Limb Myokymia in Guillain-Barré Syndrome

Kuttiappan, Gunasekaran; Sivakumar, S; Thiruvarutchelvan, K

doi:10.4103/0028-3886.279682

Cited by 6 publications

(3 citation statements)

References 8 publications

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“…Focal myokymias are often seen on the face and especially in the eyes. [ 5 6 ] To the best of our knowledge, a case that developed myokymia in the pediatric age group and on peroneus longus muscles has not been reported before in the literature.…”

Section: Discussionmentioning

confidence: 99%

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Botulinum Toxin Type A for the Treatment of Limb Myokymia

Işıkay¹

2022

Annals of Indian Academy of Neurology

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Myokymia is a rare neuromuscular disorder and limb involvement is not common in this disease. To the best of our knowledge, isolated peroneus longus muscle myokymia was not reported before in the literature; and for that reason treatment protocols were not established. Botulinum toxin type A (BoNT-A), which is used in the treatment of a variety of neurologic disorders, was also defined as a treatment option in myokymia. Herein, we will report three cases of peroneus longus muscle myokymia in children in the absence of any other neurological findings, and the successful results of treatment with local BoNT-A injections. BoNT-A is a safe and effective treatment in myokymia when administered by an experienced clinician and should always be considered when the disorder is persistent and affecting the life of the patient.

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Section: Discussionmentioning

confidence: 99%

“…Both auto-excitation and changes in the microenvironment of these axons are of great importance in the formation of myokymic discharges. [ 5 6 7 ]…”

Section: Discussionmentioning

confidence: 99%

Botulinum Toxin Type A for the Treatment of Limb Myokymia

Işıkay¹

2022

Annals of Indian Academy of Neurology

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“…Secondary acquired PNHS also exist and originate from a diverse spectrum of disorders damaging peripheral nerves, such as polyneuropathies (especially in the context of irradiation) and toxins (insecticide, toluene, lead, etc.) [7 ▪ ,8 ▪ ,9]. There is no consensus on the diagnostic process to follow in secondary PNHS, but an autoimmune and paraneoplastic screening similar to that in primary PNHS is indicated.…”

Section: Introductionmentioning

confidence: 99%

Neuromuscular hyperexcitability syndromes

Wel

Claeys

2021

Current Opinion in Neurology

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Purpose of reviewTo provide an update on recent developments regarding acquired, antibody-mediated, neuromuscular hyperexcitability syndromes, including Isaac's and Morvan's syndromes, cramp-fasciculation syndrome and rippling muscle disease, and their genetic differential diagnoses.Recent findingsAntibodies in auto-immune peripheral nerve hyperexcitability syndromes (PNHS) are directed against CASPR2 and LGI1, proteins of the voltage-gated potassium channel (VGKC) complex. We discuss the significance of ‘double-negative’ VGKC antibodies in PNHS and the rationale for ceasing VGKC antibody testing (but testing CASPR2 and LGI1 antibodies instead) in clinical practice. Recent case reports also expand the possible clinical phenotypes related to CASPR2/LGI1 antibodies, but the interpretation of these findings is complicated by the frequent association of antibody-mediated neuromuscular hyperexcitability syndromes with other auto-immune disorders (e.g. myasthenia gravis).Finally, a hereditary origin of neuromuscular hyperexcitability should always be considered, even in non-VGKC-related genes, as evidenced by the recently discovered high frequency of HINT1 mutations in people of Slavic origin.SummaryThis review provides an update on recent clinical, immunological and genetic developments in neuromuscular hyperexcitability syndromes. We also provide a guide for the clinician for diagnosing and managing these disorders in clinical practice, with a special focus on the main differential diagnoses.

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Eribulin Mesylate-related Multifocal Demyelinating Neuropathy with Myokymia in a Breast Cancer Patient

et al. 2021

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We herein report a 48-year-old woman receiving eribulin mesylate for breast cancer who presented with gait disorder, distal limb paresthesia, and weakness progressing monthly. A nerve conduction study indicated demyelination with multifocal conduction block. Considering the immune-mediated pathology of her condition, she was administered intravenous immunoglobulin. Her neurological symptoms improved promptly after intravenous immunoglobulin therapy and eribulin withdrawal. Furthermore, the limb myokymia seen at the time of admission disappeared. Her symptoms continued to improve without additional treatment. We conclude that eribulin was a rare cause of demyelinating neuropathy with multifocal conduction block derived from immune-mediated pathology.

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Limb Myokymia in Guillain-Barré Syndrome

Cited by 6 publications

References 8 publications

Botulinum Toxin Type A for the Treatment of Limb Myokymia

Botulinum Toxin Type A for the Treatment of Limb Myokymia

Neuromuscular hyperexcitability syndromes

Eribulin Mesylate-related Multifocal Demyelinating Neuropathy with Myokymia in a Breast Cancer Patient

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