Myelin formed by the oligodendroglia in the CNS differs chemically and immunologically from myelin, which is formed in the periphery of Schwann cells. Therefore, some diseases that affect the myelin affect (such as Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, polyneuropathy some other peripheral nerves.) Primary rather the peripheral nerves, others primarily affect the central nervous system (see table: diseases involving can cause demyelination in the CNS). The areas most commonly affected in the CNS are the brain, spinal cord and optic nerve.

Myelin sheaths cover many nerve fibers in the central and peripheral nervous system; they accelerate the axonal transmission of neural impulses. Diseases that affect myelin interrupt nerve conduction; the symptoms may reflect deficiencies in any part of the nervous system. Myelin formed by the oligodendroglia in the CNS differs chemically and immunologically from myelin, which is formed in the periphery of Schwann cells. Therefore, some diseases that affect the myelin affect (such as Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, polyneuropathy some other peripheral nerves.) Primary rather the peripheral nerves, others primarily affect the central nervous system (see table: diseases involving can cause demyelination in the CNS). The areas most commonly affected in the CNS are the brain, spinal cord and optic nerve. Demyelination is often secondary to an infectious, ischemic, metabolic, or hereditary disorder or a toxin (e.g., b. Alcohol, ethambutol). In primary demyelinating diseases, the cause is unknown, but an autoimmune mechanism is suspected because the disease often follow a viral infection or viral vaccination. Demyelination tends to be segmental or flick shaped distribution, it can affect various areas simultaneously or sequentially. Remyelination occurs frequently during repair, regeneration, and complete recovery of neural function. However, extensive loss of myelin usually leads to subsequent axonal degeneration and often to the degeneration of the cell body; both can be irreversible. Demyelination should be considered in any patient with unexplained neurological deficits. The following features speak for primary demyelinating diseases. Diffuse or multifocal deficits Sudden or subacute onset, particularly in young adults beginning within weeks after infection or vaccination deficits, which increase and decrease symptoms that indicate a certain demyelinating disorder (eg . unexplained optic neuritis or internuclear ophthalmoplegia in favor of multiple sclerosis) Specific studies and treatment depend on the particular disorder. Diseases that can cause demyelination in the CNS category disorders hereditary diseases phenylketonuria and other aminoacidurias M. Tay-Sachs, Niemann-Pick disease and Gaucher’s disease Hurler syndrome Krabbe and other leukodystrophies * * Adrenoleukodystrophien Adrenomyeloneuropathy * Hereditary Liver and optic atrophy related mitochondrial disorders hypoxia and ischemia carbon monoxide toxicity and other syndromes of delayed cerebral hypoxic ischemic demyelination Progressive subcortical demyelination Malnutrition The osmotic Demyelinisierungssyndrom †, formerly central pontine myelinolysis can be caused by too rapid correction of hyponatremia. Demyelination of the corpus callosum (Marchiafava-Bignami disease) Vitamin B12 deficiency Direct entry of virus into the CNS progressive multifocal leukoencephalopathy Subacute sclerosing panencephalitis Tropical spastic paraparesis / HTLV-1 associated myelopathy Primary demyelinating diseases Recurrent, progressive diseases (multiple sclerosis and its variants) monophasic disorders such as optic neuritis, acute transverse myelitis, acute disseminated encephalomyelitis and acute hemorrhagic Leukenzephalitis NMO toxins alcohol Ethambutol * Some subtypes can also cause peripheral demyelination. The osmotic † Demyelinisierungssyndrom can also be caused by sodium currents. HTLV-1 = human T-lymphotrophic virus first

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