Multiple Sclerosis and Hyperbaric Oxygen Therapy

MAIN PAGE

MS THEORIES

MULTIPLE SCLEROSIS DISEASE MODELS

HISTORY OF MULTIPLE SCLEROSIS

THE VASCULAR THEORY

HISTORY OF HBOT AND MULTIPLE SCLEROSIS

STUDY RESULTS

OTHER RESOURCES

SITEMAP

CONTACT US

OTHER NATIONAL HYPERBARIC WEBSITES

HISTORY OF MULTIPLE SCLEROSIS

YEAR

HISTORY

Around 1395

Fifteen year old Lydwina of Schieden fell while iceskating. Her progressive disability is posited as the earliest written record of an individual with multiple sclerosis. She was canonized as the Dutch patron Saint of Ice Skaters by the Roman Catholic Church in 1890.

1838

Medical drawings documented what is recognized today as multiple sclerosis.

1868

Jean-Martin Charcot, professor of neurology at the University of Paris, wrote the first comprehensive description of Multiple Sclerosis and the brain damage the disease caused. He named the disease for the widespread scarring, may found in a symmetrical pattern near the cerebrum's lateral ventricles.

1878

French histologist Dr. Louis Ranvier discovered and described myelin. As well as the gaps (nodes of Ranvier) between the myelin sheaths of individual nerve cells. In 1919, spinal fluid abnormalities were noted—their significance puzzled experts for decades.

Early 1890s

Dr. Sigmund Freud, psychologist, treated his nanny for “Creeping Paralysis,” attributing the condition to female hysteria, a diagnosis which explained female symptoms for years to follow. As a result, multiple sclerosis received little or no extensive research until recently. Male symptoms were attributed to multiple sclerosis.

1925

Lord Edgar Douglas Adrian tested electrical conductivity in the central nervous system of multiple sclerosis patients. He proved that demyelinated nerves do not conduct electrical impulses well. The same type of sensory impulse testing is still used today.

1928

Researchers identified the oligodendrocyte cell that makes myelin.

1935

Dr. Thomas Rivers demonstrated that nerve tissue, not viruses, produced an MS-like illness in animals. Experimental allergic encephalomyelitis (EAE) reinforced present auto-immunity theories, demonstrating the potential for the body to generate an immunologic attack against itself.

1938

Dr. V.B. Dolgopol described a case of optic neuritis and attributed it to Devic’s syndrome, thought to be a subclass of multiple sclerosis.

1965

Multiple sclerosis researchers discovered that blood cells react against a protein in nerve insulating myelin.

1992

The 16th edition of the Merck Manual described multiple sclerosis as follows:

  • Plaques or islands of demyelination along with destruction of both oligodendroglia and perivascular inflammation are disseminated through the CNS, primarily in the white matter, with a predilection for the lateral and posterior column (esp. in the cervical and dorsal regions), the optic nerves and periventricular areas.

  • Tracts of the midbrain, pons and cerebellum also are affected, cell bodies and axons usually are preserved, especially in early lesions. Later, axons may be destroyed, usually in the long tracts, and fibrous gliosis - this is what gives the tracts their 'sclerotic' appearance - Often both early and late lesions may be found simultaneously. Chemical changes in lipid and protein constituents of myelin have been demonstrated in and around the plaques.

  • The course is highly varied and unpredictable and in most patients, remittent. At first, months or years of remission may separate episodes, especially when the disease begins with retrobulbar neuritis (optic neuritis), but usually the intervals of freedom grow shorter, and eventually permanent, progressive disability occurs. Some remissions have even lasted 25 years or more. However, some patients have very frequent attacks and are rapidly incapacitated; in a few, particularly when onset is in middle age, the disease course is progressively and unremittingly downhill, and occasionally it is fatal within a year.