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Myelin sheath is a fatty product formed from specific neuroglial cells that provides numerous vital supporting functions as well as increases the rate of conduction of action potentials for some central and peripheral nervous system neurons. An axon wrapped in myelin sheath is said to be myelinated fibers, as such, axons not wrapped in myelin are non-myelinated fibers. In the central nervous system, the myelinated fibers have the collective name of white matter, and the nonmyelinated fibers are collectively known as gray matter as they look white and gray respectively on gross inspection of the brain in sagittal cross-section. Myelin is formed via oligodendrocytes and Schwann cells in the central and peripheral nervous systems respectively. Many physiologic complications and clinical symptoms can arise from the malformation and destruction of myelin.

Myelin sheath formation initiates in the CNS of the human embryo at about four months gestation. Oligodendrocytes can myelinate multiple axons at the same time (up to 50), and as such, any given myelinated neuron in the central nervous system can undergo myelination by several oligodendrocytes. Myelination of neurons in the peripheral nervous system commences between the twelfth and eighteenth week of gestation. Unlike oligodendrocytes, Schwann cells surround only a single axon. Schwann cells also play a role in peripheral neuron regeneration after an injury. Disruptions of myelin sheath formation and/or autoimmune-related destruction of myelin sheath can often lead to serious neurological complications. These disruptions are commonly referred to as demyelinating diseases. The most common demyelinating disease is multiple sclerosis. Multiple sclerosis is an autoimmune disorder with the patients' own antibodies directing their efforts against the myelin sheath in their central nervous system. Multiple sclerosis has a prevalence of about one in every thousand persons in the United States with women being affected with the disease two times as much as men. Histologically, multiple sclerosis shows abrupt edges of demyelinated plaque when stained with specific myelin stains. More specifically, light microscopy can view active plaques, in which there is active and progressive demyelination with PAS-stain positive breakdown product and lipid-rich macrophages present, as well as inactive plaques, in which there is no active demyelination taking place, and thus no myelin or myelin degradation products are found. That said, in inactive plaques, there is a reduction of oligodendrocytes nuclei, and there’s an increase in astrocytic proliferation. The third type of plaques seen in multiple sclerosis patients demonstrates non-abrupt borders between the normal and demyelinated tissue. These “shadow plaques” are theorized to be due to oligodendrocytes that did not get destroyed and that partially re-myelinate the damaged tissue. Multiple sclerosis typically presents clinically with visual disturbances such as diplopia and monocular blindness as well as peripheral symptoms of muscle weakness, sensory deficits, and subsequently ataxia.

Disruptions of myelin sheath formation and/or autoimmune-related destruction of myelin sheath can often lead to serious neurological complications. These disruptions are commonly referred to as demyelinating diseases. The most common demyelinating disease is multiple sclerosis. Multiple sclerosis is an autoimmune disorder with the patients' own antibodies directing their efforts against the myelin sheath in their central nervous system. Multiple sclerosis has a prevalence of about one in every thousand persons in the United States with women being affected with the disease two times as much as men. Histologically, multiple sclerosis shows abrupt edges of demyelinated plaque when stained with specific myelin stains. More specifically, light microscopy can view active plaques, in which there is active and progressive demyelination with PAS-stain positive breakdown product and lipid-rich macrophages present, as well as inactive plaques, in which there is no active demyelination taking place, and thus no myelin or myelin degradation products are found. That said, in inactive plaques, there is a reduction of oligodendrocytes nuclei, and there’s an increase in astrocytic proliferation. The third type of plaques seen in multiple sclerosis patients demonstrates non-abrupt borders between the normal and demyelinated tissue. These “shadow plaques” are theorized to be due to oligodendrocytes that did not get destroyed and that partially re-myelinate the damaged tissue. Multiple sclerosis typically presents clinically with visual disturbances such as diplopia and monocular blindness as well as peripheral symptoms of muscle weakness, sensory deficits, and subsequently ataxia. The cause of multiple sclerosis remains unknown. However, there has been a higher prevalence of multiple sclerosis in regions more north of the equator than those close or south of the equator; this leads many researchers to believe there’s a genetic and environmental component. Guillain-Barre syndrome is another demyelinating disorder, but unlike multiple sclerosis, there is autoimmune destruction of the myelin sheath in the peripheral nervous system as opposed to the central nervous system.

The cause of multiple sclerosis remains unknown. However, there has been a higher prevalence of multiple sclerosis in regions more north of the equator than those close or south of the equator; this leads many researchers to believe there’s a genetic and environmental component. Guillain-Barre syndrome is another demyelinating disorder, but unlike multiple sclerosis, there is autoimmune destruction of the myelin sheath in the peripheral nervous system as opposed to the central nervous system. Guillain-Barre is rarer than multiple sclerosis, only affecting one in every one hundred thousand persons every year and affects males and females equally.[11][12][13] Guillain-Barre syndrome typically presents as an ascending paralysis and muscle weakness, with it’s most severe and life-threatening complication being respiratory depression. The cause of Guillain-Barre disease is also not yet known, but triggers include microbial infection, traumatic surgery, or, very rarely, vaccination.[14][15][16]