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Multiple sclerosis vision loss could be helped by common allergy drug

Staff writer |
An antihistamine that is sold over the counter to treat allergies has been shown to partially reverse vision damage in people with multiple sclerosis (MS).

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Results of the study are being presented at the American Academy of Neurology's 68th Annual Meeting in Vancouver, Canada.

The drug, called clemastine fumarate, is a histamine H1 antagonist, which means it blocks histamine action at the H1 receptor, relieving allergic symptoms.

Vision damage is a hallmark of multiple sclerosis (MS), a disease of the central nervous system. It involves disrupted communication between the brain and other parts of the body.

MS is primarily regarded as an autoimmune disease, whereby the body launches an attack on its own myelin, which is the protective coating around the nerves.

First symptoms of MS typically appear between 20-40 years of age. The usual first symptoms are blurred or double vision, red-green color distortion or blindness in one eye.

Additionally, most people with MS encounter muscle weakness and difficulty with coordination and balance, which may be severe enough to hinder walking or standing.

Because the immune system destroys myelin, it eventually damages the nerves themselves. Signals to and from the brain become much slower. As a result, optic nerve damage is common in MS.

For their study - led by Dr. Ari Green, of the Multiple Sclerosis Center at the University of California-San Francisco (UCSF) - the researchers used 50 participants with MS and optic neuropathy, which is damage to the nerve that sends signals from the eye to the brain.

Over the course of 5 months, the participants - who were of an average age of 40 and who had MS for an average of 5 years - performed vision tests at the beginning and end of the study.

The researchers note that all participants had evidence of a stable chronic optic neuropathy, which means they were not recovering from their vision damage.

For one visual test, the researchers recorded the time it took for a signal to travel from the retina to the visual cortex. For a participant to be included, they had to have a transmission delay longer than 118 milliseconds in at least one eye, as well as evidence that they had a sufficient amount of nerve fibers to reinsulate.

According to the team, improvement in transmission delay is a biomarker of myelin repair.

During the first 3 months of the study, participants were either given clemastine fumarate or a placebo. Then, for the second 2 months, the participants initially given the placebo were given the drug, and vice versa.

Results showed that the patients who were taking the drug exhibited reduced delays in each eye - an average of about 2 milliseconds.


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