In the decade after World War I, MS research grew more sophisticated. Abnormalities in spinal fluid were noted for the first time in 1919, though their significance was a puzzle. Myelin, which had been discovered in 1878 by Dr. Ranvier, was studied intensively under the microscope and the cell that makes myelin, the oligodendrocyte, was discovered in 1928.

The first electrical recording of nerve transmission, by Lord Edgar Douglas Adrian in 1925, established techniques needed to study the activity of nerves and launched a series of experiments to determine just how the nervous system works. Ultimately, six Nobel Prizes were awarded for these studies. The resulting knowledge included clarification of the role of myelin in nerve conduction and a realization that demyelinated nerves cannot sustain electrical impulses.

At this time, scientists suspected that some form of toxin or poison caused MS. Because most MS damage occurs around blood vessels, it seemed reasonable that a toxin circulating in the bloodstream leaked out into the brain, even though no researcher could find a trace of it.

Just before World War II, an important breakthrough occurred. An animal model of MS was developed out of research on vaccines. It had been known that people vaccinated against viral illnesses, especially rabies, sometimes developed a disease resembling MS. It had been assumed that this occurred because the virus in the vaccines was not completely inactivated.

In 1935, Dr. Thomas Rivers at the Rockefeller Institute in New York City demonstrated that nerve tissue, not viruses, produced the MS-like illness. By injecting myelin he knew to be virus-free into laboratory animals under the proper conditions, he could induce their immune systems to attack their own myelin, producing a disease very similar to MS.

This laboratory animal form of MS, called experimental allergic encephalomyelitis, or EAE, would later become an important model for studying the immunology and treatment of MS. In fact, it paved the way to modern theories of autoimmunity, for it demonstrated how the body can generate an immunologic attack against itself.

But most doctors in the 1930s were still analyzing toxins or checking blood circulation in MS. The importance of EAE to MS was virtually ignored.

Instead, a flurry of experiments in lab animals demonstrated that blocking the blood supply to the brain sometimes caused myelin to die. The damage looked a bit like MS. Doctors wondered if MS was caused by circulation problems, and they tried therapies to stimulate blood flow including blood thinners and drugs to dilate blood vessels. X-rays were also used to treat MS, although more for their novelty than for any sound scientific reason.

It would be many years before the essential similarity of EAE and MS was understood and a link between the immune system and MS was forged.

Reference

Written by Loren A. Rolak, MD. Reproduced by permission from the National Multiple Sclerosis Society, USA. © NMSS, 2003