Glaterimer acetate and Spasticity...what next?

Meca-Lallana JE, Hernández-Clares R, Carreón-Guarnizo E.Spasticity in multiple sclerosis and role of glatiramer acetate treatment. Brain Behav. 2015 ;5(9):e00367. doi: 10.1002/brb3.367. Epub 2015 Jul 14.

INTRODUCTION:Spasticity is one of the most disabling and difficult-to-treat symptoms shown by patients with multiple sclerosis, who often show a suboptimal and unsatisfactory response to classic treatment and new available nonpharmacological alternatives. Due to the progressive nature of this condition, the early management should be essential to improve long-term outcomes.
METHODS:We performed a narrative literature review of the contribution of spasticity to the burden of multiple sclerosis and the potential role of classic disease-modifying drugs.
RESULTS:Added to the underlying pathophysiology of spasticity, certain external factors and drugs such as interferon may exacerbate the existing condition, hence their awareness is crucial as part of an effective management of spasticity. Furthermore, the evidence for the effectiveness of glatiramer acetate in preventing spasticity in naïve patients and in those switching from interferon should not be ignored.
CONCLUSIONS:This literature review proposes the examination of spasticity and the influence of classic disease-modifying agents on the level of existing condition among the variables to be considered when deciding on therapy for multiple sclerosis in clinical practice.

You know we like to post on the different actions of glatermirer acetate...but now the attention is drawn to spasticity....Come one what's next? 


Glaterimer is a group of amino acids...are they going to get into the brain to stop spasticity...unlikely but could GA inhibit spasticity , unlikely but could it block the disease process that leads to nerve damage then yes because it blocks relapses which are damaging and by accumulating less damage you are less likely to develop spasticity....What do I know and no doubt you may put me right with your experiences.

However what next GA and bladder, GA and continenence, GA and vision, GA and ....In the words of a Golch Advert..,Schtop!
However, the point is if you convert to GA then your chances of developing spasticity may be less that if you took interferon beta. I am sure if you take a more effective DMT then your chances of spasticity will be lower too

CoI We are developing a potential spasticity treatment.

Ehling R, Di Pauli F, Lackner P, Rainer C, Kraus V, Hegen H, Lutterotti A, Kuenz B, De Zordo T, Schocke M, Glatzl S, Löscher WN, Deisenhammer F, Reindl M, Berger T.Ehling R, Di Pauli F, Lackner P, Rainer C, Kraus V, Hegen H, Lutterotti A, Kuenz B, De Zordo T, Schocke M, Glatzl S, Löscher WN, Deisenhammer F, Reindl M, Berger T. 

Data from in vitro and animal studies support a neuroprotective role of glatiramer acetate (GA) in multiple sclerosis (MS). We investigated prospectively whether treatment with GA leads to clinical and paraclinical changes associated with neuroprotection in patients with relapsing-remitting (RR) MS. Primary aim of this clinical study was to determine serum BDNF levels in RR-MS patients who were started on GA as compared to patients who remained therapy-naive throughout 24months. Secondary outcomes included relapses and EDSS, cognition, quality of life, fatigue and depression, BDNF expression levels on peripheral immune cells (FACS, RT-PCR), serum anti-myelin basic peptide (MBP) antibody status, evoked potential and cerebral MRI studies. While GA treatment did not alter serum levels or expression levels on peripheral immune cells of BDNF over time it resulted in a transient increase of serum IgG antibody response to MBP, mainly due to subtype IgG1 (p<0.05), after 3months. However, no significant differences were found between GA treated and therapy-naive patients with regard to serum BDNF and intracellular BDNF expression levels, nerve conduction (including median and tibial nerve somatosensory, pattern-shift visual and upper and lower limb motor evoked potentials) or MRI (including volume of hyperintense lesions, volume of hypointense lesions after CE, mean diffusivity and fractional anisotropy) outcome parameters. In conclusion, our findings do not support a major impact of GA treatment on paraclinical markers of neuroprotection in human RR-MS.

In this study they did not find evidence to support an effect on neuroprotection and it failed to influence primary progressive disease so this conclusion may have been expected

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