Neuropsychologic status in multiple sclerosis after treatment with glatiramer

Citation
A. Weinstein et al., Neuropsychologic status in multiple sclerosis after treatment with glatiramer, ARCH NEUROL, 56(3), 1999, pp. 319-324
Citations number
50
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ARCHIVES OF NEUROLOGY
ISSN journal
00039942 → ACNP
Volume
56
Issue
3
Year of publication
1999
Pages
319 - 324
Database
ISI
SICI code
0003-9942(199903)56:3<319:NSIMSA>2.0.ZU;2-F
Abstract
Background: Glatiramer acetate (Copaxone) therapy reduces clinical disease activity in relapsing-remitting multiple sclerosis (MS). Objective: To study the effect of glatiramer therapy on neuropsychologic fu nction as part of a randomized, placebo-controlled, multicenter trial. Methods: Two hundred forty-eight patients with relapsing-remitting MS and m ild to moderate disability (Expanded Disability Status Scale score, <5.0) w ere tested before and 12 and 24 months after randomization to administratio n of glatiramer acetate, 20 mg/d, or matching placebo. Neuropsychologic tes ts examined 5 cognitive domains most often disrupted in patients with MS: s ustained attention, perceptual processing, verbal and visuospatial memory, and semantic retrieval. Results: Baseline neuropsychologic test performance was similar in both tre atment groups and was within normal range, except for impaired semantic ret rieval. Mean neuropsychologic test scores were higher at 12 and 24 months t han at baseline, and no differences were detected between treatment groups over time. No significant interactions were detected between treatment and either time or baseline impairment. Conclusions: Our 2-year longitudinal study showed no effect of glatiramer t herapy on cognitive function in relapsing-remitting MS. Although it is poss ible that glatiramer therapy has no effect on cognitive function, the lack of measurable decline in cognitive function in both patient groups for 2 ye ars limits the opportunity for glatiramer to demonstrate a therapeutic effe ct by minimizing such decline. Emerging treatments for MS should continue t o be examined for their effect on cognitive impairment because it can be a critical determinant of disability. A greater understanding of the natural history of cognitive decline in MS is essential for a rational design of th ese drug trials.