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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-8-30
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1460-2156
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
133
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2727-33
pubmed:meshHeading
pubmed-meshheading:20736187-Action Potentials, pubmed-meshheading:20736187-Adult, pubmed-meshheading:20736187-Aged, pubmed-meshheading:20736187-Aged, 80 and over, pubmed-meshheading:20736187-Amyotrophic Lateral Sclerosis, pubmed-meshheading:20736187-Cerebral Cortex, pubmed-meshheading:20736187-Electroencephalography, pubmed-meshheading:20736187-Electromyography, pubmed-meshheading:20736187-Evoked Potentials, Motor, pubmed-meshheading:20736187-Female, pubmed-meshheading:20736187-Humans, pubmed-meshheading:20736187-Isaacs Syndrome, pubmed-meshheading:20736187-Male, pubmed-meshheading:20736187-Middle Aged, pubmed-meshheading:20736187-Motor Neurons, pubmed-meshheading:20736187-Neural Conduction, pubmed-meshheading:20736187-Peripheral Nerves, pubmed-meshheading:20736187-Probability, pubmed-meshheading:20736187-Reaction Time, pubmed-meshheading:20736187-Transcranial Magnetic Stimulation
pubmed:year
2010
pubmed:articleTitle
Corticomotoneuronal function and hyperexcitability in acquired neuromyotonia.
pubmed:affiliation
Neuroscience Research Australia, Barker Street, Randwick, Sydney, NSW 2031, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't