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Acute Motor Axonal Neuropathy (acute + motor_axonal_neuropathy)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Case report: Hepatitis A preceding Guillain,Barré Syndrome,

JOURNAL OF MEDICAL VIROLOGY, Issue 8 2006
Shobha D. Chitambar
Abstract A case of acute hepatitis A with Guillain,Barré Syndrome subtype AMAN (acute motor axonal neuropathy) in a 17-year-old male is reported. Serum and cerebrospinal fluid were positive for anti-hepatitis A virus (HAV) IgM, IgG, and IgA. The onset of the syndrome was evident in week 3 of illness. The remarkably high titers of serum anti-HAV IgG appeared unique to a hepatitis A patient with the syndrome. Phylogenetic analysis of the HAV genome detected in the serum and feces revealed genotype IIIA, circulating commonly in Pune, western India. J. Med. Virol. 78:1011,1014, 2006. © 2006 Wiley-Liss, Inc. [source]

Clinical presentation and prognosis of childhood Guillain,Barré syndrome

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 7-8 2008
Jung Hwan Lee
Aim: Guillain,Barré syndrome (GBS) is an acute inflammatory polyneuropathy commonly characterised by rapidly progressive, symmetric weakness and areflexia. This study is to assess the clinical characteristics of paediatric GBS, as well as its long-term functional prognosis. Methods: We retrospectively assessed the clinical manifestations, results of electrodiagnostic tests, functional status and prognosis of 56 children diagnosed with GBS. Based on clinical and electrophysiological findings, the patients were classified as having acute inflammatory demyelinating polyradiculoneuropathy ([AIDP]n = 34), acute motor axonal neuropathy ([AMAN]n = 14), acute motor and sensory axonal neuropathy (n = 1) and Miller Fisher syndrome ([MFS]n = 7). Results: Upper respiratory infection was the most frequent preceding event, and limb weakness was the most frequent symptom at GBS onset. There was no significant difference in the mean time from the onset of illness to nadir between any of these groups. Both the AIDP and AMAN groups showed significantly poorer functional status, measured by the Hughes scale, than the MFS group. Two years after nadir, however, the three groups did not differ significantly. Functional status at nadir, as estimated by the Hughes scale, is a more important factor than electrophysiological types in predicting long-term outcome. Conclusion: The most common symptom at onset in paediatric GBS was limb weakness. Functional status at nadir in AMAN was not significantly different from that of AIDP, and both types achieved good functional outcome for ambulation after 2 years. Functional status at nadir was more important than the electrophysiological type in predicting long-term outcomes. [source]

Ganglioside mimicry and peripheral nerve disease

MUSCLE AND NERVE, Issue 6 2007
Nobuhiro Yuki MD
Abstract Four criteria must be satisfied to conclude that a given microorganism causes Guillain,Barré (GBS) or Fisher (FS) syndrome associated with anti-ganglioside antibodies: (1) an epidemiological association between the infecting microbe and GBS or FS; (2) isolation in the acute progressive phase of illness of that microorganism from GBS or FS patients with associated anti-ganglioside IgG antibodies; (3) identification of a microbial ganglioside mimic; and (4) a GBS or FS with associated anti-ganglioside antibodies model produced by sensitization with the microbe itself or its component, as well as with ganglioside. Campylobacter jejuni is a definitive causative microorganism of acute motor axonal neuropathy and may cause FS and related conditions. Haemophilus influenzae and Mycoplasma pneumoniae are possible causative microorganisms of acute motor axonal neuropathy or FS. Acute and chronic inflammatory demyelinating polyneuropathies may be produced by mechanisms other than ganglioside mimicry. Muscle Nerve, 2007 [source]

Time course of axonal regeneration in acute motor axonal neuropathy

MUSCLE AND NERVE, Issue 6 2007
Noriko Tamura MD
Abstract Patients with acute motor axonal neuropathy (AMAN) generally recover well. We reviewed clinical and electrophysiologic recovery in 13 patients for up to 5 years. Twelve patients showed rapid recovery over 12 months, whereas in the remaining one the recovery was slow and incomplete at 5 years. In AMAN, axonal degeneration appears to develop predominantly in the motor nerve terminals, and only occasionally more proximally in the nerve roots. Nerve terminal degeneration,regeneration presumably provides a mechanism for good recovery. Muscle Nerve, 2007 [source]