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In multiple sclerosis, lesions, also known as plaques, are patches of inflammation in the central nervous system (CNS) in which the nerve cells (neurons) have been stripped of their myelin, an insulating fatty protein. Lesions tend to be randomly distributed in the CNS white matter. The neurons of the white matter are responsible for sending communication signals both within the CNS and between the CNS and the rest of the body.

Demyelinated neurons do not function efficiently and it is these lesions that give rise to the symptoms of multiple sclerosis. As the disease progresses, the neurons themselves can become damaged. Modern technologies such as MRI scans and to a lesser extend CT scans can produce images of the brain and spinal cord showing the distribution of the lesions.

In relapsing-remitting MS, their is significant recovery as the inflammation dies down. Special maintenance cells called glial cells are responsible for the repair of the damaged nerves. One type of glial cell, called an oligodendrocyte, lays down new myelin and another type, called an astrocyte lays down scar tissue. In progressive forms of MS, recovery is less significant.

Examination of MRI scans show that the vast majority of lesions do not produce clinical symptoms. These are known as silent lesions. Why this is, is not well understood although it is thought that other parts of the central nervous system take over the function that was done by the damaged neurons.

Recent research indicates that there may be at least four different types of lesion indicating four different forms of multiple sclerosis or even that MS is in fact four different diseases.

At the cellular level, what happens at the site of a lesion is very complex and varied. Immune system component cells (leukocytes) especially Helper T-cells, Macrophages and possibly mast cells appear to be involved. A complex mix of cellar signalling molecules called cytokines and chemokines mediates the destruction. As well as damaging the myelin, oligodendrocytes are often killed which at the very least delays remyelination.

Lesion links:
Multiple Sclerosis of the Brain

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