitation
    Published online:
    05 March 2012
    Print publication:
    16 February 2006, pp 293-302

  • Summary

    This chapter reviews the sequence of changes in Wallerian degeneration after transection, and suggests that the late stages are similar in the disorders of axonal transport. The axons develop swellings containing densely packed accumulations of mitochondria, dense bodies and multivesicular bodies. In settings where interrupted axons survive for long periods, such as the Wallerian-like degeneration slow (Wlds) mouse, there is also an accumulation of neurofilaments. Neurofilament proteins were initially recognized to move in the slow anterograde phase of axonal transport. The importance of defects in axonal transport have become especially clear in genetic disorders where molecules involved in axonal transport have been responsible for human length-dependent neuropathies. In multiple sclerosis (MS) and other human and experimental settings with inflammatory demyelination, axonal degeneration and loss can result from focal axonal interruption consequent to the presence of nearby inflammatory cells and inflammatory mediators.