Typically it’s confined to our brain cells and is released only when it needs to send a “message” and then is immediately retracted back into the cell. But in the presence of trauma or neurodegenerative disease, vast levels of glutamate may be expelled and subsequently cause a variety of symptoms and disease activity.
Memantine has been employed in treatment for Alzheimer’s disease and seeks to suppress the excess release of glutamate with the intent to improve outcomes in patients with Alzheimer’s. While it has been shown to prevent functional disability and cognitive decline, its long-term benefit in treating this disease appears to be minimal – and by “long term” that could mean just one year’s time.
The implications for use in reducing some MS symptoms.
But the question remained as to whether this glutamate suppressor could be of use in another neurodegenerative disease such as MS. Specifically, several clinical trials sought to determine if memantne could reduce spasticity, fatigue and disability, as well as the related cognitive impairment suffered by patients. The latter is especially problematic as it affects approximately 45-65% of MS patients and causes considerable disability and lifestyle burdens.
Damage to the descending motor tracts brought about by autoimmune processes and subsequent neuroplasticity seen in MS is thought to cause disinhibition of motor reflexes leading to spasticity. Early studies involving rodent models of MS also suggest the role of glutamate toxicity in spasticity. MS-related fatigue is understood to be related to axonal injury secondary to glutamate toxicity as manifested by the reduction in N-acetylaspartate levels seen in multivoxel spectroscopic studies.1
Glutamate has been implicated in the autoimmune demyelination that we see in our MS patients as increased levels of the neurotransmitter glutamate have been identified in their brains, which lowers the levels of N-acetylaspartate (NAA) — a process that likely leads to the loss of brain volume. These findings indicate that glutamate might be a driver of neuronal cell death and disease progression in MS, and a potential target of new therapies.2
However, this trial and several others, which have been carried out to look at cognitive function, also showed no significant benefit. We do know that cognitive function is very difficult to objectively measure, particularly in a short-term study. So while more studies are warranted, the opportunity to reduce excessive glutamate in active neurological disease is one that we should continue to consider for those patients with associated symptoms.
As part of a treatment protocol…
I don’t think at this time that we should be prepared to eliminate memantine from our list of therapeutic options, especially given what we now know about the over-activation of the glutamatergic system and glutamate toxicity in neurodegeneration.
Remembering that whichever form is used it must be slowly titrated to assess patient tolerance, we generally follow these dosing practices:
For ways to naturally reduce or control glutamate levels, see:
Be sure to talk to your physician or neurology specialist if you have questions or concerns about your treatment regimen and, of course, please feel free to reach out to our office if you would like to schedule a visit.
In hope and healing,
Dr. Suzanne Gazda
1 Mehta, L. R., McDermott, M. P., Goodman, A. D., & Schwid, S. R. (2010). A randomized trial of memantine as treatment for spasticity in multiple sclerosis. Multiple sclerosis (Houndmills, Basingstoke, England), 16(2), 248–251. https://doi.org/10.1177/1352458509355462
2 Azevedo, C. J., Kornak, J., Chu, P., Sampat, M., Okuda, D. T., Cree, B. A., Nelson, S. J., Hauser, S. L., & Pelletier, D. (2014). In vivo evidence of glutamate toxicity in multiple sclerosis. Annals of neurology, 76(2), 269–278. https://doi.org/10.1002/ana.24202
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Suzanne Gazda M.D.