Clinical and Electrophysiological Features of Chronic Motor Axonal Neuropathy.
Journal
Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society
ISSN: 1537-1603
Titre abrégé: J Clin Neurophysiol
Pays: United States
ID NLM: 8506708
Informations de publication
Date de publication:
01 May 2022
01 May 2022
Historique:
pubmed:
28
8
2020
medline:
10
5
2022
entrez:
28
8
2020
Statut:
ppublish
Résumé
To determine the clinical and electrophysiological characteristics of chronic motor axonal neuropathy (CMAN) and identify the associated similarities and differences between CMAN, acute motor axonal neuropathy (AMAN), and motor neuropathy secondary to amyotrophic lateral sclerosis. The study described clinical and electrophysiological features of five patients with CMAN and compared with 20 AMAN patients, 42 amyotrophic lateral sclerosis patients and 41 healthy controls. To compare the distribution of different nerve involvement in the same limb, split ratio was introduced. Split ratio of upper limb = amplitude of compound muscle action potential abductor pollicis brevis (APB)/amplitude of compound muscle action potential abductor digiti minimi, and split ratio of lower limb = amplitude of compound muscle action potential extensor digitorum brevis/amplitude of compound muscle action potential abductor hallucis. Chronic motor axonal neuropathy patients manifested lower motor neuron syndrome with positive IgG anti-monosialoganglioside antibodies and good outcome. The CMAN patients shared similar clinical manifestation with AMAN patients except for disease course and higher Medical Research Council scores. Compared with healthy controls, the split ratio of lower limb was higher in both CMAN and AMAN, despite comparable split ratio of upper limb. There was significant difference between CMAN group and amyotrophic lateral sclerosis group in nerve involvement presented as split hand and split leg signs in amyotrophic lateral sclerosis and reverse split leg sign in CMAN. Chronic motor axonal neuropathy associated with monosialoganglioside might be a "mild" AMAN with chronic onset by similar clinical and electrophysiological features. There was a unique pattern of nerve involvement presenting as reverse split leg sign in both CMAN and AMAN.
Identifiants
pubmed: 32852287
pii: 00004691-202205000-00014
doi: 10.1097/WNP.0000000000000771
doi:
Substances chimiques
Amantadine
BF4C9Z1J53
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
317-323Informations de copyright
Copyright © 2020 by the American Clinical Neurophysiology Society.
Déclaration de conflit d'intérêts
The authors have no funding or conflicts of interest to disclose.
Références
Garg N, Park SB, Vucic S, et al. Differentiating lower motor neuron syndromes. J Neurolneurosurg Psychiatry 2017;88:474–483.
Liewluck T, Saperstein DS. Progressive muscular atrophy. Neurol Clin 2005;33:761–773.
Kim WK, Liu X, Sandner J, et al. Study of 962 patients indicates progressive muscular atrophy is a form of ALS. Neurology 2009;73:1686–1692.
Kuwabara S, Yuki N. Axonal Guillain-Barré syndrome: concepts and controversies. Lancet Neurol 2013;12:1180–1188.
Eisen A, Kuwabara S. The split hand syndrome in amyotrophic lateral sclerosis. J Neurol Neurosurg Psychiatry 2012;83:399–403.
Wang ZL, Cui L, Liu M, et al. Reassessment of split-leg signs in amyotrophic lateral sclerosis: differential involvement of the extensor digitorum brevis and abductor hallucis muscles. Front Neurol 2019;10:565.
van den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, van Doorn PA. Guillain-Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol 2014;10:469–482.
de Carvalho M, Dengler R, Eisen A, et al. Electrodiagnostic criteria for diagnosis of ALS. Clin Neurophysiol 2008;119:497–503.
Gorson KC, Ropper AH, Adelman LS, Raynor EM, Saper CB. Chronic motor axonal neuropathy: pathological evidence of inflammatory polyradiculoneuropathy. Muscle Nerve 1999;22:266–270.
Kaji R, Kusunoki S, Mizutani K, et al. Chronic motor axonal neuropathy associated with antibodies monospecific for N-acetylgalactosaminyl GD1a. Muscle Nerve 2000;23:702–706.
Riva N, Gallia F, Iannaccone S, et al. Chronic motor axonal neuropathy. J Peripher Nerv Syst 2011;16:341–346.
Pestronk A, Cornblath D, Ilyas A, et al. A treatable multifocal motor neuropathy with antibodies to GM1 ganglioside. Ann Neurol 1988;24:73–78.
Illa I, Ortiz N, Gallard E, Juarez C, Grau JM, Dalakas MC. Acute axonal Guillain-Barré syndrome with IgG antibodies against motor axons following parenteral gangliosides. Ann Neurol 1995;38:218–224.
Yuki N, Sato S, Miyatake T, Sugiyama K, Katagiri T, Sasaki H. Motoneuron-disease-like disorder after ganglioside therapy. Lancet 1991;337:1109–1110.
Yuki N. Acute motor axonal neuropathy and multifocal motor neuropathy: more in common than not. Muscle Nerve 2013;48:693–695.
Ugrenovic SZ, Jovanovic ID, Kovacevic P, Petrović S, Simic T. Similarities and dissimilarities of the blood supplies of the human sciatic, tibial, and common peroneal nerves. Clin Anat 2012;26:875–882.
Yuki N, Kuwabara S, Koga M, Hirata K. Acute motor axonal neuropathy and acute motor-sensory axonal neuropathy share a common immunological profile. J Neurol Sci 1999;168:121–126.