Visual improvement usually begins at about 4 weeks of onset, as is true of most acute manifestations of MS, perhaps sooner with corticosteroid treatment. Once improvement in neurologic function begins, it may continue for several months.
More than one-half of adult patients who present with optic neuritis will eventually develop other signs of MS. The prospective investigation of Rizzo and Lessell showed that MS developed in 74 percent of women and 34 percent of men by the 15th year after onset of visual loss; similar results were reported by the Optic Neuritis Study Group (Beck et al, 2003). The risk is much lower if the initial attack of optic neuritis occurs in childhood (26 percent developed after 40 years of followup [Lucchinetti et al, 1997]), suggesting that some instances of the childhood disease may be of a different type, perhaps viral or postinfectious. The longer the period of observation and the greater the care given to detection of mild cases, the greater the proportion of patients who are found to develop signs of MS; however, most do so within 5 years of the original attack (Ebers, 1985; Hely et al). In fact, in many patients with clinically isolated optic neuritis, MRI has disclosed lesions of the cerebral white matter—suggesting that dissemination, albeit asymptomatic, had already occurred and thereby establishing the diagnosis of MS (Jacobs et al, 1986; Ormerod et al). The Optic Neuritis Study Group has made the point, well known to neurologists, that the recurrence of optic neuritis greatly increases the chances of developing MS. Of practical value is the observation, in the study by Beck and colleagues (2003), that the risk of relapsing-remitting MS is also considerably lower (22 percent at 10 years) if the initial brain MRI fails to reveal other demyelinating lesions.
It is unclear whether optic neuritis that occurs alone and is not followed by other evidence of demyelinating disease is simply a restricted form of MS or a manifestation of some other disease process, such as postinfectious encephalomyelitis. By far the most common pathologic basis for optic neuropathy is demyelinating disease, although it is known that a vascular lesion or compression of an optic nerve by a tumor or mucocele may cause a central or cecocentral scotoma that is indistinguishable from the defect of optic neuritis. Also, there may be a special form of chronic relapsing optic neuritis that is the result of an undefined granulomatous process such as sarcoid, as suggested by Kidd and colleagues. Uveitis and sheathing of the retinal veins are other ophthalmic disorders that occur with higher than expected incidence in patients with MS. The retinal vascular sheathing is caused by T-cell infiltration, identical to that in typical plaques, but this is an infrequent finding, because the retina usually contains no myelinated fibers (Lightman et al). Optic neuritis is, of course, a common feature in neuromyelitis optica (Devic disease), discussed in a later section.
Acute Myelitis (Transverse Myelitis) (See Chap. 42)
This is the common designation for an acutely evolving inflammatory–demyelinating lesion of the spinal cord, which proves in many, but not all, instances to be an expression of MS. In this sense, the myelitic lesion is analogous to that of optic neuritis. The term transverse in relation to the myelitis is somewhat imprecise, implying that all of the elements in the cord are involved in the transverse plane, usually over a short vertical extent. Instead, in MS, the spinal cord signs are asymmetrical and incomplete and involve only a part of the long ascending and descending tracts, that is, paraplegia and complete sensory loss are unusual.