scholarly journals Acute Motor Axonal Neuropathy Accompanied with Delayed Facial Diplegia

2021 ◽  
Vol 13 (2) ◽  
pp. 40-43
Author(s):  
Byeol-A Yoon ◽  
Hyein Chung ◽  
Ja Hyeon Cho ◽  
Jong Kuk Kim
Keyword(s):  
Axonal Neuropathy ◽  
Acute Motor Axonal Neuropathy ◽  
Facial Diplegia

scholarly journals Clinical features and outcome of Guillain–Barre syndrome in Saudi Arabia: a multicenter, retrospective study

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mohammed H. Alanazy ◽  
Sawsan S. Bakry ◽  
Afnan Alqahtani ◽  
Norah S. AlAkeel ◽  
Naael Alazwary ◽  
...  
Keyword(s):  
Saudi Arabia ◽  
Clinical Features ◽  
Axonal Neuropathy ◽  
Guillain Barre Syndrome ◽  
Upper Respiratory Tract ◽  
Arab Population ◽  
Acute Motor Axonal Neuropathy ◽  
Facial Diplegia ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

Abstract Background Guillain–Barre syndrome (GBS) is an inflammatory polyradiculoneuropathy characterized by rapidly evolving weakness and areflexia, reaching nadir within 4 weeks. Data on the characteristic of GBS in Saudi Arabia are limited. This study aimed to describe the clinical, electrophysiological, and laboratory characteristics and outcome of a multicenter cohort of patients with GBS. Methods This is a retrospective multicenter nationwide study. Patients who had GBS, identified through Brighton Criteria, between January 2015 and December 2019 were included. Data collected included demographics, clinical features, cerebrospinal fluid profile, reported electrophysiological patterns, treatment, and outcome. Reported GBS subtypes were compared using chi-square, Fisher's exact, or Mann–Whitney U tests, as appropriate. Results A total of 156 patients with GBS were included (men, 61.5%), with a median age of 38 (interquartile range, 26.25–53.5) years. The most commonly reported antecedent illnesses were upper respiratory tract infection (39.1%) and diarrhea (27.8%). All but two patients (98.7%) had weakness, 64.1% had sensory symptoms, 43.1% had facial diplegia, 33.8% had oropharyngeal weakness, 12.4% had ophthalmoplegia, and 26.3% needed mechanical ventilation. Cytoalbuminological dissociation was observed in 69.1% of the patients. GBS-specific therapy was administered in 96.8% of the patients, of whom 88.1% had intravenous immunoglobulin, and 11.9% had plasmapheresis. Approximately half of the patients were able to walk independently within 9 months after discharge, and a third regained the ability to walk independently thereafter. Death of one patient was caused by septicemia. Acute inflammatory demyelinating polyradiculoneuropathy was the most commonly reported GBS subtype (37.7%), followed by acute motor axonal neuropathy (29.5%), and acute motor-sensory axonal neuropathy (19.2%). Conclusion The clinical and laboratory characteristics and outcome of GBS in the Arab population of Saudi Arabia are similar to the international cohorts. The overall prognosis is favorable.

scholarly journals Pearls & Oy-sters: Delayed Diagnosis of Acute Motor Axonal Neuropathy With Cardiac Arrest

Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000013220
Author(s):  
Sina Marzoughi ◽  
Laura Marulanda ◽  
Dian Ngo ◽  
Tychicus Chen
Keyword(s):  
Cardiac Arrest ◽  
Treatment Options ◽  
Axonal Neuropathy ◽  
Delayed Diagnosis ◽  
Rapid Progression ◽  
Acute Motor Axonal Neuropathy ◽  
Lower Extremity Weakness ◽  
Ocular Movements ◽  
Facial Diplegia ◽  
Systemic Symptoms

We present the case of a 53-year-old female who presented with right lower extremity weakness with preceding systemic symptoms including fever and chest pain. She developed rapid quadriparesis over 24 hours and had ventricular fibrillation with cardiac arrest. Examination demonstrated tetraplegia, facial diplegia with spared extra-ocular movements and areflexia. Electrodiagnostic studies including nerve conduction studies and electromyography were consistent with Acute Motor Axonal Neuropathy (AMAN). This case highlights an atypical asymmetric presentation with initially preserved reflexes, rapid progression and cardiac dysfunction that can occur independent of dysautonomia. Treatment options include intravenous immunoglobulin (IVIg) or plasmapheresis as well as supportive care and long term multidisciplinary rehabilitation and communication strategies.

Neuroleptic malignant syndrome and acute motor axonal neuropathy after Campylobacter jejuni infection

2009 ◽  
Vol 39 (3) ◽  
pp. 135-138 ◽  
Author(s):  
Y.A. Rajabally ◽  
A. Ramlackhansingh ◽  
M. Fraser ◽  
R.J. Abbott
Keyword(s):  
Neuroleptic Malignant Syndrome ◽  
Campylobacter Jejuni ◽  
Axonal Neuropathy ◽  
Acute Motor Axonal Neuropathy

scholarly journals Acute Motor Axonal Neuropathy Associated with Pandemic H1N1 Influenza A Infection

2010 ◽  
Vol 13 (1) ◽  
pp. 98-100 ◽  
Author(s):  
Marko Kutleša ◽  
Marija Santini ◽  
Vladimir Krajinović ◽  
Dinko Raffanelli ◽  
Bruno Baršić
Keyword(s):  
Influenza A ◽  
Axonal Neuropathy ◽  
H1n1 Influenza ◽  
Pandemic H1n1 ◽  
Acute Motor Axonal Neuropathy ◽  
Pandemic H1n1 Influenza

Acute Motor Axonal Neuropathy Associated with IgM Anti-GM1 following Mycoplasma pneumoniae Infection

1999 ◽  
Vol 41 (3) ◽  
pp. 175-176 ◽  
Author(s):  
J.G. Heckmann ◽  
J.B. Sommer ◽  
A. Druschky ◽  
F.J. Erbguth ◽  
A.J. Steck ◽  
...  
Keyword(s):  
Mycoplasma Pneumoniae ◽  
Axonal Neuropathy ◽  
Acute Motor Axonal Neuropathy

scholarly journals Campylobacter Species and Guillain-Barré Syndrome

1998 ◽  
Vol 11 (3) ◽  
pp. 555-567 ◽  
Author(s):  
Irving Nachamkin ◽  
Ban Mishu Allos ◽  
Tony Ho
Keyword(s):  
Molecular Mimicry ◽  
Current Knowledge ◽  
Axonal Neuropathy ◽  
Autoimmune Disorder ◽  
Acute Motor Axonal Neuropathy ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Campylobacter Species ◽  
Antecedent Infection ◽  
Different Strains ◽  
Campylobacter Infection

SUMMARY Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.

Anti-GM1b IgG antibody is associated with acute motor axonal neuropathy and Campylobacter jejuni infection

2003 ◽  
Vol 210 (1-2) ◽  
pp. 41-45 ◽  
Author(s):  
Kazue Ogawara ◽  
Satoshi Kuwabara ◽  
Michiaki Koga ◽  
Masahiro Mori ◽  
Nobuhiro Yuki ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Axonal Neuropathy ◽  
Igg Antibody ◽  
Acute Motor Axonal Neuropathy
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