AN EXPLORATION OF MULTIPLE SCLEROSIS

MS is a disease of the central nervous system. Myelin sheaths surrounding nerves in the brain and spinal cord facilitate the rapid conduction of nerve impulses to the body, and MS is the most common disorder of demyelination. Myelin is produced by oligodendrocyte cells in the connective tissue of the central nervous system, and many researchers believe that a defect in the oligodendroglial cells is the likely cause of the disease. The pathology of the disease involves an autoimmune response mediated by T helper cells in which the myelin proteins are destroyed and conduction of nerve impulses interupted. Where demyelination occurs, collagenous plaques appear, showing a relative preservation of axons but depletion of oligodendrocytes.

The disease normally follows a pattern of recurrent relapses and remission, but chronic progressive cases do occur. What is certain is that the foci of demyelination are scattered throughout the central nervous system, giving a wide range of clinical manifestations often divided into three main areas: optic nerve, brain stem, and spinal cord.

There is some thought that, contrary to what was considered to be a very limited capability of self-repair, remyelination may sometimes occur. A 1999 study found MRIs showing shadow plaques with abnormally thin myelin, raising the possibility of some remyelination by surviving oligodendrocytes or only partial loss. This same study also drew attention to subclinical cases found upon autopsy following non-MS related death.

MS is a disease of the central nervous system. Myelin sheaths surrounding nerves in the brain and spinal cord facilitate the rapid conduction of nerve impulses to the body, and MS is the most common disorder of demyelination. Myelin is produced by oligodendrocyte cells in the connective tissue of the central nervous system, and many researchers believe that a defect in the oligodendroglial cells is the likely cause of the disease. The pathology of the disease involves an autoimmune response mediated by T helper cells in which the myelin proteins are destroyed and conduction of nerve impulses interupted. Where demyelination occurs, collagenous plaques appear, showing a relative preservation of axons but depletion of oligodendrocytes.

The disease normally follows a pattern of recurrent relapses and remission, but chronic progressive cases do occur. What is certain is that the foci of demyelination are scattered throughout the central nervous system, giving a wide range of clinical manifestations often divided into three main areas: optic nerve, brain stem, and spinal cord.

There is some thought that, contrary to what was considered to be a very limited capability of self-repair, remyelination may sometimes occur. A 1999 study found MRIs showing shadow plaques with abnormally thin myelin, raising the possibility of some remyelination by surviving oligodendrocytes or only partial loss. This same study also drew attention to subclinical cases found upon autopsy following non-MS related death.