ArticleFrontiers in neurology2018
Acute Motor Axonal Neuropathy in Association with Hepatitis E.
Article in Frontiers in neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Axonal variants of Guillain-Barré syndrome: an update.Journal of neurology · 2021Review
- Neurological manifestations of hepatitis E virus infection: An overview.World journal of gastroenterology · 2021Review
- Acute Motor Axonal Neuropathy Improvement 20 Days After Hyperbaric Oxygen Therapy.International medical case reports journal · 2021Article
- Protective Effect of Hyperbaric Oxygen Treatment on Axon Degeneration after Acute Motor Axonal Neuropathy.Autoimmune diseases · 2021Article
- Guillain-Barré syndrome in a man presenting with upper extremity monoplegia.Clinical case reports · 2020Article
- A Systematic Review of the Extra-Hepatic Manifestations of Hepatitis E Virus Infection.Medical sciences (Basel, Switzerland) · 2020Review
- Hepatitis E virus-associated Guillain-Barre syndrome: Revision of the literature.Brain and behavior · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Guillain-Barré syndrome (GBS) is an acute peripheral neuropathy that develops as a result of post-infectious immune-mediated nerve injury. It can be classified into classic and variant GBS. Acute motor axonal neuropathy (AMAN) is a subtype of GBS with the key clinical features of pure motor weakness, areflexia, absence of sensory symptoms, and lack of neurophysiologic evidence of demyelination. We reported a case of acute motor axonal neuropathy in association with hepatitis E infection. A young woman was referred to us after a period of nausea, fever, and diarrhea. She had unexplained muscle weakness at admission and has been diagnosed with acute hepatitis E infection. A rigorous clinical neurological assessment revealed bilateral symmetrical weakness, which affects the lower limbs more than the upper limbs, with no evidence of sensory involvement. Neurophysiological measurements indicated acute axonal injury without clues to demyelination. A diagnosis of acute motor axonal neuropathy subtype has been made, to which she only received supportive therapy. The symptoms resolved spontaneously and full recovery of motor function was attained after 35 days of weakness onset with complete normalization of neurophysiologic parameters.
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