Acute Motor Axonal Neuropathy: Difference between revisions
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=== Aetiology === | === Aetiology === | ||
AMAN is linked to ''Campylobacter jejuni'' and Zika virus infection<ref>Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM. [[Guillain-Barre syndrome in northern China Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies.]] Brain. 1995 Jun 1;118(3):597-605.</ref><ref>Watrin L, Ghawché F, Larre P, Neau JP, Mathis S, Fournier E. [https://journals.lww.com/md-journal/fulltext/2016/04050/guillain_barr__syndrome__42_cases__occurring.50.aspx Guillain–Barré syndrome (42 cases) occurring during a Zika virus outbreak in French Polynesia.] Medicine. 2016 Apr 1;95(14):e3257.</ref> | |||
* AMAN is strongly linked to ''Campylobacter jejuni'' and Zika virus infection<ref>Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM. [[Guillain-Barre syndrome in northern China Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies.]] Brain. 1995 Jun 1;118(3):597-605.</ref><ref>Watrin L, Ghawché F, Larre P, Neau JP, Mathis S, Fournier E. [https://journals.lww.com/md-journal/fulltext/2016/04050/guillain_barr__syndrome__42_cases__occurring.50.aspx Guillain–Barré syndrome (42 cases) occurring during a Zika virus outbreak in French Polynesia.] Medicine. 2016 Apr 1;95(14):e3257.</ref> | |||
* AMAN has some documented association with hepatitis E infection<ref name=":1" /> | |||
=== Clinical features === | === Clinical features === | ||
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* Bulbar palsy in 61% of patients<ref name=":0" /> | * Bulbar palsy in 61% of patients<ref name=":0" /> | ||
However, it presents without any sensory symptoms, unlike GBS<ref name=":1">Al-Saffar A, Al-Fatly B. [[Acute Motor Axonal Neuropathy in Association with Hepatitis E.]] Front Neurol. 2018 Feb 9;9:62. doi: 10.3389/fneur.2018.00062. PMID: 29479336; PMCID: PMC5811470.</ref>. A neurophysiological screen in patients with AMAN should also show no evidence of demyelination, unlike GBS<ref name=":1" />. | However, it presents without any sensory symptoms, unlike GBS<ref name=":1">Al-Saffar A, Al-Fatly B. [[Acute Motor Axonal Neuropathy in Association with Hepatitis E.]] Front Neurol. 2018 Feb 9;9:62. doi: 10.3389/fneur.2018.00062. PMID: 29479336; PMCID: PMC5811470.</ref>. A neurophysiological screen in patients with AMAN should also show no evidence of demyelination, unlike GBS<ref name=":1" />. | ||
=== Prognosis === | |||
The prognosis of AMAN is worse compared to the other subtypes of GBS<ref>Zhang Y, Zhao Y, Wang Y. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398209/ Prognostic factors of Guillain-Barré syndrome: a 111-case retrospective review]. Chin Neurosurg J. 2018 Jun 18;4:14. doi: 10.1186/s41016-018-0122-y. PMID: 32922875; PMCID: PMC7398209.</ref>. | |||
=== References === | === References === |
Revision as of 02:58, 17 April 2024
Introduction[edit | edit source]
Acute motor axonal neuropathy (AMAN) is classified as a subtype of Guillain–Barré syndrome (GBS)[1]. The disease was first discovered in China and was nicknamed 'chinese paralytic disease'[1]. AMAN is the most common cause of flaccid paralysis in China[2]. Pathology in AMAN patients are usually limited to the motor nerve, with macrophages destroying axons while myelin remains intact, a contrast to AIDP GBS (most common form of GBS) which is known as a demyelinating disease[1]. While AMAN mainly involves axonal damage to motor nerve fibres; acute inflammatory demyelinating polyradiculoneuropathy (AIDP) involves both motor and sensory nerve fibre damage due to demyelination[1].
AMAN has an estimated prevalence of 30–65% in Asia, Central and South America[3].
Aetiology[edit | edit source]
- AMAN is strongly linked to Campylobacter jejuni and Zika virus infection[4][5]
- AMAN has some documented association with hepatitis E infection[6]
Clinical features[edit | edit source]
AMAN presents similarly in terms of clinical features as well as CSF findings to GBS[1].
- Weakness of limbs (earliest symptom is weakness of lower limbs)
- Weakness of respiratory muscles
- Gradual weakening and finally, absence of tendon reflexes
- Bulbar palsy in 61% of patients[1]
However, it presents without any sensory symptoms, unlike GBS[6]. A neurophysiological screen in patients with AMAN should also show no evidence of demyelination, unlike GBS[6].
Prognosis[edit | edit source]
The prognosis of AMAN is worse compared to the other subtypes of GBS[7].
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Lv J, Zhaori G. Collaborative studies of U.S.–China neurologists on acute motor axonal neuropathy - PMC (nih.gov) Pediatr Investig. 2022 Mar 22;6(1):1-4. doi: 10.1002/ped4.12316. PMID: 35382424; PMCID: PMC8960912.
- ↑ McKhann GM, Cornblath DR, Griffin JW, Ho TW, Li CY, Jiang Z, Wu HS, Zhaori G, Liu Y, Jou LP, Liu TC. Acute motor axonal neuropathy: a frequent cause of acute flaccid paralysis in China. Annals of neurology. 1993 Apr;33(4):333-42.
- ↑ Van den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, Van Doorn PA. Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nature Reviews Neurology. 2014 Aug;10(8):469-82.
- ↑ Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM. Guillain-Barre syndrome in northern China Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies. Brain. 1995 Jun 1;118(3):597-605.
- ↑ Watrin L, Ghawché F, Larre P, Neau JP, Mathis S, Fournier E. Guillain–Barré syndrome (42 cases) occurring during a Zika virus outbreak in French Polynesia. Medicine. 2016 Apr 1;95(14):e3257.
- ↑ 6.0 6.1 6.2 Al-Saffar A, Al-Fatly B. Acute Motor Axonal Neuropathy in Association with Hepatitis E. Front Neurol. 2018 Feb 9;9:62. doi: 10.3389/fneur.2018.00062. PMID: 29479336; PMCID: PMC5811470.
- ↑ Zhang Y, Zhao Y, Wang Y. Prognostic factors of Guillain-Barré syndrome: a 111-case retrospective review. Chin Neurosurg J. 2018 Jun 18;4:14. doi: 10.1186/s41016-018-0122-y. PMID: 32922875; PMCID: PMC7398209.