Cortical plasticity predicts recovery from relapse in multiple sclerosis

Background: Relapsing–remitting multiple sclerosis (RRMS) is characterized by the occurrence of clinical relapses, followed by remitting phases of a neurological deficit. Clinical remission after a relapse can be complete, with a return to baseline function that was present before, but is sometimes...

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Bibliographic Details
Published in:Multiple sclerosis 2014-04, Vol.20 (4), p.451-457
Main Authors: Mori, Francesco, Kusayanagi, Hajime, Nicoletti, Carolina Gabri, Weiss, Sagit, Marciani, Maria Grazia, Centonze, Diego
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Evoked Potentials, Somatosensory - physiology
Female
Humans
Immunomodulators
Long-Term Potentiation - physiology
Magnetic Resonance Imaging
Male
Medical sciences
Middle Aged
Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis
Multiple Sclerosis, Relapsing-Remitting - physiopathology
Neurology
Neuronal Plasticity - physiology
Pharmacology. Drug treatments
Recovery of Function - physiology
Recurrence
Transcranial Magnetic Stimulation
Young Adult
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Summary:Background: Relapsing–remitting multiple sclerosis (RRMS) is characterized by the occurrence of clinical relapses, followed by remitting phases of a neurological deficit. Clinical remission after a relapse can be complete, with a return to baseline function that was present before, but is sometimes only partial or absent. Remyelination and repair of the neuronal damage do contribute to recovery, but they are usually incomplete. Objective: We tested the hypothesis that synaptic plasticity, namely long-term potentiation (LTP), may represent an additional substrate for compensating the clinical defect that results from the incomplete repair of neuronal damage. Methods: We evaluated the correlation between a measure of LTP, named paired associative stimulation (PAS), at the time of relapse and symptom recovery, in a cohort of 22 newly-diagnosed MS patients. Results: PAS-induced LTP was normal in patients with complete recovery, and reduced in patients showing incomplete or absent recovery, 12 weeks after the relapse onset. A multivariate regression model showed that PAS-induced LTP and age may contribute to predict null, partial or complete symptom recovery after a relapse. Conclusion: Synaptic plasticity may contribute to symptom recovery after a relapse in MS; and PAS, measured during a relapse, may be used as a predictor of recovery.
ISSN:1352-4585
1477-0970
DOI:10.1177/1352458513512541