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Advanced Neurology





                                        REVIEW ARTICLE
                                        A novel approach to mitigate muscle atrophy in

                                        Guillain-Barre syndrome



                                        Kevin Cheung *, Sussan Askari , and Matti D. Allen 2,3
                                                    1
                                                                   2
                                        1 School of Medicine, Faculty of Health Sciences, Queen’s University, Kingston, Ontario, Canada
                                        2 Department of Physical Medicine and Rehabilitation, Faculty of Health Sciences, Queen’s University,
                                        Kingston, Ontario, Canada
                                        3 School of Kinesiology, Faculty of Arts and Sciences, Queen’s University, Kingston, Ontario, Canada



                                        Abstract

                                        Guillain-Barre syndrome (GBS) is the most common cause of acute paralytic neuropathy
                                        worldwide. GBS manifests as rapidly progressive, symmetrical numbness, paresthesia,
                                        and weakness secondary to either peripheral nerve demyelination or axonal loss.
                                        Despite  effective  disease  modifying  therapies  (e.g.,  intravenous  immunoglobulin)
                                        and individualized rehabilitation programs, many individuals recovering from
                                        GBS  experience  substantial  muscle  atrophy  and  incomplete  recovery  of  strength
                                        with resultant long-term functional impairment. This narrative review explores the
                                        therapeutic potential of omega-3 fatty acid supplementation on enhancing recovery
                                        of people with GBS. This purported benefit may occur through several potential
                                        mechanisms, supported indirectly through studies using both experimental animal
                                        and clinical human models.  These mechanisms include: (i) Anti-atrophic effects
                                        on  skeletal  muscle undergoing disuse  and  systemic  inflammation;  (ii)  the use  of
                                        omega-3s as a key building block comprising myelin; (iii) immune modulating effects
            *Corresponding author:      optimizing conditions for remyelination; and (iv) preventing excitotoxic-like neuron
            Kevin Cheung
            (Kevin.Cheung@queensu.ca)   death. The physiological mechanisms are explored in detail with examination of
                                        relevant clinical trials conducted to date. Through this exploration, there is sufficient
            Citation: Cheung K, Askari S,
            Allen MD, 2023, A novel approach   support to justify future investigations directly examining the role omega-3 fatty acid
            to mitigate muscle atrophy   supplementation may play as an adjunctive intervention that could have significant
            in Guillain-Barre syndrome.   benefit at low cost and minimal risk of adverse events.
            Adv Neuro, 2(2): 280.
            https://doi.org/10.36922/an.280
            Received: November 30, 2022  Keywords: Guillain-Barre syndrome; Fatty acids, Omega-3; Nutritional support; Muscular
                                        atrophy
            Accepted: March 27, 2023
            Published Online: April 10, 2023
            Copyright: © 2023 Author(s).
            This is an Open-Access article   1. Introduction
            distributed under the terms of the
            Creative Commons Attribution   Guillain-Barre syndrome (GBS) is an umbrella term describing a group of related
            License, permitting distribution,   autoimmune disorders of the peripheral nervous system (PNS). It is the most common
            and reproduction in any medium,
                                                                                [1]
            provided the original work is   cause of acute paralytic neuropathy worldwide . The onset of GBS is typically
            properly cited.             preceded by an infection or through an aberrant autoimmune response targeting the
                                                                   [1]
            Publisher’s Note: AccScience   PNS through molecular mimicry . Broadly, GBS can be categorized into subtypes
            Publishing remains neutral with   based on the  pathophysiological process involved:  (i) primary demyelinating (i.e.,
            regard to jurisdictional claims in
            published maps and institutional   acute inflammatory demyelinating polyneuropathy [AIDP]) and (ii) axonal loss
            affiliations.               (i.e., acute motor axonal neuropathy [AMAN] and acute motor and sensory axonal


            Volume 2 Issue 2 (2023)                         1                          https://doi.org/10.36922/an.280
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