Multiple sclerosis is an autoimmune disease characterized by the inflammatory demyelization of neurons in the central nervous system (CNS).

For the first time in history, French Neurologist Charcot has described disseminated white matter lesions within the Central Nervous System in late 19th century. On histological sections, the disseminated white matter lesions contain perivascular inflammation and demyelization, which are now characterized as pathological hallmarks for MS.

Incursion through the pathology of Multiple Sclerosis
Women with the onset of clinical symptoms occurring between fifteen and fifty years of age are most likely to develop various forms of Multiple Sclerosis. Although the exact pathogenesis of the disease is unknown, researchers believe that the clinical manifestations of MS occur as an immune reaction which consists in invading the blood-brain barrier, causing lesions at the entrance of the CNS, and perceiving the myelin basic protein (MBP) and proteolipid (PLP) as foreign. The immune system's attack on these proteins induces the damage of the protective coating of myelin and furthermore the eventual formation of lesions.

Another imminent effect of these plaques is the neuromuscular or neuro-cognitive impairment. Most common clinical symptoms of multiple sclerosis are: optic nerve dysfunction, tremors, internuclear ophthalmoplegia, sensory disturbances, upper motor neuron weakness, ataxia, and autonomic dysfunction.

Distribution and evolution of Demyelinating Plaques in Central Nervous System
Plaques may occur anywhere within the white matter of the CNS, but the most frequently in the optic nerves, the brainstem, the cerebellum and the spinal cord, as well as in the cerebral hemispheres. When adjacent to the cortex, plaques cause sub cortical myelinated fibers to spare. Plaques located nearby the gray matter rarely spread into the gray matter, including deep nuclei and the cortex.

It is not clear how the lesions evolve over time. While the typical clinical course of multiple sclerosis is characterized by relapsing and progressive disability, there have been cases of subclinical MS where the diagnosis can be confirmed only by the presence of large confluent, demyelinating plaques found only upon autopsy.

MRI investigations have demonstrated that blood-brain barrier is disrupted at the onset of symptoms, but it is still unknown whether demyelination precedes or succeeds inflammation. It is currently thought that demyelination can be produced directly or indirectly by acute inflammatory response of plasma cells, lymphocytes, and macrophages. There are myelin fragments and/or myelin breakdowns in the macrophages from those lesions. Lymphocytes play a role in pathologic processes by direct mechanism (cell-mediated immunity and antibody) or indirectly, by secreting lymphokines and cytokines.

Assessment of Severity and Possibility for Remyelination
The severity of demyelination may be assessed by relative preservation or destruction of oligodendrogliocytes. Early in the course of the disease, more oligodendrogliocytes are preserved in the plaque, which explains why some degree of remyelination remains possible. Some patience may experience a complete loss of oligodendrogliocytes. Unfortunately, for this specific category of patients, possibility of remyelination dramatically decreases.
Regardless how the pathological process evolves from inflammation to demyelination, the effects of loss of myelin by the nerve fibers are quite severe.