Not only does it get better with plasmapheresis and human immune globulin infusions, but it also responds to immunosuppressant medications, including Prednisone.However, in distinction to GBS, the condition relapses off of immunosuppressants and also can have some spontaneous waxing and waning of symptoms.This usually produces weakness of the extremities and axial musculature, which can evolve to respiratory motor failure and asphyxiation if support is not available.Prior to availability of artificial respiratory support, the mortality rate was 60%.
Multiple sclerosis has been defined as "multiple white matter lesions separated in space and time".These are considered to be "dysmyelinative" disorders, or leukodystrophies (i.e., metachromatic leukodystrophy, Krabbe's disease) and not demyelinative even though both conditions tend to strike white matter pathways. Frankfurt dating app Central nervous system myelin and peripheral nervous system myelin are antigenically different (as befits the fact that CNS myelin derives from oligodendroglia and PNS myelin comes from Schwann cells).In this condition, peripheral nerves (actually, usually at the level of the proximal nerve roots) show inflammatory infiltrates with cells involved in cell-mediated immunity.Because cell mediated immunity is involved, the condition appears to depend more on local cytokine production than the development of circulating antibodies.
This condition often involves the largest sensory nerve fibers as well.Because the largest, most heavily myelinated sensory fibers are the muscle stretch fibers, and since these fibers and the motor axons are direct parts of the reflex arc, deep tendon reflexes are almost always lost very early in the course of the condition, even in muscles that are not yet clinically weak.However, these conditions are not considered "demyelinating" due to their nonspecific and secondary effects on myelin.Additionally, there are metabolic disorders of myelination characterized by the accumulation of abnormal breakdown products.Therefore, some demyelinating disorders attack the central nervous system (the prototype is multiple sclerosis), while others affect the peripheral nervous system (the prototype being Guillain-Barre syndrome).
There is evidence that the Guillain-Barre Syndrome (GBS) is mediated by immune attack on peripheral nerve myelin.
Nonetheless, plasmapheresis (which removes significant amounts of circulating antibodies) and human immune globulin infusions (which modulate the immune system by unclear mechanisms) are capable of limiting the acute damage in the condition (these help only if done early in the clinical course).
The major pathologic changes, as would be expected with an autoimmune disease, include perivascular inflammatory infiltrate, along with demyelination in the affected nerve roots and nerves.
The more severe the actual damage to underlying axons (as a byproduct of a severe immune attack on the myelin sheath) the more likely there is to be residual.
Electromyography is able to determine how much axonal damage there has been.