11 Comments
Nov 3Liked by Gavin Giovannoni

Prof G, I found this anticholinergic burden calculator. Might be helpful to share with pwms.

https://www.acbcalc.com/

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Apr 1, 2023Liked by Gavin Giovannoni

This study came out a few months after this post.

A population-based nested case-control study was conducted in patients treated with OAB medications in Ontario, Canada. A total of 11 392 patients aged ≥66 yr with a new diagnosis of dementia between 2010 and 2017.

Conclusions: Older adults receiving solifenacin and darifenacin in the 6 mo prior to diagnosis, and those receiving solifenacin, darifenacin, tolterodine, or fesoterodine in the year prior to diagnosis, have increased odds of incident dementia, compared with those receiving mirabegron. Oxybutynin and trospium were not associated with dementia, likely due to a protopathic bias. Careful drug selection is warranted when treating patients with OAB.

https://pubmed.ncbi.nlm.nih.gov/34742663/

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thank you for posting this where people like me will find it!

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Jul 8, 2021Liked by Gavin Giovannoni

I really appreciate your raising awareness about the issue of anticholinergics. I was able to suggest SNRIs to my neurologist instead of TCAs when we started talking about trying medications for neuropathic symptoms, and I’ll be aware of what medications to watch out for in the future if I ever start having bladder issues.

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Jul 8, 2021Liked by Gavin Giovannoni

I've just started talking to a doc about bladder management meds and this is thus very timely, thanks!

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The best remyelination/neurorestorative therapy available for MS is early highly-effective DMTs. Switching off inflammation when you are young gives your nervous system the best chance of recovering. The older you get the less likely you are to recover. Similarly, the more disabled you are the less recovery, which is likely to be biological.

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RE: "Not taking a remyelination agent because you don’t notice any improvement does not sound like a very preventive strategy to me."

Show me the data? Sadly we have no licensed remyelination therapy.

The closest we get to a positive trial was the opicinumab trial and it was a small subset who appeared to respond, i.e. patients in the sweet spot. When we enriched the next phase 2b/3 trial for these sorts of patients the trial was sadly negative.

The point I am making is that you can take clemastine and live with a 7-point IQ hit, but there is no guarantee that it is working. If I had MS I wouldn't be taking clemastine off-label for this reason. I assume you are aware that many pwMS are on clemastine in the hope it is helping them.

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What therapy are referring to? There are none that I am aware of.

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This blog post is about clemastine and other anticholinergics that pwMS are using as putative remyelination agents.

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In relation to clemastine, it may also be speeding up cognition loss in pwMS. The latter is based on the well-described link between anticholinergic exposure and dementia risk.

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