At least initially, most patients have the relapsing-remitting form, which is characterized by episodes of neurologic impairment followed by complete or nearly complete recovery. Later, neurologic impairment progresses continuously, with or without superimposed relapses, in what is called the secondary progressive form. The clinical deficits are largely due to nerve-conduction blocks resulting directly from demyelination and indirectly from inflammation. Inflammation results in the local production of nitric oxide by macrophages, which are abundant in the early lesions. Nitric oxide causes graded, dose-dependent conduction block in central nerve fibers.
Remissions occur when the inflammation subsides and conduction is restored.
Initially, this is probably due to the insertion of new sodium channels into denuded axon membranes. Recent functional MRI studies in patients recovering from optic neuritis provide evidence that adaptive changes in neuronal function may also contribute to the recovery process. Two mechanisms might play a part. First, the recovery processes just described might fail, perhaps as a result of repeated inflammatory attacks on the same nerve fibers. This is known to occur in chronic inflammatory demyelinating peripheral neuropathy.