In a study published in the Proceedings of the National Academy of Science, a team of researchers from the University of Wisconsin–Madison (WI, USA) discovered that changes in the speed of electrical signals across the optic nerves may reflect recovery from myelin loss in multiple sclerosis (MS).
For many MS patients, symptoms – such as numbness, weakness and vision problems – come and go, due to them developing a relapsing–remitting disease. Further, with time, patients develop progressive MS, which damages axons by eating away at the myelin.
“There are many treatments for people with relapsing–remitting disease which are quite successful in a lot of patients,” commented Ian Duncan, Neuroscientist at the University of Wisconsin–Madison’s School of Veterinary Medicine. “And then there are the unlucky people who start out with primary progressive disease, or whose relapsing–remitting MS becomes what’s called secondary progressive MS. There are no effective treatments for them.”
Due to there not currently being an effective treatment, progressive MS has piqued the interest of pharmaceutical companies who are working to find drugs that can restore lost myelin in order to support nerve signaling.
In order to confirm the presence of myelin in the central nervous system to assess the effectiveness of new treatment, cutting into nerve tissue to take samples is required, however, this process is very destructive in human patients.
When monitoring MS patients, clinicians often use a non-invasive test called visual evoked potential (VEP), which flashes a series of lights into the eye. This prompts a recognizable electrical signal from the light to get from the retina down the optic nerve to the brain and can be recorded using electrodes on the scalp.
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“There’s a time lag between the flashes of light and the brain activity. That’s called the latency,” explained Duncan. “When that latency increases, it’s taking longer for the signal from the lights to get from the retina down the optic nerve to the brain. As MS progresses and demyelination of axons in the optic nerve worsens, the latency grows because the axons are not conducting the signal as well as healthy nerves.
“If we could prove that a decrease in latency in the VEP truly reflected remyelination of nerve axons, then you’d have it,” Duncan added. “You’ve got a way to tell if there’s improvement in a patient, an outcome measure that can show whether the drug you are testing is successfully promoting myelin repair.”
The team were able to demonstrate that changes in VEP latency track demyelination and myelination in a feline model. The researchers fed the cats irradiated food for several months to induce severe myelin loss throughout the nervous system, especially along their optic nerves. When the cats returned to their regular diets, nerve function was restored due to extensive myelin repair.
Tissue samples confirmed the return of myelin along the nerves axons as the latency times decreased. The researchers reported that normal latency of the VEP of cats is 50–60 ms, which goes up to 90–110 ms at the height of disease and then returns to 60–70 ms at recovery.
“Latency doesn’t fully recover because the myelin sheath in remyelination remains thinner than the original myelin,” commented Duncan. “But we know from previous studies that thin myelin is enough to restore function and sufficient to protect nerve fibers in the long run.”
Therefore, the findings from this study support that VEP is a true measure of remyelination, which can be used to accurately quantify the remyelination effect of new MS drugs being developed.
Source: University of Wisconsin-Madison. Flashing lights may provide vital first test of MS drug success. Press release: www.wisc.edu/