Long term effects of baclofen

Natale M, D’Oria S, Nero VV, Squillante E, Gentile M, Rotondo M. Long-term effects of intrathecal baclofen in multiple sclerosis. Clin Neurol Neurosurg. 2016;143:121-125.

OBJECTIVES:Spasticity is associated with various neurological conditions. In this study the authors analyzed the long term effects of intrathecal baclofen therapy in multiple sclerosis and evalued the benefits of the treatment on spasticity, disability, pain, spasm frequency and rated the incidence of side effects.
PATIENTS AND METHODS:A records of 123 patients, with a severe, progressive and refractory to medical therapy spasticity from different causes, underwent baclofen pump placement, after a bolus test, from 2000 to 2012,under Department of Neurosurgery at the Second University of Naples/Italy. We present our experience in treating 28 subjects that was affected by multiple sclerosis. For all patients we reviewed long-term response to therapy, surgical technique, surgery- and pump-related complications. Every patients were evaluated by means of the Modified Ashworth Scale (MAS), Penn Spasm Frequency Scale (SFS), Visual analogue Scale For Pain (VAS), Barthel index (BI) and Self Rating Depression Scale (SDS) 
RESULTS: During follow up the mean MAS score for upper and lower extremities decrease significantly. Also SFS’s decrease was statistically significant. This resulted in a dramatic improvement of BI. Furthermore, we observed a marked improvement in VAS and SDS.
CONCLUSIONS:Intrathecal baclofen provides effective long-term treatment of spasticity multiple sclerosis related. ITB therapy increases the quality of lifestyle and functional independence in appropriately selected cases.

Oral baclofen use can be associated with unwanted sedative side-effects and so people may use intrathecal baclofen. this is dosed so it keeps the baclofen out of the brain and can reduce cogfog. Indeed if you spasticity team can get on top of the activity of intrathecal baclofen, I have seen it where the other meds can be withdrawn and reduce the side effects that you may not even be fully aware of. This is because the neuros slowly increase you doses so that you don’t appreciate how sedating it is until you stop. As this paper shows there can be very good efficacy.

When  I saw the title however, I was hoping for something different. Baclofen is a GABA agonist and so promotes inhibitory nervous signals. Therefore it will block glutamate an excitatory molecule. Too much excitation leads to calcium entering the cell and too much of this causes damage and nerve death. 

Therefore can baclofen actually slow progression. 
The answer is…..I don’t know and suspect no one knows because the data is not being collcted because it is a symptom control drug. 

However this is a theorectical possibility. 

Developing a symptom control treatment may be the quickest way to get a neuroprotective drug to people with MS as you have a few month trial compared to a many years of trial. From a pharma prospective a neuroprotective will cost more than a symtom control drug I suspect.

CoI. I have been trying to develop something that can compete with balcofen


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  • The logic behind your sodium channel blockers as neuroprotectants may apply to symptomatic treatments: less overload on the nerves which perhaps do not have to work too hard to overcome deficiencies fixed by the symptomatic treatment, leading to some protection in the long run.

  • When I saw the call of this publication to Blog thought the study had also spoken about the GABA agonism promoted by Baclofen, and prevent neuronal death.
    I hope VSN16R has the same effect, perhaps has a "plus" for neuroprotection…

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