Conduction block in acute motor axonal neuropathy

Kokubun, Norito; Nishibayashi, Momoka; Uncini, Antonino; Odaka, Masaaki; Hirata, Koichi; Yuki, Nobuhiro

doi:10.1093/brain/awq260

Cited by 167 publications

(140 citation statements)

References 44 publications

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“…[18][19][20][21] In the current study, we found significant associations of reversible conduction failure with IgG anti-GM1, -GalNAc-GD1a, -GD1b, and -LM1/GA1 antibodies. Reversible conduction failure was first described in 1998 and this was followed by reports of similar findings in other cohorts.…”

Section: Resultssupporting

confidence: 60%

Antibodies to single glycolipids and glycolipid complexes in Guillain-Barré syndrome subtypes

et al. 2014

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Objective: To comprehensively investigate the relationship between antibodies to single glycolipids and their complexes and Guillain-Barré syndrome subtypes and clinical features.Methods: In acute sera from 199 patients with Guillain-Barré syndrome, immunoglobulin G (IgG) antibodies to glycolipids and ganglioside complexes were tested using ELISA against individual antigens from single glycolipids including gangliosides (LM1, GM1, GM1b, GD1a, GalNAc-GD1a, GD1b, GT1a, GT1b, GQ1b) and a neutral glycolipid, asialo-GM1 (GA1), and antigens from the combination of 2 different glycolipids. Based on serial nerve conduction studies, the electrodiagnoses were as follows: 69 demyelinating subtype, 85 axonal subtypes, and 45 unclassified.Results: Significant associations were detected between acute motor axonal neuropathy subtype and IgG antibodies to GM1, GalNAc-GD1a, GA1, or LM1/GA1 complex. Reversible conduction failure was significantly associated with IgG antibodies to GM1, GalNAc-GD1a, GD1b, or complex of LM1/GA1. No significant association was demonstrated between acute inflammatory demyelinating polyneuropathy and any of the glycolipids or ganglioside complexes. Antiganglioside complex antibodies alone were detected in 7 patients (5 axonal subtype). Conclusions:The current study demonstrates that antibodies to single glycolipids and ganglioside complexes are associated with acute motor axonal neuropathy or acute motor conduction block neuropathy but not acute inflammatory demyelinating polyneuropathy. Classification of evidence:This study provides Class II evidence that antibodies to glycolipids are increased in patients with acute motor axonal neuropathy and acute motor conduction block neuropathy but not acute inflammatory demyelinating polyneuropathy. Neurology ® 2014;83:118-124 GLOSSARY AIDP 5 acute inflammatory demyelinating polyneuropathy; AMAN 5 acute motor axonal neuropathy; AMCBN 5 acute motor conduction block neuropathy; GBS 5 Guillain-Barré syndrome; GSC 5 ganglioside complex; Ig 5 immunoglobulin; NCS 5 nerve conduction study.Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy with 2 major subtypes: acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).1 Within the axonal subtype, there are now recognized variants evident on nerve conduction studies (NCS), which demonstrate early reversible conduction failure, referred to as acute motor conduction block neuropathy (AMCBN).2 There is robust evidence that immunoglobulin G (IgG) anti-ganglioside antibodies are associated with the pathogenesis of AMAN, whereas the target antigens in AIDP remain elusive. The patients who were seronegative for antibodies to single gangliosides were found to have anti-GSC antibodies. The authors have since described further associations between anti-GSC antibodies and variants of GBS. This includes antibodies to LM1 and its complexes in AIDP, 5 to complex of GM1 and GalNAc-GD1a (GM1/GalNAc-GD1a) in AMCBN,6 and to complexes of GD1a/GD1b and GD1b/GT1b in pa...

