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"It began around 1975-76. At the time, no one spoke about multiple sclerosis. It was only 10 years later that I heard the term for the first time," Jean-Marie recalls. "In a sense, I'm lucky. How the disease evolves is already known," he explains.

Jean-Marie first arranged how he would handle the disease in his daily life: "When I first needed a wheelchair, in 1989, I had already organized my existence: installed a ramp leading up to my house and got a motorized chair to go downstairs to get into my car (I still drive), adapted the bath room, the width of the doorways… I never gave up and I participate actively in organizations like the French Association of Paralytics."

For him, his hopes for the future are not only in the possibilities of research, the doors and windows that might suddenly open (he had his first MRI only a few months ago), but also in the improvement of the daily existence of patients and the institution of a "culture of exchange" with the medical establishment that would be a relief to patients that are often fragile. A global approach that Jean-Marie sees developing.

What is peculiar to this disorder is its tendency to evolve through discrete attacks that are unpredictable. No one sign suffices to identify the disease. It's their association and their recurrent nature that suggests the diagnosis. Progress in magnetic resonance imagery (MRI) now permits early confirmation of the diagnosis and appropriate treatment, which is usually corticoids administered during attacks, immunomodulators to prevent the attacks, or immunosuppressants to control aggressive forms of the disease.

Multiple sclerosis is characterized by the destruction of the myelin sheath (the insulation that covers the axons (nerve fibres) of neurons in the brain and spinal cord. The resulting lesions form disseminated patches that are inflammatory to begin with, but end up forming permanent scars. The known genetic factors that predispose to the disease do not explain why it develops, except in a few rare hereditary forms. Environmental factors probably play a role, but this has not been proven. The initial event is the entry of inflammatory cells into the central nervous system. Segmental myelin destruction is observed later. The mechanisms underlying this polymorphic disease are still not well understood. Research, here again, is focused on how to cure, prevent or repair the damage done by the disease. It is therefore essential to come to understand how and why myelin is destroyed and nerve cells die. The discovery of neuroprotective treatments and techniques leading to myelin repair inspires hope.
 
       
The goal of the ICM, a research foundation recognized of public utility, is to support the development of research on the brain and spinal cord, in any way possible.