Light bulb moments in multiple sclerosis (MS)

In 1421, Saint Lidwina was ice skating in Schiedam, Holland, when she suddenly became weak and fell, breaking a rib at age 15. Her fall was the first sign of her disease, which progressively worsened until both legs were paralysed. Historians consider Lidwina one of the first documented cases of MS.1

In the 1830s, French anatomist Jean Cruveilhier and Scottish pathologist Robert Carswell independently, but simultaneously, were the first to describe and illustrate the nervous system lesions that develop in MS.2, 3

Dr. Jean-Martin Charcot, a professor at the University of Paris, treated a young woman with tremors and slurred speech. Following her death, he identified plaques on her brain, which he named sclerose en plaques. He linked these plaques to his other clinical observations and became the first to diagnose MS as a distinct disease.3, 4

In 1878, French scientist Dr. Louis Ranvier discovered myelin, which protects and supports nerve cells and is damaged in patients with MS.4

Based at the University of Edinburgh, pathologist Dr. James Dawson made a breakthrough in the pathology of MS in 1916 when he first described microscopic myelin damage and blood vessel inflammation occurring in the brain.8

In 1933, American scientist Dr. Thomas Rivers proved that MS was not a viral disease when he was able to show that the symptoms of MS could be recreated in animals by injecting healthy myelin and causing an autoimmune response. This animal form of the disease was called experimental allergic encephalomyelitis (EAE).4

In 1959, American neuroimmunologist Dr. Philip Paterson determined that T cells are involved in EAE when he transferred the disease from one animal to another through an injection of these immune cells.5, 6

In 1960, a group of scientists detected another type of immune cell, called a B cell, in the cerebrospinal fluid (CSF) of people with MS, which was a major step forward in diagnosis.7

Over the next two decades, the role of the human immune system in MS was further explored. Between 1960 and 1970, multiple scientists confirmed that MS is an immune-mediated disease.8,9

In 1981, British researcher Dr. Ian. R. Young used Magnetic Resonance Imaging (MRI) to look at the brain of a person with MS. Following the first scan, it became apparent that even when the patient showed no symptoms, an MRI could be used to identify signs of the disease.8

Neurologist John Kurtzke established the Expanded Disability Status Scale (EDSS), which is used to assess people with MS in clinical practice and clinical studies.10 Some of the measures include visual function, coordination and difficulty moving limbs.

In the 1990s, the first treatments were developed to help control, but not cure, MS signs and symptoms. Several injectable treatments were approved to reduce the frequency of nervous system attacks for people with relapsing MS (RMS), the most common form of the disease.8 Since then, additional medicines that slowed accumulation of disability were developed.

New treatments with different modes of action and routes of administration were developed and approved for RMS. Most treatments target the function of T cells as their primary mechanism of efficacy.

For the past two decades, scientists have continued to study MS. The latest research suggests that B cells play an important role in MS disease progression.11, 12 In countries around the world, there now exists a disease-modifying medicine to treat primary progressive multiple sclerosis.

References

1. Medaer, R. (1979). Does the history of multiple sclerosis go back as far as the 14th century? Acta Neurologica Scandnavica. 60(3):189–92.

2. Murray, T. (2009). Robert Carswell: The First Illustrator of MS. The International MS Journal. 2009. 16, 98–101.

3. Compston, A., Lassmann, H., McDonald, I. (2006). McAlpine's Multiple Sclerosis (Fourth Edition). London: Churchill Livingstone. 3–6.

4. Rolak, L. (2003). MS: The Basic Facts. Clinical Medicine & Research. 1 (1), 61–62.

5. Paterson, P. (1960). Transfer Of Allergic Encephalomyelitis In Rats By Means Of Lymph Node Cells. The Journal of Experimental Medicine. 111, 119–1947.

6. Fletcher, J et al. (2010). T cells in multiple sclerosis and experimental autoimmune encephalomyelitis. Clinical and Experimental Immunology. 162, 1–11.

7. Holmøy, T. (2009). The Discovery of Oligoclonal Bands: A 50-Year Anniversary. European Neurology. 62, 311–315.

8. Rolak, L. (2009). The Basic Facts: The History of MS. National MS Society. 1–11.

9. Steinman, L. (2003). Optic Neuritis, A New Variant of Experimental Encephalomyelitis, A Durable Model for All Seasons, Now In Its Seventieth Year. The Journal of Experimental Medicine. 197 (9), 1065–1071.

10. Kurtzke, J. (1983). Rating neurologic impairment in multiple sclerosis: An expanded disability status scale (EDSS). Neurology. 33, 1444–52.

11. Disanto G, Morahan JM, Barnett MH, Giovannoni G, Ramagopalan SV. (2012). The evidence for a role of B cells in multiple sclerosis. Neurology. 78 (11), 823–32.

12. Hauser, S. et al. (2008). B-Cell Depletion with neuroparalytic accidents in Relapsing–Remitting Multiple Sclerosis. New England Journal of Medicine. 358, 676–88