Tavist

[agate]

How's that neighbor doing? The one whose house your mother brought you to?

Sounds as if Howie just had to do something dramatic. This would have been before he heard about thongs.

[Howie]

I have no idea how that neighbor's doing, but she's probably gone by now. Our first house was one street over from my Granny, Dad's mom. I don't remember the whole thing, but was told about it later. It's strange how the brain, and memory work.

You have no memory at all when you are a newborn. What's to remember? But even now, you don't remember EVERY day of your life, just the good and bad experiences you remember, but not every day.

I have a feeling, that's a good thing.

[SalpalSally]

Poor Howie, can't get a break...LOL

[Lazarus]

I posted this study on MSWorld and this is the answer I got. Macular degeneration is unrelated to MS, the effects MS can have on the retina, and optic neuropathy. The occurrence of macular degeneration in a person with MS doesn't mean that MS caused it.

" And unfortunately, the article copied earlier is old and outdated. Although anti-LINGO-1 showed the ability to remyelinate nerves, the effect was not significant. In the clinical trial, it failed to meet its primary endpoints, and had no effect on the restoration of people's vision. All of the assertions by people of the Internet that it was going to be a cure for anyone and everyone who had lost vision due to MS-related optic neuritis -- especially years ago -- were 100% false. There may be a use for anti-LINGO somewhere in the future, but for now its use for improvement of vision is a dead end.

As someone who has lost a significant amount of visual field because of recurrent optic neuritis, I can say it would have been great to have something to bring my vision back. But it isn't going to happen, and the hopes for anti-LINGO's affects on vision were unrealistic from the start.

Plus, I spent years taking Tavist, and no improvements came from that, either.

Some people seem to thrive on the roller coaster of getting hopes up about possible treatments that don't even on the surface have much going for them, and then having those hopes crushed, but I'm not one of them. Nor do I want to participate in or promote those unlikely hopes. Life with MS is hard enough already. "



"

[Howie]

Linda, I had a detached retina, and had to have eye surgery to correct it. Vision is fine now.

What caused it, I have no idea, but I didn't have a fall, and MS was never mentioned as the cause. I suspect it was just age. It seems to happen to mostly older people.

So in one day, I lost all vision in one eye, and got it all back in one day. Talk about an emotional roller coaster!

[agate]

One person has gone on record as saying Tavist didn't work for her/him. Do we know that that person was taking the same form of Tavist the researchers used, and at the same dosage? And that is just one person.

Others might be helped. I say it's too soon to give up on Tavist--or anything else. We don't have to get our hopes up every time some new "remedy" comes down the pike. If you never hope for anything, you're never disappointed.

But on the other hand I don't see declaring the Tavist idea to be useless unless it's had more scientific testing with large numbers of people involved.

[Lazarus]

Linda, I had a detached retina, and had to have eye surgery to correct it. Vision is fine now.

What caused it, I have no idea, but I didn't have a fall, and MS was never mentioned as the cause. I suspect it was just age. It seems to happen to mostly older people.

So in one day, I lost all vision in one eye, and got it all back in one day. Talk about an emotional roller coaster!

Hi Howie,
I wanted to make it clear that what I posted was a response to the Tavist article that was posted by someone from MSWorld forums. Not sure if it is right but it made me think I should check the research out again.
Linda

[agate]

Linda, the copied article was the one from Medscape that I posted earlier in the Tavist thread. I wouldn't call it old since it's from April 2016 and is related to the latest AAN annual conference in that month.

[Sunshine]

I do not think they published the dose. They said their dose was higher than the usual dose prescribed for Tavist as an allergy drug.

[Sunshine]

I would ignore that post from MSWORLD. I am pretty sure they are getting good prelim findings on anti Lingo for remylenation. Unsure if it helps vision, can't recall.

The person sounds defeated and discouraged, and I feel badly for her. But she is not a researcher or Doctor, so take it with a grain of salt.

[agate]

Apparently there were some good results for anti-LINGO-1 for optic neuritis:

Only registered and activated users can see links., Click Here To Register...

Yes, the poster sounds discouraged, and it's very easy to get discouraged and very very tired of seeing first one treatment and then another being offered, with each one of them causing problems.

[Lazarus]

Linda, the copied article was the one from Medscape that I posted earlier in the Tavist thread. I wouldn't call it old since it's from April 2016 and is related to the latest AAN annual conference in that month.

Thanks very much. I will repost this answer on the thread I answered on MSWorld. Yeah!

