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