Monday, 5 December 2011

Research: DMT Influence Level of Spasticity

Meca-Lallana et al. Spasticity improvement in patients with relapsing-remitting multiple sclerosis switching from interferon-β to glatiramer acetate: The Escala Study. J. Neurol Sci 2011 [Epub]

OBJECTIVE: To evaluate changes in spasticity in MS patients switching from IFN-β to GA.

METHODS: Observational, multicentre study in patients with relapsing-remitting MS (RRMS) and spasticity switching from IFN-β to GA. The primary endpoint comprised changes on Penn Spasm Frequency Scale (PSFS), Modified Ashworth Scale (MAS), Adductor Tone Rating Scale (ATRS), and Global Pain Score (GPS) at months 3 and 6 after starting GA.

RESULTS: Sixty-eight evaluable patients were included (mean age, 41.7 ± 9.5 years; female, 70.6%; mean time from MS diagnosis to starting GA, 7.6 ± 5.7 years). Previous treatments were subcutaneous IFN-β1a in 42.6% patients (e.g. Rebif), intramuscular IFN-β1a in 41.2% (e.g. Avonex) and IFN-β1b (e.g. betaseron) in 32.4%, whose mean durations were 3.5±3.3, 2.7±2.5 and 4.4±3.6years, respectively. Statistically significant reductions in mean scores on all spasticity measurements were observed from baseline to month 3 (PSFS, 1.7±0.9 vs 1.4±0.6, p<0.01; MAS, 0.7±0.5 vs 0.6±0.5, p<0.01; highest MAS score, 1.9±0.8 vs 1.7±0.8, p<0.01; ATRS, 1.6± 0.6 vs 1.4 ±0.6, p<0.01; GPS, 29.4 ± 22.1 vs 24.7 ± 19.4, p<0.01) and from baseline to month 6 (PSFS, 1.7±0.9 vs 1.3±0.6, p<0.01; MAS, 0.7±0.5 vs 0.5±0.5, p<0.01; highest MAS score, 1.9±0.8 vs 1.5±0.9, p<0.01; ATRS, 1.6±0.6 vs 1.3±0.6, p<0.01; GPS, 29.4±22.1 vs 19.1±14.8, p<0.01).

CONCLUSION: Spasticity improvement in terms of spasm frequency, muscle tone and pain can be noted after three months and prolonged for six months of GA treatment.

"It is difficult to provide a working mechanism for this obervation, except perhaps that disease modification by these drugs limit the triggers of spasticity."

"One mechanism may be due that IFN-β exacerbates spasticity due to activating the immune system; similar to what we see when someone with MS gets and infection. By stopping the IFN-β it  then resolves and this observation has nothing to do with GA."

"As always with science, these results will need to be confirmed."

The figure below explains the mechanism of some of the drugs we currently use for treating MS-related spasticity.


2 comments:

  1. For those who deal with spasticity issues and are on a beta-interferon, should they ask their neuro to switch them to Copaxone or another DMT?

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  2. Re"For those who deal with spasticity issues and are on a beta-interferon, should they ask their neuro to switch them to Copaxone or another DMT?"

    It will depend on how bad the problem is. Spasticity can be anything from a minor to a severe problem, with pain and disabling spasms. It could cause poor sleep hygiene, etc. On the other side of the coin is well your MS is being controlled or not controlled by IFNbeta. Therefore, the call is an individual one that needs to considered carefully. Again I would like to see these results reproduced.

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