[agate]

More on this. Allerhist-1 or Tavist-1 (generic name: clemastine fumarate) is getting some attention again. This was a small study but the results of a phase 2 clinical trial were published in The Lancet, and that's not a journal that publishes just any old thing.

Article about it in Medical News Today, October 13:

MS could be reversed with existing allergy drug



By Tim Newman


A drug used to treat allergies has been shown to increase nerve speed in MS patients.

In a recent phase II clinical trial, an over-the-counter allergy drug was shown to improve nervous system function in patients with multiple sclerosis.

Multiple sclerosis (MS) is an autoimmune disease affecting more than 2.3 million people around the world. The condition attacks myelin, or the waxy coat around nerves, and compromises the nerves' ability to transmit messages.

Over time, as the nerves' function is steadily reduced, a range of symptoms - including problems with vision, muscle weakness, difficulty walking, and issues with balance and coordination - develop.

Current treatment focuses on preventing the immune system from causing further damage, and as it stands, no drugs can repair the damaged myelin.

Discovering a medication capable of rebuilding the damaged myelin would be a huge step forward. And according to the latest study, this may be just around the corner.
New MS drug on the horizon?

In 2014, studies carried out by Prof. Jonah R. Chan at the University of California, San Francisco showed that clemastine fumarate may be a candidate for the treatment of MS.

Because of the potential importance of the findings, the drug quickly progressed to clinical trials. This week, the results from a phase II clinical trial on clemastine fumarate are published in The Lancet.

Clemastine fumarate was first approved by the Food and Drug Administration (FDA) in 1977. It is an antihistamine medication for allergies and has been available over the counter since 1993. Its potential to treat MS is therefore as surprising as it is welcome.

According to principal investigator Dr. Ari Green, "To the best of our knowledge, this is the first time a therapy has been able to reverse deficits caused by MS. It's not a cure, but it's a first step toward restoring brain function to the millions who are affected by this chronic, debilitating disease."


The team studied the effects of clemastine fumarate on 50 individuals with long-standing MS over a 5-month period. Because the visual system is often one of the first to be affected, the researchers measured so-called visual evoked potentials (VEPs). This is a well-established method of assessing how quickly nerves conduct messages.


VEPs were measured by showing participants flickering patterns on a screen. Electrodes placed over the visual areas of the brain detected how long it took signals to travel from the eye to the relevant area of the brain.

For 90 days, half of the participants were given clemastine fumarate, and the other half received a placebo. Next, the groups were switched: the placebo group was given the drug and vice versa. Neither the participants nor the researchers knew which individuals were receiving the active treatments.

The analysis showed that the drug increased the speed of the neural signals from the eye to the back of the brain. Even once the experimental group stopped taking the medication and moved on to the placebo, the increased speed persisted.

"People thought we were absolutely crazy to launch this trial," comments Prof. Chan, "because they thought that only in newly diagnosed cases could a drug like this be effective - intuitively, if myelin damage is new, the chance of repair is strong."

In the current study, the researchers were not able to measure myelin regrowth using MRI scans. However, this is primarily due to limitations in technology, and as Prof. Chan says, "We still don't have imaging methods that have been proven to be able to detect re-myelination in humans."

Regardless of this, the evidence that re-myelination occurred is strong; there are no alternative explanations as to how VEPs could have increased.

Also, in vitro studies in human cells have shown that clemastine fumarate can stimulate activity in oligodendrocytes, which are cells that produce myelin in the central nervous system.

There is still a long path ahead, but the results are encouraging. Dr. Green is cautious not to jump the gun, saying, "By no means do we want to suggest that this is a cure-all." But it is difficult not to be excited at the potential of this drug.

Only registered and activated users can see links., Click Here To Register...

[agate]

I wonder about this statement in the article:

Regardless of this, the evidence that re-myelination occurred is strong; there are no alternative explanations as to how VEPs could have increased.

Human error in the testing might explain the increase in the VEPs, maybe?

I mentioned in another thread that I asked the neuro how I could have positive Babinski signs bilaterally during one neuro exam, and a year later normal plantar reflexes--i.e., no Babinski signs--because central nervous system damage is supposed to be permanent. It will always and forever show up on tests, I thought.

She said that the test is hard to interpret because sometimes it's not properly done, or the examiner can't say for sure what the big toe is doing, or whatever.

Seems to me that the same kind of thing might happen during a visual evoked potentials test even though it's just the patient viewing a checkerboard screen. There could still be errors in how the test is done.

Neurology seems like a very imperfect science, still.

[Frog42]

Neurology seems like a very imperfect science, still.

Agreed. Most neuros do have immense egos though.