Document Detail

Corticomotoneuronal function and hyperexcitability in acquired neuromyotonia.
MedLine Citation:
PMID:  20736187     Owner:  NLM     Status:  MEDLINE    
Acquired neuromyotonia encompasses a group of inflammatory disorders characterized by symptoms reflecting peripheral nerve hyperexcitability, which may be clinically confused in the early stages with amyotrophic lateral sclerosis. Despite a clear peripheral nerve focus, it remains unclear whether the ectopic activity in acquired neuromyotonia receives a central contribution. To clarify whether cortical hyperexcitability contributes to development of clinical features of acquired neuromyotonia, the present study investigated whether threshold tracking transcranial magnetic stimulation could detect cortical hyperexcitability in acquired neuromyotonia, and whether this technique could differentiate acquired neuromyotonia from amyotrophic lateral sclerosis. Cortical excitability studies were undertaken in 18 patients with acquired neuromyotonia and 104 patients with amyotrophic lateral sclerosis, with results compared to 62 normal controls. Short-interval intracortical inhibition in patients with acquired neuromyotonia was significantly different when compared to patients with amyotrophic lateral sclerosis (averaged short interval intracortical inhibition acquired neuromyotonia 11.3 +/- 1.9%; amyotrophic lateral sclerosis 2.6 +/- 0.9%, P < 0.001). In addition, the motor evoked potential amplitudes (acquired neuromyotonia 21.0 +/- 3.1%; amyotrophic lateral sclerosis 38.1 +/- 2.2%, P < 0.0001), intracortical facilitation (acquired neuromyotonia -0.9 +/- 1.3%; amyotrophic lateral sclerosis -2.3 +/- 0.6%, P < 0.0001), resting motor thresholds (acquired neuromyotonia 62.2 +/- 1.6%; amyotrophic lateral sclerosis 57.2 +/- 0.9%, P < 0.05) and cortical silent period durations (acquired neuromyotonia 212.8 +/- 6.9 ms; amyotrophic lateral sclerosis 181.1 +/- 4.3 ms, P < 0.0001) were significantly different between patients with acquired neuromyotonia and amyotrophic lateral sclerosis. Threshold tracking transcranial magnetic stimulation established corticomotoneuronal integrity in acquired neuromyotonia, arguing against a contribution of central processes to the development of nerve hyperexcitability in acquired neuromyotonia.
Steve Vucic; Benjamin C Cheah; Con Yiannikas; Angela Vincent; Matthew C Kiernan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-23
Journal Detail:
Title:  Brain : a journal of neurology     Volume:  133     ISSN:  1460-2156     ISO Abbreviation:  Brain     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-30     Completed Date:  2010-09-20     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  0372537     Medline TA:  Brain     Country:  England    
Other Details:
Languages:  eng     Pagination:  2727-33     Citation Subset:  AIM; IM    
Neuroscience Research Australia, Barker Street, Randwick, Sydney, NSW 2031, Australia.
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MeSH Terms
Action Potentials / physiology
Aged, 80 and over
Amyotrophic Lateral Sclerosis / pathology
Cerebral Cortex / pathology*
Electroencephalography / methods
Electromyography / methods
Evoked Potentials, Motor / physiology*
Isaacs Syndrome / complications*,  pathology*
Middle Aged
Motor Neurons / physiology*
Neural Conduction / physiology
Peripheral Nerves / physiopathology
Reaction Time / physiology
Transcranial Magnetic Stimulation / methods

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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