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Section: Resultssupporting

confidence: 60%

Antibodies to single glycolipids and glycolipid complexes in Guillain-Barré syndrome subtypes

et al. 2014

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“…The reduction of CMAP amplitude and FR was equally seen in the ulnar, median, peroneal, and tibial nerve. Prolonged DML, CB, and slowing in mo- tor conduction velocity indicated the presence of demyelination [14]. Our results showed they were more frequently found in the ulnar and peroneal nerve than the median and tibial nerve.…”

Section: Discussionsupporting

confidence: 48%

Very Early Neurophysiological Study in Guillain-Barre Syndrome

Jin

Qin

et al. 2018

Eur Neurol

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Purpose: The diagnosis of Guillain-Barre syndrome (GBS) in the very early stage may be challenging. Our aim was to report the neurophysiological abnormalities in GBS within 4 days of clinical onset. We expected that GBS will be diagnosed by the assistance of neurophysiological study in the very early stage. Methods: We prospectively recruited patients with a diagnosis of GBS discharged from First Affiliated Hospital of Xi’an Jiaotong University and Xi Jing Hospital. Patients were classified into 3 groups according to the onset of symptoms to electromyography examination interval (OEI). The neurophysiological findings were carried out using standard procedures. All patients were examined by the same experienced neurophysiologist. Results: There were not significant group differences in abnormal rate, distal motor latency (DML), motor nerve conduction velocity (MNCV), F response (FR), compound muscle action potential (CMAP), conduction block (CB), sensory nerve action potential (SNAP), and sensory nerve conduction velocity among OEI ≤4 days, 4< OEI ≤10 days, and OEI > 10 days groups. Motor nerves were more affected than sensory nerves in neurophysiological presentation in very early stage patients. The difference of motor nerves and sensory nerves was statistically significant in lower limbs, but was not in upper limbs. In motor nerve conduction studies, the abnormal rate of DML, MNCV, FR, CB was more common seen in ulnar and peroneal nerve than median and tibial nerve, the abnormal rate of CMAP was the same in ulnar, median, peroneal and tibial nerve. In sensory nerve conduction studies, the abnormal rate of ulnar nerve and median nerve was higher than the superficial peroneal nerve and sural nerve. The OEI was not correlated with the SNAP decrease rate of median (r = 0.10, p = 0.23) and ulnar (r = 0.26, p = 0.06) but was statistically correlated with sural SNAP decrease rate (r = 0.29, p = 0.04). The sural-sparing pattern phenomenon was the most commonly discovered phenomenon in very early stage patients (OEI ≤4 days), followed by patients with 4< OEI ≤10 days, ultimately found in patients with OEI > 10 days. Conclusions: We suggest performing neurophysiological examination as soon as possible for suspected GBS patients, particularly focusing on multi-spots inspection of ulnar and peroneal nerves, and paying close attention to sural-sparing patterns.

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“…The prevention of conduction in AMAN generally occurs in the first three weeks of the disease, and it is mostly reversible. It was reported that performing serial electrophysiological testing is useful for understanding the pathophysiology of AMAN (4). While the findings of laboratory and CSF evaluations were normal and ENMG examination revealed normal Figure 1.…”

Section: Discussionmentioning

confidence: 97%

Severe Pure Acute Motor Axonal Neuropathy

Taşdemir¹,

Karakoç²,

Oktayoğlu³

et al. 2015

Erciyes Med J

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Acute motor axonal neuropathy (AMAN) is a subtype of Guillain-Barré syndrome. Characteristic electrophysiological features of AMAN are reduced amplitude or absence of muscle action potentials. Our patient described progressive weakness in his leg and was not able to independently walk; he had a feeling weakness in his arms within 24 h after the onset of symptoms. He was diagnosed with AMAN according to the clinical and electrophysiological features. He could independently walk after two years following intensive physical therapy and monitoring. Neurologists and physiatrist should conduct long term monitoring and rehabilitation for patients with AMAN because neurological deficits may persist for a long time.

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Conduction block in acute motor axonal neuropathy

Cited by 167 publications

References 44 publications

Antibodies to single glycolipids and glycolipid complexes in Guillain-Barré syndrome subtypes

Antibodies to single glycolipids and glycolipid complexes in Guillain-Barré syndrome subtypes

Very Early Neurophysiological Study in Guillain-Barre Syndrome

Severe Pure Acute Motor Axonal Neuropathy

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