ECTRIMS eLearning

Inclusion of brain atrophy in no evidence of disease activity (NEDA) improves the ability to detect good long term responders
Author(s):
J.L. Ruiz Peña
,
J.L. Ruiz Peña
Affiliations:
G. Navarro Mascarell
,
G. Navarro Mascarell
Affiliations:
M. Rus
,
M. Rus
Affiliations:
F. Damas
,
F. Damas
Affiliations:
S. Eichau
,
S. Eichau
Affiliations:
M.A. Gamero Garcia
,
M.A. Gamero Garcia
Affiliations:
J.M. Garcia Moreno
,
J.M. Garcia Moreno
Affiliations:
D. Paramo Caminoa
,
D. Paramo Caminoa
Affiliations:
E. Pacheco
,
E. Pacheco
Affiliations:
S. Perez
,
S. Perez
Affiliations:
G. Izquierdo Ayuso
G. Izquierdo Ayuso
Affiliations:
ECTRIMS Learn. Ruiz Pena J. 09/14/16; 145613; EP1518
Juan Luis Ruiz Pena
Juan Luis Ruiz Pena
Contributions
Abstract

Abstract: EP1518

Type: ePoster

Abstract Category: Therapy - disease modifying - Long-term treatment monitoring

Background: No evidence of disease activity 3 (NEDA 3) defined as absence of magnetic resonance imaging activity (new T2 lesions), relapses and disability progression is used as a measure of treatment response in relapsing remitting multiple sclerosis (RRMS). Brain atrophy, which occurs rapidly in patients with MS, is an objective measure of disease worsening and progression.

Objective: To determine the percentage of patients with NEDA 3 in the first year of treatment and calculate the impact of adding brain atrophy (NEDA 4) to detect good long term responders

Methods: 41 patients (11 male and 30 female) with Relapsing Remitting MS and a Kurtzke Expanded Disability Scale Score (EDSS) of 0-5.0 were included in a prospective, longitudinal study of Fingolimod in RRMS. All patients were followed up for a mean period of 30 months. Every three months disability was assessed by different neurological scale. Percentage of Brain Volume Change (PBVC) between month 12 and baseline was measured by using an automated web version of Siena (Neuroresearch).

Results: At the first year, 20% of patients on fingolimod 0.5 mg achieved NEDA 3. Adding Brain Atrophy, the proportions of patients achieving NEDA 4 was 14%. The 15% of patients with NEDA 3 worsened after two years while none of the patients with NEDA 4 did it.

Conclusions: NEDA 4 improves the ability of NEDA 3 to detect good long-term responders, by working with both markers of inflammation and neurodegeneration. The dissemination of new automated methods for measuring brain atrophy will facilitate their use, with the consequent benefit for the patients. Furthers studies are needed.

Disclosure: Nothing to disclose

Abstract: EP1518

Type: ePoster

Abstract Category: Therapy - disease modifying - Long-term treatment monitoring

Background: No evidence of disease activity 3 (NEDA 3) defined as absence of magnetic resonance imaging activity (new T2 lesions), relapses and disability progression is used as a measure of treatment response in relapsing remitting multiple sclerosis (RRMS). Brain atrophy, which occurs rapidly in patients with MS, is an objective measure of disease worsening and progression.

Objective: To determine the percentage of patients with NEDA 3 in the first year of treatment and calculate the impact of adding brain atrophy (NEDA 4) to detect good long term responders

Methods: 41 patients (11 male and 30 female) with Relapsing Remitting MS and a Kurtzke Expanded Disability Scale Score (EDSS) of 0-5.0 were included in a prospective, longitudinal study of Fingolimod in RRMS. All patients were followed up for a mean period of 30 months. Every three months disability was assessed by different neurological scale. Percentage of Brain Volume Change (PBVC) between month 12 and baseline was measured by using an automated web version of Siena (Neuroresearch).

Results: At the first year, 20% of patients on fingolimod 0.5 mg achieved NEDA 3. Adding Brain Atrophy, the proportions of patients achieving NEDA 4 was 14%. The 15% of patients with NEDA 3 worsened after two years while none of the patients with NEDA 4 did it.

Conclusions: NEDA 4 improves the ability of NEDA 3 to detect good long-term responders, by working with both markers of inflammation and neurodegeneration. The dissemination of new automated methods for measuring brain atrophy will facilitate their use, with the consequent benefit for the patients. Furthers studies are needed.

Disclosure: Nothing to disclose

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