Document Detail


Natalizumab prevents the accumulation of cortical lesions in relapsing remitting multiple sclerosis: a preliminary report.
MedLine Citation:
PMID:  20535514     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Natalizumab has been demonstrated to be highly effective in reducing measures of disease activity, such as clinical relapse rate, and gadolinium (Gd)-enhancing and new or enlarging T2 lesions appearance in patients with relapsing remitting multiple sclerosis (RRMS). Up to date, no data on the effect of natalizumab on cortical pathology have been published. We studied the efficacy of natalizumab in preventing the accumulation of new cortical lesions (CL) in 35 RRMS patients treated for 1 year. While confirming the high impact of natalizumab in reducing the relapse rate (>90%, 85% relapse-free patients) and white matter (WM) pathology (80% patients free from new T2 WM lesions, 97% patients free from new T1 Gd-enhancing lesions), we found that this monoclonal antibody was highly effective in reducing the appearance of new CL (86% patients free from new CL). Our findings indicate a relevant activity of natalizumab against cortical inflammation in RRMS.
Authors:
F Rinaldi; M Calabrese; D Seppi; M Puthenparampil; P Perini; P Gallo
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology     Volume:  31 Suppl 3     ISSN:  1590-3478     ISO Abbreviation:  Neurol. Sci.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-02-18     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100959175     Medline TA:  Neurol Sci     Country:  Italy    
Other Details:
Languages:  eng     Pagination:  317-20     Citation Subset:  IM    
Affiliation:
Department of Neurosciences, The Multiple Sclerosis Centre of Veneto Region, University Hospital of Padova, Via Giustiniani 5, 35128, Padua, Italy, francyrinaldi@yahoo.com.
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