• José Eustasio Meca-Lallana, Pedro de Mingo-Casado, Manuel Amorin-Díaz, María Luisa Martínez-Navarro, and Andrés Fernández Barreiro.
• Department of Neurology, Multiple Sclerosis Unit, Hospital Universitario Virgen de la Arrixaca, Murcia, Spain. pmecal@gmail.com
• Clin Ther. 2010 Jun 1; 32 (6): 1061-6.

BackgroundTreatment with interferon-beta (IFN-beta) has been related to worsening of muscle spasticity in patients with multiple sclerosis (MS). However, there are no specific data on the effects of glatiramer acetate (GA) on spasticity.ObjectiveThe aim of the present study was to assess the effects of GA on spasticity in patients with relapsing-remitting MS who had been previously treated with IFN-beta or were treatment naive.MethodsTwo cohorts of MS patients with spasticity who were about to begin treatment with GA at the approved dosage (20 mg/d) were enrolled in the study: patients who were being switched from IFN-beta due to adverse events or lack of efficacy (cohort 1) and patients who were treatment naive (cohort 2). The follow-up periods for cohorts 1 and 2 were 18 and 12 months, respectively. Patients' physical condition was assessed at baseline and at the end of follow-up using the Modified Ashworth Scale (MAS), Penn Spasm Frequency Scale (PSFS), Global Pain Score (GPS), Adductor Tone Rating Scale, Expanded Disability Status Scale (EDSS), and neurophysiologic tests (latency and amplitude of the Hoffmann reflex [H reflex] in the soleus, and ratio of maximum H reflex to maximum motor response [H/M ratio] in the lower limb). The frequency and severity of adverse events were recorded throughout follow-up, and investigators rated the causal relationship to GA (unrelated, unlikely, possibly, or probably).ResultsTwenty-eight patients were included in the study, 13 in cohort 1 and 15 in cohort 2. All patients were white. Cohort 1 was 76.9% female, with a mean (SD) age of 39.85 (9.25) years; cohort 2 was 66.7% female, with a mean age of 40.73 (11.52) years. Cohort 1 had significant reductions from baseline to the end of follow-up in mean scores on the MAS for the right hemibody (from 1.85 [0.61] to 1.18 [0.60]; P = 0.002) and left hemibody (from 1.86 [0.55] to 1.27 [0.65]; P = 0.045), PSFS (from 2.00 [0.91] to 0.36 [0.81]; P = 0.002), and GPS (from 47.69 [13.94] to 24.09 [17.15] mm; P = 0.002). The changes from baseline were not significant on the mean Adductor Tone Rating Scale, EDSS, H-reflex latency or amplitude on either side, or lower-limb H/M ratio on either side. Cohort 2 had significant reductions from baseline in H-reflex latency on the left side (from 30.31 [2.44] to 28.75 [2.01]; P = 0.005) and H/M ratio on the right side (from 0.45 [0.15] to 0.35 [0.19]; P = 0.025). There were no significant changes in mean scores on the MAS for either hemibody, PSFS, GPS, Adductor Tone Rating Scale, EDSS, H-reflex latency on the right side, H-reflex amplitude on either side, or lower-limb H/M ratio on the left side. Sixteen patients experienced a total of 28 adverse events. Seven mild adverse events were considered related to GA: local reaction at the injection site (3 patients); headache/migraine, anxiety, and skin reaction (1 patient each); and an unspecified adverse drug reaction (1 patient). Two serious adverse events (pyelonephritis and pyrexia) occurred during the study, neither of them considered related to GA.ConclusionsIn this pilot study in patients with relapsing-remitting MS, GA treatment did not increase spasticity. Furthermore, the results suggest that GA may reduce spasticity in patients previously treated with IFN-beta. These findings support the conduct of large randomized controlled trials of the effects of GA on spasticity.

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