In the central nervous system, myelin can undergo assessment via the use of anti-proteolipid protein and anti-myelin basic protein immunohistochemical stains; this is because both the myelin basic protein and proteolipid protein are present in oligodendrocytes as well as myelin sheath in the central nervous system.[7]

Myelin can be seen using light microscopy using various histological methods, such as but not limited to: hematoxylin and eosin, Luxol fast blue and plastic (paraffin) embedding. These histological methods pronounce myelin and typically makes it appear as peripheral rings surrounding an axon when looking at a transverse section and as long parallel projections when viewing a longitudinal section. The nuclei of oligodendrocytes and Schwann cells are visible on hematoxylin & eosin staining; this presents as circular basophilic nuclei with a perinuclear halo giving a “fried-egg” appearance and as longitudinal basophilic nuclei proximal to an axon respectively. Light microscopy is one of the most commonly used methods used to assess the presence of specific pathology in nervous tissue.[8][9]

Myelin can be seen on transmission electron microscopy typically as a thick dark outline surrounding myelinated nerve fibers. In research, the use of three-dimensional electron microscopy can be used to view various injuries and disease processes related to the myelin sheath. This technique is typically not used clinically but has prospects to be advantageous to further the understanding of various pathophysiologic processes.[5][10]

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.

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]

Demyelinating diseases such as multiple sclerosis and Guillain-Barre syndrome have a progressive and devastating effect on affected patients. There has not been an approved treatment to reverse the demyelinating process in these diseases. However, there is an array of medications that can be used to slow the progression and to treat the symptoms that may arise from them. That said, these medications are not without potential shortfalls and side-effects. For example, beta interferons are commonly prescribed to the patients to help slow the progression of disease in multiple sclerosis. However, the use of beta interferons have been shown to induce flu-like symptoms as well as liver damage, but it is still widely used in many patients due to the therapeutic effects of the drug outweighing its potential adverse side-effects.[17][18]