During an attack of multiple sclerosis, the immune system triggers inflammation along nerves and in glial cells. Oligodendrocytes are damaged and myelin is damaged and detaches from the axon. Messages that pass along a demyelinated nerve are delayed or blocked. Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system.
In this disorder, the immune system attacks the myelin sheath, or the cells that produce and maintain it. Demyelination can cause a wide range of neurological symptoms during MS exacerbations. In severe cases, damage to myelin can result in hardened scars that are permanent and cause long-lasting symptoms. The demyelination of axons that maintain their structural integrity and the response of neurons to axon demyelination appear to provide at least a partial basis for the remissions commonly seen in MS.
In the relapsing-remitting type of MS, exacerbations are followed (usually in a few weeks or a few months) by remissions in which there is clinical recovery. Clinical deficits in MS are, in part, the result of interruption of conduction in demyelinated axons. Clinical recovery seems to reflect the restoration of safe impulse conduction in some demyelinated axons that acquire a higher than normal number of sodium channels, 1-3 This molecular remodeling of demyelinated axons provides an instructive example of adaptive neural plasticity. By understanding the molecular mechanisms involved in this type of neural plasticity, it is conceivable that, in the future, it will be possible to induce or enhance remissions.
Steroid injections or plasma exchange (PLEX) can reduce spinal cord swelling and relieve other symptoms. A number of medications, including antidepressants and pain relievers, can help treat specific symptoms. Multiple sclerosis (MS) is generally considered an autoimmune disease, in which autoreactive T cells enter the central nervous system (CNS) from the peripheral circulation and induce an inflammatory cascade that results in demyelination and axonal loss. In conclusion, CNS demyelination, which can result from multiple pathophysiological mechanisms, induces important changes in the axon: some are adaptive and others are harmful.
Demyelination has important consequences for the axon, both by altering the conduction of impulses and by modifying the axolemma and membrane components. Perhaps the redistribution of Nav1.2 along bare axons could be an adaptive response that supports the conduction of action potentials in demyelinated axons. In addition to its known antiviral and proinflammatory action, the overexpression of IFN-gamma in the CNS could participate in demyelination. Such antibodies could cause demyelination through several effector mechanisms, such as antibody-dependent cell-mediated cytotoxicity, the release of inflammatory mediators by stimulating Fc receptors on natural killer cells, macrophages or mast cells, myelin opsonization or complement activation (Archelos and Hartung, 2000).
Demyelinating diseases, such as multiple sclerosis (MS), involve damage to myelin, the protective layer of nerve cells. On the contrary, there is increasing evidence to suggest that cytotoxic CD8+ T cells may play a crucial role in demyelination. This neurophysiology is likely associated with the positive paroxysmal symptoms that are so characteristic of MS, such as tonic spasms, paroxysmal dysarthria and ataxia, paresthesia, and pain. There is no cure for demyelinating diseases, but disease-modifying therapies can alter the progression of the disease in some patients.
This increase in caliber has been related to the fact that the neurofilaments of these enlarged demyelinated axons are loosely packed together, perhaps reflecting the increased permeability of the demyelinated axolemma. Segmental demyelination results in blocking conduction or slowing conduction through adaptive responses, in particular related to modifications in the distribution of voltage-gated sodium channels along the denudate axon. There is no cure, but some people can control their symptoms well with steroids and drugs that calm the immune system. .
